Manish Chandra Prabhakar MGIMS

Reference- Harrison's Internal Medicine 18th edition

Stroke Focal seizures (Todds Palsy) Migraine Intracranial neoplasm, Cerebral abscess Head injury Subdural hematoma Epidural hematoma Hyperglycemia , Hypoglycemia Acute conversion reaction Focal encephalitis,meningitis Drug overdose cocaine, amphetamine Hypertensive encephalopathy Metabolic encephalopathy Cardiac syncope or syncope from other causes Postcardiac arrest ischemia

Reference- Harrison's Internal Medicine 18th edition 2

Diagnosis
Seizures (postictal)

Comments
Focal deficits likely are caused by seizure-induced neuronal dysfunction (reversible). May occur with simple partial or generalized seizures. Spontaneous resolution occur over hours (may last up to 48 hours) Aphasia or hemiplegia may be present. Variable drowsiness or obtundation. Blood glucose usually <45 mg/dl. Resolution of symptoms with IV glucose. Etiologies include hyperosmolar hyperglycemia, hyponatremia, and hepatic encephalopathy. May be associated with altered level of consciousness, poor attention, or disorientation (eg, delirium) asterixis. Diagnosis of exclusion. Conversion disorder is the most common psychiatric diagnosis. Comorbid psychiatric problems are common. Paresis, paralysis, and movement disorders are common. Imaging evidence or history of remote stroke is often apparent. Previous deficit may have resolved completely.
3

Hypoglycemia

Metabolic encephalopathy

Conversion reaction

Reactivation of prior deficits

History Neurologic examination

Reference- Harrison's Internal Medicine 18th edition

1.

The time of symptom onset

If patient is able to provide information family or friends

2.

The nature of symptoms

Abruptly: vascular etiology Risk factors for vascular disease, history of seizures , migraine, insulin use or drug abuse Accompanying symptoms (severe thunderclap headache subarachnoid Hemorrhage)
Reference- Harrison's Internal Medicine 18th edition

History of the Present Illness Time of symptom onset Evolution of symptoms, recovery Convulsion or loss of consciousness at onset Headache Chest pain at onset Medical History Prior intracerebral hemorrhage, h/o stroke, Recent head trauma h/o myocardial infarction

Surgical History- Recent surgical procedures

Medications- Anticoagulant therapy Review of SystemsGastrointestinal or genitourinary bleeding Reference- Harrison's Internal Medicine
18th edition 6

3.

Record:

Vital signs Blood glucose level of consciousness severity of deficits Presence of bowel or bladder incontinence

Reference- Harrison's Internal Medicine 18th edition

Identify signs of lateralized hemispheric or brainstem dysfunction consistent with focal cerebral ischemia. Level of consciousness, the presence of a gaze deviation, aphasia, neglect or hemiparesis

Reference- Harrison's Internal Medicine 18th edition

Validated 15-item scale used to assess key components of the standard neurologic examination and measure stroke severity (lyden et al, 1999) It assess level of consciousness, ocular motility, facial and limb strength, sensory function, coordination , language, speech and attention. Scores range from 0 (normal) to 42 (maximal score). It predicts short-term and long-term neurologic outcomes . (Adams et al, 1999)
Reference- Harrison's Internal Medicine 18th edition 9

Category
1a. Level of consciousness

Scale Definition
0= Alert 1= Not alert, arousable 2= Not alert, obtunded 3= Unresponsive 0= Answers both correctly 1= Answer once correctly 2= Answer neither correctly 0= Performs both tasks correctly 1= Performs one task correctly 2= Performs neither task 0= Normal 1= Partial gaze palsy 2= Total gaze palsy 0= No visual loss 1= Partial hemianopsia 2= Complete hemianopsia 3= Bilateral hemianopsia

Category
5a. Left motor arm

Scale Definition
0= No drift 1= Drift before 10 seconds 2= Falls before 10 seconds 3= No effort against gravity 4= No movement 0= No drift 1= Drift before 10 seconds 2= Falls before 10 seconds 3= No effort against gravity 4= No movement 0= No drift 1= Drift before 5 seconds 2= Falls before 5 seconds 3= No effort against gravity 4= No movement 0= No drift 1= Drift before 5 seconds 2= Falls before 5 seconds 3= No effort against gravity 4= No movement 0= Absent 1= One limib 2= Two limbs

1b. Questions

5b. Right motor leg

1c. Commands

6a. Left motor leg

2. Gaze

3. Visual fields

6b. Right motor leg

4. Facial palsy

0= Normal 1= Minor paralysis 7. Ataxia 2= Partial paralysis Reference- Harrison's Internal Medicine 3= Complete paralysis 18th edition

10

Category

Scale Definition

8. Sensory

0= Normal 1= Mild loss 2= Severe loss 0= Normal 1= Mild aphasia 2= Severe aphasia 3= Mute or global aphasia 0= Normal 1= Mild 2= Severe

9. Language

10. Dysarthria

11. 0= Normal Extinction/inattenti 1= Mild on 2= Severe

Reference- Harrison's Internal Medicine 18th edition
11

Cardio-vascular system Carotid bruit Cardiac murmur Irregularly irregular heart rhythm Unequal extremity pulses Other Signs of head or neck trauma (occult cervical spine injury) Rales on chest examination (Pneumonia) Bilateral asterixis (metabolic encephalopathy).
Reference- Harrison's Internal Medicine 18th edition 12

a neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 hours that are presumed to be of a non-traumatic vascular origin

Reference- Harrison's Internal Medicine 18th edition

13

Transient Ischemic Attack Stroke in evolution RIND ( Reversible Ischemic Neurological Deficit)

Reference- Harrison's Internal Medicine 18th edition

14

Brief episodes of focal neurological deficits lasting 2-3 minutes to at most a few hours but no longer than 24 hours leaving no residual deficits with complete functional recovery.

Reference- Harrison's Internal Medicine 18th edition

15

a focal brain ischemia in which the deficit improves over a maximum of 72 hours deficits may not completely resolve in all cases

Reference- Harrison's Internal Medicine 18th edition

16

An unusual condition in which a restricted neurological deficit spreads relentlessly over a small period of time, usually hours, to involve adjacent functional areas supplied by the affected artery.

Reference- Harrison's Internal Medicine 18th edition

17

Hypertension ( Systolic or diastolic) Smoking Atrial Fibrillation Myocardial Infarction Hyperlipidemia Diabetes Congestive Heart Failure Acute Alcohol abuse TIA >70% occlusion of the carotid arteries Oral contraceptives in women Hypercoagulopathy Polycythemia and Hemoglobinopathy Age, Gender(Male : Female 3:2), Race, Prior Stroke, and Heredity
Reference- Harrison's Internal Medicine 18th edition 18

3-4% of strokes occur in people aged 15-45 Sickle Cell anemia, tuberculosis Hypercoaguable states

Drugs

Pregnancy, OCP use, antiphospholipid antibodies, protein C and S deficiencies,nephrotic syndrome Cocaine, amphetamines

Reference- Harrison's Internal Medicine 18th edition

19

Ischemic (85% of stroke, Embolic or Thrombosis) Hemorrhagic (15% of stroke)

Reference- Harrison's Internal Medicine 18th edition

20

Acute Stroke Ischemic (85%) Hemorrhagic (15%) Subarachnoid H.

Thrombotic (55%)
Lacunar (20%) Large vessel (35%)

Embolic (30%)

Intracerebral & Cerebellar H

Subdural & Extradural H. and Hematoma

Artery-artery embolism

Cardioembolic
AF, IHD, VHD,
21

Reference- Harrison's Internal Medicine 18th edition

Usually develops at night during sleep Symptoms perceived in morning Suspect in h/o hypercoaguable states, atherosclerosis and collagen vascular disorders

Reference- Harrison's Internal Medicine 18th edition

22

Occurs at any time Frequently during periods of vigorous activity Hx of Atrial fibrillation, valvular vegetations, thromboembolism from MI, ulcerated plaques in carotid system Seizures in 20% of cases

Reference- Harrison's Internal Medicine 18th edition

24

Reference- Harrison's Internal Medicine 18th edition

25

Occur during stress or exertion Focal deficits rapidly evolve Signs of raised ICT Confusion, coma or immediate death

Reference- Harrison's Internal Medicine 18th edition

26

Loss of Consciousness Headache Vomiting Previous TIA Gradual Onset

Ischemic -ve -ve -ve +ve +ve

Hemorrhagic +ve +ve +ve -ve -ve (Sudden and maximal) +ve Moderate/ Severe

Relation with activity BP

-ve
-ve/mild
Reference- Harrison's Internal Medicine 18th edition

27

Reference- Harrison's Internal Medicine 18th edition

28

Left (Dominant) Hemisphere Stroke: Common Pattern Aphasia , Difficulty reading, writing, or calculating Majority of right handed and most left handed patients have dominance for speech and language located in the left hemisphere Left hemisphere infarction is characterized by aphasia (both motor [Brocas] and sensory [Wernickes]) and apraxia Right Hemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze

Reference- Harrison's Internal Medicine 18th edition

29

Right (Non-dominant) Hemisphere Stroke: Common Pattern Less predictable syndromes Left Hemiparesis Left-sided sensory loss

Poor left conjugate gaze Dysarthria Attention defects: extinction and neglect Spatial disorientation Behavioral changes: acute confusion and delirium Defect of left visual field
Reference- Harrison's Internal Medicine 18th edition 30

Reference- Harrison's Internal Medicine 18th edition

31

Reference- Harrison's Internal Medicine 18th edition

32

Reference- Harrison's Internal Medicine 18th edition

33

Stroke Syndromes

Large-vessel stroke within anterior ciculation

Large-vessel stroke within posterior ciculation

Small-vessel disease of either vascular bed

Internal carotid artery and Its branches

PCA

Basilar Artery

ACA

MCA

Vertebral and posterior inferior cerebellar Reference- Harrison's Internal Medicine arteries
18th edition

34

Reference- Harrison's Internal Medicine 18th edition

35

Anterior Circulation From carotid system Supplies 80% of brain

Posterior Circulation From vertebral system Supplies 20% of brain

Reference- Harrison's Internal Medicine 18th edition

36

CA arises from the innominate artery on the right and

aortic arch on the left. At level of upper neck CA

branches into internal and external

the internal carotid artery terminates into the middle (MCA) and anterior (ACA) cerebral arteries

Reference- Harrison's Internal Medicine 18th edition

37

Reference- Harrison's Internal Medicine 18th edition

38

Reference- Harrison's Internal Medicine 18th edition

39

The ACA is divided into two segments: the precommunal (A1) which connects the internal carotid artery to the anterior communicating artery

the postcommunal (A2) segment - distal to the anterior communicating artery .

The A1 segment gives rise to several deep penetrating branches that supply the anterior limb of the internal capsule, the anterior perforate substance, amygdala, anterior hypothalamus, and the inferior part of the head of the caudate nucleus. A2 segment - Supplies basal and medial aspects of the cerebral hemispheres, extends to anterior two thirds of Reference- Harrison's Internal Medicine parietal lobe.
18th edition

40

Reference- Harrison's Internal Medicine 18th edition

41

Reference- Harrison's Internal Medicine 18th edition

42

SIGNS AND SYMPTOMS

STRUCTURES INVOLVED

Paralysis of opposite foot and leg A lesser degree of paresis of opposite arm Cortical sensory loss over toes, foot, and leg a Urinary incontinence

Motor leg area Arm area of cortex or fibers descending to corona radiata Sensory area for foot and leg Sensorimotor area in paracentral lobule Medial surface of the posterior frontal lobe; likely supplemental motor area probably cingulate gyrus and medial inferior portion of frontal, parietal, and temporal lobes Frontal cortex near leg motor area callosum
43

Contralateral grasp reflex, sucking reflex

Abulia (akinetic mutism), slowness, intermittent interruption, lack of spontaneity, whispering, distraction to sights and sounds Impairment of gait and stance (gait apraxia) Dyspraxia of left limbs

Corpus Reference- Harrison's Internal Medicine 18th edition

MCA supply the lateral surface of the hemisphere except for (1) frontal pole and a strip along the superomedial border of the

frontal and parietal lobes supplied by the ACA

(2) lower temporal and occipital pole convolutions supplied by PCA

The proximal MCA (M1 segment) gives rise to penetrating branches (lenticulostriate arteries) - supply the putamen, outer globus pallidus, posterior limb of the internal capsule, the

adjacent corona radiata, caudate 18th edition nucleus .

Reference- Harrison's Internal Medicine

44

In the sylvian fissure, the MCA divides into

superior and inferior

divisions (M2 branches)

Branches from the superior division supply the frontal and superior parietal cortex and those of the inferior division Supply the inferior parietal and temporal cortex
Reference- Harrison's Internal Medicine 18th edition

45

Reference- Harrison's Internal Medicine 18th edition

46

If the entire MCA is occluded at its origin contralateral hemiplegia, hemianesthesia, homonymous hemianopia, and gaze preference to the ipsilateral side. Dysarthria is common because of facial weakness. When the dominant hemisphere is involved, global aphasia is present when the nondominant hemisphere is affected, anosognosia, constructional apraxia, and neglect are found .

Reference- Harrison's Internal Medicine 18th edition

47

Partial syndromes due to embolic occlusion of a single branch include hand, or arm and hand, weakness alone or facial weakness with Broca aphasia, with or without arm weakness

A combination of sensory disturbance, motor weakness, and Brocas aphasia suggests that an embolus has occluded the proximal superior division and infarcted large portions of the frontal and parietal cortices .
Wernicke's aphasia without weakness involvement of the inferior division of the MCA supplying the posterior part (temporal cortex) of the dominant hemisphere Hemineglect or spatial agnosia without weakness indicates involvement of inferior division of the MCA in the nondominant hemisphere
Reference- Harrison's Internal Medicine 18th edition 48

Signs and symptoms: Structures involved Paralysis of the contralateral face, arm, and leg; sensory impairment over the same area : Somatic motor area for face and arm and the fibers descending from the leg area to enter the corona radiata and corresponding somatic sensory system

Motor aphasia: hemisphere

Motor speech area of the dominant

aphasia, word deafness, anomia, jargon speech, sensory agraphia, acalculia, alexia, finger agnosia, right-left confusion (the last four comprise the Gerstmann syndrome): Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere
Reference- Harrison's Internal Medicine 18th edition 49

Anosognosia , unilateral neglect, agnosia for the left half of external space, dressing "apraxia," constructional "apraxia," distortion of visual coordinates, inaccurate localization in the half field, impaired ability to judge distance, upsidedown reading, visual illusions: Nondominant

parietal lobe

Optic radiation deep to second temporal convolution

Homonymous hemianopia: Paralysis of conjugate gaze to the opposite side:

Frontal eye field

Reference- Harrison's Internal Medicine 18th edition

50

This artery arises from the internal carotid artery and supplies the posterior limb of the internal capsule and the white matter

posterolateral to it

The complete syndrome of anterior choroidal artery occlusion consists of contralateral hemiplegia, hemianesthesia and

homonymous hemianopia.

Since this territory is also supplied by penetrating vessels of the proximal MCA and the posterior communicating and posterior choroidal arteries, minimal deficits may occur, and patients frequently recover substantially.
Reference- Harrison's Internal Medicine 18th edition 51

With a competent circle of Willis, occlusion may go unnoticed. If the thrombus propagates up the internal carotid artery into the MCA or embolizes it, symptoms are identical to proximal MCA occlusion. When the origins of both the ACA and MCA are occluded at the top of the carotid artery, abulia or stupor occurs with hemiplegia, hemianesthesia, and aphasia or anosognosia.
Reference- Harrison's Internal Medicine 18th edition 52

In addition to supplying the ipsilateral brain, the internal carotid artery perfuses the optic nerve and retina via the ophthalmic artery.

In 25% of symptomatic internal carotid disease, recurrent transient monocular blindness (amaurosis fugax) warns of the lesion.

Reference- Harrison's Internal Medicine 18th edition

53

2 Vertebral arteries basilar artery posterior cerebral arteries

Reference- Harrison's Internal Medicine 18th edition

54

In 75% of cases, both PCAs arise from bifurcation of basilar artery; in 20%, one has its origin from ipsilateral internal carotid artery; in 5%, both originate from respective ipsilateral ICA

Two clinical syndromes are commonly observed with occlusion of the PCA: (1) P1 syndrome: midbrain, subthalamic, and thalamic signs, due to disease of the Proximal P1 segment of the PCA or its penetrating branches (thalamogeniculate, posterior choroidal )

(2) P2 syndrome: cortical temporal & occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery.
Reference- Harrison's Internal Medicine 18th edition 55

Reference- Harrison's Internal Medicine 18th edition

56

P1 Syndromes

Infarction usually occurs in the ipsilateral subthalamus and medial thalamus and in the ipsilateral cerebral peduncle and midbrain.
A third nerve palsy with contralateral ataxia (Claude's syndrome) or with contralateral hemiplegia (Weber's syndrome) may result. ataxia - the red nucleus or dentatorubrothalamic tract contralateral hemiballismus - subthalamic nucleus Extensive infarction in the midbrain and subthalamus occurring with bilateral proximal PCA occlusion presents as coma, unreactive pupils, bilateral pyramidal signs, and decerebrate rigidity.

Occlusion of the penetrating branches of thalamic and thalamogeniculate arteries produces less extensive thalamic & thalamocapsular lacunar syndromes.
The thalamic Djrine-Roussy syndrome consists of contralateral Reference- Harrison's Internal Medicine hemisensory loss followed later by an agonizing, searing or burning pain in the 57 18th edition

P2 Syndromes Occlusion of the distal PCA causes infarction of the medial temporal and occipital lobes. Contralateral homonymous hemianopia with macula sparing is the usual manifestation. If the visual association areas are spared and only the calcarine cortex is involved, the patient may be aware of visual defects. Medial temporal lobe and hippocampal involvement may cause an acute disturbance in memory, particularly if it occurs in the dominant hemisphere. If the dominant hemisphere is affected and the infarct extends to involve the splenium of the corpus callosum, the patient may demonstrate alexia without agraphia. Visual agnosia for faces, objects, mathematical symbols, and colors and anomia with paraphasic errors may also. Occlusion of the posterior cerebral artery can produce visual hallucinations Reference- Harrison's Internal Medicine 18th edition of brightly colored scenes and objects

58

Bilateral infarction in the distal PCAs produces cortical blindness (blindness with preserved pupillary light reaction). The patient is often unaware of the blindness or may even deny it (Anton's syndrome). Patients may experience persistence of a visual image for several minutes despite gazing at another scene (palinopsia) or an inability to synthesize the whole of an image (asimultanagnosia). Embolic occlusion of the top of the basilar artery can produce any or all of the central or peripheral territory symptoms. The hallmark is the sudden onset of bilateral signs, including pupillary asymmetry or lack of reaction to light
Reference- Harrison's Internal Medicine 18th edition 59

The vertebral artery, which arises from the innominate artery on the right and the subclavian artery on the left, consists of four segments. V1 extends from its origin to its entrance into the 6 th transverse vertebral foramen. V2 traverses the vertebral foramina from C6 to C2.

V3 passes through the transverse foramen and circles around the arch of the atlas to pierce the dura at the foramen magnum.

V4 segment courses upward to join the other vertebral artery to form the basilar artery; only the fourth segment gives rise to branches that supply the brainstem and cerebellum.

The posterior inferior cerebellar artery (PICA) in its proximal segment supplies the lateral medulla and, in its distal branches, the inferior surface of the cerebellum.

Reference- Harrison's Internal Medicine 18th edition 60

If the subclavian artery is occluded proximal to the origin of the vertebral artery, there is a reversal in the direction of blood flow in the ipsilateral vertebral artery. Exercise of the ipsilateral arm may increase demand on vertebral flow, producing

posterior circulation TIAs, or "subclavian steal.

Reference- Harrison's Internal Medicine 18th edition

61

Branches of the basilar artery supply the base of the pons and superior cerebellum and fall into three groups: Paramedian , 710 in number, which supply a wedge of pons on either side of the midline

short circumferential, 57 in number, that supply the lateral two-thirds of the pons and middle and superior cerebellar peduncles bilateral long circumferential (superior cerebellar and anterior inferior cerebellar arteries), which course around the pons to supply the cerebellar hemispheres.
Reference- Harrison's Internal Medicine 18th edition 62

Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower basilar artery) On side of lesion Paralysis with atrophy of one-half half the tongue:

Ipsilateral twelfth nerve

On side opposite to lesion Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over one-half the body: Contralateral

pyramidal tract and medial lemniscus

63

Lateral medullary syndrome (occlusion of any of the five vessels may be

responsible vertebral, posterior inferior cerebellar, superior, middle or inferior lateral medullary arteries)

On side of lesion Pain, numbness, impaired sensation over one-half the face: Descending tract and

nucleus fifth nerve

Ataxia of limbs, falling to side of lesion: restiform

body, cerebellar hemisphere, cerebellar fibers, spinocerebellar tract

Nystagmus , diplopia , vertigo, nausea, vomiting:

Vestibular nucleus

Horner's syndrome ( miosis , ptosis , decreased sweating): Descending

sympathetic tract

Reference- Harrison's Internal Medicine 18th edition

64

Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag reflex:

Issuing fibers ninth and tenth nerves Loss of taste: Nucleus and tractus solitarius
Numbness of ipsilateral arm, trunk, or leg: Cuneate

and gracile nuclei

Weakness of lower face:

Genuflected upper motor neuron fibers to ipsilateral facial nucleus

On side opposite to lesion Impaired pain and thermal sense over half the body, sometimes face:

Spinothalamic tract

Reference- Harrison's Internal Medicine 18th edition

65

Total Unilateral medullary syndrome (occlusion of vertebral artery) Combination of medial and lateral syndromes Lateral pontomedullary syndrome (occlusion of vertebral artery) Combination of lateral medullary and lateral inferior pontine syndrome Basilar artery syndrome Combination of brainstem syndromes plus those arising in PCA distribution Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities): Bilateral long

Paralysis or weakness of all extremities, plus all bulbar musculature: Corticobulbar and corticospinal tracts

tract; cerebellar and peripheral cranial nerves

bilaterally

Reference- Harrison's Internal Medicine 18th edition

66

Medial Superior pontine syndrome (paramedian branches of upper basilar

artery)

On side of lesion Cerebellar ataxia (probably):

Superior and/or middle cerebellar peduncle

Internuclear ophthalmoplegia:

Medial longitudinal fasciculus

Myoclonic syndrome, palate, pharynx, vocal cords, respiratory apparatus, face, oculomotor apparatus, etc.: central tegmental

bundle, dentate projection, inferior olivary nucleus

On side opposite lesion Paralysis of face, arm, and leg: Rarely touch, vibration, and position are affected: Medial

Corticobulbar and corticospinal tract lemniscus

67

Lateral superior pontine syndrome (Syndrome of superior

cerebellar artery) On side of lesion Ataxia of limbs and gait, falling to side of lesion:

Middle and superior cerebellar peduncles, superior surface of cerebellum, dentate nucleus

Dizziness, nausea, vomiting; horizontal nystagmus: Vestibular

nucleus

Paresis of conjugate gaze (ipsilateral): Pontine

contralateral gaze

Reference- Harrison's Internal Medicine 18th edition

68

Miosis, ptosis, decreased sweating over face (Horner's syndrome):

Descending sympathetic fibers Tremor:Dentate nucleus, superior cerebellar peduncle

On side opposite lesion Impaired pain and thermal sense on face, limbs, and trunk: Spinothalamic

tract

Impaired touch, vibration, and position sense :

Medial lemniscus (lateral portion) Reference- Harrison's Internal Medicine

18th edition

69

Medial midpontine syndrome (paramedian branch of midbasilar artery) On side of lesion Ataxia of limbs and gait (more prominent in bilateral involvement):

Pontine nuclei

On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar

and corticospinal tract

Variable impaired touch and proprioception when lesion extends posteriorly: Medial

lemniscus

70

Lateral midpontine syndrome (Short circumferential artery)

On side of lesion Ataxia of limbs: Middle

cerebellar peduncle

Paralysis of muscles of mastication: Motor fibers

or nucleus of fifth nerve

Impaired sensation over side of face: Sensory

fibers or nucleus of fifth nerve

On side opposite lesion Impaired pain and thermal sense on limbs and trunk:

Spinothalamic tract

71

Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery)

On side of lesion Paralysis of conjugate gaze to side of lesion (preservation of convergence): Center for

conjugate lateral gaze Nystagmus: Vestibular nucleus

Ataxia of limbs and gait: Likely

middle cerebellar peduncle

Diplopia on lateral gaze:

Abducens nerve

On side opposite lesion Paralysis of face, arm, and leg:

Corticobulbar and corticospinal tract in lower pons

Impaired tactile and proprioceptive sense over half of the body: Medial lemniscus
72

Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery)

On side of lesion Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopsia:

Vestibular nerve or nucleus Facial paralysis: Seventh nerve lateral gaze

Paralysis of conjugate gaze to side of lesion: Center for conjugate

Deafness, tinnitus: Auditory nerve

or cochlear nucleus Ataxia: Middle cerebellar peduncle and cerebellar hemisphere

Impaired sensation over face:

Descending tract and nucleus fifth nerve

On side opposite lesion Impaired pain and thermal sense over one-half the body (may include face): Spinothalamic tract

Reference- Harrison's Internal Medicine 18th edition

73

Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries) On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil:

Third nerve fibers

On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and

corticospinal tract descending in crus cerebri

Reference- Harrison's Internal Medicine 18th edition

74

Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery)

On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers

and/or third nerve nucleus

On side opposite lesion Hemiataxia , hyperkinesias, tremor:

Red nucleus, dentatorubrothalamic pathway Reference- Harrison's Internal Medicine

18th edition

75

Brain Stem Stroke: Common Pattern

Hemiparesis or tetraparesis Sensory loss Diplopia Facial numbness Facial weakness (lower motor neurone) Nystagmus, vertigo Dysphagia, Dysarthria Ataxia, hiccups, vomiting Horner's syndrome Altered consciousness Crossed signs
Reference- Harrison's Internal Medicine 18th edition 76

Small penetrating branches

HT, DM, Atherosclerosis

Pure motor hemiplegia Lenticulostriate territory Pure sensory stroke Lat. Thalamus Clumsy hand dysarthria ataxic hemiparesis ataxia

Reference- Harrison's Internal Medicine 18th edition

77

Reference- Harrison's Internal Medicine 18th edition

78

occurs in vulnerable areas supplied by distal distribution cerebral arteries during periods of hypotension infarction between the anterior and middle cerebral arteries presents with hemiparesis and hemianesthesia, predominantly in the leg dominant hemisphere infarctions: decrease in verbal ability with preserved comprehension Infarction involving the posterior watershed area presents with homonymous hemianopia +/hypoesthesia in the face and legs
Reference- Harrison's Internal Medicine 18th edition 79