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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
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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.
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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
Speech area (Wernicks )
- 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

Occipital

Facilitates voluntary movement of


skeletal muscle
Understanding of spoken and
written words
Promotes vocalization of words

Receives and interpret olfactory and


auditory stimuli
Promotes recognition of pain,
coldness, light touch (Contralateral
reception)
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 from 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
o Has two hemispheres
o 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.
glossopharynge
al
X. Vagus

XI. Spinal
accessory
XII. hypoglosal

Sensory
Mixed
Mixed

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

Blood
vessel
of
external Dilated
genitalia
Integumentary system
Secretion of sweat
No direct effect
Pilomotor muscles
No direct effect
Adrenal medulla

No direct effect

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

Autonomic Nervous System


o Controls involuntary or automatic body functions
o 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
Heart
Lungs
GIT
Motility
Tone sphincters
Urinary bladder
Bladder muscle
Sphincter
Liver

Sympathetic
Increased rate and
contractility
Relaxation

Parasympathetic
Decreased rate and
contractility
Contraction

Decreased Contraction

Increased
Relaxation

Relaxation

Contraction

Contraction
Glycogenolysis

Relaxation
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, L45, 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
General appearance
State of consciousness
Arousal component
Content component
Mood and effect-changes in the nervous system
Thought content
Intellectual capacity

1.
2.

3.
4.
5.

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
VIII.
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 globe
strokes 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, widebased 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. Increased ICP
b. Stroke, hematoma, intracranial hemorrhage
c. Tumors
d. Infections
e. 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
Eye opening responses
4 Opens eyes spontaneously
3 Opens eyes in response to voice
2 Opens eye in response to painful stimuli
1 Does not open eyes
Best verbal response
5
Oriented
4
Confused
3
Utters inappropriate words
2
Incomprehensible words
1
None
Best motor response
6
Obeys command
5
Localizes pain
4
Withdraws with painful stimuli
3
Flexion (Decorticate posturing)
2
Extension (Decerebrate posturing
1
None
Total 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)
NEUROLOGIC DISORDER
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
Muscle Functioning
Muscle Function Loss
Injury
remaining
Cervical, above
None
All including respiration
C4
C5
Neck, scapular elevation
Arm, chest, all below
chest
C6-C7
Neck, some chest
Some arm, fingers, some
movement, some arm
chest movement all below
movement
chest
Thoracic
Neck, arms (full), some
Trunk, all below chest
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 rtpa)

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 li-chewing, 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
emotional
stress
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 inhibitors- transmit
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

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
e.

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 46 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 acid-base 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 anti-inflammatory
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.