Study Guide The Neuroscience and Neurological Disorders

Study Guide The Neuroscience and Nervus System Disorders
STUDY GUIDE THE NEUROSCIENCE AND NERVUS SYSTEM DISORDERS
Planners
IA Sri Wijayanti IA Sri Indrayani
Putu Gede Sudira Ni Made Susilawathi
Ni Putu Sriwidyani Ni Putu Witari
Anna Marita Gelgel Sri Maliawan
Kumara Tini Dewi Sutriani Mahalini
Ketut Widyastuti
Contributors
I Nyoman Mangku Karmaya I Komang Arimbawa
D.A. Inten Dwi Primayanti Putu Pramana
I Wayan Sugiritama Ketut Widyastuti
I Made Jawi IA Sri Indrayani
Ni Putu Sriwidyani Ni Made Susilawathi
I Nyoman Wande Ni Putu Witari
DPG Purwa Samatra Sri Maliawan
I Made Oka Adnyana Nyoman Golden
IGN Budiarsa Tjokorda GB Mahadewa
Thomas Eko Purwata I Wayan Niryana
AAA Putri Laksmidewi Dewi Sutriani Mahalini
Anna Marita Gelgel Made Widhi Asih
Kumara Tini IA Sri Wijayanti
IB Kusuma Putra Putu Gede Sudira
Editors
Putu Gede Sudira
Layout
Rizky Darmawan
First Edition September 2017

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system,
or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or
otherwise without prior written permission of the publisher.
Published by Department of Medical Education Medicine Programme, Faculty of Medicine,
Universitas Udayana.
Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017
2
CONTENTS
STUDY GUIDE THE NEUROSCIENCE AND NERVUS SYSTEM DISORDERS .......................... 2

CONTENTS........................................................................................................................................... 3
PREFACE ............................................................................................................................................. 5
CURRICULUM MAP............................................................................................................................. 6
GENERAL CURRICULUM OF NEUROSCIENCE AND NERVUS SYSTEM DISORDERS .......... 7
PLANNERS AND LECTURERS........................................................................................................ 13
FACILITATORS .................................................................................................................................. 14
LEARNING ACTIVITY ........................................................................................................................ 15
IMPORTANT INFORMATIONS ......................................................................................................... 15
STUDENT PROJECT......................................................................................................................... 16
ARTICLE REVIEW ASSESSMENT FORM ...................................................................................... 18
ARTICLE REVIEW ASSESSMENT FORM ...................................................................................... 19
SELF ASSESSMENT ......................................................................................................................... 20
ASSESSMENT METHOD .................................................................................................................. 20
GENERAL TIME TABLE FOR A AND B CLASSES ........................................................................ 20
TIME TABLE OF CLASSES .............................................................................................................. 21
LEARNING PROGRAMS ................................................................................................................... 29
LECTURE 1......................................................................................................................................... 29
LECTURE 2......................................................................................................................................... 32
LECTURE 3......................................................................................................................................... 34
LECTURE 4......................................................................................................................................... 37
LECTURE 5......................................................................................................................................... 40
LECTURE 6......................................................................................................................................... 42
LECTURE 7......................................................................................................................................... 44
LECTURE 8......................................................................................................................................... 47
LECTURE 9......................................................................................................................................... 51
LECTURE 10 ...................................................................................................................................... 57
LECTURE 11 ...................................................................................................................................... 62
LECTURE 12 ...................................................................................................................................... 66

3
LECTURE 13-14 ................................................................................................................................. 69

LECTURE 15 ...................................................................................................................................... 71
LECTURE 16 ...................................................................................................................................... 73
LECTURE 17 ...................................................................................................................................... 75
LECTURE 18 ...................................................................................................................................... 80
LECTURE 19 - 20 ............................................................................................................................... 84
LECTURE 21 ...................................................................................................................................... 86
LECTURE 22 -23 ................................................................................................................................ 91
LECTURE 24 ...................................................................................................................................... 94
LECTURE 25 ...................................................................................................................................... 98
LECTURE 26 .................................................................................................................................... 100
LECTURE 27 .................................................................................................................................... 102
LECTURE 28 .................................................................................................................................... 104
LECTURE 29 .................................................................................................................................... 107
LECTURE 30 .................................................................................................................................... 114
LECTURE 31 .................................................................................................................................... 117
LECTURE 32 .................................................................................................................................... 119
LECTURE 33 .................................................................................................................................... 121
REFERENCES ................................................................................................................................. 123

4
PREFACE
The medical curriculum has become increasingly vertically integrated, with stronger basic
concept and support by clinical examples and cases to help in the understanding of the
relevance of the underlying basic science. Basic science concepts may help in the
understanding of the pathophysiology and treatment of diseases. Neuroscience and nervus
system disorders block has been written to take account of this trend, and to integrate core
aspects of basic science, pathophysiology and treatment into a single, easy to use revision aid.
The neuroscience and nervus system disorders block will refresh neuroscience of basic
anatomy, histology, physiology of human neurological system, pharmacology of different
classes of nervus system related drugs, symptom and signs of major neurological diseases and
its pathophysiology and basic principle concept to education, prevention, treatment and
rehabilitation in nervus system disorders in patient, family and community. This study guide is
developed by the academic staffs from various departments: Anatomy, Physiology, Histology,
Pharmacology, Anatomy and Clinical Pathology, Neurology, Pediatric Neurology,
Aneshtesiology, Neurosurgery and Radiology.
The learning process will be carried out for 3 weeks (15 working days) and 1 week for
Basic Clinical Skills starts from September 26th, 2017 as shown in the time table. The final
examination will be conducted on October 26th, 2017 in the form of Multiple Choice Questions.
The learning situation include lecture, individual learning, small group discussion, plenary
session, practice, and clinical skills.
Most of the learning material should be learned independently and discuss in Small Group
Discussion by the students with the help of facilitator. Lecture is given to emphasize the most
important thing of the material. In small group discussion, the students gave learning task to
lead their discussion.
This simple study guide need more revision in the future, so that the planners kindly invite
readers to give any comments and critics for its completion. Thank you.
Planners

5
CURRICULUM MAP

6
GENERAL CURRICULUM OF NEUROSCIENCE AND NERVUS SYSTEM
DISORDERS
Aims:
Comprehend the structure, physiology, and pathology of the nervus system.
Interpret the laboratory and imaging examination of the nervus system disorders.
Diagnose and treat the patient with common nervus system disorders.
Plan education, prevention, management and rehabilitation of nervus system disorders
to patient, family and community.
Learning outcomes:
Concern about the size of problem and diversity of nervus disease in the community.
Able to describe the structure and function of the nervus system.
Able to interpret the result of examination (physical, laboratory, and imaging studies).
Able to explore patients with nervus problem.
Able to manage major and common nerurological diseases
Able to implement rehabilitation of nervus diseases.
Curriculum contents:
Structure and function of the nervus system.
Physiology of the CNS, PNS, ANS.
Symptoms and signs of neurological disease.
Pathophysiology of nervus system disorders.
Basic physical, laboratory, electrocardiography and imaging examination.
Interpretation of examination results.
Drugs that commonly used in nervus system disorders.
Basic principles of education, prevention, treatment and rehabilitation in nervus system
disorders in patient, family and community.
Curriculum structure:
Structure of curriculum mainly is derive from general competences of Indonesian general
practioner. Those competences in diagnosing diseases and doing clinical skills should be
mastered by all the general practioners here. Local values of our institutions are also considered
as added values in this curriculum.

8

9

10

11

12
PLANNERS AND LECTURERS
NO NAME DEPARTMENT PHONE

Prof. Dr. dr. I Nyoman Mangku Karmaya, M.
1 Anatomy 0811387105
Repro, PA(K)
2 dr. D.A. Inten Dwi Primayanti, M.Biomed Fisiology 081337761299
3 dr. I Wayan Sugiritama, M.Kes Histology 08164732743
4 Dr. dr. I Made Jawi,M.Kes Pharmacology 08179787972
5 Dr. dr. Ni Putu Sriwidyani, Sp.PA Anatomy Pathology 081337115012
6 Dr. dr. I Nyoman Wande, Sp.PK Clinical Pathology 08124686885
7 Dr. dr. DPG Purwa Samatra, Sp.S(K) Neurology 08123918731
8 Dr. dr. I Made Oka Adnyana, Sp.S(K) Neurology 0817347697
9 dr. IGN Budiarsa, Sp.S Neurology 0811399673
10 Dr. dr. Thomas Eko Purwata, Sp.S(K) FAAN Neurology 08123948477
11 Dr. dr. AAA Putri Laksmidewi, Sp.S(K) Neurology 0811388818
12 Dr. dr. Anna Marita Gelgel, Sp.S(K) Neurology 08113980999
13 dr. Kumara Tini, Sp.S, FINS Neurology 081238701081
14 dr. IB Kusuma Putra, Sp.S Neurology 085738534259
15 dr. I Komang Arimbawa, Sp.S Neurology 081338226892
16 dr. Ketut Widyastuti, Sp.S Neurology 08123634110
17 dr. Ida Ayu Sri Indrayani, Sp.S Neurology 081246751536
18 dr. Ni Made Susilawathi, Sp.S(K) Neurology 08124690137
19 dr. Ni Putu Witari, Sp.S Neurology 081338724040
20 Prof. Dr. Dr. Sri Maliawan, Sp.BS(K) Neuro-surgery 0811398466
21 Dr. dr. Nyoman Golden, Sp.BS(K) Neuro-surgery 0811380037
Dr. dr. Tjokorda GB Mahadewa, M.Kes, Sp.BS(K)
22 Neuro-surgery 0818484654
Spinal
21. dr. I Wayan Niryana,M.Kes,Sp.BS(K) Neuro-surgery 08179201958
22. dr. Dewi Sutriani Mahalini, Sp.A Pediatric 08123641466
23 dr. I Wayan Niryana, M.Kes,Sp.BS(K) Neuro-surgery 08179201958
24 dr. Made Widhi Asih, Sp.Rad(K) Radiology 081916442626
25 dr. IA Sri Wijayanti,M.Biomed, Sp.S Neurology 081337667939
26 dr. Putu Gede Sudira, Sp.S Neurology/ DME 081805633997

13
FACILITATORS
Regular Class (Class A)

Venue
No Name Group Departement Phone
(2ndfloor)
A1 Physiology 08123924477 2nd floor:
1 Prof. dr. I D P Sutjana, M.Erg
R.2.01
Dr. dr. Desak Made A2 Biochemistry 081338776244 2nd floor:
2
Wihandani, M.Kes R.2.02
Dr. dr. BK. Satriyasa, A3 Pharmacology 087777790064 2nd floor:
3
M.Repro R.2.03
dr. I Nyoman Gede Wardana, A4 Anatomy 087860405625 2nd floor:
4
M.Biomed R.2.04
dr. Luh Olivia Saraswati A5 Cardiology 081330530247 2nd floor:
5
Suastika, Sp.JP, FIHA R.2.05
Dr. dr. Ni Nyoman Sri A6 Microbiology 08553711398 2nd floor:
6
Budayanti, Sp.MK (K) R.2.06
dr. IGN Sri Wiryawan, A7 082341768888 2nd floor:
7 Histology
M.Repro R.2.07
dr. Ni Luh Pt. Ratih Vibriyanti A8 Dermatovener 081337808844 2nd floor:
8
Karna, Sp.KK ology R.2.08
dr. Ni Putu Wardani, A9 DME 08113992784 2nd floor:
9
M.Biomed, Sp.An R.2.21
A10 Internal 08123853700 2nd floor:
10 dr. I Ketut Mariadi, Sp.PD
Medicine R.2.22
English Class (Class B)

Venue
No Name Group Departement Phone
(2ndfloor)
Dr. dr. I Made Sudarmaja, B1 Parasitology 081239539945 2nd floor:
1
M.Kes R.2.01
dr. Pande Putu Yuli B2 Radiology 081327941987 2nd floor:
2
Anandasari, Sp.Rad R.2.02
B3 Pharmacology 08179787972 2nd floor:
3 Dr. dr. I Made Jawi, M.Kes
R.2.03
dr. IGAB. Krisna Wibawa, B4 Surgery 08123858698 2nd floor:
4
Sp.B(K)V R.2.04
B5 DME 081805633997 2nd floor:
5 dr. Putu Gede Sudira, Sp.S
R.2.05
dr. I Gusti Ngurah Mayun, B6 081237395050 2nd floor:
6 Histology
Sp.H.K R.2.06
Dr. dr. I Wayan Weta, MS, B7 Public Health 081337005360 2nd floor:
7
SpGK R.2.07
Prof. Dr. I Nyoman Adiputra, B8 Physiology 0811397971 2nd floor:
8
M.O.H. PFK R.2.08
Dr. dr. I Nyoman Bayu 2nd floor:
9 B9 Obgyn 081339550423
Mahendra, Sp.OG (K) R.2.21
Prof. dr. Ketut Tirtayasa, MS, B10 08123623422 2nd floor:
10 Physiology
AIF, AIFO, Sp.Erg R.2.22

14
LEARNING ACTIVITY
There are several types of learning activity:

Lecture
Plenary session
Independent learning based on the lectures topic
Small group discussion to solve the learning task
Practicing
Student project
Clinical skill and demonstration
Self assessment at the end of every topic
Lecture will be held at room 4.02 (4th floor), while discussion rooms available at 2nd floor
(room 2.01-2.08, 2.21 and 2.22).
IMPORTANT INFORMATIONS
Meeting of the students representative
In the middle of block schedule, a meeting is designed among the student representatives
of every small group discussions, facilitators, and resource persons. The meeting will discuss
the ongoing teaching learning process, quality of lecturers and facilitators as a feedback to
improve the next process. The meeting will be taken based on schedule from Department of
Medical Education and/ or during Student Project Presentation Day.

15
STUDENT PROJECT
Title of student project

Group Topic Evaluator
A1 Dystonia & Sindrom Tourettes Dr. dr. DPG Purwa Samatra, Sp.S(K)
A2 Normal Pressure Hydrocephalus Dr. dr. AAA Putri Laksmidewi, Sp.S(K)
A3 Childhood Brain Tumors Dr. dr. Nyoman Golden, Sp.BS(K)
A4 Neuromyelitis Optica dr. Putu Witari, Sp.S
A5 Sindrom Tolosa Hunt Dr. dr. Made Oka Adnyana, Sp.S(K)
A6 Arteriovenous Malformation dr. I Wayan Niryana, M.Kes, Sp.BS(K)
A7 Neuronitis Vestibularis dr. Ida Ayu Sri Indrayani, Sp.S
A8 Beckers Dystrophy dr. Dewi Sutriani Maharini, Sp.A
A9 Cerebral Angiography dr. Made Widhi Asih, Sp.Rad(K)
A10 Polymyositis dr. IA Sri Wijayanti, M.Biomed,Sp.S
B1 Subdural Haematoma Prof. Dr. dr. Sri Maliawan, Sp.BS(K)
Dr. dr. Thomas Eko Purwata, Sp.S(K)
B2 Tabes Dorsalis
FAAN
Dr. dr. Tjokorda GB Mahadewa, M.Kes
B3 Brown-Sequard Syndrome
Sp.BS(K)Spinal
B4 Tindakan DSA Pada Stroke Iskemik dr. IGN Budiarsa, Sp.S
B5 Wallenberg Syndrome dr. IB Kusuma Putra, Sp.S
B6 Vegetative state dr. I Komang Arimbawa, Sp.S
B7 Thoracic Outlet Syndrome Dr. dr. Putu Pramana, Sp.An, KMN.,M.Kes
B8 Temporal Lobe Epilepsy Dr. dr. Anna Marita, Sp.S(K)
B9 Cytomegalovirus Encephalitis dr. Putu Gede Sudira, Sp.S
B10 Therapeutic Spinal Tap dr. Putu Gede Sudira, Sp.S
About Topic, Presentations place and schedules, Task rules, Assessment, and Evaluator will
be discussed at lecture of block introduction on September 26th, 2017.
Student project consist of 6 10 pages, 1.5 space, font times new romance 12. Outline of report
must follow below guidance and consist of preface, table of content, Introduction
(Pendahuluan), Content (Isi, sesuai topik yang dibahas), Summary (Ringkasan), Refferences:
(Daftar Pustaka) Van Couver style.

16
TITLE
(subject/ topic: choose from compentency list)
Members Name and Student Registered Number
Faculty of Medicine
Udayana University
2017
______________
Example:
Journal
Sheetz MJ, King GL. Molecular understanding of hyperglycemias adverse effect for
diabetic complications. JAMA. 2002;288:2579-86.
Textbook
Libby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A, Kasper D,
Hoster S, Longo D, Jamason S (eds). Harrisons principles of internal medicine. 15th ed.
New York: McGraw Hill; 2001. p. 1977-82.
Internet
WHO. Obesity: preventing and managing the global epidemic. Geneva: WHO 1998.
[cited 2005 July]. Available from:
http://www.who.int/dietphysicalactivity/publications/facts/ obesity/en.

17
ARTICLE REVIEW ASSESSMENT FORM

Faculty of Medicine, Udayana University
___________________________________________________________________________
Block : The Neuroscience and Nervus System Disorders
Name : ________________________________________
Student No. (NIM) : ________________________________________
Facilitator : ________________________________________
Title : ________________________________________
________________________________________
Time table of consultation
Point of discussion Week Date Tutor sign
1. Title 1
2. Refferences 1
3. Outline of paper 2
4. Content 3
5. Final discussion 4
Assessment
A. Paper structure : 7 8 9 10
B. Content : 7 8 9 10
C. Discussion : 7 8 9 10
Total point : ( A + B + C ) : 3 = _____________
Denpasar, ______________________
Name of Facilitator

18
ARTICLE REVIEW ASSESSMENT FORM

Faculty of Medicine, Udayana University
___________________________________________________________________________
Block : The Neuroscience and Nervus System Disorders
Name : ________________________________________
Student No. (NIM) : ________________________________________
Facilitator : ________________________________________
Title : ________________________________________
________________________________________
Assessment
A. Paper structure : 7 8 9 10
B. Content : 7 8 9 10
C. Discussion : 7 8 9 10
Total point : ( A + B + C ) : 3 = _____________
Denpasar, ______________________
Name of Evaluator

19
SELF ASSESSMENT
Self assessment of each lecture will be given after each lecture session, and will be
marked. This mark can determine whether the student pass this block or not. Any final mark
between 62 - 64 will be reconsidered with self assessments mark to see the students status.
Any student with self assessments mark 65 or more will pass this block. And for the lower one
will have to attend the remedial examination. It is important to do this self assessment
cautiously, because this activity may be your ticket to pass this block just at first examination.
ASSESSMENT METHOD
Assessment in this theme consists of:
SGD : 5%
Final Exam : 80%
Student Project : 15%
Final mark 65 or more considered to pass this block. Certain conditions applied for those
with final mark between 62 64. These students will be analyzed using their self assessments
mark. Students with final mark 62 64 and self assessments mark equal or more than 65 will
also considered pass this block. The value of marking:
A 80
B+ >70-79
B 65-70
GENERAL TIME TABLE FOR A AND B CLASSES

CLASS A CLASS B
TIME ACTIVITIES TIME ACTIVITIES
08.00-09.00 Lecture 09.00-10.00 Lecture
09.00-10.30 Independent learning 10.00-11.30 Student project
10.30-12.00 SGD 11.30-12.00 Break
12.00-12.30 Break 12.00-13.30 Independent learning
12.30-14.00 Student project 13.30-15.00 SGD
14.00-15.00 Plenary session 15.00-16.00 Plenary session

20
TIME TABLE OF CLASSES

DAY/DATE Class A Class B ACTIVITY VENUE PIC
Lecture 1 dr. IA Sri

08.00-09.00 11.00-12.00 Highlight in Neuroscience Class room Wijayanti,
& neurological disorders M.Biomed, Sp.S
Prof. Dr. dr. I

Lecture 2 Nyoman Mangku
09.00-10.00 12.00-13.00 Class room Karmaya,
Anatomy of CNS & PNS
M.Repro, PA(K)
dr. I Wayan
Lecture 3
10.00-11.00 13.00-14.00 Class room Sugiritama,
Histology of CNS & PNS M.Kes
1
12.30-14.00 09.00-10.00 Independent learning
Tue
Sep 26,
11.00-12.00 14.00-15.00 SGD Disc room Facilitator
2017
12.00-12.30 10.00-10.30 Break
12.30-14.00 10.30-11.00 Student project
Prof. Dr. dr. I

Nyoman Mangku
Karmaya,
14.00-15.00 15.00-16.00 Pleanary Day 1 Class room M.Repro, PA(K)/
dr. I Wayan
Sugiritama,
M.Kes
dr. D.A. Inten Dwi

Lecture 4
08.00-09.00 10.00-11.00 Class room Primayanti,
Physiology of CNS & PNS M.Biomed
Lecture 5
dr. Ni Putu Sri
2 09.00-10.00 11.00-12.00 Neuropathology of CNS & Class room Widyani, Sp.PA
Wed PNS
27,
2017
12.00-12.30 12.00-12.30 Break
12.30-14.00 12.30-13.30 Student project

21
dr. D.A. Inten Dwi

Primayanti,
14.00-15.00 15.00-16.00 Pleanary Day 2 Class room M.Biomed / dr. Ni
Putu Sri Widyani,
Sp.PA
Lecture 6
Dr.dr. I Nyoman
08.00-09.00 10.00-11.00 Clinical Pathology: Class room
Wande, Sp.PK
Cerebrospinal analysis
Lecture 7
Pharmacology: Drugs Dr.dr. I Made
09.00-10.00 11.00-12.00 Class room
used for seizure disorders Jawi, M.Kes
& Parkinsonism
3 12.00-12.30 12.00-12.30 Break

Thu
Sep 28, 12.30-14.00 12.30-13.30 Student project
2017 Dr.dr. I Nyoman
14.00-15.00 15.00-16.00 Pleanary Day 3 Class room Wande, Sp.PK/

Dr.dr. I Made
Jawi, M.Kes
Lecture 8 dr. Dewi Sutriani

08.00-09.00 10.00-11.00 Class room Mahalini, Sp.A
Febrile Seizure
Lecture 9
Dr.dr. Anna
09.00-10.00 11.00-12.00 Seizure, Epilepsy, and Class room Marita, Sp.S(K)
Status Epilepticus
4
Mon
Oct 2, 11.00-12.30 13.30-15.00 SGD Disc room Facilitator
2017
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project

dr. Dewi Sutriani
Mahalini, Sp.A/
14.00-15.00 15.00-16.00 Pleanary Day 4 Class room Dr.dr. Anna
Marita, Sp.S(K)

22
Lecture 10 Dr.dr. AAA. Putri

08.00-09.00 10.00-11.00 Dementia, Post Traumatic Class room Laksmidewi,
Sp.S(K)
Amnesia
Dr.dr. DPG.
Lecture 11
09.00-10.00 11.00-12.00 Class room PurwaSamatra,
Parkinson Disease Sp.S(K)

5
Tuesday 11.00-12.30 13.30-15.00 SGD Disc room Facilitator
Oct 3,
2017 12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project
Dr.dr. AAA. Putri

Laksmidewi,
14.00-15.00 15.00-16.00 Pleanary Day 5 Class room Sp.S(K)/ Dr.dr.
DPG. Purwa
Samatra, Sp.S(K)
Dr.dr. Thomas
Lecture 12
08.00-09.00 10.00-11.00 Class room Eko Purwata,
Neuropathic Pain Sp.S(K), FAAN
Lecture 13 Dr.dr. Made Oka

09.00-10.00 11.00-12.00 Migrain, Neuralgia Class room Adnyana,
Sp.S(K)
Trigeminal

6
Wednesday
Oct 4, 2017 12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project
Dr.dr. Thomas
Eko Purwata,
Sp.S(K), FAAN/
14.00-15.00 15.00-16.00 Pleanary Day 6 Class room Dr.dr. Made Oka
Adnyana,
Sp.S(K)
Dr.dr. Made Oka

Lecture 14
Adnyana,
08.00-09.00 10.00-11.00 Tension Type Headache, Class room Sp.S(K)
Cluster Headache

23
dr. Made
Lecture 15 WidhiAsih,
09.00-10.00 11.00-12.00 Imaging: X-ray of skull Class room Sp.Rad(K)
and Spine
7
Thu Oct 5, 10.00-11.00 09.00-10.00 Independent learning
2017
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project
Dr.dr. Made Oka

Adnyana,
14.00-15.00 15.00-16.00 Pleanary Day 7 Class room Sp.S(K)/ dr.
Made WidhiAsih,
Sp.Rad(K)
Dr.dr. Putu
Lecture 16
08.00-09.00 11.00-12.00 Class room Pramana, Sp.An.,
Acute and reffered pain KMN., M.Kes
Lecture 17 dr. Ketut

09.00-10.00 12.00-13.00 Vertigo, Bells palsy, and Class room Widyastuti, Sp.S
Meniere Disease

10.00-11.00 13.00-14.00 Neurological aspect of Class room Indrayani, Sp.S
Hearing Loss and Tinnitus
8 12.30-14.00 09.00-10.00 Independent learning

Fri
2017
12.00-12.30 10.00-10.30 Break
12.30-14.00 10.30-11.00 Student project
Dr.dr. Putu
Pramana, Sp.An.,
KMN., M.Kes/dr.
14.00-15.00 15.00-16.00 Pleanary Day 8 Class room Ketut Widyastuti,
Sp.S/ dr. IA Sri
Indrayani, Sp.S

24
Lecture 19 dr. IGN Budiarsa,

08.00-09.00 11.00-12.00 Stroke I: TIA, Cerebral Class room Sp.S
Infarction, ICB, SAH

dr. IGN Budiarsa,
Lecture 20 Sp.S
09.00-10.00 12.00-13.00 Class room
Stroke II: Management
dr. I Wayan
Lecture 21
Niryana,M.Kes,
9 10.00-11.00 13.00-14.00 Stroke III: Surgical Class room Sp.BS(K)
Mon Management of Stroke
Oct 9,
12.00-12.30 10.00-10.30 Break
12.30-14.00 10.30-11.00 Student project

dr. IGN Budiarsa,
Sp.S/ dr. I Wayan
14.00-15.00 15.00-16.00 Pleanary Day 9 Class room Niryana,
M.Kes,Sp.BS(K)
Lecture 22 Dr.dr. Tjokorda

Complete Spinal GB Mahadewa,
08.00-09.00 10.00-11.00 Class room M.Kes,
Transaction, Acute Sp.BS(K)Spinal
Medullary Compression
Lecture 23 Dr.dr. Tjokorda

Prehospital& Initial GB Mahadewa,
09.00-10.00 11.00-12.00 Class room M.Kes,
Management of spine & Sp.BS(K)Spinal
spinal cord injury
10
Tue 10.00-11.00 09.00-10.00 Independent learning
Oct 10,
2017 11.00-12.30 13.30-15.00 SGD Disc room Facilitator
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project
Dr.dr. Tjokorda
GB Mahadewa,
14.00-15.00 15.00-16.00 Plenary Day 10 Class room M.Kes,
Sp.BS(K)Spinal

25

08.00-09.00 10.00-11.00 Neuropathy, CTS, TTS, Class room Wijayanti,
M.Biomed, Sp.S
Peroneal Palsy

09.00-10.00 11.00-12.00 HNP, Radicular Class room Wijayanti,
M.Biomed, Sp.S
Syndrome
11
Wed
Oct 11, Disc room Facilitator
11.00-12.30 13.30-15.00 SGD
2017
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project

dr. IA Sri
14.00-15.00 15.00-16.00 Plenary Day 11 Class room Wijayanti,
M.Biomed, Sp.S
Lecture 26 dr. KumaraTini,

Coma, Encephalopathy, Sp.S, FINS
08.00-09.00 10.00-11.00 Class room
Hipertensive
Encephalopathy,
Lecture 27 dr. IB. Kusuma

09.00-10.00 11.00-12.00 Class room
Putra, Sp.S
Neurogenic Bladder
Thu
2017
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project

dr. KumaraTini,
Sp.S, FINS/ dr.
14.00-15.00 15.00-16.00 Plenary Day 12 Class room IB. Kusuma
Putra, Sp.S
Lecture 28 dr. Made

08.00-09.00 10.00-11.00 Meningitis, Ensefalitis, Class room Susilawathi,
Sp.S(K)
13 Cerebral Malaria
Fri Lecture 29 dr. Putu Gede
Oct 13, 09.00-10.00 11.00-12.00 CNS Infection HIV AIDS, Class room Sudira, Sp.S
2017 Spondylitis TB, Rabies

26
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project

dr. Made
Susilawathi,
14.00-15.00 15.00-16.00 Plenary Day 13 Class room Sp.S(K)/ dr. Putu
Gede Sudira,
Sp.S
Lecture 30 dr. Putu Witari,

08.00-09.00 10.00-11.00 Tetanus Neonatorum, Class room Sp.S
Tetanus, Poliomyelitis
Lecture 31 dr. Komang

09.00-10.00 11.00-12.00 Guillain Barre Syndrome, Class room Arimbawa, Sp.S
Myasthenia Gravis

Mon Oct 16,
2017 11.00-12.30 13.30-15.00 SGD Disc room Facilitator
12.30-13.00 12.00-12.30 Break
13.00-14.00 12.30-13.30 Student project
dr. Putu Witari,

14.00-15.00 15.00-16.00 Plenary Day 14 Class room Sp.S/ dr. Komang
Arimbawa, Sp.S
Lecture 32 Prof. Dr.dr. Sri

Traumatic Brain Injury, Maliawan,
08.00-09.00 10.00-11.00 Class room Sp.BS(K)
Prehospital & Initial
Management
Lecture 33 Dr.dr. Nyoman

09.00-10.00 11.00-12.00 Brain Tumor and Class room Golden, Sp.BS(K)
15
Tue Oct 17, Treatment Options
2017
12.30-13.00 12.00-12.30 Break

27
13.00-14.00 12.30-13.30 Student project
Prof. Dr.dr. Sri

Maliawan,
14.00-15.00 15.00-16.00 Plenary Day 15 Class room Sp.BS(K)/ Dr.dr.
Nyoman Golden,
Sp.BS(K)
16
08.00 - Student Project
Wed Oct 18, 08.00 - Finish Auditorium Team
Finish Presentation
2017
17 08.00-10.00 Basic Clinical Skill 1: dr. Putu Witari,

Skills Sp.S
Thu Oct 19, 10.00-12.00 Fungsi Luhur, saraf
Laboratory
2017 kranialis
Skills dr. IA Sri

18 Basic Clinical Skill 2: Wijayanti,
Laboratory
Fri Oct 20, 08.00-10.00 10.00-12.00 Sistem Motorik, M.Biomed, Sp.S
2017 Koordinasi dan sensorik
Basic Clinical Skill 3: Skills dr. Putu Gede

- Refleks fisiologis, Laboratory Sudira, Sp.S
19 patologis dan primitif
Mon - Pemeriksaan tulang
08.00-10.00 10.00-12.00
Oct 23, belakang
2017 - Tanda perangsangan
meningeal dan tanda
ischialgia
Basic Clinical Skill 4: Skills dr. IA Sri
20 Pemeriksaan Diagnostik Laboratory Indrayani, Sp.S
Tue Radiologi (CT-skenotak

08.00-10.00 10.00-12.00
Oct 24, dan interpretasinya),
2017 Punksi Lumbal dan
elektrodiagnostik lainnya
21
Wed Oct 25, Pre- Evaluation Break
2017
22
Thu Oct 26, Examination
2017
Class Room : R. 4.02 (4th Floor)

NB. Kuliah Dr.dr. I Nyoman Wande, Sp.PK, dipindahkan ke Hari Jumat, 13 Oktober 2017.

28
LEARNING PROGRAMS
LECTURE 1
HIGHLIGHT NEUROSCIENCE AND NEUROLOGICAL DISORDERS
dr. Ida Ayu Sri Wijayanti, M.Biomed, Sp.S*
*Neurology Department, School of Medicine, Faculty of Medicine, Universitas Udayana
Basic structure
The nervous system consists of the brain, spinal cord and peripheral nerves. It is made up
of nerve cells, called neurons, and supporting cells called glial cells.
There are three main kinds of neurons. Sensory neurons are coupled to receptors
specialised to detect and respond to different attributes of the internal and external environment.
The receptors sensitive to changes in light, sound, mechanical and chemical stimuli subserve
the sensory modalities of vision, hearing, touch, smell and taste. When mechanical, thermal or
chemical stimuli to the skin exceed a certain intensity, they can cause tissue damage and a
special set of receptors called nociceptors are activated; these give rise both to protective
reflexes and to the sensation of pain.
Motor neurons, which control the activity of muscles, are responsible for all forms of
behaviour including speech. Interposed between sensory and motor neurons are Interneurones.
These are by far the most numerous (in the human brain). Interneurons mediate simple
reflexes as well as being responsible for the highest functions of the brain. Glial cells, long
thought to have a purely supporting function to the neurons, are now known to make an
important contribution to the development of the nervous system and to its function in the adult
brain. While much more numerous, they do not transmit information in the way that neurons do.
Neurons have an architecture that consists of a cell body and two sets of additional
compartments called processes. One of these sets are called axons; their job is to transmit
information from the neuron on to others to which it is connected. The other set are called
dendrites - their job is to receive the information being transmitted by the axons of other
neurons. Both of these processes participate in the specialised contacts called synapses.
Neurons are organised into complex chains and networks that are the pathways through which
information in the nervous system is transmitted.
The brain and spinal cord are connected to sensory receptors and muscles through long
axons that make up the peripheral nerves. The spinal cord has two functions: it is the seat of
simple reflexes such as the knee jerk and the rapid withdrawal of a limb from a hot object or a
pinprick, as well as more complex reflexes, and it forms a highway between the body and the
brain for information travelling in both directions.
Anatomy of the Brain
The brain consists of the brain stem and the cerebral hemispheres. The brain stem is
divided into hind-brain, mid-brain and a between-brain called the diencephalon. The hind-brain
is an extension of the spinal cord. It contains networks of neurons that constitute centres for the
29
control of vital functions such as breathing and blood pressure. Within these are networks of
neurons whose activity controls these functions. Arising from the roof of the hind-brain is the
cerebellum, which plays an absolutely central role in the control and timing of movements.
The midbrain contains groups of neurons, each of which seem to use predominantly a
particular type of chemical messenger, but all of which project up to cerebral hemispheres. It is
thought that these can modulate the activity of neurons in the higher centres of the brain to
mediate such functions as sleep, attention or reward. The diencephalon is divided into two very
different areas called the thalamus and the hypothalamus: The thalamus relays impulses from
all sensory systems to the cerebral cortex, which in turn sends messages back to the thalamus.
This back-and-forward aspect of connectivity in the brain is intriguing - information doesnt just
travel one way. The hypothalamus controls functions such as eating and drinking, and it also
regulates the release of hormones involved in sexual functions.
The cerebral hemispheres consist of a core, the basal ganglia, and an extensive but
thin surrounding sheet of neurons making up the grey matter of the cerebral cortex. The basal
ganglia play a central role in the initiation and control of movement. Packed into the limited
space of the skull, the cerebral cortex is thrown into folds that weave in and out to enable a
much larger surface area for the sheet of neurons than would otherwise be possible. This
cortical tissue is the most highly developed area of the brain in humans. It is divided into a large
number of discrete areas, each distinguishable in terms of its layers and connections. The
functions of many of these areas are known - such as the visual, auditory, and olfactory areas,
the sensory areas receiving from the skin (called the somaesthetic areas) and various motor
areas. The pathways from the sensory receptors to the cortex and from cortex to the muscles
cross over from one side to the other. Thus movements of the right side of the body are
controlled by the left side of the cortex. Similarly, the left half of the body sends sensory signals
to the right hemisphere such that, for example, sounds in the left ear mainly reach the right
cortex. However, the two halves of the brain do not work in isolation - for the left and right
cerebral cortex are connected by a large fibre tract called the corpus callosum.
The cerebral cortex is required for voluntary actions, language, speech and higher
functions such as thinking and remembering. Many of these functions are carried out by both
sides of the brain, but some are largely lateralised to one cerebral hemisphere or the other.
Areas concerned with some of these higher functions, such as speech (which is lateralised in
the left hemisphere in most people), have been identified. However there is much still to be
learned, particularly about such fascinating issues as consciousness, and so the study of the
functions of the cerebral cortex is one of the most exciting and active areas of research in
Neuroscience.
Fundamental of Neurological Disorders
The clinical history is of paramount importance in neurology, perhaps more so than in any
other medical specialty. It is indispensable as a diagnostic instrument, it serves to establish a
doctorpatient relationship built on trust, and it is a prerequisite for the success of any
treatment that will follow. The history should always be taken with utmost care.

30
The type of neurological disturbance from which a patient is suffering can usually be
determined from a carefully obtained clinical history even before the physical examination or
any further tests are performed. In many patients, the history alone permits the assignment of a
precise diagnosis, but only if the physician has been listening closely to the patient. Skillful
history taking is the distinguishing mark of a good clinician.
In any branch of clinical medicine, not just in neurology, a good history can be obtained
only if the patient has confidence in the physician. Introduce yourself to the patient and take the
history in a place offering the necessary privacy and discretion. The patient should be
comfortably seated and emotionally at ease, as far as the circumstances allow, and must not
feel rushed. If someone else is present during the interview, e. g., a medical student, introduce
this person and make sure the patient really has no objection to his or her presence. Persons
other than the physician taking the history should behave discreetly and keep themselves
somewhat in the background. The history should be detailed and complete and should be taken
by, or under the supervision of, an experienced clinician, as far as possible. While interviewing
the patient, observe these principles: in the beginning the patient should be doing most of the
talking and you should say as little as possible.
Every patient has the right to be treated courteously and tactfully and to receive the
physicians full attention during an appropriately set period. You should perform a meticulous
physical examination only after you have listened carefully to the patients story and filled it out
with further, detailed questioning. The patient has the right to a full explanation of your findings
and of what they imply about his or her illness. You should explain these matters truthfully, in
language that the patient can understand and with due respect for his or her feelings. You will
often find yourself having to steer a difficult course between bluntness and euphemism.
The history and physical examination are two independent and equally important
components of clinical diagnostic assessment. They must complement each other and should,
to some extent, be performed in parallel. The experienced clinician, while listening to the
patients history, will already be thinking of specific abnormalities to look for on physical
examination. If the examination should then reveal other, perhaps unexpected findings, the
clinician can amplify the history by asking further, specific questions. Ideally, the clinician will be
able to make the diagnosis from the history and physical examination alone.

31
LECTURE 2
ANATOMY OF NERVUS SYSTEM
Prof. Dr. dr. I Nyoman Mangku Karmaya, M.Repro, PA(K)*
*Anatomy Department, School of Medicine, Faculty of Medicine, Universitas Udayana
The needs of living things for feeding, feeling safe, comfortable and finding a partner to
breed need information from outside or from within the body to be able to respond in an integral
way. The creature required cells that have specialization easy to receive and convey stimulus.
These cells are called nerve cells. In the body thenerve cells are arranged in the Central
Nervous System (CNS), Peripheral Nervous Syatem (PNS) and Autonomic Nervous System
(ANS). By its nature nerve cells are divided into motor and sensory nerves. Neuro anatomy
studies the nervous system, its organization and its functions.
The CNS is tubular shaped with a swollen cranial part, consisting of the brain, brainstem
and spinal cord. The CNS consists of many nuclei and nerve fibers arranged in tract. That
brings the sensory stimuli of the spinal cord to the higher centers called tractus ascendens
carrying sensory impulses. The down fibers from the brain to the spinal cord is called tractus
descendentes carrying motor sensoric.
The PNS is nerve fibers that comes out of the CNS and serves all the organs of the body,
both motor and sensory. The CNS consists of 12 pairs cranial nerves (nervi craniales) coming
out from the brain stem and consist of 31-32 pairs peripheral nerves.
The ANS is motoric in nature serving smooth muscle existing in the internal organs
(visceral organs), glandular muscles and also serve the heart muscle.
Neural cells at both the center and the periphery are maintained by glial cells In its
function nerve cells need the help of other nerve cells to convey messages either to the center
or to the periphery. The relationship between nerves is called a synapse. Communication in
synapses is done through a chemical substance called neurotransmitter.
Learning Task.
1. Draw a chart of a nerve cell, its parts and its types!
2. Explain what are synapses, neurotransmitters and types of synaptic anatomical
relationships!
3. Explain the properties of the nerves according to the impulse it carries!
4. Describe all parts of the CNS as well as its function!
5. Explain the anatomy of PNS, the amount and its nature!
6. Name all cranial nerves and their properties!
7. Explain about SSO and its properties!
8. What is the difference between sympathetic and parasympathetic nerves?
9. Distinguish the tract and nerve fibers. Between nuclei and ganglion. Between afferent
and afferent fibers!
10. Explain segmental, intersegmental and supra segmental reflexes!
11. Describe neuroglia and its function!

32
Case 1
A young man complained every sport his lips always dry. Conversely if sleep like runny.
1. What autonomous nerve is active in active motion / exercise and during sleep?
2. Describe the location of the sympathetic nerve center, the organ served, and its effects!
3. Explain the location of the parasympathetic center, the organ served and its effects!
Case 2.
A housewife suffers a spinal fracture from trauma. The mother experiences muscle paralysis as
well as loss of skin sensation from below the navel down. There is hyperreflesi in the knee joint.
Doctors suspect damage has occurred on Upper Motor Neuron due to spinal cord injury.
1. Draw the cross-sectional chart of the spinal cord, its parts and its functions!
2. Explain what is meant by Upper Motor Neuron and Lower Motor Neuron! Differences
between tractus ascendentes and descendentes!
Case 3.
When a new wake up a father can not move half his body, his lips can not close tight and one
eyelid can not be blinked and unclear voice. Suspected the father suffered a stroke involving the
cranial nerve.
1. Name the cranial nerves, the structure served and their nature!
Case 4.
When your bare feet step on a lit cigarette butt, you pull your legs very fast. The reflex
movements we have are useful to protect our bodies from danger.
1. Explain what the monsinaptic reflex and the polysinaptic and its components!
2. What's segmental, intersegmental and suprasegmental responses?

33
LECTURE 3
HISTOLOGY OF NERVUS SYSTEM
Dr. Wayan Sugiritama, M.Kes*
*Histology Department, School of Medicine, Faculty of Medicine, Universitas Udayana
Abstract:
Anatomically, the nervous system is divided into the central nervous system (CNS),
consisting of the brain and the spinal cord; and the peripheral nervous system(PNS), composed
of nerve fibers and small aggregates of nerve cells called nerve ganglia. Structurally, nerve
tissue consists of two cell types: nerve cells, or neurons, which usually show numerous long
processes; and several types of glial cells, which have short processes.
The brain contains about 1012 neurons, each of which has a cell process (axon and
dendrite) through which it establishes contacts with hundreds of other neurons. The spaces
between neurons are occupied by neuroglia which have short processes, support and protect
neurons, and participate in neural activity, neural nutrition, and the defense processes of the
CNS.
Brain and spinal cord are covered by three layers of connective tissue, meningens. The
outermost layer is the dura mater, the innermost is the pia mater, and an intermediate layer
between these is the arachnoid.
The nerve of PNS consists of varying numbers of myelinated and unmyelinated axons
originating from neurons located in the brain, spinal cord, or ganglia. Functionally, the PNS is
divided into a sensory (afferent) component, which receives and transmits impulses to the CNS
for processing, and a motor (efferent) component, which originates in the CNS and transmits
impulses to effector organs throughout the body. The motor component is further subdivided as:
somatic system and autonomic system.
A major function of the CNS is to receive sensory stimuli from various parts of the body
and to analyze this information and respond by generating signals that are transmitted over
PNS to initiate and integrate muscular, secretory, and other activities in the body. The function
of the CNS is not limited to integration of information from the periphery, it is also engaged in
less well understood endogenous neural activity that underlies consciousness, memory,
reasoning, and regulation of behavior.
Trigger Case 1:
A 22-year-old male had a severe, traumatic injury on his head and lower back after a
motorcycle accident. He referred to the hospital in unconscious state. There was large
hematoma on his head and abrasion on lower back. A CT-Scan was done and found subdural
hematoma and brain edema. The surgical was done to safe his life. When the patient
conscious he cannot feel and move both of his leg. Neurological examination found there was
decreased of motoric and sensory function on his leg.

34
Learning Tasks:
1. Differentiate the histological structure of the cerebellum with the cerebrum!
2. Describe the structure of connective tissue that covered the brain!
3. Why subdural space considered as potential space and what are its clinical importance?
4. Decreased of motoric and sensory function on patients leg may caused by spinal cord
injury, please explain its structure!
5. On the accident, peripheral nerve system (PNS) may have injured, explain the microscopic
structure of Peripheral Nervous system (PNS), and its classification!
6. Explain the regeneration of the brain and nerve after the injury!
Trigger Case 2:
A one-year-old boy referred to the neurologist with enlargement of the head, vomiting and
fatigue. On examination the doctor found decreased of muscular function. A lumbar puncture
was done to measure the intracranial pressure and collect the sample of cerebrospinal fluid
(CSF). There was an increase of intracranial pressure and the composition of CSF was normal.
He was diagnosed with hydrocephalus.
Learning Tasks:
1. Explain the structure of plexus choroideus which is produce the CSF!
2. Explain the production and absorption of CSF (cerebrospinal fluid)!
3. Explain the role of the blood-CSF barrier in maintained the chemical stability of the CSF!
4. Describe the structure of neuroglial cell which is have a role in circulation of CSF!
Trigger Case 3
A two-year-old girl admitted to the hospital with high body temperature followed by
seizures and decrease of consciousness. A CSF examination found a sign of infection and the
working diagnosis is encephalitis.
Learning Tasks:
1. Explain the structure of high selective barrier between blood borne substances and
neural tissue of CNS!
2. How this barrier can protect the neural tissue of CNS from dangerous substances (e.g.
microorganism) on the blood, explain your answer!
3. What is the clinical importance this barrier in treatment of disease in CNS, explain your
answer!
Self Assessment
1. Explain the general structure of neuron!
2. Mention and explain classification of neuron according to their structure and their
function!
3. Explain the Nislls Bodies!
4. Mention the type and explain the function of neuroglial cells!
5. Mention and explain various types of synapses between neuron!
6. Brain consist of...................................and................................
7. White matter is composed mostly by................., and Gray Matter is composed mostly
by......................
8. Differentiate the histological structure between cerebrum and cerebellum
9. Connective tissue that covered the brain and spinal cord is called by, its
outermost layer is... intermediate layer is., and the innermost layer is..
10. Blood-brain barrier is composed by.......
35
11. Cerebro spinal fluid (CSF) is produced by..................

12. Connective tissue which covers a nerve is....................., covers each bundle of nerve
fiber is................., and covers a nerve fiber is............
13. Myelin sheath in CNS is produced by...............and in PNS by........
14. Explain the classification of the nerves!
15. Differentiate the structure of somatic and autonomic nervous system!
16. Ganglia are..................., there are two types of ganglia :................and.............

36
LECTURE 4
PHYSIOLOGY OF NERVUS SYSTEM
dr. I Dewa Ayu Inten Dwi Primayanti, M.Biomed*
*Physiology Department, School of Medicine, Faculty of Medicine, Universitas Udayana
The nervous system is unique in the vast complexity of thought processes and control
actions it can perform. It receives each minute literally millions of bits of information from the
different sensory nerves and sensory organs and then integrates all these to determine
responses to be made by the body.
The nervous system consist of a highly complex aggregation of cells, part of which is a
communication network and another part a supportive matrix. The communication network is
formed by neurons, which are the functional cellular units of nervous system. The nervous
system includes both sensory (input) and motor (output) system interconnected by complex
integrative mechanisms. The nervous system divided into the Central Nervous System (CNS)
and the Peripheral Nervous System. The central nervous system includes the brain and
spinal cord. The peripheral nervous system has afferent ( sensory) neurons that bring
infoemation into the Central Nervous System , and efferent neurons that carry information away
from the CNS back to various parts of the body. The efferent neurons include somatic motor
neurons, which control skeletal muscles, and autonomic neurons, which control smooth and
cardiac muscle, gland and some adipose tissue. Autonomic neurons are subdivided into
sympathetic and parasympathetic branches.
Neurons have a cell body with a nucleus and organelles to direct cellular activity,
dendrites to receives incoming signals and an axon to transmit electrical signal from the ceel
body to the axon terminal.
The nervous system is composed primarily of two cell types are found in central nervous
system & peripheral nervous system. The neuron is the basic structural and functional unit of
the Nervous System which typically consist of a cell body (soma), several dendrites, and a
single axon. Neuron structure is related to function, which have receptive and integrative zone
(dendrite and cell body), trigger zone (axon hillock), and conductive region (axon) especially in
terminal end of axon has secretive synaptic transmitter.
The four major types of glial cells (Neuroglia ) in the central nervous system are
astrocytes, oligodendrocytes, microglia, and ependymal cells. Glial cells help support the
neuron both physically and metabolically. For instance function of the astrocytes as glue,
scaffold, establishing blood brain barrier, repair brain injuries and neural scar formation, take up
glutamate and GABA, take up excess K+ ECS, and enhance synaptic formation and to
strengthen synaptic transmission. oligodendrocytes form myelin sheath, line internal cavity of
the Central nervous system contribute to the formation CSF (ependymal cells), microglia as
scavenger.
Neuron communicate with muscle, gland, and other neurons at junction its called
neuromyal junction, neuroglandular, and synapses. Synapses are found in dendrite, soma, and
axon (axodendrtic, axosomatic, axoaxonic synapses). Synaptic transmission involves release of
neurotransmitter from the presynaptic cell, diffusion of neurotransmitter across the synaptic cleft
37
and binding of neurotransmitter to receptors on the postsynaptic cell. It ends when the
neurotransmitter dissociates from the receptor and is removed from the synaptic cleft.
Much of the activity in the Nervous system arises from mechanism that stimulate sensory
receptor located at the distal termination of sensory neuron. Signal travel over peripheral nerves
to reach the spinal cord and are then transmitted throughout the brain. Incoming sensory
massages are processed and integrative with information stored in various pools of neurons
such that the resulting signals can be used to generate appopriate motor response
LEARNING TASK
1. Describe functional type of neurons : afferent, autonomic, brain, central, efferent, enteric,
parasympathetic, peripheral, sensory, somatic motor, spinal, sympathetic!
2. Explained about:
a. Polarization, depolarization, repolarization and hyperpolarization.
b. Action potential, grade potential ( Explain how the graded potential and action
potential differ !)
c. Resting membrane potential.
d. Ion channels ( List four major type of ion channels, are they chemically-gated,
mechanically-gated or voltage-gated?)
3. Define three ways neurotransmitters are removed from the synapse, explained it!
4. What is the function of the mitokondria in a cell and how do mitokondria get to the axon
terminal?
5. The nervous system secretes neurocrines. Mention its and the receptor location!
6. What do you know about:
a. EPSP ( excitatory postsynaptic potential) and IPSP ( Inhibitory postsynaptic
potential)?
b. Fast synaptic potential & slow synaptic potential?
7. A man falls into deep sleep with one arm under his head. This arm is paralyzed when
he awakens, but it tingles, and pain sensation in it is still intact. What is the reason for
the loss of the motor function without loss of pain sensation is that in the nerves to his
arm?
8. What is the primary function of myelin, microglia, ependymal cells?
9. Please explain the function of the brain based on the region!
10. A woman was walking in the park. She saw a very beautiful flower. She was very happy
and picked the flower. Explain the neuro-physiological processes that occur in that
woman!
SELF ASSESSMENT
1. Describe the structure of neuron and explain significance of its principal regions!
2. Classify neurons on the basis of their structure and function!
3. Describe the location, the major types, and functions of the supporting cells!
4. Explain how the graded potential and action potential differ!
5. Define polarization, depolarization, repolarization and hyperpolarization!
6. Explain the actions of voltage regulated Na+ and K+ channels and describe the event
that occur during the production of an action potential!
7. Explain how action potentials are regenerated a long myelinated and non myelinated
axon!
8. Describe the events that occur in the interval between the electrical excitation of axon
and the release of neurotransmitter!
38
9. Compare the characteristics of EPSPs and action potential!

10. Explain the synaptic transmission exhibits special characteristic!
11. Explain how sensory receptors are categorizeds. Give examples of functional of
functional categories and explain how tonic and phasic receptors differ!
12. Describe the classification of the sensory division sensory receptors!
13. Give examples of different types of cutaneous receptors (somatosensory receptors) and
describe the neural pathways for the cutaneous senses!
14. Explain how the mechanical energy is tranduced/ converted into nerve impulses by the
organ Corti and how pitch perception is accomplished!
15. Give examples the following modalities are tested: sense of pain, temperatur, touch,
vibration, and sense of positition!
16. Distinguish between and compare monosynaptic and polysynaptic reflexes.

39
LECTURE 5
NEUROPATHOLOGY OF NERVUS SYSTEM
Dr. dr. Ni Putu Sriwidyani, Sp.PA*
*Pathology of Anatomy Department, School of Medicine, Faculty of Medicine, Universitas Udayana
ABSTRACT
The principal function unit of the central nervous system is the neuron. Of all the cells in
the body, neurons have a unique ability to receive, store, and transmit information. Neurons of
different types and in different locations have distinct properties, including functional roles,
distributions of their connections, neurotransmitters used, metabolic requirements, and levels of
electrical activity at a given moment. A set of neurons may thus show selective vulnerability to
various insults because it shares one or more these properties. The CNS is affected by a
number of unique neurological disorders, and also responds to common insults in a manner that
is distinct from other tissues. In central nervous system pathology will discussed about cerebral
edema, hydrocephalus, and raised intracranial pressure and herniation, and some common
central nervous system diseases.
The two components of peripheral nerves are axons and myelin sheaths made by
Schwann cells. Injuries to either of these components may result in a peripheral neuropathy. In
peripheral nerve diseases will discussed about general type of peripheral nerve injury, anatomic
patterns of peripheral neuropathies and some specific peripheral neuropathies.
Case 1
A 45 year old, previously healthy man has developed headaches over the past month.
There are no remarkable findings on physical examination. A cerebral angiogram shows a 7 mm
saccular aneurysm at the trifurcation of the right middle cerebral artery.
Question:
1. What is the abnormal vascular disease found in this man?
2. What is the complication of this abnormality
Case 2
A 72 year old woman falls down the stairs. She does not lose consciousness. About 36
hours later, she develops a headache and confusion and is taken to the emergency department.
On physical examination, she is conscious and has a scalp contusion on the occipital. What is
the most likely location of an intracranial hemorrhage in this patient?
Case 3
A 25 year old female has been experiencing episodes of numbness and tingling in her
right and left hands for several months. This problem typically occurs near the end of the day
and makes it difficult to use her computer keyboard. The thumb and first two fingers are most
affected. There is no pain or swelling, and she does not recall any trauma to her upper
extremities. What condition most likely caused her problem?

40
SELF ASSESMENT
Describe and give some example of:
1. Cerebral edema, hydrocephalus, and raised intracranial pressure.
2. Malformation and developmental disease.
3. Trauma affecting CNS.
4. Cerebrovascular disease.
5. CNS Infection.
6. Demyelinating disease.
7. Degenerative disease of CNS.
8. Tumors of CNS.
9. General type of peripheral nerve injuries.
10. Anatomic patterns of peripheral neuropathies.
11. Some specific peripheral neuropathies.

41
LECTURE 6
CEREBROSPINAL FLUID ANALYSIS
Dr. dr. I Nyoman Wande, Sp.PK*
*Clinical Pathology Department, School of Medicine, Faculty of Medicine, Universitas Udayana
Abstract
The cerebrospinal fluid (CSF) is a dynamic, metabolically active substance that has many
important functions. It is invaluable as a diagnostic aid in the evaluation of inflammatory
conditions, infectious or non infectious, involving the brain, spinal cord, and meninges. CSF is
obtained with relative ease by lumbar puncture (LP). Alterations in CSF constituents may be
similar in different pathologic processes and cause difficulties in interpretation. Combining a set
of CSF variables referred to as routine parameters (i.e. determination of protein, albumin,
immunoglobulin, glucose, lactate, and cellular changes, as well as specific antigen and antibody
testing for infectious agents) will increase the diagnostic sensitivity and specificity.
CSF should be analysed immediately after collection. If storage is needed 12 ml of CSF

should be partitioned into three to four sterile tubes. Albumin CSF/serum ratio (Qalb) should be
preferred to total protein measurement and normal upper limits should be related to patients
age. Elevated Qalb is a non-specific finding but occurs mainly in bacterial, cryptococcal, and
tuberculous meningitis, leptomingeal metastases as well as acute and chronic demyelinating
polyneuropathies. Pathological decrease of the CSF/serum glucose ratio or an increase in
lactate concentration indicates bacterial or fungal meningitis or leptomeningeal metastases.
Intrathecal immunoglobulin G synthesis is best demonstrated by isoelectric focusing followed by
specific staining. Cellular morphology (cytological staining) should be evaluated whenever
pleocytosis is found or leptomeningeal metastases or pathological bleeding is suspected.
Computed tomography-negative intrathecal bleeding should be investigated by bilirubin
detection.
Learning Objective
1. Describe the formation and location of cerebrospinal fluid (CSF)!
2. Describe the appearance and state the composition of normal CSF!
3. Understand the clinical significance of performing a spinal tap and accurately evaluating
CSF!
4. Discuss the importance and significance of utilizing the properly collected CSF specimen
for chemistry, hematology, microbiology and immumologic testing!
5. Know how to examine and report the appearance of CSF.
6. Be able to perform a manual white blood cell chamber count on a CSF specimen.
7. Be able to correctly calculate the white blood cell count for CSF specimens when given
the results of a chamber count performed using various dilutions.
8. Know the significant laboratory results expected to be obtained from patients with
meningitis caused by viral, bacterial or fungal infections.

42
Scenario 1:
A man, 30 years old, came to the emergency room with complain about unconscious.
Previously the patient had a bloody cough for 3 months, night fever and body weight decreased
since 4 months ago. On physical examination was found: unconscious patient, blood pressure
130/80 mmHg, pulse rate: 100 times/ minute, respiration rate: 40 times/ minute, axillary
temperature 37,90C. Patients planned to do cerebrospinal fluids analysis.
Learning task:
1. What is a lumbar puncture (spinal tap) and how is it performed?
2. Which of the following is an abnormal cerebrospinal fluid (CSF) finding?
3. Which of the following CSF results suggests fungal meningitis?
4. Which of the following is true about the CSF changes in patients with tuberculous
meningitis?
5. Which of the following is most likely to cause a low CSF glucose?
Scenario 2:
A man, 25 years old, came to the emergency room with complain about Seizures.
Previously the patient had a cephalgia for 3 months, impaired vision since 1 months ago. On
physical examination was found: conscious patient, blood pressure 120/80 mmHg, pulse rate:
80 times/minute, respiration rate: 25 times/minute, axillary temperature 36,50C. Patients planned
to do cerebrospinal fluids analysis.
1. Are there other reasons to do a lumbar puncture?
2. Why do I need a spinal tap? Why can't my blood or urine be tested?
3. What other tests may be done in addition to CSF analysis?

43
LECTURE 7
PHARMACOLOGY: DRUGS USED FOR SEIZURE DISORDERS & PARKINSONISM
& OTHER MOVEMENT DISORDERS
Dr. dr. I Made Jawi, M.Kes*
*Pharmacology Department, School of Medicine, Faculty of Medicine, Universitas Udayana
AIMS
1. Describe the rationale drugs used to treat each type of seizure.
2. Describe the desired therapeutics outcomes for seizure disorders.
3. Develop a education plan for people diagnosed with a seizure disorder.
LEARNING OUTCOMES
Apply concepts and principles of drugs used for seizure.
CURRICULUM CONTENT
1. Basic pharmacology of anti seizure drugs
- Drugs used in partial seizures & generalized tonic-clonic seizures.
- Drugs used in generalized seizures.
- Other drugs used in management of epilepsy.
2. Clinical pharmacology of anti seizure drugs
- Management of epilepsy.
- Special aspect of the toxicology of anti seizure drugs.
ABSTRACT
Seizures are the result of the sudden, excessive firing of a small number of neurons and
the spread of electrical activity to adjacent neurons. There are several types and many causes
of seizures. Identification of the cause of seizure activity is important in determining the type of
therapy required. Contributing factors (e.g., head injury, fever, hypoglycemia, drug overdose)
must be specifically treated to correct the underlying cause before chronic anticonvulsant
therapy is started. Once the underlying cause is treated, it is rare that chronic antiepileptic
therapy is needed. If the seizures are chronic and recurrent, the patient is diagnosed as having
epilepsy. Epilepsy is treated almost exclusively with anticonvulsant medications. The goals of
therapy are to reduce the frequency of seizure activity and minimize the adverse effects of the
medicine. To attain this, therapy must be individualized to consider the type of seizure activity
and the age, gender, and concurrent medical condition of the patient. Patients as well as their
families require education and support regarding their responbilities in managing epilepsy.
SCENARIO
Mr X, 45 years old, suddenly had a tonic clonic seizure while attending a seminar. When his
family notified of this and his need for transportation home, his wife tells you he has not been
taking his medications regulary.

44
LEARNING TASK
1. Describe how you as a doctor would address this situation!
2. Describe anti seizure drugs using in seizure patients!
3. Describe adverse effect of anti seizure drugs using in seizure patients!
SELF ASSESMENT
1. What is the definition of fetal hydantoin syndrome!
2. Which one of antiseizure drugs can cause gingival hyperplasia!
3. Can you describe the interaction of antiseizure drugs with the other drugs!
4. What is the treatment of patient with status epilepticus!
AIMS
1. Describe the rationale drugs used to treat parkinsons disease.
2. Describe the desired theraupetic outcomes for parkinsons disease.
3. Develop a education plan for people diagnosed with parkinsons disease.
LEARNING OUTCOMES
Apply concepts and principles of drugs used for parkinsons disease.
CURRICULUM CONTENT
Drug therapy for Parkinsons Disease
- Drug class: Dopamine Agonists
- Drug class: COMT Inhibitor
- Drug class: Anti cholinergic Agents
- Drug class: Miscellaneous Anti parkinsonism Agents
ABSTRACT
Parkinsons disease is a progressive neurologic disorder caused by deterioration of
dopamine-producing cells in the portion of the brain responsible for maintenance of posture and
muscle tone and the regulation of voluntary smooth muscles. Normally a balance exists
between dopamine, an inhibitory neurotransmitter, and acetylcholine, an excitatory
neurotransmitter and acetylcholine, an excitatory neurotransmitter. The symptoms associated
with Parkinsons disease develop because of a relative excess of acetylcholine in the brain. The
goal of treatment is to restore dopamine neurotransmitter function as close to normal as
possible and relieve symptoms caused by excessive acetylcholine. Therapy must be
individualized, but selegiline therapy is often started first to slow the development of symptoms.
As selegiline becomes less effective, levodopa is started with or without selegiline. Dopamine
agonists (amantadine, bromocriptine, pergolide, ropinirole, pramipexole) may be added to
directly stimulate dopamine receptors. Entacapone may be added to levodopa therapy to
reduce the metabolism of levodopa, prolonging its action. Anti cholinergic agents may be added
at any time to reduce the effects of the excessive acetylcholine. Non pharmacologic treatment
(e.g., diet, exercise, physical therapy) of Parkinsons disease is equally important in maintaining
the long-term well being of the patient.

45
SCENARIO
Mrs X, 55 years old, is being started on an anti cholinergic drug as part of the treatment plan for
Parkinsons disease.
LEARNING TASK
1. What symptoms can be expected to improve?
2. What problems could also arise from starting this medication?
3. Discuss the normal course of progsession of Parkinsons disease and include the
rationale for drug therapy to alleviate the symptoms!
4. List drugs which will give to the patient who has parkinsonism!
5. Explain why do you choose L-dopa and not dopamine to treat Parkinsons disease!
6. Explain why levo-dopa could not be combined with pyridoxine!
7. Describe the benefit combination of levodopa with carbidopa in the treatment of
Parkinsonism!
8. Describe why dipenhydramine used to treat Parkinsonism caused by neuroleptic!
SELF ASSESMENT
1. Describe the rationale drugs used to treat parkinsons disease!
2. Describe the side effect of drugs that used for parkinsons disease!
3. Develop an education plan for people diagnosed with parkinsons disease!

46
LECTURE 8
FEBRILE SEIZURE IN CHILDREN
dr. Dewi Sutriani Mahalini, Sp.A*
*Paediatry Department, School of Medicine, Faculty of Medicine, Universitas Udayana
Aims:
Describes concepts, definition, pathophysiology, classification, diagnosis and management of
febrile seizures in children.
Learning outcome:
1. Describe definition and classification of febrile seizure in children!
2. Describe etiology and risk factors of febrile seizure in children!
3. Describe the sign, symptom and diagnosis criteria of febrile seizure in children!
4. Describe the management of febrile seizure and long term management for prevention
recurrent seizure!
5. Describe the necessary information and education about febrile seizure for parents and
social environment!
1. Definition, etiology and pathophysiology of febrile seizure in children.
2. Classification of febrile seizure,
3. Recommendation for management febrile seizure in children.
4. Recommendation for immediate medical management of acute seizure and status
epilepticus.
5. Risk factors of recurrent febrile seizures and genetic epilepsy with febrile seizures plus
(GEFS+).
6. Long term management for prevention of recurrent febrile seizure (intermittent and long
term prophylaxis).
Abstract
Febrile seizures (FS) are the most common seizure disorder in childhood. Seizures with
fever occur in 3- 5% of children in North America and Europe, and in up to 14% of children in
Asia. It affects both boys and girls equally, mainly between 6 and 36 months with a peak at an
age of 18 months.
A febrile seizure (FS) is a disorder that presents between 6 months and 5 years of age
with convulsions and fever (temperatures above 38oC) but without evidence of intracranial
infection or defined cause. It is defined as a seizure occurring in the context of a febrile illness,
not secondary to a central nervous system (CNS) infection or an altered metabolic state in
children who have not had neonatal or previous afebrile seizures.
There are two main clinical forms: Simple febrile seizure are a short generalized seizure,
duration lasting than 15 minutes, not recurring within 24 hours, occurring during a febrile
episode, not caused by an acute disease of the nervous system. Simple febrile seizures usually
occurring during the first 24 hours of a febrile illness. Complex febrile seizure are a focal or
generalized and prolonged seizure, duration greater than 15 minutes, recurring more than once
47
in 24 hours. Complex febrile seizure also associated with post-ictal neurologic abnormalities,
more frequently a post ictal palsy (Todds palsy) or with previous neurologic deficits.
The risk factors for developing febrile seizures are multiple and include both genetic
factors such as positive family history of FS and environmental factors such as day care
attendance, specific infections, neuronal abnormality and prolonged stay in a neonatal unit.
Approximately 30-40% of children who have a febrile seizure will have a recurrence,
usually within 12 months. A higher risk of recurrence exists if the first seizure occurs when there
is a history of febrile seizure or epilepsy in the family, the age is younger than 12 months when
first febrile seizure occurred, temperature less than 39oC when seizures, the short time interval
between the onset of fever and seizures.
The etiology of FS is multifactorial; an autosomal dominant inheritance with reduced

penetrance has been described in several families. Several chromosomal loci have been
identified, particularly those on 19q and chromosome 2. Gene mutations on voltage gated ion
channels such as the alpha 1 subunit, the alpha 2 subunit and beta 1 subunit of sodium channel
(SCN1A, SCN2A, and SCN1B) and those affecting the gamma amino butyric acid (GABA)
receptor have been shown to be strongly associated with the epilepsy syndrome of genetic
epilepsy with febrile seizures plus (GEFS+).
Although a change in body temperature is required for occurrence of FS, the convulsions
are not specifically related to the rise in temperature or height of the temperature. They are
considered to be due to increased neuronal excitability due to release of various pyrogens.
Diagnosis is essentially based on history taking and physical examination. The initial
evaluation is intended to exclusion of intracranial process or metabolic disorder. Immediate
medical management includes treatment of the seizure if still continuing. Benzodiazepines
administered rectally, buccally or nasally are useful for rapid control. Diazepam over the first 24-
48 hours of each febrile illness has been in use since 1978 for intermittent prophylaxis; however
its efficacy in the meta-analysis is controversial. Long term treatment with sodium valproate may
be beneficial in children with very frequent atypical febrile seizures, particularly those with
recurrent prolonged seizures, duration of seizures more than 15 minutes, focal seizures, or in
children with neurological disorders before or after seizures (such as cerebral palsi,
hydrocephalus, hemiparesis).
Case 1
A girl, 12 months of age, came to the emergency unit with main complaint seizure.
Seizure occur once at 2 hours before admission, the duration 5 minutes, the type of seizure were
generalized tonic, with both eyes looking upward. A few minutes after seizure finished, she cried
loudly. The physical examination revealed: alert, respiration 28 times/minutes, pulse 100
times/minutes, temperature 39.5oC. The urination was clear and yellow, but the patient had
vomiting about 5 times/day and diarrhea 4 times since 2 days before admission.

48
Case 2
A boy, 4 years of age, came to the emergency unit with main complaint serial seizure. The
first seizure occur 4 hours before admission, second seizure occur since 15 minutes ago and the
seizure still continued until the patient arrive at emergency unit and still continued after
treatment with diazepam rectally. Type of seizure were generalized tonic clonic, both eyes
looking upward. She look weak after seizure and still unconscious. The past history were patient
already had seizure 3 times episode since 12 months of age.
History of delivery were spontaneous, birth body weight 2000 grams and severe asphyxia.
The physical examination revealed: respiration rate 30 times/minutes, pulse 120 times/minutes,
rectal temperature 40.0oC. She also had history of cough and difficult breathing since 3 days
before admission. The urination was clear and yellow, defecation was normal.
Case 3
A boy, 3 years of age, came to the emergency unit with main complaint serial seizure. The
first seizure occur 5 hours before admission, he looks weak after seizure and crying loudly 10
minutes later. Second seizure occur since 20 minutes ago and the seizure still continued until the
patient arrive at emergency unit. Patient had been treated with diazepam rectally twice
prehospital, but the seizure still continued. Type of seizure were tonic clonic and just affect the
right limbs. He look weak after seizure and still unconscious. The past history: patient already
had seizure, 2 times episodes since 8 months of age, history of delivery were sectio cesarea from
mother with severe preeclampsia, the baby was preterm and had severe asphyxia. The physical
examination revealed, respiration 54 times/minutes, pulse 120 times/minutes, rectal temperature
39,5oC. The neurological examination revealed bad posture with limbs spasticity. He had been
diagnosed with Cerebral palsy & failure to thrive. He also had history of cough and difficult
breathing since 1 days before admission. The urination was clear and yellow, defecation normal.
Learning task
Answer the questions below for all three cases above!
1. What is the diagnosis and differential diagnosis? Explains the reason of your answers?
2. What are the risk factor of recurrent seizure in this patient?
3. What are past history of seizure that you need to know for long term management?
4. Explain possible causes or etiology of the acute seizure?
5. What are the necessary diagnosis work up to support your diagnosis?
6. What are the management for acute seizure?
7. Explain long term management to the patient!
8. What are information and education that should be you done?

49
Self assessment
1. Describe definition of febrile seizure in children!
2. Describe classification of febrile seizure in children and its differentiation!
3. Describe etiology and patophysiology of febrile seizure in children!
4. Describe the management of acute seizure in emergency unit!
5. Describe the long term management for prevention recurrent seizure!
6. Describe prognosis of febrile seizure and risk factors that influences its!
References
1. Ismael S, Pusponegoro HD, Widodo DP, Mangunatmadja I, Handryastuti S, Editor.
Rekomendasi penatalaksanaan kejang demam. UKK Neurologi IDAI, 2016.
2. Ismael S, Pusponegoro HD, Widodo DP, Mangunatmadja I, Handryastuti S, Editor.
Rekomendasi penatalaksanaan status epilepticus. UKK Neurologi IDAI, 2016.
3. American Academy of Pediatrics. Febrile Seizures: guideline for the neurodiagnostic
evaluation of the child with a simple febrile seizure. Pediatrics 2011;127: 389
4. Hampers LC, Spina LA. Evaluation and management of pediatric febrile seizures in the
emergency department. Med Clin N Am 2011; 29:8393.
5. Kasperaviciute D, Catarino CB, Matarin M, Leu C, Novy J, Tostevin A, et al. Epilepsy,
hippocampal sclerosis and febrile seizures linked by common genetic variation around
SCN1A. Brain 2013; 136: 314050
6. Duba CM, Brewstera AL, Barama TZ. Febrile seizures: Mechanisms and relationship to
epilepsy. Brain Dev. 2009; 31(5): 36671.

50
LECTURE 9
SEIZURE, EPILEPSY AND STATUS EPILEPTICUS
Dr. dr. Anna Marita Sinardja, Sp.S(K)*
Aims:
Describe the pathophysiology, diagnosis, early manage and referral patient with seizures.
Learning Outcome:
1. Describe the role of neurotransmitters on patophysiology of seizures!
2. Describe the neurological sign and symptom of seizures!
3. Describe the classification of epilepsy!
4. Describe the Electroencephalography in diagnose of epilepsy!
5. Describe early patients management with seizures and epilepsy with anti epileptic
drugs (AEDs), indications and side effects!
Curiculum Contents:
1. The anatomy of cerebral cortex, sub cerebral cortex and hyppocampus.
2. The role of neurotransmitters in seizure and epilepsy.
3. The classification of epilepsy.
4. The etiology of epilepsy.
5. The role of anti epileptic drugs (AEDs).
6. The adverse effect of AEDs.
7. The psychosocial aspect of epileptic patients.
Abstract
Epilepsy is a condition characterized by repeated seizures due to a disorder of the brain

cells. It is a life-long tendency, though the seizures may start at any time during life and occur
sporadically or frequently. Some of the epilepsies are confined to particular age groups. Some
suffer from it their whole lives and others only for a few years. Epilepsy may develop after a
particular identifiable event (e.g., asphyxia, head injury, meningitis), in which case it is called
symptomatic epilepsy, or it may develop without any identifiable cause, and then it is called
idiopathic epilepsy.
A seizure is a result of excessive nerve-cell discharges in the brain. It is seen as a sudden

abnormal function of the body, often with loss of consciousness, an excess of muscular activity,
or sometimes a loss of it, or an abnormal sensation. The excessive nerve-cell discharges or
excitation may remain in a small area of the brain (a localized lesion or focus) giving rise to
partial (focal) seizures, or start immediately in the whole brain or spread from the small area
(focus) to the whole brain and spinal cord giving rise to generalized seizures. Not only may
these discharges vary in site, but also in severity and extent, therefore a wide variation of
clinical forms is seen. A seizure is also referred to as a convulsion, fit, or attack. However, the
words convulsion or fit are usually used to refer to seizures with tonic-clonic muscle
movements.

51
According to 1981 International League Against Epilepsy classification of epilepsy;

A. General epilepsy;
1. Tonic clonic (grand mal); loss of consciousness, fall, convulsions, muscle rigidity.
2. Absence; brief loss of consciousness and staring
3. Myoclonic; sporadic (isolated), jerking movements
4. Clonic; repetitive, jerking movements
5. Tonic; muscle stiffness, rigidity
6. Atonic; loss of muscle tone Partial Seizures
B. Partial/Focal Epilepsy;
1. Simple (awareness is retained);
a. Partial Motor; jerking, muscle rigidity, spasms, head-turning
b. Sensory; unusual sensations affecting either the vision, hearing, smell, taste or
touch
c. Autonomic; stomach sensation
d. Psychological; memory or emotional disturbances
2. Complex (Impairment of awareness); automatisms such as lip smacking, chewing,
fidgeting, walking and other repetitive involuntary movements
3. Partial seizure that becomes generalized seizure; begins as partial (simple or
complex) and evolves into grand-mal seizure.
The mechanism of epilepsy and seizure

The underlying mechanism of epilepsy is all about the imbalance between excitatory and
inhibitory neurons with its neurotransmitter such as gamma amino butyric acid (GABA) for
inhibition and glutamate for the excitatory actions.
Etiology of epileptic seizures

1. Epilepsy
2. Metabolic; hypoglycaemia, electrolyte imbalance
3. Infection; intracranial, extracranial
4. Trauma; birth trauma, head injury
5. Anoxia; birth asphyxia
52
6. Toxic; drugs, CO poison

7. Space occupying lesion
8. Circulatory disturbances; stroke, vascular anomalies
9. Cerebral oedema; hypertensive encephalopathy, eclampsia
10. Congenital; malformations of the brain (hydrocephalus)
11. Degenerative diseases; Niemann-Pick disease, cerebromacular degeneration
12. Genetic
13. Cryptogenic
Diagnosis
Diagnosis epilepsy based on the clinical manifestations from history taking and supporting
diagnosis results.
Differential diagnosis
Vasovagal syncope
Cardiac arrhythmia
Transient cerebral ischaemic attack
Hypoglycaemic attack
Panic attack
Non-epileptic attack disorder (NEAD)
Cataplexy
Investigation
EEG: help to support the diagnosis, determine seizure type and syndrome
MRI: is imaging investigation of choice for people with epilepsy
Other tests
1. Serum biochemical profile including plasma electrolytes, renal and liver function,
glucose, calcium, magnesium are essential.
2. ECG
Management
Selection of AED therapy will depend on the seizure type;
1. For partial seizures, the drug of first choice is carbamazepine. Valproate and phenytoin
followed by topiramate, lamotrigine and clobazam may be used as second choice and
add on therapy.
2. For generalised seizures, valproate should be the drug of choice. The second choice will
depend on the seizure type.
-absence seizure: lamotrigine, clonazepam.
-myoclonc seizure: lamotrigine, clonazepam, phenobarbitone
-generalised tonic clonic seizure; phenytoin, carbamazepine, phenobarbitone,
clonazepam, clobazam, lamotrigine
3. For unclassified seizures; in patients less than 25 years ageuse valproate, and for those
over 25 years age use carbamazepine.

53
Start with a single drug at a low dose. Gradual dose increments (to prevent adverse
effects) should be made up to the optimal dose for seizure control. If seizures continue despite
optimal dosage, it should be built up to a maximum tolerated dose unless side effects occur.
Patients should be reviewed regularly and investigations (eg liver profile) done if side effects are
suspected. If seizures continue despite the maximally tolerated dose of the first AED, review the
diagnosis, the seizure type / syndrome, dosage and frequency of administration and
compliance. If the initial AED has failed or has to be withdrawn due to adverse effects, then
monotherapy using the second choice AED may be tried. The second drug should be built up to
an optimal dose and then the initial drug should be tapered off slowly. All attempts should be
made to control the epilepsy on monotherapy. At least two attempts at monotherapy should be
tried before considering a combination.
If symptoms are not adequately controlled on monotherapy, an appropriate second choice

AED should be combined. If the added second drug is unhelpful, it should be gradually
withdrawn, and another AED should be tried. If the second drug is also only partially helpful,
either the first or second drug may be tailed off, depending on the relative efficacy, side effects
and tolerance, and another drug tried.
If symptoms are not adequately controlled on several attempts with two drug
combinations, a third AED may be added. The aim of treatment is to maintain the patient on the
minimum number of drugs required to achieve adequate symptom control. If trials of
combination therapy do not bring about worthwhile benefit, treatment should revert to the
regimen (monotherapy or combination therapy) that has proved most acceptable to the patient
(considering seizure frequency and tolerability of side effects).
Withdrawal of AED therapy should be considered in patients who have been seizure free
for at least 3 years. Decision to continue or withdraw medication should be made after a full
discussion of the risks and benefits of withdrawal. When AED treatment is being discontinued, it
should be done slowly (at least over 2-3 months) and one drug should be withdrawn at a time.
Care should be taken when withdrawing benzodiazepines and barbiturates. In the event of
seizure recurrence following withdrawal of AEDs the patient should be referred to a specialist.
All individuals with epilepsy should have access via their specialist to a tertiary service when
circumstances require.
Psychososial aspect of epilepsy

The following issues should be discussed with patients during visits:
1. epilepsy in general
2. diagnosis and treatment options
3. medication and side effects
4. seizure type(s), triggers and seizure control
5. first aid, safety and injury prevention at home and work
6. road safety and driving regulations
7. stigma and life style
8. prognosis
9. sudden death in epilepsy (SUDEP)
10. status epilepticus
54
STATUS EPILEPTICUS
This is a true neurologic emergency with high mortality rate. Status epilepticus (SE) is a
neurological emergency resulting from prolonged clinical or electroencephalographic seizure
activity.
Classifications;
1. convulsive status epilepticus
2. non convulsive status epilepticus
Definition
1. convulsive status epilepticus (CSE); continuous convulsive seizures lasting more than 5
minutes or two or more seizures during which the patient does not return to baseline
consciousness.
2. Non convulsive status epilepticus (NCSE); change in mental status from baseline for at
least 30 minutes associated with ictal discharges on EEG.
Etiology
In adults, SE is more often of acute symptomatic etiology and the common etiologies
include: central nervous system (CNS) infections, acute strokes, hypoxic encephalopathy,
metabolic causes and low AED levels. No clear etiology can be identified in 20% of cases. Of
the acute symptomatic etiology, cerebrovascular disease is the predominant cause in developed
countries, more so in the elderly
Management
Patients must be brought to hospital at the earliest. Stage for management;
1. Premonitory stage; prolonged seizure at home/before hospitalization; rectal diazepam
0.5 mg/kg
2. First stage; at hospital; oxygen, stabilize airway, respiration and hemodynamic
parameters. Obtain IV access. Random blood glucose, liver function test, renal function
test, electrolytes and blood urea nitrogen, monitor ECG and SpO2. Consult neurologist.
3. Second stage; established status epilepticus; phenytoin 15-20 mg/kg IV at maximum
rate 50 mg/minute.
4. Third stage; refractory status epilepticus; if the seizure persists until more than 60
minutes admit patient to intensive care unit in a specialized centr3. Prepare to
mechanically ventilate and obtain central venous pressure access and continuous
hemodynamic monitoring through arterial line. Start EEG monitoring.
Case 1
A 12 years old boy, came to emergency department with seizures after having a motor
accident. He fell into right sided and hit his right head to the ground. Before the seizures he felt
headache in his right sided then felt something weird to his body. His eyes and head was
looking at the right sided followed by jerking of the left arm, while he was fully alert. After a
moment then both his arms & limbs were stiff followed by stomping movement. When this
happened, he lost conciousness. The seizure was less than 2 minutes long. After the seizure
ended, he slowly regained conciousness.
55
Learning task
1. What is the diagnosis and the type of epilepsy?
2. Explain why a traumatic brain injury can caused a covulsion?
3. What is the diagnostic investigation plan?
Self assessment
1. Describe the function of neurotransmitters!
2. Describe how an accident can cause a seizures!
3. Describe the classification of epilepsy especially in this case!
4. Describe the diagnostic investigation in patient with seizures!
Describe the TOPICAL DIAGNOSIS in patient with:

1. Right sided hemiplegia
2. Left sided superior extremity monoplegia
3. Left sided N III paralyzed with hemiplegia alternan
4. Tetraplegia
5. Paraplegia.
Case 2
A 9-year-old boy came to the clinic since he has been having spells in which he suddenly
stops what he was previously doing and stares for about one minute. He cannot recall what
happened during the spell itself. Sometimes it happened while he was writing at school and that
event stop the activity suddenly. After the attack he regained consciousness and back to activity
and didnt remember what has had happened.
Learning task
1. What is the diagnosis of the patient?
2. What kind of the drugs you can give to the patient?
Case 3
A woman 20 years old came to emergency department with unconsciousness after having
massive seizures attack. She has medical history of having general epilepsy with phenytoin in
treatment for 6 months. She stoped the treatment a week ago by herself.
Learning task
1. What is the diagnosis of this case?
2. What is the management of this case?

56
LECTURE 10
DEMENTIA (VASCULAR DEMENTIA & ALZHEIMER DEMENTIA)
Dr. dr A.A. Ayu Putri Laksmidewi, Sp.S(K)*
Aims:
Able to establish tentative diagnosis, provide initial management and refer patient with
Vascular Dementia (VaD) and Alzheimer Dementia (AD).
Learning outcome:
1. Able to describe physiology and etio-pathogenesis of VaD and AD.
2. Able to describe how to implement general strategy and neuropsychological approach to
the patient with VaD and AD.
3. Able to describe management by making initial assessment, providing initial
management and referring patient with VaD and AD.
4. Able to describe the prognosis of VaD and AD.
Module Dementia:
1. Cognitive impairment, demonstrated by memory loss and impairment of language,
praxis, recognition or abstract thinking.
2. The cognitive impairment is chronic and progressive, and results in functional decline.
3. Delirium must be ruled out.
(Delirium is a disturbance in awareness, attention and cognition developing over a short period
of time and represents a decline from baseline. Delirium tends to fluctuate in severity temporally
and is a result of another medical condition or withdrawal or exposure to toxins).
Table 1. Comparison of Vascular Dementia and Alzheimers dementia.

Vascular Dementia Alzheimers Dementia
Gender Male > female Female > male
Genetic involvement Not clear Suspected
Onset Relatively sudden Insidious
Course Stepwise progression Gradual and progressive
Somatic complaints Common Rare
Hypertension More common Less common
Focal Neurological sign Present Unusual
Personality Well preserved Disintegration
Insight Preserved Lost early
Affect Depression, Anxiety, Lability Affect blunted
Scenario 1 :
A 57-years-old man, came to the hospital with chief complaint of difficulty in recalling
recent memories. This patient had a 6-months history of memory impairment. He had been
diagnosed with cerebrovascular diseases (stroke) 1.5 years ago. He is known to have high
blood pressure and diabetes mellitus.

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Learning Task:
1. What questions should you ask this patient? What kind of point should you make in the
questions so that a good history on the memory impairment can be taken? (key:
fundamental four and secret seven)
2. What kind of physical examination, neurological examination and neurobehaviour
examination will you do?
3. How to diagnose this patient and what are the differential diagnosis?
4. How to decide the staging in this dementia patient?
5. Please explain the etio-pathogenesis and pathophysiology of vascular dementia!
6. Please write down the tests that can be used to screen or to diagnose dementia patient!
Self Assessment :
1. Describe the history taking on the memory impairment!
2. Describe the neurological and neurobehavior examination!
3. Describe the causes of dementia!
4. Describe the management of dementia!
5. Describe the prognosis for this patient!
Scenario 2 :
A 65 years old woman came with complaint of slowly progressed memory and cognitive
impairment that had started since approximately 5 years ago. She had no known history of
high blood pressure, stroke, diabetes, or head injury.
Learning Task :
questions so that a good history on the memory impairment can be taken? (key:
fundamental four and secret seven)
2. What kind of physical examination, neurological examination and neurobehavioral
examination will you do?
4. How to decide the staging in this dementia patient?
5. Please explain the etio-pathogenesis and pathophysiology of vascular dementia!
6. Please write down the tests that can be used to screen or to diagnose dementia patient!
Self Assessment :
2. Describe the neurological and neurobehavior examination!
3. Describe the causes of dementia!
4. Describe the management of dementia!

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Module : Post Traumatic Amnesia
Aims :
Describe diagnosis, neurobehavior problems management of patient with Post Traumatic
Amnesia
Learning outcome
1. Describe pathobiology of Traumatic Brain Injury.
2. Describe neurological and neurobehavioral examination for patient with Post Traumatic
Amnesia.
3. Describe management of patient with Post Traumatic Amnesia.
4. Describe psychosocial aspect of patient with Post Traumatic Amnesia
Abstract Traumatic Brain Injury (TBI)

Traumatic Brain Injury (TBI) refers to an alteration in brain function or other evidence of
brain pathology resulting from an impact and/ or acceleration/ initialization of the brain.
Additionally a milder form of TBI is clinically termed a concussion.
The TBI can be classified as primary and secondary or focal and diffuse injury. It is called
primary when induced by mechanical force and occurs at the moment of injury. The two main
mechanism that cause primary injury are contact and acceleration-deceleration. Contrarily,
secondary injury is not mechanically induced and may be delayed from the moment of impact or
superimpose injury on a brain already affected by a mechanical injury.
The TBI causes both an acute injury due to direct damage and disruption of brain tissue
and neural circuit, secondary or delayed injury from other sources. These include ongoing
hemorrhage, hypoxia, ischemia, elevated intracranial pressure, changes in metabolic function,
coagulopathy and or pyrexia and dementia.
Post traumatic amnesia (PTA) is the time elapsed from injury to the moment when
patients can demonstrate continuous memory of what is happening around them. Aside from
the Glasgow Coma Scale (GCS) and duration of loss of consciousness, PTA is one of the
indicators of severity in TBI. PTA is common early after TBI. Its pathophysiology is poorly
understood. The hippocampus is central to memory processing and normally shows strong
functional connectivity to nodes within a large-scale intrinsic connectivity network that is called
the default mode network (DMN).
The TBI severity spectrum ranges from mild impact with no behavioral syndromes,
resulting in no lasting structural injury and producing only transient and temporary changes in
neurologic function to patients in prolonged coma/ vegetative state from catastrophic brain
injury. Cognitive impairments after a concussion can include difficulty concentrating, difficulty
remembering, feeling in a frog, feeling slowed down, forgetting recent events, confusion,
repeating question, answering slowly and amnesia.

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Amnesia
Amnesia is a severe, isolated disturbance of declarative memory in the absence of other
forms of cognitive dysfunction. Amnesia is typically divided into two aspects: retrograde
amnesia and anterograde amnesia. Retrograde amnesia is associated with a loss of memory
for prior events; this likely results from an inability to retrieve those memories from our memory
storage, which relate to an inability to identify appropriate cues for memory retrieval.
Anterograde amnesia is an inability to form new memories, likely as a result of damage to the
temporal or frontal lobes or the white matter connecting them. Post- traumatic amnesia is a
period of both retrograde and anterograde amnesia in those with moderate to severe TBI. The
retrograde amnesia component may prevent patients from knowing their family members,
friends and information that defines who they are, occupation. The anterograde amnesia
component prevents new memory accrual, including memory for those providing the patients
care.
Patients are unable to acquire new memories (anterograde amnesia) or recall recent
memories (retrograde amnesia). Other memories remain intact, including remote memory,
working memory and semantic memory.
Bilateral lesions of the Papez circuit and related areas can cause an amnestic syndrome,
while unilateral lesions can produce a milder, but often clinically relevant, memory deficit.
The Papez circuit includes the medial temporal lobes (hippocampus and entorhinal
cortex), the diencephalon (fornix and mammillary bodies; dorsomedial and anterior nuclei of the
thalamus), and the basal forebrain cholinergic nuclei (medial septal nuclei and the diagonal
band of Broca)
As an indicator of severity of TBI, the duration of PTA is important to observe. This is the
Cantu grading of Brain Injury:
Grade I : No loss of consciousness (LOC); PTA lasting < 30 minutes.
Grade II : LOC < 1 minute or PTA > 30 minute but < 24 hours
Grade III : LOC > 1 minute or PTA > 24 hours
PTA is also staged into mild, moderate and severe based on the duration: < 24 hours: > 24
hours - < 7 days ; and > 7 days respectively
The management for PTA depends on the severity of brain trauma. The mild PTA requires
cognitive therapy and stimulation but it is important not to burden the patient during the acute
phase with too much information and complex tasking. Moderate and severe PTA, especially
following a coma, needs more complex cognitive rehabilitation and requires long periods of
treatment and as of now no single medication is proven effective to fasten the recovery.
Scenario:
A 25 years old man, was brought to the Emergency Room following a bike accident with
no helmet on. Witness account stated he got head injury upon impact on the ground and was
unconscious for roughly a minute. He was slightly somnolent on examination, and unable to
recall the accident or what happened up until the point he was moved to the ER bed. Family
mentioned a perfectly healthy background and no history of serious illness in the past.

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Learning task :
questions so that a good history can be taken? (key: fundamental four and secret seven)
2. What kind of physical examination, neurological examination, neurobehavioral
examination and will you do?
4. How to decide the grading for the patients condition?
5. Please explain the pathophysiology of post traumatic amnesia!
6. Please explain your plan of care of this patient!
Self Assessment:
2. Describe the neurological and neurobehavioral examination!
3. Describe the tyoe of injuries that can cause the post traumatic amnesia!
4. Describe the management and neurocognitive-restoration for the PTA!

61
LECTURE 11
PARKINSON DISEASE
Dr. dr. DPG Purwa Samatra, Sp.S(K)*
Introduction
Parkinson's disease is a progressive disorder of the nervous system that affects

movement. It develops gradually, sometimes starting with a barely noticeable tremor in just one
hand. But while a tremor may be the most well-known sign of Parkinson's disease, the disorder
also commonly causes stiffness or slowing of movement. Although Parkinson's disease can't be
cured, medications may markedly improve your symptoms. In occasional cases, your doctor
may suggest surgery to regulate certain regions of your brain and improve your symptoms.
Patophysiology.
The symptoms associated with Parkinsons disease are the result of the loss of a number
of neurotransmitters, most notably dopamine. Symptoms worsen over time as more and more of
the cells affected by the disease are lost. The course of the disease is highly variable, with
some patients exhibiting very few symptoms as they age and others whose symptoms progress
rapidly.
Parkinsons is increasingly seen as a complex neurodegenerative disease with a

sequence of progression. There is strong evidence that it first affects the dorsal motor nucleus
of the vagus nerve and the olfactory bulbs and nucleus, then the locus coeruleus, and
eventually the substantia nigra. Cortical areas of the brain are affected at a later stage. Damage
to these various neuronal systems account for the multi-faceted pathophysiologic changes that
cause impairments not just to the motor system but also to the cognitive and neuropsychological
systems.

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Parkinson's signs and symptoms :

Tremor. A tremor, or shaking, usually begins in a limb, often your hand or fingers. You
may notice a back-and-forth rubbing of your thumb and forefinger, known as a pill-rolling
tremor. One characteristic of Parkinson's disease is a tremor of your hand when it is
relaxed (at rest).
Slowed movement (bradykinesia). Over time, Parkinson's disease may reduce your
ability to move and slow your movement, making simple tasks difficult and time-
consuming. Your steps may become shorter when you walk, or you may find it difficult to
get out of a chair. Also, you may drag your feet as you try to walk, making it difficult to
move.
Rigid muscles. Muscle stiffness may occur in any part of your body.
Impaired posture and balance. Your posture may become stooped, or you may have
balance problems as a result of Parkinson's disease.
All above are Cardinal Sign and Symptoms
Another Sign and symptom
Loss of automatic movements. In Parkinson's disease, you may have a decreased
ability to perform unconscious movements, including blinking, smiling or swinging your
arms when you walk.
Speech changes. You may have speech problems as a result of Parkinson's disease.
You may speak softly, quickly, slur or hesitate before talking. Your speech may be more
of a monotone rather than with the usual inflections.
Writing changes. It may become hard to write, and your writing may appear small.
The cause of Parkinson's disease is unknown, but several factors appear to play a role,
including:
Your genes. Researchers have identified specific genetic mutations that can cause
Parkinson's disease, but these are uncommon except in rare cases with many family
members affected by Parkinson's disease.
However, certain gene variations appear to increase the risk of Parkinson's disease but
with a relatively small risk of Parkinson's disease for each of these genetic markers.
Environmental triggers. Exposure to certain toxins or environmental factors may
increase the risk of later Parkinson's disease, but the risk is relatively small.
Researchers have also noted that many changes occur in the brains of people with Parkinson's
disease, although it's not clear why these changes occur. These changes include:
The presence of Lewy bodies. Clumps of specific substances within brain cells are
microscopic markers of Parkinson's disease. These are called Lewy bodies, and
researchers believe these Lewy bodies hold an important clue to the cause of
Parkinson's disease.
Alpha-synuclein is found within Lewy bodies. Although many substances are found
within Lewy bodies, scientists believe an important one is the natural and widespread
protein called alpha-synuclein (A-synuclein). It's found in all Lewy bodies in a clumped
form that cells can't break down. This is currently an important focus among Parkinson's
disease researchers.

63
Diagnose
No specific test exists to diagnose Parkinson's disease. Your doctor trained in nervous
system conditions (neurologist) will diagnose Parkinson's disease based on your medical
history, a review of your signs and symptoms, and a neurological and physical exam.
Imaging tests such as MRI, ultrasound of the brain, SPECT and PET scans may
also be used to help rule out other disorders. Imaging tests aren't particularly helpful for
diagnosing Parkinson's diseases
Medications include:
Levodopa : Drugs of Choise Levodopa, the most effective Parkinson's disease
medication, is a natural chemical that passes into your brain and is converted to
dopamine.
Carbidopa-levodopa. Levodopa, the most effective Parkinson's disease medication, is
a natural chemical that passes into your brain and is converted to dopamine.Levodopa is
combined with carbidopa , which protects levodopa from premature conversion to
dopamine outside your brain, which prevents or lessens side effects such as nausea.
Dopamine agonists. Unlike levodopa, dopamine agonists don't change into dopamine.
Instead, they mimic dopamine effects in your brain.
MAO-B inhibitors. These medications include selegiline (Eldepryl, Zelapar) and
rasagiline (Azilect). They help prevent the breakdown of brain dopamine by inhibiting the
brain enzyme monoamine oxidase B (MAO-B). This enzyme metabolizes brain
dopamine. Side effects may include nausea or insomnia.
Catechol-O-methyltransferase (COMT) inhibitors. Entacapone (Comtan) is the
primary medication from this class. This medication mildly prolongs the effect of
levodopa therapy by blocking an enzyme that breaks down dopamine.
Anticholinergics. These medications were used for many years to help control the
tremor associated with Parkinson's disease. Several anticholinergic medications are
available, including benztropine (Cogentin) or trihexyphenidyl.
Amantadine. Doctors may prescribe amantadine alone to provide short-term relief of
symptoms of mild, early-stage Parkinson's disease. It may also be given with carbidopa-
levodopa therapy during the later stages of Parkinson's disease to control involuntary
movements (dyskinesias) induced by carbidopa-levodopa.
Surgical procedures
Deep brain stimulation. In deep brain stimulation (DBS), surgeons implant electrodes
into a specific part of your brain. The electrodes are connected to a generator implanted
in your chest near your collarbone that sends electrical pulses to your brain and may
reduce your Parkinson's disease symptoms.

64
Trigger / scenario
A 62 year old man, Balinese, Hinduism came to hospital with main complaint tremble of
both hand since six month ago. On examination we found resting tremor on the right hand more
severe then left hand.
1. What are other things that have to be asked in this patient?
2. What are the physical examination that you should look in this patient ?
3. How to make proper diagnosis in this patient ?
4. What is your diagnostic procedures suggestion ?
5. What is diffrential diagnosis of this patient ?
6. What is the management of this patient ?
7. What other education should be given to this patient ?
8. When this patient should be referred to neurologic expertise?
Learning task.
1. What are the pathology and pathogenesis of PD ?
2. Please describe pathophysiology of PD.
3. What are diagnostic criteria in PD?
4. Please describe management of PD.
5. Please describe differential diagnosis of PD.
6. Please describe what synmptoms and sign non motor Parkinson disease?
7. Please describe about dyskinesia, on of phenomenone, freezing ?
Self assesment
1. Please describe basal ganglia component.
2. Please describe circuit of basal ganglia.
3. Please describe role of neurotransmitter in basal ganglia.
References :
1. Parkinson Disease and Movement Disorders by : T.N Mehrotra, Kalyan
B.Bhattachharyya.
2. Principles and Practice of Moveement Disorders by : Stanley Fahn, Joseph Jankovic,
Mark Hallet.

65
LECTURE 12
NEUROPATHIC PAIN
Dr. dr. Thomas Eko Purwata, Sp.S(K), FAAN*
Aims:
Know the current definition of neuropathic pain, the epidemiology, classification and
etiological, anatomical or mechanism based of neuropathic pain. Clinical characteristic,
diagnostic work-up including history, clinical examination and treatment of neuropathic pain.
Learning outcome
1. Definition
Recognize that neuropathic pain is a consequence of injury or disease affecting the
somatosensory system.
2. Epidemiology
- Know that painful peripheral neuropathy is common complication in HIV/AIDS,
diabetes, alcoholism and vasculitis.
- Know that 4 out of 5 patients with idiopathic polyneuropathy and 1 in 3 patients with
Guillain Barr syndrome have neuropathic pain.
- Know that peripheral neuropathic is common after surgical procedure, as well as during
treatment with chemotherapeutic agents.
3. Etiology
- Know the common causes for neural damaged and subsequent pain i.e.: metabolic
disease, infection, ischemia, injury, entrapment, connective tissue disease, AIDS,
malignancy, drugs and toxins.
- Know that neuropathic pain may develop without any identifiable cause (e.g.,
intercostal neuralgia, idiopathic polyneuropathy).
- Know that painful neuropathy may be the first manifestation of a systemic disease.
4. Clinical characteristic of neuropathic pain
- Know the common symptoms associated with neuropathic pain e.g., burning pain,
electric shock-like pain, pain paroxysm, dysesthesia and paresthesia.
- Know the common signs associated with neuropathic pain including positive
(mechanical and thermal allodynia and hyperalgesia, temporal and spatial summation),
negative (sensory loss, weakness and muscle atrophy) and other signs (neuroma
signs, referred sensation, swelling, skin flare and discoloration, hyperhidrosis and
trophic changes).
- Know that the patient with neuropathic pain may have concomitant non-neuropathic
pain.
- Know that questionnaires have been developed to differentiate neuropathic pain from
non-neuropathic pain, e.g., the LANSS Pain Scale and the Neuropathic Pain
Questionnaire or to measure various characteristics, e.g., the Neuropathic Pain Scale
and the Neuropathic Pain Inventory.
5. Pathological changes in nervous system
- Know the pathological changes that occur the affected nerves e.g. Wallerian
degeneration, sprouting and neuroma formation.
66
6. Know pathophysiological mechanisms in peripheral and central nervous system.

7. Know diagnostic work-up including history, clinical examination and treatment of
neuropathic pain.
Abstract
The new definition of neuropathic pain according International Association for Study of
Pain (IASP) is a consequence of injury or disease affecting the somatosensory system. For the
vast majority of neuropathic pain diagnostic entities, there is no precise information about
percentage of subjects reporting neuropathic pain. However it has been estimated that about
5% of patient with traumatic injury suffer from pain. Further about 8 % of stroke patients suffer
from central neuropathic pain as do about 28% of patients with multiple sclerosis and about
75% of patients with syringomyelia.
Neuropathic pains are classified according either to the etiological diagnosis of the
neuropathy (e.g., painful diabetic neuropathy, postherpetic neuralgia or post traumatic
neuralgia), or to the anatomical site of the lesion (e.g., central or peripheral pain).
Basic research in animal models of neuropathic pain indicates that multiple
pathophysiological mechanism may be at play in neuropathic pain condition.
Clinical characteristic of neuropathic pain were varied. The common symptoms associated
with neuropathic pain e.g., burning pain, electric shock-like pain, pain paroxysm, dysesthesia
and paresthesia. The symptoms of neuropathic pain including positive (mechanical and thermal
allodynia and hyperalgesia, temporal and spatial summation), negative (sensory loss, weakness
and muscle atrophy) and other signs (neuroma signs, referred sensation, swelling, skin flare
and discoloration, hyperhidrosis and trophic changes).
Diagnostic work-up including collection of medical history, focused at exploring the onset
of pain and posssible association with current diseases, trauma, surgery etc.
Therapeutic intervention applied in neuropathic pain consist of pharmacological and
nonpharmacological approach.
Common pharmacological approaches used for neuropathic pain including: sodium and
calcium channel blocker, NMDA receptor blocker, antidepressant, anti convulsan and opioid.
NSAID is not responsive for treatment neuropathic pain.
Scenario
A 55 years old man complaint parasthesia in both his legs accompanied by electric shock
like pain especially in bed time. Patient refused use blanked when he sleeps although the
weather is very cool, the reasons were he felt pain on his legs when contact with contact with
blanked. Past history: he has been suffering diabetes since 6 years ago, with un controlled
blood glucose.
Learning task:
1. What is the type of the pain in this patient?
2. Describe the pathophysiology of the pain in this patient!
3. What is the management of this patient?

67
Self assesment
1. What is the classification of neuropathic pain?
2. Explain the mechanism of neuropathic pain!
3. Explain the clinical manifestation of neuropathic pain!
4. Explain the management of neuropathic pain!
Learning Resource
1. Justins DM. Pain an Update Review. IASP Press, Seattle, 2005
2. Bonica Management of Pain, 2001
3. Loeser JD. The Kyoto protocol of IASP Basic Pain Terminology Pain 137 (2008), 473-7
4. Mogil J. Pain 2010 an Updated Review. IASP Press, Seattle, 2010.

68
LECTURE 13-14
HEADACHE (TENSION TYPE HEADACHE, CLUSTER HEADACHE, MIGRAIN) AND
TRIGEMINAL NEURALGIA
Dr. dr. Made Oka Adnyana, Sp.S(K)*
Aims
Diagnosis work up, management of primary headaches (tension type headache, cluster
headache, migraine), and trigeminal neuralgia.
Learning outcome
1. To describe the definition of headache.
2. To describe the pathophysiology of headache.
3. To differentiate primary and secondary of headache.
4. To diagnosis primary headaches (tension type headache, migraine, and cluster
headache).
5. How to manage primary headache (pharmacology, non pharmacology), and trigeminal
neuralgia.
Curiculum content
1. Nerve innervation of head.
2. Pain sensitive structures of the head.
3. Physiology of trigeminal nociception.
4. Classification of primary headaches.
5. Clinical sign and symptom of primary headaches.
6. Treatment of primary headaches.
Abstracts
Headache is the most common complaint in neurology medical practice. Headache
divided into primary and secondary. In differentiating both classes, we need to find the red flag
sign. Secondary headache is assumed for their existence. Red flag sign are sign and symptoms
those need further investigation because of their more dangerous underlined disease. Primary
headache consist of tension type headache, migraine, cluster headache and other primary
headache.
To diagnose primary headache we need more about of headache, because physical
examination and laboratory result usually normal.
Treatment of primary headache consist of pharmacology (analgetic) and
nonpharmacology management. Treatment with analgetic must be carefully, because over use
of analgetic could make a drug over use headache.
Trigeminal neuralgia is a group of symptoms characterized by severe pain attacks
accompanied sudden spasm of the face in a short time, which is limited to the areas served by
dermatomes of the trigeminal nerve. Between attacks there is usually pain free. Treatment of
trigeminal neuralgia is with anticonvulsants and surgery.

69
Trigger/scenario.
A 20 years old woman, came to the neurology clinic, with complain of headache, tight or
pressing sensation on head, bilateral each episode lasts in 4 hours. Headache attacks 15
times/month.
Learning task.
1. What symptom we should ask to the patient?
2. What is diagnosis of this case?
3. How to manage this patient?
A 21 yers old boy complain of unilateral headache since yesterday. He experienced

severe pain around the eye ball. With red and watery eye as well. While having the attack in
experienced vomitting, nausea. First attack was occurred at age of 20, happened 8 times/ day
without remission And finally the distance between eyelids got smaller when he had headache.
Learning task
1. What other symptom we should know to diagnose this case?
2. What could be the possible diagnosis?
3. How is the management?
A 20 years old men complain unilateral headache since 5 days ago. She experienced
several pain in the left side of head. She also experienced blured vision about 60 minute before
headache. Blurred vision lasting about 25 minutes. 2-3 days before attack he suffer from
depression, loss appetite. Headache attack 3 time/ weeks. First attack was occurred by age 15
years old. Her mother has the same symptom.
Learning task
1. What other symptom we should know to diagnose this case?
Self assessment
1. Describe pain sensitive structure of the head!
2. Describe pathophysiology of headache!
3. How to differentiate primary and secondary headache!
4. Describe what is the red flag!
A 40 years old man complaints severe pain on left side of the face especially when
washing the face, sensation of pain as such as burning and lasting a few minutes.
Learning task
1. What other symptom we should know to diagnosis this case?
Self assessment
1. Describe anatomy of trigeminal nerve!
2. Describe pathophysiology neuralgia trigeminal!
3. How to How to differentiate primary and secondary headache, trigeminal neuralgia, and
primary headache (cluster headache)?
70
LECTURE 15
NEURORADIOLOGY OF BRAIN AND SPINE
dr. Made Widhi Asih, SpRad(K)*
*Radiology Department, School of Medicine, Faculty of Medicine, Universitas Udayana
Aim
Describe the neuroimaging modalities for brain and spine.
Learning outcome
1. Know the neuroimaging modalities for brain and spine.
2. Understand the basic principle of each neuroimaging modality.
3. Understand the advantage and disadvantage of each neuroimaging modality.
4. Be able to choose the appropriate radiology examination for neurology case.
Abstract
Neuroradiology is a subspeciality of radiology focusing on the diagnosis of abnormalities
of the central nervous system, peripheral nervous system, spine, head, and neck
using neuroimaging techniques.
Some of the most common imaging modalities used in neuroradiology include CT or
Computed Tomography scanning and MRI or Magnetic Resonance Imaging. Plain radiography
is utilized on a limited basis and ultrasound is used in limited circumstances, in particular in the
pediatric population. Angiography is another common modality which looks inside the blood
vessels. Traditionally angiography has involved the use of X-ray technology, but more and more
angiograms are using CT or MRI technology instead. The CT or MR Angiography is an
examination used for diagnosis of vascular abnormalities or diagnosis and characterization of
masses or other lesions related to vascular myelography is another imaging modality commonly
used in neuroradiology which using a contrast agent to detect pathology in the spinal cord. All
modalities used in several ways to image the nervous system, however they each have their
advantages and disadvantages, which should be considered in determining the modalities that
will be chosen in neurological cases.
Case 1
An old man was escorted by his family to the hospital with complaints of upper and lower
extremity weakness since yesterday morning. History of hypertension for 5 years, no previous
history of trauma.
Learning Task
1. What is the differential diagnosis of this patient?
2. What is radiology examination will you suggest?
3. When did you need to add the contrast agent during the examination?
Self Assessment
1. Explain the advantages and disadvantages of CT and MRI!
2. Explain how to prepare the patient before radiological examinations that require contrast!

71
Case 2
A 34-year-old male comes with pain, tingling and numbness in her left lower extremity
since 6 months ago and get worsen since the last month. There is an excessive gym history
Learning Task :
1. What is the possibility diagnosis of this patient?
2. What is conventional radiology examination will you suggest?
3. What is advanced radiology modality that should be chosen for this case?
Self Assessment
1. Explain what should be evaluated on the vertebral X Ray
2. Explain why conventional myelography is rarely done today
Case 3
A 2-month-old male infant comes with a seizure complaint and a head size larger than
normal. The history of labor is normal.
Learning Task
2. What is conventional radiology examination will you suggest for measure the head size ?
3. What is advanced radiology modality that safe for this patient should be chosen?
Self Assessment
1. Explain the radiological sign of increase intracranial pressure on skull X-ray!
2. Explain the basic workings of a radiology modality for assessing the baby's brain safely!
Learning Resources
1. Wiliam Herring, MD. Learning Radiology : Recognizing the Basics. Saunders; 3rd ed;
April 30, 2015
2. Michael Y.M. Chen, Thomas L. Pope David J. Ott, Basic Radiology. Lange : 2nd ed,
2011; 325 396
3. David Sutton. Radiology and Imaging for Medical Student. Elsevier Health Sciences. 7th
ed, Sept 1998.

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LECTURE 16
ACUTE AND REFERRED PAIN
Dr. dr. I Putu Pramana Suarjaya, Sp.An. KMN, KNA, M.Kes*
*Anesthesiology Department, Faculty of Medicine, Universitas Udayana
AIMS
Describe mechanism of Acute and Referred Pain and function of pain.
LEARNING OUTCOMES
Apply its concepts and principles in acute pain patient setting.
CURRICULUM CONTENTS
1. Describe basic mechanism of pain
2. Describe neuronal circuit processing of pain
3. Describe role of neurotransmitter in central and peripheral nervous system
ABSTRACTS OF LECTURES
Pain is a personal, subjective experience that involves sensory, emotional and
behavioural factors associated with actual or potential tissue injury, or described in term of such
damage. What patients tell us about their pain can be very revealing, and an understanding of
how the nervous system responds and adapts to pain in the short and long term is essential if
we are to make sense of patients experiences.
Although acute pain and associated responses can be unpleasant and often debilitating,
they serve important adaptive purposes. They identify and localize noxious stimuli, initiate
withdrawal responses that limit tissue injury, inhibit mobility thereby enhancing wound healing,
and initiate motivational and affective responses that modify future behavior. Nevertheless,
intense and prolonged pain transmission, as well as analgesic undermedication, can increase
postsurgical/traumatic morbidity, delay recovery, and lead to development of chronic pain. The
wide area of discomfort surrounding a wound, or even a wound that has healed long ago, such
as an amputation stump, is a natural consequence of the plasticity of the nervous system.
An understanding of the physiological basis of pain is helpful to the sufferer, and the
professional who have to provide appropriate treatment. Understanding the anatomical
pathways and neurochemical mediators involved in noxious transduction, transmission,
modulation and pain perception is key to optimizing the management of acute pain.
According to the International Association for the Study of Pain (IASP), pain is defined as
An unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in term of such damage (IASP 1979). With regard to a more recent
classification, pain states may be characterized as physiologic pain, nociceptive/inflammatory
pain (acute pain) , or neuropathic pain (chronic pain).
Physiologic pain defines rapidly perceived nontraumatic discomfort of very short duration.
Physiologic pain alerts the individual to the presence of a potentially injurious environmental
stimulus, such as a hot object, and initiates withdrawal reflexes that prevent or minimize tissue
injury.
Nociceptive pain (acute pain) is defined as noxious perception resulting from cellular
damage following surgical, traumatic, or disease-related injuries. Nociceptive pain has also
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been termed inflammatory pain because peripheral inflammation and inflammatory mediators
play major roles in its initiation and development. In general (but not always) the intensity of
nociceptive pain is proportional to the magnitude of tissue damage and release of inflammatory
mediators.
Neuropathic pain (chronic pain) is defined by the International Association for the Study of
Pain as pain initiated or caused by a pathologic lesion or dysfunction in peripheral nerves and
CNS. Neuropathic pain is usually constant and described as burning, electrical, lancinating, and
shooting.
A major barrier to appropriate pain management is a general misperception that pain and
nociception are interchangeable terms. This encourages the belief that every individual will
experience the same sensation if given the same stimulus.
Non Steroid Anti-inflamations Drugs (NSAIDs) have analgesic, anti-inammatory, and
antipyretic properties. They are indicated in the relief of mild to moderate pain associated with
injury, inammation in skin, ligaments, muscles or bone, postoperative pain, dysmenorrhea,
headache, and renal or biliary colic. They can be used in conjunction with opioids for more
severe pain.
Worldwide, opioids remain the mainstay for the treatment of moderate to severe acute
pain. An opioid is any substance with a pharmacological action at the opioid receptor; an opiate
is a naturally occurring opioid.
Referred pain, also called reflective pain, is pain perceived at a location other than the site
of the painful stimulus. An example is the case of angina pectoris brought on by a myocardial
infarction (heart-attack), where pain is often felt in the neck, shoulders, and back rather than in
the thorax (chest), the site of the injury. The International Association for the Study of Pain has
not officially defined the term; hence several authors have defined the term differently.
CASE
A 45 years old woman was admitted to emergency unit with broken left lower arm and
bruishing in her left foot due to motorcycle accident. She was fully conscious. She was crying for
those pain. It was so painful, she told the physician at the emergency unit. After through
examination and diagnosis was made, she brought to the operating theatre for close reduction
for the broken left lower arm and wound toilette under general anesthesia. The anesthesiologist
gave some non steroid anti-inflammation drug and opioid analgesic after the procedure. She
looks comfortable in post anesthesia care unit and discharge at the same day, given oral
analgesic (and antibiotics).
LEARNING TASK
1. Describe mechanism/ pathophysiology of pain in this patient?
2. How should we manage the pain in this patient?
3. What is the risk of under-treatment in the acute pain patients?
SELF ASSESMENT
1. What is meant by analgesia?
2. What is hyperalgesia?
3. What is the goal of Pain therapy?
4. What is neuroplasticity in pain and explain the mechanism?
74
LECTURE 17
VERTIGO, BELLS PALSY, MENIERE DISEASE
dr. Ketut Widyastuti, Sp.S*
AIMS:
Describe diagnosis, initial management and rehabilitation therapy for Vertigo, Meniere
disease and Bells Palsy.
LEARNING OUTCOME:
1. Describe vestibular system anatomy and function and how it relates to the clinical exam
and vestibular function tests.
2. Distinguishes vestibular and non vestibular vertigo symptom.
3. Distinguishes between peripheral vestibular vertigo and central vestibular vertigo.
4. Describe a detailed examination of the patient with vertigo including the patient history
and subjective exam, include Romberg Test, Fukuda Test and Dix Hallpike.
5. Describe the various appropriate treatment for BPPV and Meniere Disease.
6. Describe the rehabilitation treatment for vertigo.
Curriculum contens:
1. History taking of Dizziness and vertigo.
2. Physical Examination of vertigo patients.
3. Treatment and rehabilition management for vertigo.
4. Prognosis in vertigo cases.
ABSTRACTS
The CNS coordinates and integrates sensory input from the visual, vestibular, and
proprioceptive systems. Vertigo arises from a mismatch of information from two or more of the
involved senses, caused by dysfunction in the sensory organ or its corresponding pathway.
Visual inputs provide spatial orientation. Proprioceptors help relate body movements and
indicate the position of the head relative to that of the body. The vestibular system (via the
otoliths) establishes the body's orientation with respect to gravity. The cupulae's sensors track
rotary motion. The three semicircular canals sense orientation to movement and head tilts and
are filled with a fluid called endolymph. The endolymphatic sac produces glycoproteins that
create an osmotic sink necessary to maintain flow.
Vertigo refers to the subjective feeling of movement of self or the environment in the
absence of true movement. Vertigo is a frequent symptom that results from a variety of
etiologies, some benign and others serious. One of the more important differentiating features is
determining if the vertigo has a peripheral or central etiology.
Peripheral vertigo generally refers to vertigo which arises from dysfunction of the
vestibular apparatus in the inner ear or its connecting vestibular nerve (CN VIII). In addition to
hearing, the inner contains the bony labryinth where the semicircular canals and utricle/saccule
are located. These structures sense linear and angular motion, and are essential in the
maintenance of balance and various vestibular reflexes.

75
Central vertigo results from dysfunction of the central connections of the vestibular
apparatus including the vestibular nuclei in the brainstem and their connections, especially to
the cerebellum. The vestibular nerve (CN VIII) is usually considered part of the peripheral
vestibular system (essentially being a peripheral nerve).
Benign Paroxysmal Positional Vertigo (BPPV) is caused by displacement of the otoconia
from the utricular membrane, causing an alteration in the hemodynamics of the inner ear.
Consequently, the fluid within the inner ear lags behind movements of the head, which leads to
vertigo and nystagmus. BPPV is the most common cause of vertigo. BPPV is thought to
arise due to the displacement of otoconia (small crystals of calcium carbonate) from the
maculae of the inner ear into the fluid-filled semicircular canals. These semicircular canals
are sensitive to gravity and changes in head position can be a trigger for BPPV.The
posterior canal is the most commonly affected site, but the superior and horizontal canals
can be affected as well.
BPPV can be classified as cupulolithiasis and canalithiasis. Cupulolithiasis is when
the otoconia are adhered to the cupula and canalithiasis is when the otoconia are free
floating in the canal. Additionally, the type of nystagmus that a patient may display can be
classified as geotropic or apogeotropic. Geotropic describes the nystagmus as a horizontal
beat towards the ground. Apogeotropic describes the nystagmus as a horizontal beat
towards the ceiling.
Meniere disease also called endolymphatic hydrops, is a disorder that can affect hearing
and balance to a varying degree. Meniere disease is chronic disorder in inner ear. It is
characterized by episodes of vertigo, low-pitched tinnitus, and hearing loss. The hearing loss is
fluctuating rather than permanent, meaning that it comes and goes, alternating between ears for
sometime, then becomes permanent with no return to normal function. The condition affects
people differently; it can range in intensity from being a mild annoyance to a lifelong condition.
Meniere often begins with one symptom, and gradually progresses. However, not all symptoms
must be present to confirm the diagnosis although several symptoms at once is more conclusive
than different symptoms at separate times.
According guidelines of the American Academy of Otolaryngology-Head and Neck
Surgery (AAO-HNS), Meniere disease have four symptoms:
1. Attacks of rotational vertigo that can be mild to severe, unpredictable, and minimal 20
minutes for 1 episode, but generally no longer than 24 hours.
2. Fluctuating, progressive, unilateral (in one ear) or bilateral (in both ears) hearing loss,
usually in lower frequencies. Getting worsen during attack.
3. Unilateral or bilateral tinnitus, with characteristic low frequency or roaring noise.
4. A sensation of fullness or pressure in one or both ears.
SELF DIRECTING LEARNING

Basic knowledge that must be known:
1. Describe the other types of peripheral vertigo!
2. Describe the types of central vertigo!
3. Management of central vertigo and other peripheral vertigo.

76
Scenario 1
A 43-year old-man rolled over in the bed early morning and feeling sudden dizziness that
room was spinning around him. The spinning sensation occur less than 1 minute and
accompanied by nausea and vomiting. This had never happened to him before. The patient
denied tinnitus, hearing loss, recent viral illness and head trauma.
Learning Task
1. Take the history (remember the secret seven and fundamental four) that is needed to
make the diagnosis
2. Describe the physical examination of the patient (general neurologic and neurootologic
examination)
3. How to distinguishes patient with vestibular and non vestibular vertigo?
4. How to differentiate between peripheral and central vestibular vertigo?
6. Explain the patophysiology of that diagnosis!
7. What is the initial management of this patient ?
8. What is the prognosis of the patient?
Self Assessment
1. How to do a good history taking in vertigo cases?
2. How to do a good physical examination in vertigo cases?
3. What is the etiology of peripheral and central vertigo?
4. What is the pathogenesis of Benign Paroxysmal Positional Vertigo(BPPV) and Menieres
disease?
5. When do you refer the patient with vertigo?
Scenario 2
A woman, 36 years old, experiences episodic vertigo within 1 year, accompanied by
nausea, hear roaring noise and fullness in her ears, and there also hearing loss that more
severe in right ear. One week before the symptoms appear, she feel tired and eat much salty
food.
Learning task
1. Take the history (remember the secret seven and fundamental four) that is needed to
make the diagnosis!
2. Describe the physical examination of the patient (general neurologic and neurootologic
examination)!
4. Describe the supporting examination for this case
5. Explain the patophysiology of that main diagnosis
7. What is the prognosis of that patient ?

77
BELLS PALSY
Aims
Describe diagnosis, management and referral patients with facial palsy
Learning outcome
1. Diagnosis of Bells Palsy
2. Differential Diagnosis of Bells Palsy
3. Management for Bells Palsy
4. Prognosis of Bells Palsy
5. Further investigations and referrals
Curriculum contens:
1. History taking of Bells Palsy
2. Physical Examination of facial palsy patients
3. Investigation routine and specific of Bells Palsy
4. Management for Bells Palsy
Abstracts
Bells Palsy is clinical syndrome of idiopathic acute unilateral facial paralysis. Patients may
report the exposure to cold preceded their symptoms. The face often described as feeling stiff
and numb without any objective sensory deficit. Decrease tearing and hyperacusis may appear
in some cases may precede weakness.
The condition is thought to be related to a viral infection, the swollen nerve being entrapment in
the facial canal. Although not life threatening, BellsPalsy may have severe functional, aesthetic,
and psychological consequences.
Self directing learning

1. The anatomy of Facial nerve
2. Facial Palsy
3. Bells Palsy
4. Factors that affect Bells Palsy
Scenario
A 24-year old-medical student came to the policlinic with fascial weakness since just wake
up. He was unable to move the left side of his face. On examination was found : left nasolabial
sulcus is flatter than the right side, left corner of lip and eye difficult to close while grimacing He
worried that a serious problem, possibly a stroke, might be have occurred. He had influenza-
like symptoms the week before this sudden attack.

78
Learning task:
1. From the history above, what need to be asking to the patient? (remember the secret
seven and fundamental four)
2. Describe the physical examination of patient!
4. Where is topical diagnosis base on facial nerve pathway?
5. How to differentiate between facial palsy in Bells Palsy and Stroke patient?
6. Explain the pathogenesis from the main diagnosis that has been mention above!
7. What is the management of this patient?
8. When do we start to rehabilitate the patient?
9. What is the prognosis of that patient?
10. When do you refer the patient with Facial Palsy?
Self assessment
1. How to do a good history taking in Facial Palsy cases?
2. How to do a good physical examination in Facial Palsy cases?
3. When do you refer the patient with Facial Palsy?
Refferences
1. PERDOSSI. Pedoman dan Tatalaksana Vertigo 2012
2. Adam and Victors. Principles of Neurology 8th.
3. Pedoman Tata Laksana Vertigo, Kelompok Studi Vertigo Perhimpunan Dokter Spesialis
Saraf Indonesia (Perdossi), 2012
4. Bhattacharyya N, Baugh R.F, Orvidas L dkk. Clinical Practical Guideline: Benign
Paroxysmal Positional Vertigo. J Otolaryngology-Head and Neck Surgery 2008;139: 47-
81

79
LECTURE 18
NEUROLOGICAL ASPECT OF HEARING LOSS AND TINNITUS
dr. Ida Ayu Sri Indrayani, Sp.S*
AIM
To be able to describe the conditions of hearing loss and tinnitus, to know the current
definition of hearing loss and tinnitus, as well as its etiology and the underlying mechanisms
hearing loss and tinnitus, clinical presentation, and diagnostic work-up, including clinical
examination and early management of hearing loss and tinnitus.
LEARNING OUTCOMES:
1. To understand the degree of hearing loss and definition of tinnitus.
2. To understand the neuroanatomy of ears, neurophysiology of hearing, and how to
perform the eighth nerve neurological examination.
3. To understand and be able to explain the etiology and underlying mechanisms hearing
loss and tinnitus.
4. To be able to obtain a comprehensive history, perform a clinical examination and assess
the hearing loss and tinnitus.
5. To understand the early management and diagnostic planning for hearing loss and
tinnitus, as well as to know when, how, and to whom the patient shall be referred to (i.e.
whether to a neurologist or and ENT doctor).
ABSTRACT
In order to be able to understand the underlying mechanism of hearing loss, one shall
comprehend the definition of pure tone, noise, and frequency (wherein the amount of vibrations
per second is stated in Hertz [Hz]), and sound in the first place. Furthermore, sound intensity is
stated in decibel (dB), hearing capacity, and the degree or severity of hearing loss. Moreover,
one shall also understand the neuroanatomy and neurophysiology of hearing process, as well
as to learn how to perform the eighth cranial nerve (i.e. the vestibulocochlear nerve). As widely
known, vestibulocochlear nerve consists of two different functional components, which are the
vestibular nerve that is responsible for balance, and cochlear nerve which is responsible for
hearing.
Vestibular nerve delivers impulses which originated from organs whose its function is to
maintain balance (e.g. semicircular duct, utricle, and sacculus). It records the movement and
position of the head with its relation to maintain and adjusting the balance. On the other hand,
cochlear nerve is responsible for hearing impulses delivery which originates from the organ of
Corti inside the cochlea.
The external ear consists of an earlobe which projects to the ear canal until it terminates in
the tympanic membrane. Furthermore, the middle ears shape is like a cubicle with its outer,
frontal, lower, and posterior borders consist of tympanic membrane, Eustachian tube, and
jugular vein, respectively. Meanwhile, the posterior border consists of aditus and antrum and
vertical part of the facial canal, whereas the upper border consists of tympanic tegmen
(meninges/brain parenchyma). In addition, the inner border from cranial to caudal are horizontal
semicircular canal, facial canal, oval window, round window, and promontorium. Middle ear
80
consists of cochlea which consists of three semicircular canals. Meanwhile, the tympanic and
vestibuli ducts can be seen at the tip of the cochlea. The tympanic duct or scala tympani and the
vestibular duct or scala vestibuli contain perilymph, while the cochlear duct or scala media
contains endolymph. It is worth mentioning that perilymph has different composition when
compared with endolymph in terms of sodium and other ionic compositions. This is essential for
hearing process.
Physiology of hearing involves someone who can hear voices or noises due to the
conducted vibrations via either air or bone, which the former is considered to be better. Sound
vibration is captured by the earlobe and then transmitted to the ear canal until it vibrates the
tympanic membrane. This vibration is then further conveyed to the hearing bones which in turn
be transmitted to the perilymph inside the scala vestibuli. Furthermore, it presses the endolymph
and subsequently push the basal membrane, thus bulging out downward and moves the
perilymph inside the scala tympani. On resting period, the tip of hair cells are on a convoluted
formation, which straighten up upon the movement of the basal membrane. These physical
stimuli are initiated by the ion gradient between potassium and sodium to generate action
potential which is transmitted to the eighth nerve branch, and ultimately be passed to the
primary hearing area in the brain (i.e. Broamann area 39-40) via the central nervous system in
the temporal lobe.
Hearing disturbance can happen on outer, middle, or inner ear. Hearing problem in the
outer and middle ear can cause conductive healing loss, while problems in the inner ear can
cause sensorineural deafness.
Hearing loss can be divided into three types, i.e. conductive, sensorineural, or mixed
hearing loss. In conductive hearing loss, there is an impaired sound conduction due to a
disorder or disease in the outer or middle ear. Meanwhile, on nerve deafness (i.e. perception or
sensorineural hearing loss), the problem exists in the cochlea (i.e. inner ear), on the eighth
cranial nerve, or located in the primary auditory area in the temporal lobe (Broadmann 39-40).
Hearing capacity can be measured and tested using audiological test, comprising basic
audiology (1), tuning fork test (2), and whispering test (3). Pure tone audiometry and special
audiology test which uses biometric device are typically done by an ENT doctor.
The neurological functions of hearing can examined through (1) tuning fork. This test is a
qualitative assessment, similar to Rinne, Schwabach, and Weber tests. This test is conducted
by using the tuning fork with common accepted frequencies, such as 512, 1024, and 2048 Hz.
In order ease the clinical interpretation, the aforementioned tests are performed simultaneously.
Meanwhile, further supporting examinations can also be done, including radiological
assessments using head contrast-CT scan or MRI, and neurophysiological examination like
Auditory Evoked Potential (BAEP) which is usually done by a neurologist.
Various disorders can induce hearing loss, for example conductive hearing loss can be
caused by an infection (Eustachian tube blockade, otitis media, otosclerosis, tympanic-sclerosis,
hemotympanum, and hearing bone dislocation) on the outer and middle ear. Meanwhile,
sensorineural (perceptive hearing loss) can be due to aplasia or congenital factor, viral or
bacterial labyrinthitis, drug intoxication, acoustic trauma, or head trauma. On the other hand,
retrocochlear sensorineural hearing loss can be caused by cerebellopontine angle tumors, like,
for instance, acoustic neuroma, in which clinical neurological deficits can be readily observed
such as facial hemiparesis due to facial nerve palsy, chronic progressive headache, multiple

81
myeloma, brain damage and hemorrhage, meningitis (meningitis Suis), and other brain
disturbances.
Tinnitus is an abnormally heard sound which is derived from inside of the head. Tinnitus
can be classified as objective and subjective. Tinnitus can be divided according to its intensity,
i.e. high- or low-pitched tinnitus. Tinnitus can appear in a continuous manner or wax and wane.
Tinnitus is usually linked to sensorineural and conductive hearing loss. Low-pitched tinnitus with
conduction problem is usually caused by a blockade, tumor, or middle and outer ear infection. In
addition, low-pitched tinnitus with pulsation in the absence of any hearing problem is a sign of
early jugular glomus tumor. On the other hand, objective tinnitus is often caused by vascular
problems. Disorder of the jugular vein in the form of an aneurysm can cause a tinnitus with a
similar rhythm to the heart beat.
Tinnitus treatment is a complex issue, along with difficulties in determining its cause, albeit
the cure can be pursued by treating the underlying cause. Often times, the masking and
diversion efforts of tinnitus can become a practical solution which can readily be trained and
adapted to the patient, for instance, the patient is asked to mask the tinnitus by listening to the
load noise of a cooling fan, air conditioner, or radio. The patient shall be given detailed
information regarding his/her illness, thus providing reassurance instead of panic, in which the
latter can sometimes be able to exacerbate the tinnitus complaints. It should also be explained
to the patient that tinnitus is difficult to treat and it is advisable to self-train and adapt to this
disorder.
SCENARIO CASE
A 43 y.o right-handed woman presents to the neurological clinic with hearing loss, facial
paralysis, and headache. Her story began one month ago with a sudden decrease in hearing on
her right ear. One week prior to this visit, she began to notice weakness of the right face, which
has now progressed to complete paralysis. Over last 3 months she had an intermittent right
occipital headache, clumsiness and postural imbalance if she turns quickly. She denies any
change in her voice or difficulty with swallowing or swallowing difficulty. Her past medical history
is unremarkable. She is currently not on any medications except birth control pills. Her physical
examination shows a 43 y o woman that has an obvious right facial paralysis. Her pulse is 62
beats/ min; blood pressure 118/62 mm Hg; and temperature 36.7 C ( 98,6 F). The Head and
face bear no lesions. Her voice is normal, but her speech is slightly distorted because of the
facial paralysis. Her extra occular movements are normal. Her eye grounds do not show any
papil oedema. Her ears have normal tympanic membranes. The Weber test tuning fork
lateralizes to the left ear. Air conduction is louder than bone conduction in both ears. There is no
neck lymphadenopathy or other masses. An Audiogram shows a mild sensorineural hearing
loss in the right ear; the left ear has normal hearing. An Auditory brain steam response is
abnormal for the right ear; it is normal for the left ear.
SELF ASSESSMENT
1. What is the most likely neuroanatomical etiology and the diagnosis?
2. Why can the patient suffer from hearing problem and facial weakness?
3. What is the next diagnostic step?
4. When and where will you refer the patient?

82
LEARNING RESOURCES:
1. Claudia Krebs,Weinberg, Akesson. Neuroscience, Wolters Kluwer heath .Lippincott
Williams & Wilkins.2012.
2. Fakultas Kedokteran Universitas Indonesia,. Buku Ajar Ilmu Kesehatan Telinga Hidung
Tenggorokan; Ed 4, hal 9-84.2000
3. E. Sukardi. Neuroanatomia Medica. Universitas Indonesia Press.1984.
4. Toy,Simpson,Pleitez, Rosenfield, Tintner. Case Files.432-440. Mc Graw Hill. New
York.2008.

83
LECTURE 19 - 20
STROKE: TIA, CEREBRAL INFARCTION, ICB, SAH AND ITS MANAGEMENT
dr. IGN Budiarsa, Sp.S*
Aims
Describe diagnosis, management and referral patients with stroke.
Learning outcome:
Describe pathogenesis, clinical aspect, examination, and management of stroke patient.
Curriculum contents
1. Ischemic stroke.
2. Hemorrhagic stroke.
Abstract
Stroke is a clinical diagnosis made on the characteristic temporal profile of neurological
symptoms and signs, as examplified by the WHO definition: Rapidly developing clinical signs of
focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer, or
leading to death, with no apparent cause other than of vascular origin.
Stroke is the third most common cause of death worldwide (after coronary heart disease
and all cancers combined) and the major cause of disability. The most frequent cause of stroke
is a localized disturbance of cerebral circulation, i.e., cerebral ischemia/infarction (ischemic/non
hemorrhagic stroke). Ischemic stroke classification is base on five subtype: large artery
atherothrombosis-thromboembolism, embolism from the heart, small vessel disease, uncertain
cause, and rare causes. Less common are hemorrhagic stroke (spontaneous intra cerebral
hemorrhage and subarachnoid hemorrhage). Subarachnoid hemorrhage is the exception to this
definition and usually presents without focal neurological deficits.
Stroke typically manifest abruptly, resulting in a maximum deficit usually within hours and
lasting longer than 24 hours. If a patients focal neurological deficit lasts less than 24 hours, it is
arbitrarily defined as a TIA (transient ischemic attack). Clinical history, examination and
investigation will separate infarction and hemorrhage. When a clear account of symptoms is
available, the clinical diagnosis of stroke works well and the risk of mistaking a nonvascular
lesion for stroke is very small. When the history is not so clear, however, because the patient is
unconscious, confused, or aphasic and the event has no reliable witnesses, the diagnosis is
more difficult and the chance of misdiagnosis is high. In these situations, CT (computed
tomography) or MRI (magnetic resonance imaging) is important to exclude non-stroke
diagnoses such as traumatic subdural hematomas or malignancy.
Treatment aims, prevent progression of present event, prevent immediate complication
and the development of subsequent event, rehabilitation and stroke prevention.

84
Trigger/scenario
A 67 years old women with a history of type 2 diabetes mellitus and atrial fibrillation
pressents to the emergency room with left body weakness and slurred speech. The onset was
sudden while she was brushing) her teeth 2 hours ago, and she was brought immediately to the
emergency room. Physical exam findings include blood pressure of 105/90 and irregularly
irregular heartbeat. GCS 15. Paralysed from the left side of the body, with the face and upper
extremity being worse than the lower extremity. Routine chemistries and cell counts are normal.
Self assessment
2. What is the diagnosis tools you made to make definite diagnosis?
Learning Task
1. Pathogenesis of stroke.
2. Clinical aspect and diagnostic tools for stroke.
3. Management and prevention of stroke.
Trigger/scenario
A 53 years old women with a history of type 2 diabetes mellitus and atrial fibrillation
pressents to the emergency room with slurred speech and right body weakness. The onset was
sudden while she was swimming 1 hour ago, and she was brought immediately to the
emergency room. Physical exam findings include blood pressure of 95/70 and irregularly
irregular heartbeat. GCS 15. Paralysed from the right side of the body, with the face and upper
extremity being worse than the lower extremity. Routine chemistries and cell counts are normal.
Self assessment
2. What is the diagnosis tools you made to make definite diagnosis?
Learning Task
1. Pathogenesis of stroke.
2. Clinical aspect and diagnostic tools for stroke.
3. Management and prevention of stroke.

85
LECTURE 21
SURGICAL ASPECT OF CEREBROVASCULAR ACCIDENTS (CVA)
dr. I Wayan Niryana, M.Kes, SpBS(K)*
*Surgery Department, School of Medicine, Faculty of Medicine, Universitas Udayana
AIMS
Provide initial assessment and management, established tentative diagnosis, proposed
definitive management, and prognosis patient with CVA.
LEARNING OUTCOME
The student know what is management and the surgical indication of CVA
CURRICULUM CONTENTS
Cerebrovascular Accidents (CVA)
1. Etiology and Pathophysiology of Cerebrovascular disease.
2. Clinical Features and Investigations of Cerebrovascular disease.
3. Management and Surgical Indication for Cerebrovascular disease.
ABSTRACTS
Due to the improvement of the treatment of ischemic heart disease over ischemic or
hemorrhagic brain disease over the last 10 years, more and more patients can benefit from non
surgical and surgical intervention. The nineties have been called the decade of the brain in
developed countries where brain attack has been treated as aggressively as heart attacks. Thus
it is now the time for all developing countries to follow the same pathway.
Next to heart disease and cancer, cerebrovascular disease is the most frequent cause of
death in the western world. And at least one-half of all neurological patients in general have
some type of cerebrovascular disease. The term cerebrocvascular disease denotes any
abnormality of the brain resulting from a pathologic process of blood vessels, be they arteries,
arterioles, capillaries, veins, or sinuses. The pathologic change in the vessels takes the form of
occlusion by thrombus or embolus, or of rupture, and the resulting abnormalities in the brain are
of two types: ischemia, with and without infarction, and hemorrhage. Rarer forms of
cerebrovascular disease are those due to altered permeability of the vascular wall and
increased viscosity or other changes in the quality of blood. The latter changes underlie the
strokes that complicate diseases such as sickle-cell anemia and polycythemia and account for
the headache, brain edema, and convulsions of hypertensive encephalopathy.
From all of Cerebrovascular accidents 25% present with intracerebral haematoma (ICH)
and account for 2-4% of all deaths. They are twice as common as SAH. Over two thirds are
known to be fatal. The patients are usually middle aged or over, with a male preponderance.
The incidence is about 1 per 10,000 with a 30day mortality of 44%.
Etiology: There are two categories, primary and secondary.

Primary ICH:
It is associated with hypertension and distinct from hemorrhagic infarcts. It has been
suggested that hypertensive changes in the arterial wall, such as, hyaline degeneration, and
micro aneurysms are at fault. Another suggestion is the thin walled vessels (such as
86
lenticulostriates), originating directly from the main vessel are subjected to higher intravascular
pressure than the cortical vessels and tend to rupture. Eighty percent of them are
supratentorial. Mostly, the location is central and deep.
Secondary ICH:
It is associated with a medical condition other than hypertension, representing about 20%
of all ICHs. They may be due to:
Coagulopathies (10-15%)-Among these, platelet disorders are important. About 5% of those
receiving heparin, irrespective of the dosage, develop thrombocytopenia. The platelet defects
may be hereditary (Von Willebrands disease) or acquired through drugs (Aspirin, penicillin, or
new cephalosporins) or through disease (myeloproliferative and dysplastic disorders, uremia,
cirrhosis, SLE, multiple myeloma).
Arterio Venous Malformations (AVMs (7%) represent a heterogeneous group with different
histological types (cavernoma, AVMs, venous angioma and capillary telangiectosis).
Vasculopathies (5%), such as cerebral amyloid angiopathy, polyarterites nodosa and
necrotizing vasculopathy in drug abusers, tend to produce multiple subcortical haematomas.
Tumors (2%) such as glioblastoma and metastasis tumors such as, melanoma,
choriocarcinoma, renal cell carcinoma and bronchogenic carcinoma, are the most frequent
tumors in producing ICH.
Pathophysiology:
The haematomas may be massive (>5cm) with extension into the ventricles or may be
small (<1.5 cm). The extravagated blood forms a roughly circular or oval mass which grows in
volume for a brief period. Adjacent brain tissue is displaced and compressed resulting in
extensive edema and ischemia. Ischemic area may be much larger than the area of clot.
Cerebellar and brainstem ICH may produce obstructive hydrocephalus which may add to the
problems. In large hemorrhage, there is midline shift and the vital centers are
compromised. Rebleeding is rare. Resolving haematomas may develop into a cyst over a period
of months, with a gliotic wall which may be orange colored due to haemosiderin laden
macrophages.
Clinical features:
It depends on the site and size of the hematoma. Sudden headache, vomiting with
depressed level of consciousness and focal signs is the usual mode of presentation. Absence of
neck stiffness may help to exclude SAH. The large ones are usually associated with LOC. In
putaminal ICH, the patient develops sudden hemiplegia with conjugate horizontal gaze deviation
towards the clot. Speech may be involved if the dominant hemisphere is involved. In thalamic
ICH, the findings are as in putaminal ICH; in addition, there may be neck retraction, paralysis of
vertical gaze with upward gaze palsy, inequality of pupils, and skew deviation with the contra
lateral eye being displaced downward and medially.
Cerebellar ICH presents with severe headache, nausea and vomiting and imbalance and
depressed level of consciousness. Pontine ICH present with coma, pin point pupils and
decerebrate rigidity. Cortical ICH may present with headache and seizures.

87
Investigations:
The CT Scan will reveal the clot and other associated features such as midline shift and
hydrocephalus. A contrast CT may suggest a vascular problem, which may necessitate an
angiography. The MRI gives a better delineation of the above; in addition the age of the
haematoma can be guessed. MRI may suggest an associated AVM. Angiography (CT
Angiography (CTA), MR Angiography (MRA), Digital Substraction Angiography (DSA)
should be carried out whenever there is a suggestion of vascular malformation, in the absence
of previous hypertension or coagulopathies before a life saving clot evacuation. When surgery is
not planned, the angiography can wait for few weeks to avoid a false negative angiography.
Coagulation studies must be done as a routine in addition to ECG, chest X-ray and other
general investigations.
Management:
Supportive care control of hypertension, reduction of ICP without compromising the CPP
and prevention of complications are the mainstay. Fluid and electrolytes and tissue oxygenation
must be closely monitored. The aim is to avoid secondary events. An aggressive decrease of
high BP may lead to cerebral ischemia. Ideally, it should not be lowered below 150mm Hg
systolic and 100 mm of Hg diastolic.
Should general measures to control the raising ICP fail, hyperventilation may help; but
must be employed with careful watch on pCo2, arterial blood pressure and preferably with ICP
monitoring as well. The CPP should not be compromised. Osmotherapy with mannitol may help
only when the serum osmolality is lower than 300 mosm/kg.Prophylactic anti convulsant therapy
is advised by most physicians with no supporting evidence.
The role of surgical intervention is controversial. Neurosurgeons and neurologists
advocate that large cerebellar hemorrhages with compression of the brain stem or obstruction of
the fourth ventricle should be surgically removed as soon as possible. Surgical removal of large
lobar hemorrhages in young patients who are clinically deteriorating has also been
recommended based on anecdotal experience. On the other hand, the results of such surgery in
hematomas within the basal ganglia and other deep structures are unacceptable. Standard
craniotomy for surgical removal of primary brain stem or thalamic hemorrhages has been all but
abandoned because of the extremely poor outcomes in almost all patients.
Craniotomy: Craniotomy and evacuation of the clot has been the standard approach for
removal of intraparenchymal hemorrhage. In addition a decompressive craniectomy with a
duraplasty is preferred by some. Its major advantage is adequate exposure to remove the clot. It
is not difficult or time-consuming. The major disadvantage of a more extensive surgical
approach is that it may lead to further brain damage, particularly in patients with deep-seated
hemorrhages. In addition, the effectiveness of clot removal by craniotomy is far from ideal.
Nonrandomized treatment series of patients with cerebellar hemorrhage report good outcomes
for surgically treated patients who have large (>3 cm) cerebellar hemorrhages or cerebellar
hemorrhages with brain stem compression or hydrocephalus. In these patients, medical
management alone often results in bad outcomes. Smaller cerebellar hemorrhages without brain
stem compression that are managed medically do reasonably well.
Guidelines for the Management of Spontaneous Intracerebral Hemorrhage (A Guideline for
Healthcare Professionals From the American Heart Association/American Stroke Association)
Stroke. 2015;46:000-000.
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Surgical Treatment of ICH: Recommendations

1. Patients with cerebellar hemorrhage who are deteriorating neurologically or who have
brainstem compression and/or hydrocephalus from ventricular obstruction should
undergo surgical removal of the hemorrhage as soon as possible (Class I; Level of
Evidence B). Initial treatment of these patients with ventricular drainage rather than
surgical evacuation is not recommended (Class III; Level of Evidence C). (Unchanged
from the previous guideline)
2. For most patients with supratentorial ICH, the usefulness of surgery is not well
established (Class IIb; Level of Evidence A). (Revised from the previous guideline)
Specific exceptions and potential subgroup considerations are outlined below in
recommendations 3 through 6. 3. A policy of early hematoma evacuation is not clearly
beneficial compared with hematoma evacuation when patients deteriorate (Class IIb;
Level of Evidence A). (New recommendation)
4. Supratentorial hematoma evacuation in deteriorating patients might be considered as
a life-saving measure (Class IIb; Level of Evidence C). (New recommendation)
5. DC with or without hematoma evacuation might reduce mortality for patients with
supratentorial ICH who are in a coma, have large hematomas with significant midline
shift, or have elevated ICP refractory to medical management (Class IIb; Level of
Evidence C). (New recommendation)
6. The effectiveness of minimally invasive clot evacuation with stereotactic or
endoscopic aspiration with or without thrombolytic usage is uncertain (Class IIb; Level of
Evidence B). (Revised from the previous guideline)
Outcome:
The natural course of spontaneous ICH leads to a 30-day mortality rate of 45%. The
patient's initial level of consciousness, hemorrhage size, and intraventricular extension of blood
has proven to be accurate predictors of outcome. Less commonly, age, sex, hypertension, and
mass effect may indicate harmful effects on outcome in patients with ICH.
The author recommends that patients with smaller hematomas who are alert, stable, or
improving should be treated medically and the patients with larger hematomas who show
progressive neurological deficit, prolonged functional impairment, and intracranial hypertension
should be treated surgically. Patients with a GCS score <4 should also be treated medically
because they uniformly die or have extremely poor functional outcome that cannot be improved
by surgery. Easily accessible supratentorial hematomas with mass effect, especially in the
young and in those with a GCS score >5, must be evacuated. The aim of surgery should be the
removal of as much of the clot as possible, with minimal disruption of surrounding brain tissue. If
possible, surgery should also remove the underlying cause of hemorrhage, such as an
arteriovenous malformation, and prevent complications of ICH such as hydrocephalus and mass
effect of the blood clot. More complete clot removal may decrease elevated ICP and local
pressure effects of the blood clot on the surrounding brain. Stereotactic aspiration may be
associated with better outcomes than standard craniotomy; but this hypothesis has yet to be
tested in a randomized study. Ultra-early removal of ICH by localized, minimally invasive
surgical procedures is promising but untested. Further study of the dynamics of hemorrhage and
additional results are needed prior to making a decision on how to divide patient management
into the two categories of surgical and nonsurgical treatment.
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SCENARIO
Male patient, 35 years old was referred to the Emergency room on a face mask
oxygenation, with Infusion lines at right arm with large caliber of needle, warmed crystalloids
has been administered. The blood pressure is 160/100 mmHg, heart rate 60x/mnt, Respiration
rate 20x/mnt. Pupil round an equal, size: right side 5mm, left side 3mm, with left hemi paresis.
His eyes are open with pain stimuli and his GCS was E2V2M4. Neck stiffness was negative.
History: When he was watching TV, suddenly he got severe headache, seizure, vomiting and
then after that he looks decreased of consciousness. No history of hypertension before. History
of headache on and off since 5 years ago.
LEARNING TASKS
1. What is the clinical diagnosis and differential diagnosis?
2. What is the investigation that need for this patient?
3. How is the initial management for this patient?
4. When should you suggest to doing surgery for this patient?
5. How should you explain the prognosis of the patient to the family?
SELF ASSESMENT
1. Explain the Cerebrovascular Anatomy that supplies the brain and cerebellum!
2. Learn about clinical features, investigations and differentials diagnosis of
cerebrovascular disease!
3. Learn about emergency management: medical and surgical aspect of CVA!
4. Learn about how to explain the prognosis of CVA!

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LECTURE 22 -23
COMPLETE SPINAL TRANSECTION AND ACUTE MEDULARRY COMPRESSION
AND PREHOSPITAL & INITIAL MANAGEMENT OF SPINE& SPINAL CORD INJURY
Dr .dr. Tjok Gde Bagus Mahadewa, M.Kes, Sp.BS(K)Spinal*
Aims:
Provide initial assessment and management, established tentative diagnosis, proposed
definitive management, and rehabilitation method or refer patient Complete Spinal Transection
Learning outcome:
The student can provide initial assessment and management, established tentative
diagnosis, proposed definitive management, and rehabilitation method or refer patient with
Complete Spinal Transection
Complete Spinal Transection:
1. Evaluate and appropriately manage for suspected Complete Spinal Transection.
2. Determine appropriate patient disposition and definitive management for Complete
Spinal Transection.
3. Proposed rehabilitation method or refer patient with Complete Spinal Transection.
Abstracts
It is estimated that the prevalent population of people in America with a spinal cord injury
(SCI) is approximately 200.000-400.000 people. The incidence is about 40 per million people
and about 11.000 new cases per year. SCI is caused by both trauma and by disease processes
(non-traumatic SCI) such as spinal cord infection and infarction. Mostly (50,7%) affected
cervical level, frequently at C5 level, using American Spinal Cord Injury Association (ASIA)
Impairment Scale is determined 49% in ASIA A (Complete Impaired). Typically people who
acquire a traumatic SCI are young and male, whilst non-traumatic SCIs occur more often in later
life and with a more even gender split. Most spinal cord injury causes permanent disability or
loss of movement (paralysis) and sensation below the site of the injury AKA Complete Spinal
Transection. Paralysis that involves the majority of the body, including the arms and legs, is
called quadriplegia or tetraplegia. When a spinal cord injury affects only the lower body, the
condition is called paraplegia. Many scientists are optimistic that important advances will occur
to make the repair of injured spinal cords a reachable goal. In the meantime, treatments and
rehabilitation allow many people with spinal cord injury to lead productive, independent lives.
Today, there's still no way to reverse damage to the spinal cord. But modern injuries are
usually less severe, partial spinal cord injuries. And advances in recent years have improved the
recovery of people with a spinal cord injury and significantly reduced the amount of time
survivors must spend in the hospital. Researchers are working on new treatments, including
innovative treatments, prostheses and medications that may promote nerve cell regeneration or
improve the function of the nerves that remain after a spinal cord injury. In the meantime, spinal
cord injury treatment focuses on preventing further injury and enabling people with a spinal cord

91
injury to return to an active and productive life within the limits of their disability. This requires
urgent emergency attention and ongoing care.
Emergency actions
Urgent medical attention is critical to minimizing the long-term effects of any head or neck
trauma. So treatment for a head and spinal cord injury often begins at the scene of the accident.
If you suffer a head or neck injury, you'll likely be treated by paramedics and emergency
workers who will attend to three immediate concerns:
Maintaining your ability to breathe
Keeping you from going into shock
Immobilizing your neck to prevent further spinal cord damage
Emergency personnel typically immobilize the spine as gently and quickly as possible
using a rigid neck collar and a rigid carrying board, which they'll use to transport you to the
hospital. In the emergency room, doctors focus on maintaining your blood pressure, breathing
and neck stabilization and avoiding possible complications, such as stool or urine retention,
respiratory or cardiovascular difficulty, and formation of deep vein blood clots in the extremities.
You may be sedated so that you don't move and sustain more damage while undergoing
diagnostic tests for head and spinal cord injury. If you do have a spinal cord injury, you might
be admitted to the intensive care unit for treatment. You may even be transferred to a regional
Complete Spinal Transection center that has a team of neurosurgeons, orthopedic surgeons,
spinal cord medicine specialists, psychologists, nurses, therapists and social workers with
expertise in brain and spinal cord injury.
Early stages of treatment

In the early stages of decreases of consciousness, paraplegia or quadriplegia, your doctor
will treat the injury that caused the loss of function. Immediate treatment may include:
Medications. Methylprednisolone (Medrol) is a treatment option for acute spinal cord injury.
This corticosteroid seems to cause some recovery in people with a spinal cord injury if given
within eight hours of injury. Methylprednisolone works by reducing damage to nerve cells and
decreasing inflammation near the site of injury.
Immobilization. You may need traction to stabilize your spine and bring the spine into proper
alignment during healing. Sometimes, traction is accomplished by placing metal braces,
attached to weights or a body harness, into your skull to hold it in place. In some cases, a rigid
neck collar also may work.
Surgery. Often, emergency surgery is necessary to remove fragments of bones, foreign
objects, herniated disks or fractured vertebrae that appear to be compressing the spine. Surgery
may also be needed to stabilize the spine to prevent future pain or deformity. Controversy exists
regarding the best time to perform surgery. Some surgeons believe it should be performed as
soon as possible in most circumstances, while others believe it's safer to wait for several days
before attempting any surgery. Research has not clearly proved which approach is better.
Persisting SCI impacts on every aspect of a person's life: health status, physiological,
active community participation, psychological, social, reproductive, economic, employment,
educational and recreation. An SCI will affect people in variable ways, depending on the level of
the spinal cord lesion and the completeness of the injury. Generally all people with SCI have
some degree of motor or sensory loss and a disrupted autonomic nervous system. This has a
profound effect on a person's health, function and physiology. The most important factors
92
predicting functional outcome are the neurological level and degree of completeness of spinal
cord lesion. However, a range of other medical and non-medical factors can influence outcome,
including age, body shape and weight, associated injuries, pre-existing disease, spasticity and
contractures, living arrangements and family support, level of education and financial resources.
Functional goals are based on sequential organization of spinal segments and capacity of
spared muscle groups to perform specific activities of daily living, qualified by other factors such
as those listed above.
When working with patients to establish wheeled mobility goals, it is essential to
understand the individual impact of a person's SCI and other health issues associated with co-
morbid conditions and with ageing. Pre-morbid lifestyle and interests, personality characteristics
and coping style, degree of social support and economic circumstances will all be important
factors influencing adjustment and eventual outcome. Within the learning modules is information
about establishing and assessing a patients health status. For people who require wheeled
mobility, the effective prescription and use of a wheelchair enables and empowers them to
participate in life and interact in their community. Many patients with a spinal cord injury will
spend most of their waking hours in their wheelchair; each patient is unique and has highly
individual and, over time, changing needs. It is no longer acceptable, to prescribe a wheelchair
and seating system without careful consideration of the patients goals and postural, pressure,
functional, safety and environmental needs. A correctly prescribed wheelchair and seating
system will optimize function, address the impact of environmental factors, correct and prevent
postural and pressure issues and meet a patient's community participation needs
Scenario
Male patient, 25 years old as a passenger of a public transportation, had a head on
collision. The driver was died immediately at the scene. The patient was referred to the
Emergency room as being immobilized on a long spine board and semi rigid cervical collar. On
a face mask oxygenation, with Infusion lines at both arms with large caliber of needles, warmed
crystalloids has been administered. The blood pressure is 85/40 mmHg, heart rate 130x/mint,
Respiration rate 40x/mint, shallow respiration pattern, with an obvious injury on the chest wall.
His eyes are open and well respond to verbal stimuli. He can lift up his shoulder but cannot
elevate his elbows neither his legs.
1. What is the working diagnosis?
2. How is the prompt management for this patient?
3. How should you explain the prognosis of the patient to the family?
Learning tasks
1. Learn about Initial Assessment and Management for Spinal Injury.
2. Learn about Brain and Spinal Injury diagnosis and management for Spinal Injury.
3. Learn about rehabilitation methods for Spinal Injury.
4. Learn about how to refer patient with Spinal Injury
Self assessment
1. Mention several types of Spinal Injury!
2. Mention several types of Spine Fractures!
3. How can we prevent Secondary Spinal Cord Injury?
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LECTURE 24
NEUROPATHY (CARPAL TUNNEL SYNDROME, TARSAL TUNNEL SYNDROME,
PERONEAL NERVE PALSY)
Aim
Describe about focal neuropathy and nerves injury. Describe clinical characteristic, risk
factors, diagnostic work-up including history, clinical examination, imaging, and treatment of
focal neuropathy.
Learning outcome
1. Know and understand the anatomy and pathophysiology of nerves injury.
2. Be able to obtain a comprehensive history and physical examination in the assessment
of patients with focal neuropathy.
3. Understand the use of diagnostic tool for assessing focal neuropathy.
4. Understand treatment of focal neuropathy.
ABSTRACT
Neuropathy means disease or abnormality of nervous system. Neuropathies can be
sensory, motor or autonomic. Sensory nerves gives us information about the posisition of our
joints, pain and temperatures. Motor nerves stimulate muscl contraction and movement.
Autonomic nerves control functions that our odies dont consciously regulate, such sweating,
certain bowel and bladder function and heart rate.
Symptoms of neuropathy depend on both the type of nerves affected and the mechanism
that causes damage to the nerves. The most common presenting symptom is the combination
of numbess and tingling in the toes and feet. Less common neuropathies can cause weakness
or clumsiness, and it may be difficult to do certain activities, such as raising an arm over the
head, getting up from seated position or walking up stairs.
Nerve injury are quite common and may have serious implications for the patient. Most
nerve injuries result from either acute injury or chronic cumulative trauma. Focal neuropathies
result from trauma (laceration,stretch or traction, crush or compression, friction), ischemia (small
or large vessel), infiltration(neoplastic, granulomatous, inflammatory/infectious), hemorrhage,
chemical neuritis from injection of toxic agents, freezing, or radiation.
Several factors influence the susceptibility of nerves to injury. Supporting epineurial and
perineurial tissues protect nerves from compressive and traction forces, and this explains why
nerve roots, which lack these structures, are more vulnerable. Nerves are particularly at risk
when passing over hard, unyielding surfaces (ulnar nerve at the medial epicondyle) or through
fixed compartments (median nerve in the carpal tunnel); chronic compression syndromes at
these sites are called entrapment neuropathies. Nerve compression may be acute or chronic,
intermittent or progressive, and the relative contributions of mechanical and ischemic factors are
debated. Entrapped nerves observed at surgery show constriction at the entrapment site, with
proximal swelling due either to edema or, more commonly, to fibrous thickening. Acute injury,
modeled experimentally by tourniquet application, is characterized by mechanical deformation
(invagination/intussusception of myelin) at the node of Ranvier, concentrated at the cuff edges,
94
leading first to paranodal demyelination and then to segmental demyelination. More severe or
prolonged compression results in axonal degeneration.
CARPAL TUNNEL SYNDROME

Carpal tunnel syndrome (CTS), the clinical syndrome related to median nerve entrapment
at the wrist, is by far the most common entrapment neuropathy. It affects 3%5% of adults in
the United States and has a 10% lifetime risk. The highest incidence is between 40 and 60
years of age. At least half of these patients have bilateral symptoms, and approximately three-
quarters have bilateral median entrapment that is demonstrable electrophysiologically. The
dominant hand is more frequently and severely affected.
Symptoms begin with intermittent hand numbness, paresthesias, or pain in any
combination. Nocturnal symptoms interrupting sleep or present upon awakening are
characteristic, although not invariable. Symptoms are provoked by activities. Most patients feel
that the symptoms are on the palmar aspect of the fingers, but about 10% say that they are
more dorsal. With progression, sensory symptoms become more persistent, with perceived
hand weakness or clumsiness in handling objects. Sensory examination may reveal
hypesthesia or hyperesthesia in involved fingers. Weakness of thenar muscles, along with
thenar atrophy, represents more advanced median nerve compression.
Nerve conduction studies are highly sensitive in establishing median nerve entrapment at
the wrist, its severity, and its axonal versus demyelinating features. Sensory conduction is the
most sensitive measure. Both ultrasound and magnetic resonance imaging (MRI) can show
flattening of the median nerve within the carpal tunnel and swelling proximal to the lesion site.
A significant percentage (perhaps one-quarter or more) of untreated CTS will improve
spontaneously by both clinical and neurophysiologic criteria. Wrist splinting in a neutral position
and activity modifications are often adequate in mild cases with intermittent symptoms and
normal exams. Controlled trials demonstrate the short-term benefit of local corticosteroid
injection or low-dose, short-term oral corticosteroids. The response to injection may also be
helpful diagnostically in some cases where the diagnosis is uncertain and may predict a
response to carpal tunnel release (CTR).
TARSAL TUNNEL SYNDROME

Tarsal tunnel syndrome (TTS), also called posterior TTS, is an entrapment neuropathy of
the posterior tibial nerve under the flexor retinaculum at the medial ankle. Conditions associated
with TTS include ankle injury, posttraumatic fibrosis, thick flexor retinaculum, tight footwear, and
space-occupying lesions (ganglia, varicose veins, schwannoma, lipoma, abnormal muscles
within the tunnel). Ultrasonography or MRI is often helpful for anatomic definition.
Typically, there is burning or sharp foot pain, numbness, or paresthesias in the distribution
of one or more of the plantar nerves; the heel is often not involved, as the calcaneal branch may
arise proximal to the tarsal tunnel. Symptoms are aggravated by weight bearing, are relieved
with rest, and may be nocturnal.
Electrodiagnostic testing can be helpful, but may be limited and difficult to interpret in
patients who are elderly and in those with calloused feet, bilateral symptoms, or underlying
peripheral neuropathy.
Conservative therapy is initially employed in most cases without a space-occupying lesion,
and may include avoiding external compression, anti-inflammatory/neuropathic medications,
95
corticosteroid injection, and orthotics. Corticosteroid injection into the tarsal tunnel may be both
diagnostic and therapeutic. Good clinical results are often reported with surgical release of the
flexor retinaculum, including improvement in electrophysiologic parameters, but it is not
uncommon to encounter apparent failures in the EMG lab.
PERONEAL NERVE PALSY

Peroneal nerve palsy or peroneal neuropathy is the most frequent mononeuropathy
encounterd in the lower limb and the third most common focal neuropathy encountered overall,
after median and ulnar neuropathies. Most often, peroneal nerve palsy occurs at fibular neck,
where the nerve is superficial and vulnerable to injury. The most common site of injury is the
fibular head, but focal neuropathies have also been reported at the level calf, ankle and foot.
Patients usually present with a foot drop and sensory disturbance over the lateral calf and the
dorsum of foot. Clinical motor examination demonstrates weakness in ankle dorsiflexion and
great toe extension with deep fibular and eversion weakness with superficial fibular involvement.
Compressive lesions are often painless; those associated with a mass may be painful, as are
vasculitic infarcts that can occur at various points along the nerve.
Electrophysiology can localize the level of the nerve palsy, reveal the underlying
pathology, and establish the prognosis. Nerve conduction studies can document focal slowing
ofmotor conduction or conduction block at the fibular head in demyelinating lesions (recording
from the extensor digitorum brevis and, importantly, the tibialis anterior muscles). Management
depends on the etiology and pathophysiology. Known external compressive lesions are
managed conservatively.
SCENARIO
A 39 years old female came to clinic with pain and burning of 5 months duration in her
right ankle and sole. More recently, pain has occurred at rest waking her at night. She
expressed losing ability to walk, if the pain continued to progress.
LEARNING TASK
1. What other history taking, other symptoms that we should explore to diagnosis this
case?
2. What other examination that we should do to diagnosis this case?
4. What is management of this patient?
SCENARIO
A 45 years old male came to clinic with chief complaint of left leg pain. His symptoms
began after she fell of on her left hip 3 months ago. He had some weakness when walking and
his symptoms had progressed. The patient also complained of left-sided lower back and buttock
pain with movement and intermittent lightning bolt sensation to thighs.

96
LEARNING TASK
case?
SCENARIO
A 41 year old female artist presented with a 2 year history of numbness in both hands, right
greater than left. The numbness was most severe in the right thumb and was specifically
brought on by paint. Numbness, pain and tingling in both hands woke her up at night.
LEARNING TASK
case?

97
LECTURE 25
RADICULOPATHY
Aim
Describe the structure of spine and relation to nerve roots. Describe clinical characteristic,
risk factors, diagnostic work-up including history, clinical examination, imaging, and treatment of
radiculopathy.
Learning outcome
1. Know the the structure of spine and relation to nerve roots.
2. Understand and explain how cervical and back problems induced radiculopathy.
3. Be able to obtain a comprehensive history and physical examination in the assessment
of patients with radiculopathy.
4. Understand the use of diagnostic tool for assessing radiculopathy.
5. Understand treatment of radiculopathy.
Abstract
Musculoskeletal neck and back pain generally is high and midline, experienced in the
upper neck and back muscles. Radicular pain tends to occur medial to the scapula or in the
buttock with eventual radiation down the arm or leg. Because sitting increases the intraspinal
pressure, radiculopathies are classically much worse with sitting but improved with standing or
walking. Also, as a general rule, the pain is maximal proximally, whereas paresthesia and
numbness are more prominent distally. Radiculopathy is a peripheral neurologic syndrome
resulting from mechanical injury and chemical irritation of the spinal nerve roots. It may involve a
single, or multiple nerve roots. Two most common types are lumbosacral and cervical.
Obtaining a detailed history is important to establish a diagnosis of radiculopathy. The
diagnosis may be suggested by symptoms of pain, numbness, and weakness in a pattern
consistent with the distribution of a particular nerve root. Neck or back pain may also be
present. Physical examination may reveal motor and sensory deficits in the distribution of a
nerve root. In cervical radiculopathy, Spurling's test may elicit or reproduce symptoms radiating
down the arm. In the case of lumbosacral radiculopathy, a Straight leg raise maneuver may
exacerbate radiculopathic symptoms. Deep tendon reflexes may be diminished or absent in
areas innervated by a particular nerve root.
Little is known about the natural history of radiculopathy. The pathogenesis involves an
inflammatory process initiated by nerve root compression. Radiography of the spine is usually
the first diagnostic test ordered in patients who present with neck and back symptoms. MRI has
become the method of choice for imaging to detect significant soft-tissue pathology, such as
disc herniation.
There are few controlled randomized studies comparing operative with nonoperative
treatment for this condition. There is no clear evidence that surgical treatment provides better
long-term outcomes than nonoperative measures. Initial treatment should be directed at
reducing pain and inflammation. The treatment can begin with local icing, NSAIDs, and
measures that reduce the forces compressing the nerve root: relative rest; avoiding positions
98
that increase symptoms; manual traction; and, if necessary, mechanical traction. Epidural
steroids have been used in patients whose conditions have not had satisfactory responses to
medications, traction, and a well-designed physical therapy program.
Patients whose condition fails to improve with a comprehensive rehabilitation program and
selective injections should be offered a surgical evaluation. Generally, patients should show
progressive improvement over the first 6-8 weeks with conservative treatment. If there is no
significant improvement in this time frame, consider a surgical evaluation.
Self assesment
1. What is the definition of radiculopathy?
2. Why it happened most often in cervical and lumbar spine?
3. Explain the mechanism of radiculopathy!
4. Explain the diagnostic work-up for radiculopathy!
Scenario
A 43 years old man, a farmer came to the policlinic with complaint low back pain, started
suddenly after lifting heavy objects. The pain is radiating pain accompanied by paresthesia that
spreading to the right lateral side of thigh until to little toe. There were no micturition and
defection disturbances.
Learning task
2. If etiology of back pain in this patient is HNP (hernia nukleus pulposus) L4-L5, what is
the symptoms and signs ?
3. What is diagnostic work-up for this patients?
4. What is the management for this patients?
Learning Resources
1. Eubanks JD.Cervical Radiculopathy: Nonoperative Management of Neck Pain and
Radicular Symptoms. Am Fam Physician. 2010;81(1):33-40
2. Last AR, Hulber K. Chronic Low Back Pain: Evaluation and Management. Am Fam
Physician. 2009;79(12):1067-1074
3. Taylor LP, Lemming SE. Neck and Back Pain. American Academy of Neurology.
4. Ropper AH, Samuels MA, Klein JP. Pain in the Back, Neck, and Extremities. Principles
of Neurology 10th ed. 2014: 198-225

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LECTURE 26
ENCEPHALOPATHY AND COMA
dr. Kumara Tini, SpS, FINS*
AIMS
Describe neurobiology, diagnosis, initial management and referral patients with decrease of
consciousness and coma.
LEARNING OUTCOME
1. Understand neurobiology of alertness and coma.
2. Understand and able to examine patient with decrease of consciouness and coma.
3. Understand and able to describe etiology of decrease of consciouness and coma.
4. Understand and able to manage patient with decrease of consciouness and coma.
CURRICULUM CONTENS
1. History taking patients with decrease of consciousness and coma
2. Physical Examination patients with decrease of consciousness and coma
3. Initial Management patients with decrease of consciousness and coma
ABSTRACTS
Coma is a loss of consciousness involving unawareness of self, others and the external
world, and the passage of time. People with comais unable to respond to external events or
basic needs such as eating and drinking. Automatic reflex movements or abnormal body
positions may be evident n rsponse to pain or other stimuli.
Coma can result from from mechanical destruction of crucial area of the brain stem,
thalamus and cerebral cortex ( anatomic or structural coma) or from widespread (global)
disruption of brain by metabolic process (metabolic coma). Structural causes of coma include
bleeding in or around the brain (e.g., hemorrhagic stroke, subarachnoid hemorrhage, etc.) major
stroke with death of brain tissue (cerebral infarction), brain tumors, brain infection, head trauma.
While meatbolic causes can be from deprived brain oxygen (hypoxia) such as pnerumonia,
heart failure, massive blood loss. Overdose of illegal drugs, alcohol. Failure of the lungs,
kidneys, liver whivh might produse accumulation of waste products that toxic to the brain. Very
low blood sugar, extremely low or high temperature, fluid or electrolyte imbalances and certain
bacteria or viruses may result in coma
History taking, physical and neurological examnitaion are very important to delinieate
emergeny stae, etiology and to amnage patient with coma. Basic managment to maintain the
patency and adequate supply of oxygen, blood flow will prevent patient from secondary or
further brain damage despit the accurate treatment for etiology.

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1. The role ascending reticular activating System in the brainstem, thalamus and cerebral
cortex in consciousness.
2. Etiologies of coma.
3. History taking, physical and neurological examination of coma.
4. Management of patients with coma.
Scenario 1
Female 60 years old was brought to ER with decrease of consciouness. She suddenly fell
in the kitchen. Upon examintaion her GCS was examined. She opened her eyes with pain
stimuli, uttered aduh, sakit with pain stimuli and whe her sternum pressed by the examiner
fingers adequatly she was able to localized the pin stimulus. Her left extremities moved more
actively as compared to her right. BP 200/120mmHg, HR 100x/minute sinus rythm, RR
24x/minute, Temp: 37.8OC. Pupil anisocor 4mm/2mm, light reflex -/+ , dolls eye (+), corneal
reflex +/+. Left hemiplegia was noticed. She has history of hypertension and on medication
Captopril 3x25mg, she is not a diabetic patient .
Learning Task
1. What is her GCS?
2. What is the tocial diagnosis in relation to anatomical structur of consciouness? and
describe what based your answer!
3. What is the most possible diagnosis?
4. What investigation you suggest and how to manage this patient?
Self Assessment
1. Know how to examine unconsciousness or comatose patient
2. Know neurobilogy of conciouness and comatose pateint
3. Know the etiology and management of unconsciousness or comatose patient
Scenario 2
Male 50 years old was brought to ER with decrease of consciouness. Hewas complaining
about headache since int the morning . He does not have history about high blood pressure or
diabetes, recreational drugs user. Upon examination in ER his GCS was E3V4M5. Blood
pressure 240/140mmHg, HR 90x/minute, RR 20x/minute, temp 37.6oC. Pupil were isocor, light
reflex were (+) bilaterally, with intact other brainstem reflexes. No motoric deficit was noticed.
Laboratoric test within normal limit and head scan was normal
Learning Task:
1. What is the most possible diagnosis?
2. Explained the mechanism of decrease of consciouness in this patient ?
3. How to manage this patient?

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LECTURE 27
NEUROGENIC BLADDER
dr. IB Kusuma Putra, Sp.S*
Aim
Describe the the structure of urinary bladder and understand the normal micturation
mechanism and neurogenic bladder dysfunction. Explain clinical characteristic, risk factors,
diagnostic work-up including history, clinical examination and treatment of neurogenic bladder.
Learning outcome
1. Know the the structure of urinary bladder and understand how they normally operate to
control of micturition (urination).
2. Understand and be able explain that impairs bladder and bladder outlet afferent and
efferent signaling can cause neurogenic bladder.
3. Understand and be able explain pathophysiology of neurogenic bladder.
4. Be able to obstain a comprenhensive history, physical examination and assessment of
patients with neurogenic bladder.
5. Understand management of neurogenic bladder.
Abstract
Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder, is a
dysfunction of the urinary bladder due to disease of the central nervous system or peripheral
nerves involved in the control of micturition (urination).
Neurogenic bladder dysfunction, sometimes simply referred to as neurogenic bladder,
is a dysfunction of the urinary bladder due to disease of the central nervous system or
peripheral nerves involved in the control of micturition (urination). Neurogenic bladder usually
causes difficulty or full inability to pass urine without use of a catheter or other method.
Symptoms of neurogenic bladder range from detrusor underactivity to overactivity,
depending on the site of neurologic insult. The urinary sphincter also may be affected, resulting
in sphincter underactivity or overactivity and loss of coordination with bladder function. Urinary
incontinence, characterized by either the involuntary release of large volumes of urine or
continuous dribbling of small amounts, bed-wetting may occur, frequent urination, Persistent
urge to urinate despite recent voiding; constant feeling that the bladder is not completely empty,
pain or burning on urination and dribbling urine stream.
The appropriate/tepat therapy and a successful outcome are predicated upon accurate
diagnosis through a careful medical and voiding history together with a variety of clinical
examinations, including urodynamics and selective radiographic imaging studies.
Self assesment
1. What is the classification of neurogenic bladder?
2. What is causes of neurogenic bladder ?
3. Explain the mechanism neurogenic bladder!
4. Explain the diagnostic work-up neurogenic bladder!
5. Explain the treatment of neurogenic bladder!
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Scenario
A 55 years old, male, teacher presented with Spinal cord lesion T 10 after motor vehicle
accident. The injury occurred 1 hour ago. He complained of urinary retention, accompanied by
flaccid paraparesis at T10 below, and the somatic reflex activity is either depressed or absent.
Learning task
1. Explain urinary retention mechanism for this patients!
2. Explain the classification of neurogenic bladder for this patient!
3. What is diagnostic work-up for this patients?
Learning Resources
1. Wein AJ, Rackley RR. Overactive bladder: a better understanding of pathophysiology,
diagnosis and management. J Urol. Mar 2006;175(3 Pt 2):S5-10. [Medline]
2. Rackley, RR, Kim, ED. Neurogenic bladder. Avaiable at
http://emedicine.medscape.com/article/453539-overview accessed 11 April 2014
3. Wein AJ, Dmochowski RR. Neuromuscular dysfunction of the lower urinary tract. In:
Wein AJ, Kavoussi LR, Novick AC, et al, eds. Campbell-Walsh Urology. 10th ed.
Philadelphia, Pa: Saunders Elsevier; 2011:chap 65.

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LECTURE 28
CENTRAL NERVOUS SYSTEM INFECTIONS
MENINGITIS, ENCEPHALITIS AND CEREBRAL MALARIA
dr. Ni Made Susilawathi, Sp.S(K)*
AIMS
Describe diagnosis, initial management and referral patients with meningitis, encephalitis
and cerebral malaria.
LEARNING OUTCOME
1. Define of meningitis, encephalitis and cerebral malaria.
2. Describe prevalence of meningitis, encephalitis and cerebral malaria.
3. Describe common clinical presentation, Cerebrospinal fluid (CSF) finding and initial
management for the following:
a) Bacterial Meningitis
b) Viral Meningitis
c) Encephalitis
d) Cerebral malaria
4. Explain neurologic examination for meningitis, encephalitis and cerebral malaria.
5. Explain the patophysiology of Meningitis, Encephalitis and Cerebral Malaria.
6. Describe common complication of Meningitis, Encephalitis and Cerebral Malaria.
7. Discuss the need for urgent investigations and referrals.
CURRICULUM CONTENS
1. History taking patients with Meningitis, Encephalitis and Cerebral Malaria.
2. Physical Examination patients with Meningitis, Encephalitis and Cerebral Malaria.
3. Initial Management patients with Meningitis, Encephalitis and Cerebral Malaria.
ABSTRACTS
Infection can affect the function of the nervous system by damaging the brain
(encephalitis, abscess),its lining (meningitis, subdual empyema), spinal cord (myelitis, cord
compression),lumbosacral plexus, muscle and nerves. At least 1% of hospital admission relate
to infection of central nervous system (CNS), primarily bacterial meningitis. Encephalitis refers
to an acute, usually diffuse inflammatory process affecting the brain. While meningitis is
primarily an infection of the meningen,a combined meningoencephalitis my also occur.
Acute bacterial meningitis is a life-threatening neurological emergency. Early diagnosis
and effective antibiotic treatment remains the cornerstone of successful management of ABM.
Classic symptoms include headache, fever, neck stiffness and altered mental status. The
causative organism of meningitis can be predicted based on the patients age, exposure to an
epidemic, vaccination against common agents (eg, Haemophilus influenza, Streptococcus
pneumonia or Neisseria meningitides) and immune state. The key to diagnosing meningitis lies
in examining the cerebrospinal fluid (CSF) by lumbar puncture.
Viral encephalitis is an inflammation of the brain parenchyma caused by a viral vector.
Acute or subacute onset of fever, headache and altered mental status are the cardinal features
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of acute viral encephalitis. Personality change, perceptional disturbance (illusions and

hallucinations) and disorientation are common and can heralding symptoms. Herpes simplex
virus, arthropod-borne viruses and enteroviruses are the most common causes among adults.
Cerebral malaria is the most severe neurological complication of infection with
Plasmodium falciparum malaria. It is a clinical syndrome characterized by coma and asexual
forms of the parasite on peripheral blood smears. Mortality is high and some surviving patients
sustain brain injury which manifest as long-term neuro-cognitive impairments.

1. The Meningens and The cerebrospinal fluid and ventricular system.
2. The technique performing a lumbar puncture/spinal tap.
3. Cerebrospinal fluid finding in CNS infection.
Scenario 1
A 28 year-old man presents the emergency room with a severe headache, fever and
confusion and hearing loss, all of which had developed two days before visiting hospital. He is
not known to have any medical illness, and there is no history of head trauma. On examination ,
he has a temperature of 380C , Blood pressure 110/68 mmHg and pulse 100 beat/min.
Neurologic examination revealed neck rigidity and kernig sign
Learning Task
1. What is the most likely diagnosis?
2. What is the best diagnostic next step?
3. What is the appropriate theraphy?
Scenario 2
A 59 year old woman who presented to the emergency room with a three day history of
mental status changes. Three days prior admission she had eaten out and had one episode of
diarrhea. Since then she had slowly become increasingly confused. She had trouble finding the
right words and had been using incorrect word in sentence. She had no significant previous
medical history and no recent illnesses. On examination disorientated with her vital sign within
normal limit. She did not have meningeal sign.
Learning Task
1. What is the most likely diagnosis ?
2. What is the best diagnostic next step ?
3. What is the appropriate theraphy ?

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Scenario 3
A 18 years old man presented altered consciousness with high grade intermittent fever of
more than four days duration. The fever asscociated with chills and rigors. There was history of
generalized tonic clonic convulsions prior to admission. He had history of travelling to NTT. On
examination, GCS E3V3M5, Blood pressure 110/70. Respiratory and heart rate within normal
limits. He had hepatosplenomegaly with liver being aroud 4 cm pappable. He did not have
meningeal sign
Learning Task
1. What is the most likely diagnosis?
2. What is the best diagnostic next step?
3. What is the appropriate theraphy?
Self Assessment
1. Know the clinical presentation of meningitis and encephalitis and cerebral malaria.
2. Learn to develop a diagnostic strategy for the diagnosis of meningitis, encephalitis,
cerebral malaria and understand the cerebrospinal fluid finding in meningitis,
encephalitis and cerebral malaria.
3. Know strategy for meningitis, encephalitis and cerebral malaria in the emergency room.

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LECTURE 29
NEUROINFECTION 2: HUMAN IMMUNODEFICIENCY VIRUS INFECTION AND
ACQUIRED IMMUNE DEFICIENCY SYNDROME RELATED CENTRAL NERVOUS
SYSTEM INFECTION, TUBERCULOUS SPONDYLITIS, AND RABIES
dr. Putu Gede Sudira, Sp.S*
*Department of Medical Education/ Neurology Department, School of Medicine, Faculty of Medicine,
Universitas Udayana
AIMS
This lecture will help student to comprehend their basic knowledge in preclinical subjects
and relate it to clinical aspect of neuroinfection cases. There are 3 cases should be mastered in
this topic Human Immunodeficiency Virus Infection and Acquired Immune Deficiency Syndrome
(HIV/ AIDS) related Central Nervous System (CNS) Infection, Tuberculous Spondylitis, and
Rabies.
LEARNING OUTCOMES
1. Apply concepts and principles of basic preclinical in anatomy, biochemistry,
pathophysiology, pharmacology knowledge related to HIV/ AIDS related CNS Infection,
Tuberculous Spondylitis, and Rabies.
2. Able to diagnose patient with HIV/ AIDS related CNS Infection, Tuberculous Spondylitis,
and Rabies cases.
3. Choosing appropriate management to HIV/ AIDS related CNS Infection, Tuberculous
Spondylitis, and Rabies cases.
4. Understand prognosis of HIV/ AIDS related CNS Infection, Tuberculous Spondylitis, and
Rabies cases.
CURRICULUM CONTENT
Diagnosis of HIV/ AIDS related CNS Infection, Tuberculous Spondylitis, and Rabies are
listed in Indonesian Competence Standard of Doctor 2012. Their level of competency are 3A/ B,
it means that general practitioner have to notice the diagnosis and arrange initial management
or treatment before refer them to specialist.
ABSTRACT
Infection can posses in various ways and affect every part in human bodies. Intracranial
as the most secure place because of its double protection perform by blood brain barrier is no
exception. Local or systemic infection spread and destroy blood brain barrier and give
temporary or permanent damage to adjacent brain structures.
Systemic infection like HIV/ AIDS lowering body immunity and act as opportunistic
infection intracranial. Brain is the second most commonly affected organ in patients with HIV/
AIDS. Many opportunistic infections may involve the brain ranging from HIV encephalopathy,
primary lymphoma, mycobacterial, herpes simplex, cryptococcosis. But the five most frequent
conditions are cytomegalovirus, toxoplasmosis, progressive multifocal leukoencephalopathy
(PML), cryptococcosis, and HIV encephalopathy infection. They remain a major cause of
morbidity and mortality even though its number getting lower as a consequence of the
introduction of highly active antiretroviral therapy (HAART) to patient group.
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In clinical practice, the noninvasive methods are used to establish the diagnosis of these
entities. The clinical manifestations are nonspecific and depend on the type and location of the
lesions. Imaging studies, especially magnetic resonance imaging (MRI), are very useful for the
diagnosis of toxoplasmic encephalitis and PML, although in cryptococcal meningitis and
cytomegalovirus infections cases their sensitivity is lower. The presence of multiple ring-
enhancing lesions with surrounding oedema and mass effect is characteristic of toxoplasmosis.
Molecular methods applied to the cerebrospinal fluid (CSF) are essential for the diagnosis of
PML and cytomegalovirus infections. In addition, the quantification of viral DNA of both JC virus
(the causative agent of PML) and cytomegalovirus has prognostic implications and may serve to
evaluate the response to therapy. Cryptococcosis may be easily diagnosed by CSF stains and
cultures, as well as by the detection of the cryptococcal capsular polysaccharide antigen in the
blood and, especially, the CSF.
Effective treatments are available for toxoplasmosis and cryptococcosis, although adverse
effects are common and some patients may not respond to therapy. The response to
antitoxoplasmic therapy, which is usually observed within the first 2 weeks, is also used for
diagnostic purposes. In contrast, there is no specific treatment for PML, and the efficacy of
anticytomegalovirus therapy is poor and the toxicity significant. HAART has improved the
outcome of patients with AIDS who have infections of the CNS, and the initiation of this therapy
is mandatory for all patients with such infections, particularly in those conditions for which
effective therapy is not available.
Vacuolar myelopathy is the most common chronic myelopathy occurs during the late
stages of HIV infection, often in conjunction with AIDS dementia complex, peripheral
neuropathies, and opportunistic infections or malignancies of the central or peripheral nervous
system (eg, cytomegalovirus, PML, lymphoma). Vacuolar myelopathy typically presents as a
slow progression of painless leg weakness, stiffness, sensory loss, imbalance, and sphincter
dysfunction.
Electrophysiologic tests can confirm a clinical diagnosis of vacuolar myelopathy. The CSF
analysis are usually normal in HIV-1associated vacuolar myelopathy (HIVM) and it can exclude
infection like cytomegalovirus, varicella-zoster virus, herpes simplex virus, Human T-cell
lymphotropic virus (HTLV)-1, and HTLV-2. Imaging studies are often noncontributory but may
reveal unsuspected coexisting conditions such as extramedullary or intramedullary infections,
neoplasms, degenerative disk disease, or spine degenerative joint disease.
No specific treatment is currently approved for this condition, it mainly supprotive
treatment but viral control tailored to the individual patient's medical and viral history is
important, as case reports showing clinical and radiologic improvement with highly active
retroviral therapy (HAART) have been described.
Tuberculous spondylitis, also known as Pott disease, is one of the oldest demonstrated
diseases of humankind. Since the advent of antituberculous drugs and improved public health
measures, it has become rare in industrialized countries, although it is still a significant cause of
disease in developing nations. Tuberculous involvement of the spine has the potential to cause
serious morbidity, including permanent neurologic deficits and severe deformities. Medical
treatment or combined medical and surgical strategies can control the disease in most patients.
Tuberculous spondylitis manifests as a combination of osteomyelitis and arthritis that usually
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involves more than 1 vertebra. The anterior aspect of the vertebral body adjacent to the
subchondral plate is usually affected. Tuberculosis may spread from that area to adjacent
intervertebral disks. In adults, disk disease is secondary to the spread of infection from the
vertebral body. In children, the disk, because it is vascularized, can be the primary site.
Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canal can be
narrowed by abscesses, granulation tissue, or direct dural invasion, leading to spinal cord
compression and neurologic deficits. The kyphotic deformity is caused by collapse in the
anterior spine. Lesions in the thoracic spine are more likely to lead to kyphosis than those in the
lumbar spine. A cold abscess can occur if the infection extends to adjacent ligaments and soft
tissues. Abscesses in the lumbar region may descend down the sheath of the psoas to the
femoral trigone region and eventually erode into the skin.
The clinical presentation of Tuberculous spondylitis in patients infected with the human
immunodeficiency virus (HIV) is similar to that of patients who are HIV negative; however, spinal
tuberculosis seems to be more common in persons infected with HIV. The presentation of
tuberculous spondylitis depends on the following stage of disease, affected site, and presence
of complications. Potential symptoms of tuberculous spondylitis include fever and weight loss.
The average duration of symptoms at diagnosis is 4 months but can be considerably longer due
to the nonspecific presentation of chronic back pain. Back pain is the earliest and most common
symptom of tuberculous spondylitis. The pain caused by Tuberculous spondylitis can be spinal
or radicular. Neurologic abnormalities occur in 50% of cases and can include spinal cord
compression with paraplegia, paresis, impaired sensation, nerve root pain, and/ or cauda
equina syndrome. Cervical spine tuberculosis is a less common presentation but is potentially
more serious because severe neurologic complications are more likely. This condition is
characterized by pain and stiffness. Patients with lower cervical spine disease can present with
dysphagia or stridor. Symptoms can also include torticollis, hoarseness, and neurologic deficits.
Laboratorium studies used in the diagnosis of tuberculous spondylitis include the following
positive result in tuberculin skin test (PPD), elevated erythrocyte sedimentation rate (ESR), and
microbiologic studies to confirm the diagnosis. Bone tissue or abscess samples are obtained to
stain for acid-fast bacilli (AFB), and organisms are isolated for culture and susceptibility.
Procedures guided by computed tomography (CT) scanning can be used to guide percutaneous
sampling of affected bone or soft-tissue structures. It is expected that nonculture methods (DNA
amplification) using skeletal tissue samples will become additional routine diagnostic
methodologies. Their main advantages include high specificity, high sensitivity, and rapid
results.
The duration of treatment is somewhat controversial. A 4-drug regimen should be used
empirically to treat tuberculous spondylitis. Treatment can be adjusted when susceptibility
information becomes available. Although some studies favor a 6 to 9 month course, traditional
courses range from 9 months to longer than 1 year. The duration of therapy should be
individualized and based on the resolution of active symptoms and the clinical stability of the
patient. Isoniazid and rifampin should be administered during the whole course of therapy.
Additional drugs are administered during the first 2 months of therapy and are generally chosen
from among the first-line drugs, such as pyrazinamide, ethambutol, and streptomycin. In cases
of drug resistance, the use of second-line medications is indicated.

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Rabies is a viral disease that affects the central nervous system (CNS). Rabies is a highly
neurotropic virus that evades immune surveillance by its sequestration in the nervous system.
The virus is transmitted in saliva or in aerosolized secretions from infected animals, typically via
a bite. The virus is not hardy and is quickly inactivated by drying, ultraviolet rays, x-rays, trypsin,
detergents, and ether. Rabies does not cause cytotoxicity. Death occurs from global neurologic
and organ dysfunction. The virion acts in the synaptic space, where homology in amino acid
sequences between neurotransmitter receptors for acetylcholine, GABA, and glycine may afford
a mechanism for viral binding of these receptors. Thus, its action is neurotoxic, rather than
direct damage.
There are 4 clinical phases in rabies patient incubation period, prodromal period, acute
neurologic periode, and coma. During incubation period, the infected individual remains
asymptomatic. The average duration of incubation is 20-90 days and can prolong to years.
Patients may not recall exposure because of the prolonged incubation period. The shorter
duration if the patient is bitten on the head or neck or if a heavy inoculum is transferred through
multiple bites, deep wounds, or large wounds. The rabies virus is segregated from the immune
system during this period, and no antibody response is observed. During prodromal period the
virus enters the CNS. The duration of this period is 2-10 days. Nonspecific symptoms and signs
develop. Paresthesia, pain, or intense itching at the inoculation site is pathognomonic for rabies
and occurs in 50% of cases during this phase; this may be the individuals only presenting sign.
Symptoms may include the following malaise, anorexia, headaches, fever, chills, pharyngitis,
nausea, emesis, diarrhea, anxiety, agitation, insomnia, and depression. Acute neurologic period
is associated with objective signs of developing CNS disease. The duration is 2-7 days.
Symptoms include muscle fasciculations, priapism, and focal or generalized convulsions.
Patients may die immediately or may progress to paralysis, which may be present only in the
bitten limb at first but usually becomes diffuse. Patients develop agitation, hyperactivity,
restlessness, thrashing, biting, confusion, or hallucinations. After several hours to days, this
becomes episodic and interspersed with calm, cooperative, lucid periods. Furious episodes last
less than 5 minutes. Episodes may be triggered by visual, auditory, or tactile stimuli or may be
spontaneous. Seizures may occur. This phase may end in cardiorespiratory arrest or may
progress to paralysis. Another form of rabies, paralytic rabies, is also known as dumb rabies or
apathetic rabies, because the patient is relatively quiet compared with a person with the furious
form. Twenty percent of patients do not develop the furious form. Paralysis occurs from the
outset, and fever and headache are prominent. Finally the comatose periode begins within 10
days of onset, and the duration varies. Without intensive supportive care, respiratory
depression, arrest, and death occur shortly after coma.
Diagnosis of rabies mainly from anamnesis and physical examination, various supporting
examination can help to establish diagnosis. Skin biopsy from the nape of the neck to find the
Rabies antigen can be detected in cutaneous nerves by direct fluorescent antibody. Less
preferably, scraping of corneal epithelia, or corneal touch impression, for direct fluorescence
antibody can be used. This requires topical ocular anesthetic and is best performed by an
ophthalmologist. Viral cultures and polymerase chain reaction (pcr) assay from speciments
like saliva - results of saliva culture for rabies virus are positive in low yield within 2 weeks of
illness onset, cerebrospinal fluid - after the first week of illness, 80% monocytosis is observed;
protein and glucose test results are normal, or brain tissue - often postmortem; staining with
immunohistochemical or florescent antibody staining is definitive. Blood gas analysis shows
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Respiratory alkalosis resulting from hyperventilation develops in the prodromal and early acute
neurologic phases of rabies; this is followed by respiratory acidosis as respiratory depression
progresses. Hematology studies results of the white blood cell (WBC) count range from normal
to elevated, with 6-8% atypical monocytes. As the neurologic phase of rabies progresses, chest
radiographs may reveal infiltrates due to aspiration, nosocomial pneumonia, acute respiratory
distress syndrome, or congestive heart failure. Findings from magnetic resonance imaging
(MRI) and computed tomography (CT) scanning of the brain often indicate that no abnormalities
are present. Electroencephalography (EEG) findings include encephalopathic changes. Due to
generalized vasospasm of cerebral arteries during the first week of illness, EEG amplitude may
drop precipitously and mimic brain death. This may be further suggested by papillary reflex
abnormalities such as anisocoria or fixed pupils due to dysautonomia. These findings may
reverse with return of blood flow. A more reliable means of determining brain death in the case
of rabies may therefore be cerebral arterial flow scanning that demonstrates absent flow. Brain
biopsy is another option. Supraventricular tachycardia may be observed during cardiac
monitoring. Eventually, bradycardia and cardiac arrest occur.
Centres for Disease Control (CDC) and World Health Organization (WHO) recommend 2
doses of cell-culture vaccine administered intramuscularly or intradermally on days 0 and 3 for
preexposure "booster" prophylaxis. Pregnancy is not a contraindication to postexposure
prophylaxis against rabies, which is warranted to protect the life of the fetus and mother. No
adverse pregnancy outcomes have been documented with postexposure prophylaxis. No
mother-to-fetus transmission has been described, and spread of the virus is not hematogenous;
thus, neither rabies exposure nor diagnosis in the mother is an indication for pregnancy
termination. Before the onset of rabies symptoms, passive and active immunizations are
effective in preventing progression to full-blown rabies. If the patient has had no prior rabies
vaccination, if he or she is of unknown status, or if more than 5 years have passed since his or
her last vaccination, rabies vaccine and immunoglobulin should be administered as follows:
Rabies vaccine IM (deltoid) - 1 mL on days on days 0, 3, 7, and 14.
Rabies immunoglobulin - 20 IU/kg infiltrated as much as feasible around and under the
bite wound; if any left over, give IM (gluteus).
If the patient has had prior rabies vaccination, vaccine should be administered IM (deltoid) 1 mL
on days on days 0 and 3. Outside the United States, in areas where cost and vaccine supply
are limiting factors, alternatives to the IM regimens may be more feasible. In addition, rabies
vaccination may be the norm in some countries where rabies is endemic, and anamnestic
response may permit effective alternative dosing. In 1998, the World Health Organization
(WHO) released guidelines for ID use of human diploid cell vaccine (HDCV), purified chick
embryo cell vaccine, and purified duck embryo cell vaccine. The WHO published updated
postexposure prophylaxis guidelines that included ID regimens often used outside the United
States.
Symptomatic rabies cannot be managed in the outpatient setting. Intensive
cardiopulmonary supportive care is the only treatment available for patients with symptomatic
rabies. Rabies vaccination and administration of HRIG is ineffective at this point. You look tired
but please send me picture of dinosaurus to my account at night before my lecture, and do not
tell your friends to do so. Empiric treatment for rabies should be guided by local public health
recommendations, whenever feasible, taking into account whether viral shedding periods are
known for the species, the animal's history and risk for rabies exposure, and local epidemiology.
111
In most settings where rabies is a risk, prophylaxis should be initiated regardless of whether or
not the animal is in custody and being observed. Prophylaxis may be discontinued if the animal
does not develop rabies within 10 days or is found to be free of rabies upon sacrifice.
Precaution for healthcare workers to perform Universal precautions and respiratory
precautions during respiratory therapy are indicated for health care providers. Rabies
postexposure prophylaxis of health care workers is indicated only for high-risk exposures as
determined with the assistance of local infection control and public health authorities.
SCENARIO
A 20-year-old man was admitted with a 10-day history of back pain and vomiting, followed
by marked weakness of the lower limbs and confusion during the three days prior to admission.
On admission he was febrile (38 C) and confused. Physical examination was normal
except for the neurological signs of stiff neck, bilateral positive Babinski sign, and urinary
retention. Computed tomography (CT) of the brain showed no abnormalities of the cerebral
parenchyma except for a low degree of hydrocephalus. Cerebrospinal fluid (CSF) analysis
showed xanthochromic fluid that contained 59 cells/ml, 60% lymphocytes, protein 6.5 g/l,
glucose 40 mg/dl (blood glucose 94 mg/dl), and chloride 590 mg/dl. Acid-fast stains were
negative, as well as India ink and Gram stains.
Mycobacterium tuberculosis cultures were later positive. Other investigations were
normal. HIV serology was negative and the chest X-ray was normal. There was no evidence of
active or inactive extrameningeal TB.
Anti-tuberculous therapy consisting of isoniazid (INH), rifampin (RMP), pyrazinamide
(PZA), and ethambutol (EMB) in addition to IV dexamethasone 24 mg/day were initiated on the
second hospital day.
By the fourth hospital day, the patient had paraplegia, which was associated with
asymmetric sensory loss to pinprick at the level of T9 on the right and T4 on the left, and loss of
sphincter control. Deep tendon reflexes were absent and bilateral Babinski sign was found.
Magnetic resonance imaging (MRI) of the spine revealed an obliterated subarachnoidal space in
the thoracic and lumbar segments, a subarachnoid block with enhancement of nerve roots, and
thickening of the filum terminale. There was gadolinium (Gd) enhancement of the lumbar
meninges and a hypersignal T2 of the spinal cord from the fourth to ninth thoracic vertebra. IV
dexamethasone was continued for two weeks, followed by oral prednisone 1 mg/kg body weight
daily.

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LEARNING TASK
Discuss case by using Maastricht 7 jumps approach. Ideally we need to do the discussion
twice to apply this method. Pilot project to apply at our institution is considered now. We modifiy
the steps so you need to do step 1, 2, 5, and 7 today. There are steps like:
1. Clarifying Terms and Concepts. You have to find the unfimiliar terms from scenario and
make sure all members have similiar opinion on it. This helps the group to start with a
clear and common understanding of terms and concepts in the problem.
2. Defining the Problem. By reading the scenario, you clearly formulate a concrete defined
problem or propose a definition of the problem. This helps to establish the boundaries of
the problem under discussion.
3. Analyzing the problem/ brainstorming. This step is meant to refresh the knowledge
present within the group and to activate the prior knowledge. Listing to as many
explanations or alternatives as possible for the problem without excluding any
explanations is important.
4. Categorizing. This helps in defining interrelationships between previous listed
explanations. The group builds a coherent description of the explanations of the
processes, the group thinks, underlies the problem.
5. Formulating Learning Issues. Depending on the previous discussion, whatever is still not
known or unclear can be formulated into clear, well-defined learning issues for self
directed learning.
6. Self Study. This step is meant to help the student to select relevant literature sources.
Students are provided with a list of materials that are related to the problem. The
students preferably make a selection of appropriate materials from this list. After
selecting the sources, many steps follow. All group members are required to study the
resources, gain a clear understanding of the knowledge to link previous knowledge to
new attained knowledge and to prepare to report back critically on the acquired
knowledge.
7. Discussion of newly acquired knowledge. This phase is usually scheduled after a couple
of days to allow time for self study. This session lasts 1-2 hours.
During plenary session, we will randomly ask learning tasks were discussed to groups
(step no 2 and 5). Other group will try to answer and discuss it (step no 7).

113
LECTURE 30
CENTRAL NERVOUS SYSTEM (CNS) INFECTIONS: POLIOMIELITIS, TETANUS,
TETANUS NEONATORUM
dr. Ni Putu Witari, Sp.S*
Tetanus is an acute disease caused by an exotoxin of bacterium Clostridium tetani. The

etiology discovered by Carle and Rattone in 1884. The Clostridium tetani is sensitive to heat
and can not survive in the presence of oxygen. The spores of Costridium tetani are distributed in
soil and in the intestine and feces of dogs, cats, pigs, chickens, sheep, horses and rats. C.
tetani produced two exotoxins i.e tetanospasmin and tetanolysin.
The incubation period is about 8 days (range 3 to 21 days). Anaerobic conditions allow
germination of spores and production of toxins. Tetanus is characterized by muscle spasm,
initially in the jaw muscle. There are three different forms of tetanus : local tetanus, cephalic
tetanus, and generalized tetanus. Tetanus is often fatal and cause death. The complications of
tetanus are otonom disfunction, respiratory problem, renal and electrolyte dysfunction, and
nosocomial infection. The medical management of tetanus are : all wounds should be cleaned,
eradication of causative bacterial, remove unbound tetanus toxin, supportive therapy, and
immunization.
Case
A 50 year-old woman just arrived at the hospital with chief complain cant open her mouth
since yesterday.
Learninng task
1. Please do anamnesis to this patient
2. What will you find on physical examination if this patient suffered from general tetanus
Ablett score 2?
3. How to manage the patient? How is the prognosis of this patient? Why?
Self Asssessment
1. Learn about the clinical feature of tetanus
2. Learn the pathogenesis of tetanus
3. Learn the wound management
4. Learn about immunization for tetanus
POLIOMYELITIS
Poliomyelitis (polio) is mainly affects young children. Poliomyelitis caused by a virus that
invades the nervous system, and can spread from person to person. There is no cure but
preventable by safe and effective vaccines.
Most of persons who infected with polio will have no symptoms (approximately 72%),
about 24% have minor symptoms. The minor symptoms are : fever, headache, fatique, flu-like
symptoms, nausea, neck and back stiffness, pain in the limbs, which can resolve completely.
Only less than 1% result in permanent paralysis of the limbs. When the paralysis affected the
respiratory muscles, 5-10% persons infected with polio died.
114
Case
A 5 years old child, come to clinic with his parents because his left leg paralyzed since two days
ago. There is no pain or numbness on the leg.
Learning task
1. Please do anamnesis to this patient and his family
2. If it is a poliomyelitis, what will you find on clinical examination?
3. What is your differential diagnosis for this case?
4. What should you do to confirm your diagnosis?
5. How to manage the patient?
Self Assessment
1. Learn the anatomy of medulla spinalis and peripheral nerve.
2. Learn the cause of poliomyelitis.
3. Learn the clinical feature of poliomyelitis.
4. Learn the prevention of poliomyelitis.
TETANUS NEONATORUM
Tetanus neonatorum (neonatal tetanus) is a major cause of mortality in infant in
underdevelop countries. Infection results from umbilical cord contamination during unsanitary
delivery, and a lack of maternal immunization (the mother is not immune).
In tetanus neonatorum, symptoms usually appear from 4-14 days after birth, averaging
about 7 days. At the end of the first week of life, infected infants become irritable, feed poorly,
and develop rigidity with spasms. Tetanus neonatorum is a form generalized tetanus that occurs
in newborn infants without protective passive immunity. Neonatal tetanus has a very poor
prognosis.
Neonatal tetanus can be prevented by immunizing women of childbearing age with
tetanus toxoid, either during pregnancy or outside of pregnancy.
Case
A 10 days baby just arrived at the hospital with chief complain irritable and feed poorly,
since a day before.
Learninng task
1. Please do the complete anamnesis to the parents!
2. What will you find on physical examination on tetanus neonatorum? What is your
differential diagnosis? Why?
3. How to manage the patient?
4. How to prevent tetanus neonatorum?
Self Assessment
1. Learn about the clinical feature of tetanus.
2. Learn the pathogenesis of tetanus neonatorum.
3. Learn the management.
4. Learn about immunization for tetanus prevention.
115
Refferences :
1. Dian S., Tetanus., 2011., Infeksi pada Sistim Saraf., Kelompok Studi Neuro Infeksi,
Perdossi
2. Prof.dr. I Gst. Ng. Gd. Ngoerah; 1991; Dasar-Dasar Ilmu Penyakit Saraf; Airlangga
University Press
3. Centers for Diseases Control and Prevention (CDC), Global Health Polio,2013
4. World Health Organization (WHO), Poliomyelitis (Polio), 2014
5. Patrick B Hinfey, MD; Tetanus ; Mar 2014 ; Medscape
6. World Health Organization (WHO), 2008

116
LECTURE 31
PERIPHERAL DISEASE (GUILLAN-BARRE SYNDROME)
dr. Komang Arimbawa, Sp.S*
Aim
Describe the patophysiology, epidemiology, clinical presentations, diagnostic work-up,
treatment and prognosis of Guillan-Barre Syndrome (GBS).
Learning outcome
1. Understanding the patophysiology mechanism and the epidemiology of GBS.
2. Know the clinical presentations of GBS.
3. Be able to make diagnostic work-up including patient history, clinical finding and another
comprehensive tests (CSF examination, ENMG/ NCS).
4. Understanding the management of GBS.
5. Recognize the prognosis of GBS.
Abstract
Diagnosis of GBS is an acute or subacute polyneuropathy that can follow minor infective
illnesses, inoculations, or surgical procedures or may occur without obvious precipitants. Clinical
and epidemiologic evidence suggest an association with preceding Campylobacter jejuni
infection. Its precise cause is unclear, but it appears to have an immunologic basis. Patients
generally present with weakness that is symmetric, usually begins in leg, is often more marked
proximally than distally, and is sometimes so severe that it is life-threatening, especially if the
muscles of respiration or swallowing are involved. Sensory complaints while usually less
marked than motor symptoms, are also frequent. The deep tendon reflexes are typically absent.
There may be marked autonomic dysfunction with tachycardia, labile blood pressure, disturbed
sweating, sphincter disturbances and impaired pulmonary function.
The albuminocytological dissociation occur, characterized by increased protein
concentration but a normal cell count; abnormalities may not be found in the first week.
Electrophysiologic studies may reveal marked slowing of motor and sensory conduction
velocity, or evidence of denervation and axonal loss.
Plasmapheresis is best instituted early, indicated especially in patients with a severe or
rapidly progressive deficit or respiratory compromise. Intravenous immunoglobulin
(400mg/kg/day for 5 days) appears to be equally effective and should be used in preference to
plasmapheresis in adults with cardiovascular instability and in children; the two therapies are not
additive.
The disorder is self limiting and improvements occurs over the weeks or months following
onset. Approximately 70-75% of patients recover completely, 25% are left with mild neurologic
deficits and 5% are die, usually as a result of respiratory failure.

117
Self assessment
1. Explain the patophysiology mechanism of GBS!
2. Explain the clinical presentation of GBS!
3. Describe the diagnostic work-up for GBS!
4. Describe the medications approaches and prognosis for GBS!
Scenario
A 20 yrs old man complain weakness of leg muscles, suffered from 2 days ago, ascending
type, symmetrical, proximal more pronounced than distal. Previously, two weeks before he felt
weakness, he got pronounced diarrhea for 3 days, and it got improved by itself. Leg weakness
is not improved by rest. There is no complaint of sensory abnormalities, no micturition or
respiratory problem. There is also no history of trauma. From clinical finding there is flaccid
paralysis of legs with absent deep tendon reflexes.
Learning task
1. What is the possible diagnosis of this patient?
2. What is the diagnostic work up for this patient?
3. What condition should we obtain from the CSF examination and what is the
interpretation?
4. What is the management planned for this patient?
Learning resources:
1. Ropper, A., Brown, R. 2009. Adams and Victors : Principles of Neurology.
9th ed. New York: McGraw-Hill. p.1405-1414.
2. Longmore M, Wilkinson I, Turmezei T, Cheung CK. 2007. Oxford Handbook of Clinical
Medicine. 7th ed. New York: Oxford University Press.

118
LECTURE 32
TRAUMATIC BRAIN INJURY, PRE HOSPITAL AND MANAGEMENT OF
ACUTENEUROTRAUMA IN RURAL AND REMOTE LOCATION
Prof. Dr. dr. Sri Maliawan, Sp.BS(K)*
Aims
To understand traumatic brain injury
Learning Outcome
1. Comprehend the specific principles of anatomy and physiology related to brain injury.
2. Identify and discuss the principles of general management of unconscious patient.
3. Outline the method of evaluating head injury using a minineurologic examination.
4. Identify and discuss the management techniques of head injury.
Curriculum contents
1. Scalp hematoma
2. Skull fracture
3. Monro Kellie doctrine.
4. Glasgow coma scale
5. Intracranial hematoma
6. Cushing response
7. Mini neurologc examination
8. Brain death
9. CT scan
10. External and internal decompression .
Abstract
Incidence. Neurotrauma is responsible for 70% of all road fatalities and 50% of trauma
deaths. Road crashes cause 50- 60% of all head injuries. Accidental injury is the third highest
cause of death in motorised countries. The highest incidence for hospital admission in persons
under 45 years of age is form trauma.
Factor in the Rural Environment. The following factors are significant in rural trauma :
asolation and distance, medical facilities, level of neurosurgical competence, delay in definitive
care, administrative organisation, rural crash profiles, e.g., incidence of 40% fatality on
admission, more severe injuries, multiple injuries, higher incidence of single vehicle crashes,
road and environmental conditions, driver competence and fatigue and compliance with
preventive measures such as alcohol, seatbelts, helmets and speed.
Neurotrauma. Clinical factors adversely influencing outcome [death and disability]
- Severity of Primary Injury
- Intracranial Complications
- Hypoxaemia
- Hypercarbia
- Hypotension
- Anaemia
119
- Multiple Injuries
- Age
- Prolonged Prehospital Time
- Admission To Inappropriate Hospital
- Delayed Or Inappropriate Interhospital Transfer/ Retrieval
- Delay In Definitive Surgical Treatment
Learning Task
Female 40 years old a pedestrian was hit by motor bike , upon arrival to emergency
department, she able to open her eye and say painfull while she withdrawn her hand , there
are brill hematoma, rinorhea, and bloody discharge from her nose and mouth, respiratory rate
26x/mnt gurgling, Blood pressure 80/60 mmHG, and Heart rate 120x/mnt.
1. What is the clinical diagnosis base on GCS?
2. What is initial management?
3. Describe sign of skull base fracture!
4. Describe sign and symptom of intracranial hematoma!
5. Mention and explain about EDH,SDH,ICH,SAH, IVH!
Self assessment
1. What is cushing respons?
2. When do you susfect ICH develop after TBI?
3. What are indication for craniotomy and craniectomy procedures?
4. Describe lucid interval!
5. Lateralization or hemisyndrome.
6. Brain death.
Learning Resoursces
1. Sri maliawan cedera kepala
2. American college of surgeon; ATLS
3. The neurosurgical society of Australia; head injury an remote area

120
LECTURE 33
BRAIN TUMOR AND TREATMENT OPTIONS
Dr. dr. Nyoman Golden, Sp.BS(K)*
Aims
Describe the surgical management of brain tumors.
Learning outcomes
Understanding the surgical principles in the management of brain tumors
Curriculum
1. Preoperative management
2. Perioperative management
3. Operative management
4. Complications
Abstract of lecture
Before embarking surgical tumor removal, evaluation of clinical history and findings, the
results radiographic studies, benefits and risks of surgery and detailed discussion with the
patient must be completely done. The medical problems in the patients history must be
evaluated and properly treated. Brain tumor with significant brain edema, must be put on steroid
medication. Even when there is no or little edema, if it is thought that there will be lot of brain
tissue manipulation at surgery, steroid should be started at least 48 hours prior surgery.
Complicating hydrocephalus that may present in certain brain tumors must be considered
whether it gives signs and symptoms of raised intracranial pressure. When there is no symptom,
nothing needs to be done. Just before the surgery is started, make sure that manitol with a
dosage of 1-1.5g/kg has been given and this must be finished within 20-30 minutes. In addition,
many surgeons give furosemid with a dosage of 10-20 mg just after the catheter is inserted.
Antibiotic is given one hour before surgery and together with steroid are continued at 6 hours
intervals. Antiepileptic drug is given when there is a history of seizure attack.
The main goals of surgery are to provide specimen for accurate pathological diagnosis
and to reduce mass effect. Many factors must be considered in making decision for surgery,
including patients age, neurological status, general medical condition, degree of mass effect,
location of the tumor, extent of abnormality and the patients understanding of the risks and
benefits of surgery. The success of tumor removal is most likely dependent on thorough imaging
studies evaluation, understanding the normal and pathologic anatomy, proper positioning of the
patient, well-planned surgical exposure, microsurgical technique familiarity, avoidance of severe
and prolong tissue retraction and minimal exposure of normal brain tissue. For benign tumors
such as meningioma and neurinoma, complete tumor removal must be considered including
excision of affected dura and bone. To avoid severe brain retraction, internal decompression of
tumor mass must be first accomplished before removing out the capsule completely. When
some part of the tumor strongly attaches to the important structures such as nerves and brain
stem, it must be left. If the tumor is malignant such as high grade astrocytoma or glioblastoma, it

121
must be removed out as much as possible while trying to preserve function of eloquent brain
area.
The surgeon must be aware of the possibility of surgical complications. Majority of
complication can be prevented by careful preoperative planning, meticulous technique and
familiarity of using microintruments. The surgeon must be intimate with knowledge of the
predicted complication. When the patient does not recover promptly, an immediate CT scan
must be taken to evaluate the presence of hematoma, brain edema, hydrocephalus, tension
pneumocephalus and infarction. The subsequent treatments depend on the result of that scan.
Scenario
A 8 year old boy was presented with 6 months history of gastrointestinal disturbance. He
has been brought to medical attention several times, but it seemed to be not help. His school
performance was significantly distorted in the last one year. Four weeks before admission he
was noted to have difficulty in walking steadily and started to have problem with articulation. On
examination revealed bilateral of 6th nerve paralysis, disturbance of all cerebellar function and
papil edema. Head CT has been taken and he will be put on surgical tumor removal. The doctor
on duty has carefully informed the family including the aims of surgery, outcomes, postoperative
complication, adjuvant modalities following surgery and the possibility of having another surgery
for the complication caused by tumor compression.
Learning task
1. Describe the possible location of the tumor
2. Describe the most likely of the tumors histopathology
3. Describe the accompanying complication
4. Describe the management of this complication
5. Describe the preoperative management
6. Describe the surgical approach to exposure this tumor
7. Describe the surgical goals of this tumor
8. Describe the post operative complications that may appear
Self assessment
1. Explain the classification of brain tumors
2. Explain the work of manitol in reducing intracranial pressure
3. Explain how a brain tumor can cause hydrocephalus
4. Explain how the patient can get bilateral 6th nerve paralysis
5. Explain the mechanism of papil edema

122
REFERENCES
A. Student Standard References :

1. Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott &
Wilkins, 2007.
2. Gartner LP, Hiatte JL: Color Textbook of Histology, 2nd ed. Philadelphia, WB Saunders
Company, 2001.
3. Guyton AC: Textbook of Physiology, 11st ed. Philadelphia, WB.Saunders Company,
2006
4. Fox S.I.: Human Physiology, 9th ed. New York, McGraw-Hill, 2006
5. Kumar V, Cotran R S, Robbins SL: Robbins Basic Pathology, 7th ed. Philadelphia,
Saunders, 2003
6. Trevor AJ, Katzung BG, Masters: Katzung & Trevors Pharmacology, 7th ed. New York,
Lange Medical Books/Mc.Graw-Hill, 2005.
7. McPhee, S.J., Papadakis, M.A., Current Medical Diagnosis & Treatment. 47th ed. New
York, Lange Mecical Book`s/The McGraw-Hill Companies, 2008.
B. Additional Student References :

1. H2: Fowcett DW, Jensh RP: Bloom & Fawcetts Concise Histology, 2nd ed. London,
Arnold. 2002.

123

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Study Guide The Neuroscience and Nervus System Disorders

STUDY GUIDE THE NEUROSCIENCE AND NERVUS SYSTEM DISORDERS

First Edition September 2017

STUDY GUIDE THE NEUROSCIENCE AND NERVUS SYSTEM DISORDERS .......................... 2

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

LECTURE 13-14 ................................................................................................................................. 69

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

PLANNERS AND LECTURERS

NO NAME DEPARTMENT PHONE

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Regular Class (Class A)

English Class (Class B)

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

There are several types of learning activity:

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Title of student project

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

Members Name and Student Registered Number

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

ARTICLE REVIEW ASSESSMENT FORM

Block : The Neuroscience and Nervus System Disorders

Student No. (NIM) : ________________________________________

Time table of consultation

Point of discussion Week Date Tutor sign

Total point : ( A + B + C ) : 3 = _____________

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

ARTICLE REVIEW ASSESSMENT FORM

Block : The Neuroscience and Nervus System Disorders

Student No. (NIM) : ________________________________________

Total point : ( A + B + C ) : 3 = _____________

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

GENERAL TIME TABLE FOR A AND B CLASSES

TIME ACTIVITIES TIME ACTIVITIES

08.00-09.00 Lecture 09.00-10.00 Lecture

09.00-10.30 Independent learning 10.00-11.30 Student project

10.30-12.00 SGD 11.30-12.00 Break

12.00-12.30 Break 12.00-13.30 Independent learning

12.30-14.00 Student project 13.30-15.00 SGD

14.00-15.00 Plenary session 15.00-16.00 Plenary session

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

TIME TABLE OF CLASSES

Lecture 1 dr. IA Sri

Prof. Dr. dr. I

12.30-14.00 10.30-11.00 Student project

Prof. Dr. dr. I

dr. D.A. Inten Dwi

12.00-12.30 12.00-12.30 Break

12.30-14.00 12.30-13.30 Student project

Department of Medical Education - Faculty of Medicine - Universitas Udayana, 2017

dr. D.A. Inten Dwi

10.00-11.00 09.00-10.00 Independent learning

11.00-12.00 13.30-15.00 SGD Disc room Facilitator

3 12.00-12.30 12.00-12.30 Break

14.00-15.00 15.00-16.00 Pleanary Day 3 Class room Wande, Sp.PK/

Lecture 8 dr. Dewi Sutriani

13.00-14.00 12.30-13.30 Student project