The Nervous System

- Is the bodys most organized and complex structural and functional

system. It profoundly affects both psychological and physiologic
functions.
- The function of nervous system is to control motor, sensory,
autonomic, cognitive, and behavioural activities.
- It consist of two major parts:
A. Central nervous system- including the brain and the spinal
cord
B. Peripheral nervous systemwhich includes the cranial
nerves, spinal nerves and autonomic nervous sytem
- The basic functional unit of the brain is neuron. It is composed of
dendrites, cell body and an axon.
The dendrites are branch type structures for receiving
electrochemical messages.
The axon is long projection that carries electrical impulses
away from the cell body
Types:
1. Acetylcholine-muscle movement
2. Biogenic amines (thinking process)
-Dopamine -Serotonin
-Norepinephrine -Histamine
3. Amino acids
-GABA
-Peptides

- Some neurons have myelinated sheath that increases speed of

conduction.
- Nerve cell bodiues occurring in clusters are called a center.
- Neurotransmitters communicate messages from one neuron to
another or from a neuron to a specific target tissue. It potentiates,

terminates, or modulates specific action. Many disorders are due to,

at least in part, to an imbalance of neurotransmitters.

THE CENTRAL NERVOUS SYSTEM

BRAIN
It is the largest and most complex part of the nervous system. It is
composed of more than 100 billion neurons and associated fibers. The
brain is divided into three major areas:
A. Cerebrum- composed of two hemispheres, the thalamus, the
hypothalamus and the basal ganglia
B. The brain stem- includes the midbrain, pons and medulla
C. The cerebellum is located under the cerebrum and behind the brain
stem
CEREBRUM
- The outside surface of the hemispheres has wrinkled appearance
that is the result of many folded layers convulsions called gyri, which
increase the surface area of the brain accounting for the high level of
activity carried out by such a small appearing organ.
- The cerebral hemispheres are joined at the lower portion of the
fissure by the corpus callosum.
- The external or outer portion of the hemisphere \9the cerebral
cortex) is made up of gray matter. White matter makes up the
innermost layer and is composed of myelinated nerve fibers and
neuroglia cells that form tracts or pathways connecting various parts
of the brain with one another.
Both left cortex and the right cortex interpret sensory data,
store memories, learn and form concepts however each hemisphere
dominates the other in many functions.
In most people, for example, the left cortex has dominance for
systemic analysis, language and speech, mathematics, abstraction, and
reasoning.
The right cortex has dominance for assimilation of sensory
experience such as visual, spatial information, and activity such as
dancing, gymnastics, music and art appreciation.

- The cerebral hemispheres are divided into pairs of lobes as follows:

Frontal the largest lobe, located in the fron of the brain.the
major functions of this lobe are concentration, abstract
thought, information storage, or memory and motor function. It
contains Brocas area, which is located in the left hemisphere
and is critical for motor control of speech. It is also responsible
in large part for a persons affect, judgement, personality and
inhibitions
Parietal- a predominantly sensory lobe posterior to the frontal
lobe. This lobe analyzes sensory information and relays the
interpretation of this information to other cortical areas and is
essential to a persons awareness of the body position in
space, size and shape discrimination and right-left orientation.
Temporal located inferior to the frontal and parietal lobes,
this lobes contains the auditory receptive areas and plays a
role in memory of sound and understanding of language and
music
Occipital located posterior to the parietal lobe, this lobe is
responsible for visual interpretation and memory.
Area
Functions
Frontal

Controls movements of voluntary

muscle
Primary motor area

Facilitates voluntary movement of

skeletal muscle

Speech area (Wernicks )

Understanding of spoken and

written words

- Located in the posterior part

of the superior temporal
convolution
Motor area (Brocas)
- Located in the lateral, inferior
portion of the frontal lobe
Temporal
Parietal

Promotes vocalization of words

Receives and interpret olfactory and

auditory stimuli
Promotes recognition of pain,

coldness, light touch (Contralateral

reception)
Occipital

Receives and interprets visual

stimuli

- The corpus callosum, a thick collection nerve fibers that connects

the two hemispheres of the brain is responsible for the transmission
of the information from one side of the brain to the other.
- The basal ganglia are masses of nuclei located deep in the cerebral
hemispheres that are responsible fro control of fine motor
movements, including those of the hands and lower extremities
- The thalamus lies on either side of the third ventricle and acts
primarily as a relay station for all sensation except smell. All memory,
sensation and pain impulses pass through this section of the brain.
- The hypothalamus is located anterior and inferior to the thalamus
and beneath and lateral to the third ventricle. The hypothalamus
plays an important role in the endocrine system because it regulates
the pituitary secretion of hormones that influence metabolism,
reproduction, stress, response and urine production

BRAIN STEM
The brain stem consists of the midbrain, pons and medulla
oblongata:
MIDBRAIN- connects the pons and cerebellum with the
cerebral hemispheres, it contains sensory and motor pathways
and serves as the center for auditory and visual reflexes.
Cranial nerves III and IV originate in the midbrain.
PONS is situated in front of the cerebellum between the
midbrain and the medulla and between medulla and the
midbrain. Cranial nerves V through XIII originate in the pons.
Portion of pons help regulate respiratory system
Medulla-control cardiac rate, BP, respirators and swallowing

CEREBELLUM
Has two hemispheres
Coordination of skeletal muscle activity, maintenance of balance,
posture and control of voluntary movements

STRUCTURES PROTECTING THE BONE

- THE brain is contained in the rigid skull which protects from injury.
The major bones of the skull are frontal, temporal, parietal, occipital
and sphenoid bones.
- The meninges fibrous connective tissues that cover the brain and
spinal cord, provide protection, support and nourishment. The
layers of the meninges are the dura mater, arachnoid and pia mater:
Dura mater- the outermost layer, covers the brain and the
spinal cord
Arachnoid the middle membrane. It contains cerebrospinal
fluid.
Pia mater the innermost, thin transparent layer that hugs the
brain closely and extends into every fold of the brains surface

CEREBROSPINAL FLUID
- Is a clear and colorless fluid that is produced in the choroid plexus of
the ventricles and circulates around the surface of the brain and
spinal cord.
- It is important in immune and metabolic functions in the brain. It is
produced at a rate of about 500ml/day.
- The CSF may also be tested for immunoglobulins or presence of
bacteria.

THE SPINAL CORD

- Is continous with the medulla, extending from the cerebral
hemispeheres and serving as the connection between the brain and
periphery
- The bones of the vertebral column surround and protect the spinal
cord and consist of 7 cervical, 12 throracic and 5 lumbar vertebrae
and terminate in the coccyx.
- Gives rise to 31 pairs of spinal nerves (C1-C8, T1-T12, L1-L5, S1-S5,
coccygeal nerve)
- Center for conducting messages to and from the brain; a reflex center

THE PERIPHERAL NERVOUS SYSTEM

- It includes the cranial nerves, the spinal nerves and the autonomic
nervous system.

CRANIAL NERVES
- It innervate the head, the neck and special structures. There are 12
pairs of cranial nerves emerge from the lower surface of the brain
and pass through openings in the base of the skull
Cranial Nerves
I. Olfactory
II. Optic
III. Oculomotor

TYPE
Sensory
Sensory
Motor

IV. trochlear
V. trigeminal

Motor
Mixed

VI. abducens
VII. facial

Motor
Mixed

VIII. acoustic
IX.
glossopharyngeal

Sensory
Mixed

X. Vagus

Mixed

XI. Spinal
accessory
XII. hypoglosal

Motor
Motor

FUNCTION
Sense of smell
Visual acuity and visual fields
Muscles that move the eye and
lid, papillary constriction, lens
and accommodation
Muscle that move the eye
Facial sensation, corneal reflex,
mastication
Muscles that move the eye
Facial expression and muscle
movement, salivation and tearing,
taste, senasation in the ear
Hearing and equilibrium
Taste sensation in the pharynx
and tongue and pharyngeal
muscles, swallowing
Muscles of the pharynx, larynx
and soft palate, sensation in
external ear, pharynx, larynx,
thoracic and abdominal viscera,
parasympathetic innervations of
thoracic and abdominal organs
Sternocleidomastoid and
trapezius muscles
Movement of the tongue

THE SPINAL NERVES

The spinal cord is composed of 31 pairs of spinal nerves, 8 cervical,
12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal

AUTONOMIC NERVOUS SYSTEM

- Regulates the activities of internal organs of internal organs

such as the heart, lungs, blood vessels, digestive organs and

glands.
- There are two major divisions:
A. Sympathetic nervous system- were predominantly
excitatory responses, most notably the fight and flight
response
B. Parasympathetic nervous system- which controls mostly
visceral functions
Structures or Activity
Pupil of the eye
Circulatory System
Rate of force of heartbeat
Blood vessels
In heart muscle
In skeletal muscle
In abdominal viscera
And the skin
Blood pressure
Respiratory System
Bronchioles
Rate of Breathing
Digestive System
Peristaltic
movement
of
digestive tube
Muscular
sphincters
of
digestive tube
Secretion of salivary glands
Secretion of stomach, intestine
and pancreas
Conversion of liver glycogen to
glucose
Genitourinary system
Urinary bladder
Muscle walls
Sphincters
Muscle of the uterus

Parasympathetic
Effects
Constricted

Sympathetic
Effects
Dilated

Decreased

Increased

constricted
No direct effect
No direct effect

Dilated
dilated
Constricted

Decreased

Increased

constricted
Decreased

Dilated
Increased

Increased

Decreased

Relaxed

Contracted

Thin, watery saliva

Increased

Thick, viscid saliva

No direct effect

No direct effect

Increased

Contracted
Relaxed
Relaxed, variable

Relaxed
Contracted
Contracted

under

Blood vessel of external Dilated

genitalia
Integumentary system
Secretion of sweat
No direct effect
Pilomotor muscles
No direct effect
Adrenal medulla

No direct effect

some conditions;
varies
with
menstrual
cycle
and pregnancy
No direct effect

Increased
Contracted
(goose-flesh)
Secretion
of
epinephrine
and
norepinephrine

Autonomic Nervous System

Controls involuntary or automatic body functions
Has two subdivisions, serving same organ but have counterbalancing
effects; each system can inhibit the organ stimulated by the
other
Sympathetic Nervous System
originates from lateral horns of first thoracic through the
first lumbar of spinal cord (thoracolumbar)
helps the body cope with events in the external
environment
Functions mainly during stress, triggering the fight or flight
response
Increases heart rate and respiratory rate, pupil dilation,
cold, and sweaty palms
Parasympathetic Nervous System
Consist of the vagus nerves originating in the medulla of the
brain stem and spinal nerves originating from the sacral
region of the spinal cord (craniosacral)
Activates GI system
Supports restorative, resting body function through such
actions as replenishing fluids and electrolytes

Effect organ

Sympathetic

Parasympathetic

Heart

Increased rate and

contractility

Decreased rate and

contractility

Lungs

Relaxation

Contraction

Decreased Contraction

Increased

GIT
Motility
Tone sphincters

Relaxation

Urinary bladder
Bladder muscle
Sphincter

Liver

Relaxation

Contraction

Contraction

Relaxation

Glycogenolysis

None

Neurodiagnostic
Examination
Skull Films
x -ray visualization of the skull. It confirms skull fracture
remove metallic items from hair

Spine Films
X-ray visualization of the spine
Avoid flexion/rotation of spine when fracture is suspected

CT scan
Electroencephalography
Graphical recording of spontaneous electrical impulses of the
brain from scalp electrodes
Hair shampoo to remove oil/sprays- for better transmission of
electrical impulses of the brain
Avoid caffeine and other stimulants, anticonvulsants for at
least 24 hours. These substances affect electrical activities of
the heart
Wash hair after the procedure to remove EEG paste
Electricomyography (EMG) and Nerve conduction velocity
Emg records electrical activities in muscles at rest, during
voluntary contraction and in response to electrical stimulation
May be with mild discomfort due to the needles
Brain scan
Involves administration of radionuclide
Cerebral angiography
Intrarterial injection of contrast medium with simultaneous
radiographs of head and neck to visualize intracranial and
extracranial vessels
May experience hot. Flushing sensation as dye is injected
Remove metallic clips from hair
Check allergy to iodine or seafoods
Observe arterial puncture site for bleeding or hematoma.
Observe for any for any change in neurological status: due to
embolus, thrombus or vasospasm may at risk of ischemia
Bed rest may have head elevated for 6 to 8 hours. If femoral
puncture, must keep leg extended and immobile for several
hours to prevent dislodgement of clot

Lumbar tap (Lumbar puncture)

Introduction of needle into spinal subarachnoid space usually
at L3-4, L4-5, L5-S1, interevrtebral space, tp assess
cerebrospinal fluid
Encourage client to void pre procedure. To promote comfort
Assist client to fetal position to widen intervertebral spaces
Queckenstedsts may be preformed to test subarachnoid
obstruction.
Post-op: flat in bed for 6-8 hours. To prevent spinal headache
Headache may develop due to CSF leakegae: trated with
bedrest, analgesics and ice to head
Normal CSF vales: 0-15mmHg or 75 to 180mmH20
MRI
Ventriculography
Air is introduced directly into the lateral ventricles through
trephine openings (burr holes) into the skull, X-ray films are
yaken
Flat on bed for 24 to 48 hours
Monitor V/S and do neurologic checks
Severe headache last 48 hours
Observe seizure precaution
Observe respiratory difficulty

 An indication of how patient is functioning as a whole and how the

patient is adapting to the environment
1. General appearance
2. State of consciousness
Arousal component
Content component
3. Mood and effect-changes in the nervous system
4. Thought content
5. Intellectual capacity

NEUROLOGIC ASSESSMENT
I. Comprehensive History Taking
Demographic Data
Current health
Past health history
Medication history
Growth and development
Family health history
Psychosocial history
II. V/S
III.Mental Status Assessment
LOC
Orientation
Memory
Mood/affect
Intellectual performance
Judgment/Insight
Language/communication

IV.Motor System assessment-muscle strength, tone, coordination, gait

and station movement
V. Sensory Function-superficial sensation, touch/pain, temperature,
proprioception, discrimination
VI.Reflex activity
VII. Cranial nerve testing

MENTAL STATUS ASSESSMENT

WITH ABNORMAL FINDINGS
Unilateral neglect (lack of caring of the other side of the body); strokes
involving middle cerebral artery.
Poor hygiene and grooming: dementing disorders
Abnormal gait and posture: transient ischemic attacks(TIAs) , strokes,
and Parkinsons disease
Emotional swings, personality changes: strokes
Aphasia-defective or absent language function: TIAs, strokes involving
anterior/posterior artery; general term for impairment of language
Dysphonia- change in tone of voice
Dysarthria- (different in speaking); is indistinctness of words in word
articulation resulting from interference with the peripheral speech
mechanisms (e.g. muscles of the tongue, palate, pharynx, or lips)
[Phipps, 1998, p. 1901]
Decreased level of consciousness
Confusion, Coma

COGNITIVE FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS

Disorientation to time and place: stroke of right cerebral hemisphere

1. Memory deficits
2. Emotional defense
CRANIAL NERVE ASSESSMENTS
Cranial I (Olfactory): Anosmia
1. lesions of frontal lobes
2. impaired blood flow to middle cerebral artery.
Cranial II (Optic)
1. blindness in eye: strokes of internal carotid artery, TIAs
2. Homonymous hemianopia - impaired vision or blindness in
one side of both eyes; blockage of posterior cerebral artery.
3. Impaired vision: strokes of anterior cerebral artery; brain
tumors
Note:
Visual acquity-mediated by the cones of the retina
Field of vision or peripheral vision-portion of space in which
objects are visible during the fixation of vision in one direction.
The receptors for peripheral fields are the rod neurons of the
retina. (Phipps, 1998, p. 1906)
Cranial nerve III, IV, VI (Oculomotor, Trochlear, Abducens)-motor
nerves that arise from the brainstem
1. Nystagmus - involuntary eye movement; strokes of anterior,
inferior, superior, cerebellar arteries
2. Constricted pupils: may signify impaired blood flow to
vertebralbasilar arteries.
3. Ptosis (eyelid falldown); dropping of the upper eyelid over the
globestrokes of posterior inferior cerebellar artery;
myasthenia gravis, palsy of CN III

Cranial nerve V (Trigeminal)largest cranial nerve with motor and

sensory components: changes in facial sensations; impaired
blood flow to carotid artery
1. Decreased sensation of face and cornea on same side of body;
strokes of posterior inferior cerebral artery
2. Lip and mouth numbness
3. Loss of facial sensation: contraction of masseter and temporal
muscles, lesions CN V
4. Severe facial pain: trigeminal neuralgia (tic dorlourex)
Cranial VII (Facial nerve)mixed nerve concerned with facial
movement and sensation of taste
1. Loss of ability to taste
2. Decreased movement of facial muscles
3. Inability to close eyes, flat nasolabial fold, paralysis of lower face,
inability to wrinkle the forehead
4. Eyelid weakness; paralysis of lower face; paralysis of upper motor
neuron
5. Pain, paralysis, sagging of facial muscles: affected side in Bells palsy
Cranial VIII (Acoustic)composed of a cochlear division related to
hearing and a vestibular division related to equilibrium
(Phipps, 1998, p. 1909)
Decreased hearing or deafness: strokes of vertebralbasilar arteries
or tumors of CN VIII
Cranial IX(Glossopharyngeal) and cranial X (Vagus)chief function of
cranial nerve IX is sensory to the pharynx and taste to the
posterior third of tongue; cranial nerve X is the chief motor
nerve to the soft palatal, pharyngeal and laryngeal muscles
(Phipps, 1998, p. 1909)
1. Dysphagia (difficulty swallowing)
2. Unilateral loss of gag reflex
Cranial XI (Spinal accessory)motor nerve that supplies the
sternocleidomastoid muscle and upper part of trapezius
muscles
1. Muscle weakness
2. Cortralateral hemiparesis: strokes affecting middle cerebral artery
and internal artery
Cranial XII (Hypoglossal)

1. Atrophy, fasciculations (twitches): LMN disease

2. Tongue deviation toward involved side of the body

SENSORY FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS

Altered sensation occurs with variety of neurologic pathology
Altered sense of position: lesions of posterior column of spinal cord
Inability to discriminate fine touch: injury to posterior columns
MOTOR FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS
Muscle atrophy: LMNs disease
Tremors (groups, large of muscle fibers)-Parkinsons disease
(tremors at rest), multiple sclerosis (tremors observed in
activity)
Fasciculations (single muscle fiber): disease or trauma to LMN,
side effects of medications, fever, sodium deficiency, anemia
Flaccidity (decreased muscle tone): disease or trauma to LMN and
early stroke
Spasticity (increased muscle tone): disease of corticospinal motor
tract
Muscle rigidity: disease of EP motor tract
Cogwheel rigidity (muscular movement with small regular jerky
movement; parkinsons disease
Muscle weakness-in arms, legs, hands: TIAs
Hemiplegia-paralysis of half of body vertically
Flaccid paralysis: strokes of anterior spinal artery, multiple
sclerosis or myasthenia gravis
Total loss of motor function: below level of injury
Spasticity of muscle: incomplete cord injuries

CEREBELLAR FUNCTION ASSESSMENT WITH ABNORMAL FINDINGS

Ataxia (lack of coordination and clumsiness of movement,
staggering, wide-based and unbalanced gait)

Steppage gait (client drags or lifts foot high, then slaps foot onto
floor; inability to walk on heels; disease of LMN
Sensory ataxia (client walks on heels before bringing down toes and
feet are held wide apart; gait worsens with eyes closed
Parkinsonian gait (stooped over position while walking with
shuffling gait with arms held close to the side)
Rombergs test (Positive)- With feet approximated, the patient
stands with eyes open and then closed; if closing the eyes
increases the unsteadiness, a loss of proprioceptive control is
indicated
REFLEX
Hyperactive: reflexes
Decreased reflexes
Clonus of foot (Hyperactive, rhythmic dorsiflexion and plantar
flexion of foot)
Superficial reflexes (such as abdominal) and cremasteric reflex
Positive Babinski reflex (dorsiflexion of big toe)
Special Neurologic Assessment

Brudzinskis sign (pain, resistance, flexion of hips and knees when

head flexed to chest with client supine)

Positive Kernigs sign-excessive pain when examiner attempts to

straighten knees with client supine and knees and hips
flexed

Decorticate posturing (up)

Decerebrate posturing (down)

Altered Level of consciousness

1. Consciousness
Requires:
1. Arousal: alertness; dependent upon reticular activating system
(RAS); system of neurons in thalamus and upper brain stem
2. Cognition: complex process, involving all mental activities;
controlled by cerebral hemispheres
Process that affect LOC:
a.
b.
c.
d.
e.

Increased ICP
Stroke, hematoma, intracranial hemorrhage
Tumors
Infections
Demyelinating disorders

Systemic Conditions affecting LOC

Hypoglycemia
F/E imbalance
Accumulated waste products from liver or renal failure
Drugs affecting CNS: alcohol, analgesics, anesthetics
Seizure activity: exhausts energy metabolites
Level of Consciousness

Alert
Lethargic-very sleepy
Obtunded
Stuporous
Coma
Death

Client Assessment with Decreased LOC

a. Increased stimulation required to elicit response from client
b. More difficult to arouse; client agitated and confused when
awakened
c. Orientation changes: losses orientation to time first, then place,
person
d. Continuous stimulation required to maintain wakefulness
e. Client has no response, even to painful stimulation
Loss of Simultaneous Eye Movement
Loss of normal reflex functioning:
1. Dolls eye movement: eye movement in opposite direction of head
rotation (normal function of brain stem)
2. Oculocephalic reflex: eye move upward with passive flexion of neck;
downward with passive neck extension (normal function)
3. Oculovestibular response (cold caloric testing): instillation of cold
water in ear canal cause nystagmus (lateral tonic deviation of eyes)
toward stimulus (normal function)
GLASGOW RESPONSE
4
3
2
1

Eye opening responses

Opens eyes spontaneously
Opens eyes in response to voice
Opens eye in response to painful stimuli
Does not open eyes

Best verbal response

5
4
3
2
1

Oriented
Confused
Utters inappropriate words
Incomprehensible words
None

Best motor response

6
5
4
3
2
1
Total

Obeys command
Localizes pain
Withdraws with painful stimuli
Flexion (Decorticate posturing)
Extension (Decerebrate posturing
None
3-15

14 no impairment
3 compatible with brain death
7 state of coma

MOTOR FUNCTION ASSESSMENT

a. Client follows verbal commands
b. Pushes away purposely from noxious stimuli
c. Movements are more generalized and less purposeful (withdrawal,
grimacing)
d. Reflexive motor responses
e. Flaccid with little or no motor response

COMA

Irreversible coma - vegetative state

Permanent condition of complete unawareness of self and
environment, death of cerebral hemispheres with continued
function of brain stem and cerebellum
Client does not respond meaningfully to environment but has
sleep-wake cycles and retains ability to chew, swallow and
cough
Eyes may wander but cannot track objects
Minimally conscious state: client aware of environment, can
follow simple commands, indicates yes/no responses; make
meaningful movements (blink, smile)
Often results from severe head injury or global anoxia
Locked-in syndrome
1. Client is alert and fully aware of environment; intact cognitive
abilities but unable to communicate through speech or movement
because of blocked efferent pathways from brain
2. Motor paralysis but cranial nerves may be intact allowing client to
communicate through eye movement and blinking
3. Occurs with hemorrhage or infarction of pons, disorders of lower
motor neurons or muscle
Brain Death
1. Cessation and irreversibility of all brain functions
2. General criteria:
a. Absent motor and reflex movements
b. Apnea
c. Fixed and dilated pupils
d. No ocular responses to head turning and caloric stimulation
e. Flat EEG

NURSING DIAGNOSIS
Ineffective airway clearance: limit suctioning to <10-15
seconds, hyperoxygenate
Risk for aspiration
Risk for impaired skin integrity: preventive measures, continual
inspection
Impaired physical mobility: maintain functionality of joints,
physical therapy
Risk for Imbalanced Nutrition: Less than body requirements
Anxiety (of family)

SPINAL CORD INJURY

- Is primarily an injury of young adult males and 50% of those injured

are between 16 and 30 years of age.
- Motor vehicle crashes account for 48% of reported cases of SCI, with
falls 23%, violence primarily from gunshot wounds (14%),
recreational sporting activities (9%) and other events accounting for
the remaining injuries.
- The predominant risk factors for SCI include young age, male gender
and alcohol and drug use
Pathophysiology:
Damage in SCI ranges transient concussion (from which the
patient fully recovers), to concusion, laceration, and
compression of the spinal cord substance (either alone or in
combination), to complete transaction (severing) of the spinal
cord (which renders the patient paralyzed below the level of
the injury)
The vertebrae most frequently involved are the 5th, 6th and 7th
cervical vertebrae (C5 to C7), the 12th thoracic vertebrae (T12),
and the first lumbar vertebrae (L1).
SCI can be separated into two categories:
A. Primary injuries- are the result of the initial insult or
trauma and are usually permanent.
B. Secondary injuries- are usually the result of contusion,
tear injury, in which the nerve fibers begin to swell and
disintegrate
Primary concern for critical care nurses. It
reversible during the first 4 to 6 hours after injury.
Manifestations:
Subjective
Loss of sensation below level of injury

Inability to move
Objectivity
A. Early symptoms of spinal shock
Absence of reflexes below level of lesion
Flaccid paralysis below level of injury
Hypotonia results in bowel and bladder distention
Inability to perspire in affected parts
Hypotension
B. Later symptoms of spinal cord injury
Reflex hyperexcitability
State of diminished reflex hyperexcitability below site in all
instances of cord damage following hyperreflexia
In total cord damage-loss of motor and sensory function is
permanent
Sacral region-atonic bladder and bowel with impairment of
sphincter control
Lumbar region- spastic bladder and loss of bladder and anal
sphincter control
Thoracic-trunk below the diaphragm
Cervical-from neck down, if above C4 respirations and depressed
In partial cord damage, depends on the type of neurons affected
(spastic vs. flaccid)

Clinical manifestations:
Paralysis of muscles of respiration
Bradycardia
Hypotension
Urinary retention
Hypomotility
Muscle atrophy
Poikilothermia-abnormality in sensing change in temperature
The type of injury refers to the extent of injury to the spinal cord
itself.

1. Incomplete spinal cord lesions (the sensory or motor fibers, or

both, are preserved below the lesion)
are classified according to the area of spinal cord
damage;
A.1. central cord syndrome- motor deficits in the upper
extremities compared to the lower extremities, sensory loss
varies but is more pronounced in the upper extremities;
bowel/bladder dysfunction is variable or function may be
completely preserved
- caused: injury or edema of the central cord, usually of the
cervical area. May be caused by hyperextension injuries.
A.2. Anterior Cord Syndrome loss of pain, temperature and
motor function is noted below the level of the lesion; light
touch, position and vibration sensation remain intact.
- caused: the syndrome may be caused by acute disk
herniation or hyperflexion injuries associated with fracture
dislocation of vertebrae. It also may occur as a result of injury
to the anterior spinal artery, which supplies the anterior two
thirds of the spinal cord
A.3. Brown-sequard syndrome (lateral cord Syndrome)ipsilateral paralysis or paresis is noted. Together with
ipsilateral loss of touch, pressure and vibration and
contralateral loss of pain and temperature.
-caused: the lesion is caused by a transverse hemisection of
the cord 9half of the cord is transacted from north to south)
usually as aresult of knife or missile injury, fracture dislocation
of unilateral articular process, as possibly an acute ruptured
disk.
2. A complete spinal cord lesion- total loss of sensation and
voluntarymuscle control below the lesion) can result to
paraplegia or tetraplegia
Paraplegia- paralysis of the lower extremities with
dysfunction of the bowel and bladder from a lesion in the
thoracic, lumbar or sacral region of the spinal cord
Tetraplegia- paralysis of both arms and legs with
dysfunction of the bowel and bladder from alesion of the
cervical segments of the spinal cord.

MUSCLE FUNCTION AFTER SPINAL CORD INJURY (((log-rolling)

Spinal Cord
Injury

Muscle Functioning
remaining

Muscle Function Loss

Cervical, above
C4

None

All including respiration

C5

Neck, scapular elevation

Arm, chest, all below

chest

C6-C7

Neck, some chest

movement, some arm
movement

Some arm, fingers, some

chest movement all below
chest

Thoracic

Neck, arms (full), some

chest

Trunk, all below chest

Lumbo-sacral

Neck, arms, chest, turnk

Legs

Laminectomy
Autonomic dysreflexia (after spinal shock resolves)
Exaggerated autonomic response to stimuli: such as distended
bladder or bowel (e.g. pain)
Severe hypertension
Headache
Flushed skin
Diaphoresis
Nasal Congestion
Management:
emergency management: any patient who is involved in a motor
vehicle crash, a diving orcontact sports injury, a fall,or any direct
trauma to the head and neck must be considered to have SCI. Initial

care must be a rapid assessment, extrication, and stabilization or

control of life threatening injuries and transportation to the most
appropriate medical facility.
The the scene of injury patient must be immobilized on a spinal
board with head and neck maintained in a neutral position, to
prevent incomplete injury from becoming complete.
1. Place in high-Fowlers position
2. Ensure patency of urinary drainage and assess for infection.
3. Eliminate other potential stimuli
4. Notify physician: administer prescribed antihypertensive
Nursing Diagnosis
1. Impaired gas exchange related to muscle fatigue and retained
secretions.
2. Decreased cardiac output r/t venous pooling and immobility
3. Impaired skin integrity r/t immobility and poor tissue perfusion
4. Constipation r/t the injury, inadequate fluid intake, diet low in
roughage and immobility
5. Urinary retention
6. Impaired physical mobility
7. Risk for autonomic dysreflexia r/t reflex stimulation of SNS
8. Altered nutrition less than body requirements r/t increased
metabolic demand
9. Sexual dysfunction r/t inability to achieve erection or perceive
pelvic sensations

Medical Management
ImmoblizationGardner well tongs, halo external fixation
Maintenance of heart rate (Atropine) and BP (dopamine)
vasopressors
Methylprednisolone therapy
Insertion of NGT
Intubation, if needed
Indwelling urinary catheter
Stress ulcer prophylaxis (Proton-pump inhibitos, H2 blockers)
Physical therapy

STROKE/ TRANSIENT ISCHEMIC ATTACK

Stroke is a brain attack
needing emergency management, including specific
treatment and secondary and tertiary prevention
Stroke is an emergency
where virtually no allowances for worsening are tolerated
Stroke is treatable
optimally, through proven, affordable, culturally-acceptable
and ethical means
Stroke is preventable
in implementable ways across all levels of society
CEREBROVASCULAR DISORDERS- is an umbrella term that refers to a
functional abnormality of the central nervous system that occurs when the
normal blood supply to the brain is disrupted.
It can be divided into two major categories:
1. Ischemic stroke
2. Hemorrhagic sroke

Basic Location of Cerebral Aneurysm

Cerebral embolus-moving
Cerebral thrombus
Cerebral hemorrhage

Ischemic stroke-little blood flow

- Or brain attack is a sudden loss of function resulting from disruption
of the blood supply to a apt of the brain.
1. Thrombotic formation of a blood clot with coagulation the results in
the narrowing of the lumen of a blood vessel with eventual
occlusion
2. Embolic occlusion of a cerebral artery by an embolus, resulting in
necrosis and edema of the area supplied by the involved vessel
Ischemia----energy failure---- 1. Acidosis 2. Ion imbalance--intracellular calcium increased and Depolarization and increased
glutamate--- cell membrane and proteins break down, formation of
free radicals , protein production decreased---lead to cell injury and
death

Hemorrhagic stroke-disrupted blood flow

- Are caused by bleeding into the brain tissues, the ventricles or at the
subarachnoid spaces
1. Intracerebral hemorrhage stroke-bleeding within the brain caused
by a rupture of vessels
Most common in patients with hypertension, and cerebral
atherosclerosis because degenerative changes from diseases
cause rupture of the blood vessel

2. Subarachnoid hemorrhagic stroke-hemorrhage into the

subarachnoid space may 0occur as a result of an aneurysm or
Aarteriovenous malformation (AVM), trauma or hypertension.
3. Intracranial aneurysm is a dilation of the walls of cerebral artery
that develop as a result of weakness in the arterial wall. The cause of
aneurysm is unknown although research is ongoing. An aneurysm
may due to atherosclerosis which result in defect in the vessel wall
with subsequent weakness of the wall.
Development of CVA
1. Transient Ischemic attack-brief episodes of neurologic
manifestations which clear completely in less than 24 hours
2. Reversible ischemic neurologic deficit-neurologic deficits remain
after 24 hours but leaves no residual signs and symptoms after days
to weeks
3. Stroke in-evolution-progressing stroke which develops over a period
of hours or days; manifestations dont resolve and leave residual
neurologic effects
4. Completed stroke- when neurologic deficits remain unchanged over
2-3 day period

Risk Factors
Prior ischemic episodes
Cardiac disease
DM
Atherosclerotic diseasae
Hypertension, hypercholesterolemia
Polycythemia
Smoking
Oral contraceptives
Emotional stress
Obesity
Family history of stroke

Age
Warning signs that may precede CVA
Paresthesia
Transient loss of speech
Hemiplegia
Severe occipital or nuchal headaches
Vertigo or syncope
Motor or sensory disturbances (tingling transient paralysis)
Epistaxis
CLINICAL MANIFESTATIONS
Numbness or weakness of the face, arm, or leg especially on one
side of the body
Confusion or change in mental status
Trouble speaking or understanding speech
Visual disturbance
Difficulty walking, dizziness or loss of balance or coordination
Sudden severe headache
******** motor, sensory, cranial nerve, cognitive and other functions may
be disrupted
SPECIFIC DEFICITS
Dependent upon area damaged
Hemiplegia
Aphasia
- sensory/receptive-Wernicks aphasia
- motor/expressive-Brocas aphasia (able to understand the
stimuli but cannot express
Global aphasia
- Agnosia
- Dysarthria
- Incontinence
- Horners syndrome-decrease lacrimation
- Unilateral neglect

Emotional or Behavioral Reactions:

Severe mood swings
Social withdrawal
Inappropriate sexual behavior
Outbursts of frustration and/or anger
Regression to an earlier behavior
Right brain damage
Paralyzed left side
Spatial-perceptual deficits
Tend to deny or minimize
problems
Impaired judgment
Impaired time concepts
Short term span

Left brain damage

Paralyzed right side
Impaired speech/language
Impaired right and left
discrimination
Aware of deficits, depression,
anxiety
Impaired comprehension
Slow performance, cautious

Middle cerebral artery Involvement

Contralateral paralysis
Contralateral anesthesia, loss of proprioception, fine touch,
localization
Aphasia
Neglect of opposite side
Homonymous hemianopia-loss of vision for one half of the visual
field
Diagnostic procedures

CT scan-determine if vascular or nonvascular lesions

Angiography
MRI
Laboratory (CBC, PT, PTT)-not definitive to conform diagnosis

Medical management

Decreased ICP

BP management
Fluid volume management
Tissue plasminogen activator-must be given within 3 hours of onset
of manifestations and will dissolve clot; recombinant altephase
(Activase rt-pa)
Antithrombotic (aspirin, clipyridamole)-prevent platelet aggregation
Anticoagulant (heparin, clexane)
Steroids or osmotic, diuretics
Antihypertensive and diuretics

Nursing management

Hourly neurological assessment

Monitor and prevent intracranial hypertension
Positioning
- bed rest: keep mainly on unaffected side
- use of pillows to support to prevent flexion deformity,
thrombus formation
- external hip rotation
- assist in progressive activity (mobility)
- Progressive self-care (ADL)

Prevention of injury
- eyes-normal saline, artificial tears, eye patch
- side rails up
- decubitus ulcer prevention/management
- Oral mucosa care
Nutrition/prevention of aspiration
- Communication
- Others:
Reorientation
Minimize environmental stimuli
Emotional support
Rehabilitative
Discharge care

- Ways to prevent recurrence

dietary modification
Stress reduction
Smoking cessation
Exercise program
Drug compliance
- Residual deficits and balancing realistic expectation
- Special methods of feeding
- Ensure continuity of care and emotional support

Client with Seizure

Disorder
Seizures-alteration in consciousness, sensory and motor
- Abnormal motor, sensory, autonomic, or psychic activity that
result from sudden excessive discharge from cerebral neurons.
Paroxysmal motor, sensory, or cognitive manifestations of
spontaneous abnormal discharges from neurons in cerebral cortex
May involve all or part of brain consciousness, autonomic
function, motor function and sensation

Epilepsy: any disorder characterized by recurrent seizures

- Is a group of syndromes characterized by unprovoked,
recurring seizures
Categorization of seizures:
Partial seizures: activation of part of one cerebral hemisphere
a. Simple partial seizure: no altered consciousness, recurrent
muscle contraction; motor portion of cortex affected.
: generally without impairment of consciousness
b. Complex partial seizure: impaired consciousness; may engage in
automatisms (repetitive nonpurposeful activity such as lip smacking,
preceded by aura, originates in the temporal lobe)

Generalized seizures: involve electrical discharges in the

whole brain
Involves both brain hemispheres; consciousness always
impaired
Absence seizures (petit mal): characterized by sudden brief
cessation of all motor activity, blank stare and
unresponsiveness often with eyes fluttering
Grandma seizure- is characterized by an aura. It may be
flushing lights, smells, spots before the eyes, dizziness
Tonic-clonic phase: is accompanied by dyspnea,
drooling of saliva, urinary incontinence

Post ictal phase: is characterized by exhaustion,

headache, drowsiness, deep sleep of 1 to 2 hours,
disorientation
Preceded by aura, sudden loss of consciousness
Tonic phase: rigid muscles, incontinence (as muscle contracts,
bladder relax)
Clonic phase: altered contraction, relaxation, eyes roll back,
froths at mouth
Post-ictal phase: unconscious and unresponsive to stimuli
OTHER TYPES
Petit mal (absence or little sickness) is not preceeded by an
aura. There is little or no tonic-clonic movements. It is
characterized by blank facial expression and automatism like lichewing, cheek smacking. Regain of consciousness is as rapid as
it was lost; last for 10 to 20 seconds. It usually occurs during
childhood and adolescents.
Jacksonian (focal seizure)- common in clients with organic brain
lesion like frontal lobe tumor. Aura is present like numbness,
tingling, crawling feeling. It is chaeacterized by tonic clonic
movements of group of muscles e.g. hands, foot or face , then
proceeds to grand mal seizure
Psychomotor seizure- it is psychiatric component. Aura is
present 9hallucinations and illusions. It is characterized by
mental clouding 9 being out of touch with environment). The
client appears intoxicated. During the time of loss of
consciousness, there is ongoing physical activities. It is
manifested by confusion, amnesia and need fro sleep. The client
may commit violent or antisocial acts. E.g. going naked in public,
running amok, during the time of loss of consciousness
Febrile seizure this is common among children under 5 years
of age, when body temperature is rising

Status Epilepticus- a type of seizure occurring in rapid

succession and full consciousness is not regained between
seizures. Brain damae may occur secondary to prolonged
hypoxia and exhaustion. The client is often in coma for 12 to 24
hours, during which time recurring seizures occur. The attack is
usually related to failure to take prescribed anticonvulsant.
1. Continuous seizure activity, generally tonic-clonic type
2. Client at risk to develop hypoxia, acidosis, hypoglycemia,
hyperthermia, exhaustion
3. Life threatening medical emergency requiring immediate treatment:
b.
Establish and maintain airway
c.
Diazepam (Valium) and Lorazepam (Ativan) intravenously at
d.
50% Dextrose IV
e.
Phenytoin (Dilantin) IV-increase seizure threshold
f.Pentobarbital-lessen nervous irritation

Medications:
a. Manage but do not cure seizures- suppresses the abnormal
electric impulses from the seizure focus to toher cortical areas,
thus preventing the seizure but not eliminating the cause of
the seizure
Ex. Hydantoins- dialntin
Barbiturates- phenobarbital
Benzodiazepines- diazepines
Iminostilnes- carbamazepine
Key Interventions:
1. Stay with the client
2. Protect client from injury
Put padded side rails
If the client sitting or standing, ease him upto onto the floor.
Protect head with small pillow or place the head onto the lap
Do not apply restraints

Do not insert tongue blade during tonic-clonic movements

3. maintaining airway
Turn client to side
Loosen constricting clothing especially around the neck
Nursing Diagnosis:
1. Risk for Ineffective airway clearance
2. Anxiety
Interventions:
2. Assess for signs and symptoms of seizure activity such as report of
aura or twitching of muscle groups
3. Have an oral airway oxygen and suction readily available
4. Stay with client to protect him from injury and observe seizure
activity. If he is in bed, remove pillows, raise side rails, put bed on flat
position. Loosen any restrictive clothing
5. After seizure, assess respiration and pulse. If they present and he is
unresponsive turn him onto his side to keep his airway patent
6. Cover him with a blanket for warmth and privacy
7. Observe and document characteristics of the seizure
Anyiconvulsant and pregnancy
- Phenytoin, carbamazepine, trimethadione, valporic acid have
teratogenic properties.Valporic acid can cause neural tube
defect (spina bifida)
- It can cause loss of folate acid

Client with Multiple

Sclerosis
Multiple Sclerosis- is an autoimmune disorder that causes destruction of
myelin sheath of nerve fibers in the brain and spinal cord
1. Believed to be autoimmune response to prior viral infection
2. Inflammation destroys myelin leading to axon dysfunction; neurons
in spinal cord, brain stem, cerebrum, cerebellum and optic nerve
affected
3. Stressors trigger multiple sclerosisfebrile states, pregnancy,
physical exertion and fatigue and these can trigger relapses
4. Incidence is highest in young adults (20-40); onset between 20-50;
females more than males
Manifestations
1. Fatigue
2. Optic nerve involvement: blurred vision, haziness, blindness
3. Brain stem involvement: nystagmus, dysarthria (scanning speech);
cognitive dysfunction, vertigo, deafness
4. Weakness, numbness in legs, spastic paresis, bladder and bowel
dysfunction
5. Cerebellar involvement: nystagmus , ataxia, hypotonia
6. Charcoats triad
S- canning speech (repetition)
I- intention tremors
N- ystagmus
exacerbations may be aggravated by fatigue, chilling and
stress

emotional

Collaborative management:
patch the eye alternately for diplopia
provide- well balanced diet, high in fiber to prevent constipation

physical therapy to improve muscle strength and to avoid

contracture
avoid hot baths. Heat increases weakness
force fluids to prevent constipation and infection
speech therapy to relieve scanning speech
plasmapheresis: to inhibit autoimmune response
pharmacotherapyglucocorticoids
muscle relaxants- to relieve muscle spasm
immunosuppresants- to reduce relapse

Myasthenia
Gravis
Disturbance in the transmission of impulses at the myoneural
junction resulting in profound weakness (muscle of the eyes, eyelid,
chewing, swallowing, speaking and breathing)
Believed to be due to reduced acetylcholine receptors due to
destruction and blockage attributed to autoimmune process
An autoimmune disorder, characterized by varying degrees of
weakness of the voluntary muscles (Smeltzer & Bare, 2004, p. 1956)
Highest in young adult females.
Manifestations
Extreme muscle weakness, worsens as the muscle is used but
disappears with rest
Dysphagia, drooling
Diplopia (double vision)
Dysarthria
Ptosis of the eyelid (both eyes), strabismus
Myasthenia smile (nasal smile)snarl smile, mask like facial
expression
Impaired speech
Respiratory difficulty
Note:
Myasthenia gravis is purely a motor disorder with NO effect on
sensation or coordination

Diagnostic Test

 Neostigmine (Prostigmine)subcutaneous or IV administration of

tensilon (prevents enzymatic breakdown of Ach) to provide relief of
symptoms.2mg first rhen 8mg. positive tensilon test is observed as
improvement in muscular strength. Muscle weakness returns in 3 to
5 min.
The thymus gland, which is a site of acetylcholine receptor antibody
production is enlarged in myasthenia gravis
The anyidote for cholinergic is atropine sulphate
Medical Management
Pharmacologic
- Acetylcholinesterase blockers
- Corticosteroids to suppress immunity
Plasmapheresis X-ray or surgical removal of thymus (thymectomy)
COMPLICATIONS:
Myasthenic Crisis
Sudden inability to swallow or maintain respirations due to weakness
of the muscles of respiration; undermedication
Caused by undermedication or delayed medication
Exacerbation of the disease process characterized by severe
generalized muscle weakness and respiratory and bulbar weakness
that may result in respiratory failure (Smeltzer & Bare, 2004, p.1957)
Clinical manifestations: sudden marked rise of BP due to hypoxia,
increased HR, severe respiratory distress and cyanosis, Absent
cough and swallowing reflex, Increased secretions, increased
diaphoresis and increased lacrimation
Interventions: increased doses of cholinergics as long as the client
responds positively to endrophonium treatment

Cholinergic Crisis
Caused by Overdosage of anticholinergic drugs
May mimic the symptoms of exacerbation
Interventions- discontinue all cholinergic drugs until cholinergic
effects decrease, adequate ventilation, 1mg atropine sulphate
Note:

Differentiation of myasthenic crisis and cholinergic crisis can be

achieved with the edrophonium chloride (Tensilon) Test. The patient
with myasthenic crisis improves immediately following administration,
while patient with cholinergic crisis may experience no improvement or
deteriorate (Smeltzer & Bare, 2004)
Collaborative Management:
Assess swallowing and gag reflex before feeding the client. To
prevent aspiration
Administer medications 20-30 minutes before meals. To improve
ability to swallow and prevent choking
Administer medications at an exact time. To prevent myasthenic
crisis that results to respiratory distress
Protect the client from falls due to muscle weakness
Implement aspiration precautions
Start meal with cold beverage. To contract muscles of the throat and
improve ability to swallow
Promote adequate ventilation. To relieve respiratory difficulty
Avoid infections. Infection may trigger exacerbations of MG
Provide adequate rest with alternating activities
Plasmapheresis. This involves separation of antibodies from the
plasma to inhibit autoimmune response.
Avoid muscle relaxants, barbiturates, morphine sulphate,
tranquilizers, neomycin because these drugs pote4ntiate muscle
weakness because of effect on myoneural junction
Pharmacotherapy:
Acetylcholinesterase inhibitors/ cholinesterase inhibitorstransmit neuromuscular implses by preventing the destruction
of acetylcholine. Therefore there is increased muscle strength
Glucocorticoids- for anti-inflammatory effects
Antacid to prevent GI upset due to glucocorticoids
Surgery: thymectomy (surgical removal of thymus gland)- if MG is
due to thymoma
Survival guide for client with MG
Reschedule daily task to prevent weakness
Secure handicapped parking sticker
Frequent rest periods

Have alarm clock available- to take medications on time, this

prevents myasthenic crisis
Patch eye alternately for diplopia
Strat meal with cold beverage. To contract muscles of the
throat and prevent aspirations
Avoid factors that affect respiratory functions and may cause
respiratory infections:
Very hot or very cold weather
Aerosol, pesticides, cleaners
Alcohol, tonic water, cigarette smoke

TRIGEMINAL NEURALGIA
Tic Doulorex
Is a sensory disorder of the 5th cranial nerve
It is manifested by excruciating, recurrent paroxysms of sharp,
stabbing facial pain along the trigeminal nerve (lips,gums, nose,
cheeks)
Pain aggrevated by cold, washing th efface, chewing, hot or cold
foods and fluids, touch of wind on the face
Collaborative management for the client with trigeminal neuralgia
are as follows:
Instruct the client to avoid hot or cold foods and beverages
Provide liquidsand soft foods
Instruct client to chew food on the unaffected side
Pharmacotherapy:
a) Elavil (amitriptyline)
b) Lioresal (baclofen)
c) Tegretol (Carbazepine)
d) Valium (diazepam)

e) Dilantin (phenytoin)
Surgery- alcohol injection of the nerve
Neurectomy

BELLS PALSY (facial

paralysis)
Is caused by lower motor lesion of the seventh cranial nerve
Is caused by infection by infection, trauma, hemorrhage, meningitis
or a tumor
It is manifested by paralysis of one side of the face with drooping of
the eyelid on that side (ptosis)
It is accompanied by inability to raise the eyebrows, frown, smile,
close the eyelids or puff out the cheeks
No definite test
Collaborative management:
Encourage facial exercises
Protect the eyes from dryness and prevent injury
Promote frequent oral care
Instruct the client to chew on the unaffected side
Pharmacotherapy:
Steroid
analgesics

ICP
Increased blood volume, increased brain volume, increased CSF
volume
Normal pressure: 5-15 mmHg, with pressure tranducer with head
elevated 30; 60-180 cmH20, water manometer with client
lateral recumbent
Sustained increases associated with:
a. Cerebral edema
b. Head trauma
c. Tumors
d. Abscesses
e. Stroke
f.
Inflammation
g. Hemorrhage
Factors that Increases ICP
Hypercapnea, hypoxemia
Cerebral vasodilating agents
Valsalva maneuver; coughing or sneezing
Body positioning (prone, neck flexion, extreme hip flexion)
Isometric muscle contraction

Emotional upset; noxious stimuli

Arousal from sleep
Clustering of activities
Pain and agitation

ICP
Cranial insult

Tissue edema

Increased ICP

Compression of blood vessels

Decreased cerebral blood flow
Decreased oxygen with brain cell death
Edema around necrotic tissue
Increased ICP with brainstem and respiratory center compression
Carbon dioxide accumulation
Vasodilation

Increased ICP

DEATH

Pathophysiology: pressure results to lack of oxygen and blood supply

Manifestations:
Restleness- initial sign of increased ICP

Headache due to traction on pain- sensitive brain strctures and

on cranial nerves
Nausea and vomiting due to pressure at the medulla oblongata.
Vomiting may be projectile
Decreasing level of sensorium-most sensitive, reliable and earliest
indicator: due to cerebral hypoxia, interference with RAS
function
Increasing BP due to increased force of cardiac contractility, the
bodys attempt to increase cerebral tissue perfusion and
oxygeneation, decreasing pulse
Pupillary changes (a reflection of tissue shifts) diplopia,
anisucuria (unequal pupil)is due to cranial nerve III
(oculomotor) compression.
Cushings triad-increasing systolic pressure, widening pulse
pressure and bradycardia (final compensatory mechanism to
maintain CSF)
Papilledema-due to the compression of optic disc
Respiratory changes-RR is slow due to involvement of medulla
oblongata and pons
Motor changes-dependent on site of pressure; usually starts
contralaterally; then hemiplegia, decortication or decerebation
depending on pressure on brain stem
Body temperature may be hyperthermia or hypothermia due to
involvement of the hypothalamus
Dolls eye sign- dysconjugate of the eyes as the head is moved to
one side
Decortications (flexion, adduction and internal rotation of upper
extremities, lower extremities are extended) this indicates
involvement above midbrain
Decerebration (extension, adduction and internal rotation of the
arms and extension of lower extremities). This indicates
involvement of the brainstem. This indicates poor prognosis.
The client may have cardiopulmonary arrest anytime
Oculovestibular test (caloric ice water test) dysconjugate
movement of the eyes occur in response to irrigation of the ear
with cold water.
Late signs: coma, apnea, unilateral pupil changes

Medications for Increased ICP

Osmotic diuretics increases osmolarity of blood and draw fluid from
edematous brain and tissue into vascular bed
Loop diuretics such as furosemide
Antipyretics or hypothermia blanket: used to control increases in
cerebral metabolic rate
Anticonvulsants to manage seizure activity
Histamine H2 receptors to decrease risk of stress ulcers
Barbiturates: may be given as continuous infusion to induce coma
and decrease metabolic demands of injured brain
Vasoactive medicine may be given to maintain blood pressure to
cerebral perfusion
Surgery-include removal of brain tumors, burr holes, insertion of drainage
catheter or shunt to drain excessive CSF
ICP monitoring
Continuous intracranial pressure monitor is used for continual
assessment of ICP and to monitor effects of medical therapy and
nursing interventions
Risk of infection exists with invasive procedure
Nursing Diagnosis
1. Ineffective Tissue perfusion
2. Risk for infection: open head wounds and intracranial monitor device
requires meticulous aseptic technique
Anxiety (family)
Collaborative Management:
Note: increased ICP is an emergency. The cerebral cortex can tolerate
hypoxia only 4-6 minutes. The medulla oblongata can tolerate hypoxia for
10

Position: fowlers. lateral position. The HOB elevation is 15 to 30

degree, maximum of 45 degree. To promote drainage of CSF from
the subarachnoid space of the spinal cord. This position also
promotes maximum lung expansion. Caution: do not elevate HOB at
90 degree. This may cause brain herniation.
Adequate oxygenation: mechanical ventilation helps promote acidbase balance. Acidosis and alkalosis may increase ICP
Safety: prevent falls that may result from altered level of
consciousness and seizures,
Rest: physical and emotional stress may further increase ICP
Avoid factors that increase ICP as follows:
Nausea and vomiting
Valsalva maneuver
Over suctioning
Restrains application
Rectal examination
Enema
Bending or stooping
If coughing and sneezing could not be avoided, follow- through with
open mouth
Control hypertension. Hypertension reduces cerebral tissue
perfusion
Restrict fluid intake. Limit fluid intake to 1, 200 to 1,500 mls/day to
reduce CSF production
Pharmacotherapy:
Mannitol, an osmotic diuretic. It reduces cerebral edema by
increasing urine output
Lasix, a diuretic. It reduces cerebral edema by increasing urine
output
Decadron (dexamethasone), a corticosteorids. It has an antiinflammatory effect and reduces cerebral edema. This is the
only corticosteroids that can pass through blood-brain barrier
Anticonvulsant- to prebvetm seizures
Antacids to prevent GI irritation that may be induced by
decadron
Histamine- H2 receptor antagonist, to prevent stress ulcer
Anticoagulants- to prevent thromboembolism
Critical to remember:

Opiates (narcotics) and sedatives are contraindicated to the

client with increased ICP. These drugs may cause respiratory
depression and acidosis.