Cognitive and Perceptual

Disorders
Prepared by: Emman M. Parangue, R.N.
Edited by: Jane Wisdom J. Gallana, RN
01.
Overview of the
Nervous System
Overview of the Nervous System
Divisions
Central Nervous System
Brain
Spinal cord
Peripheral Nervous System
Cranial Nerves
Spinal Nerves
Cerebrum

● largest area of your brain

● consists of the right and left hemispheres
- Each hemisphere receives sensory information
from the opposite side of the body and controls the
skeletal muscles of the opposite side.
● governs sensory and motor activity and thought and
learning
Cerebrum
Cerebral cortex - responsible for the conscious activities of
the cerebrum
corpus callosum - is a nerve tract that connects
the cerebral hemisphere
basal ganglia - are several islands of gray matter
buried deep within the white matter
- regulate voluntary motor activities by modifying
instructions sent to the skeletal muscles by the
primary motor cortex
Cerebral Hemispheres

paired, collectively called cerebrum

connected by corpus callosum
surface anatomy
gyri
sulci
fissures
Cerebral Hemispheres
each cerebral hemisphere has 3 regions:
gray matter - plays a significant role in mental functions,
memory, emotions and movement.
white matter - the deeper tissue, is composed of fiber
tracts carrying impulses to, from or within the cortex
basal nuclei
Functions of Cerebrum

speech, memory, logical and emotional responses

consciousness
interpretation of sensation
voluntary movements
cerebral cortex - 5 major lobes
5 MAJOR Lobes:
1. Frontal lobe
primary motor area
Broca's area – specialized area for speaking (production of speech )
located only in one side, usually the left, causes
inability to say the words properly
● Thinking, planning, organizing, problem solving,
● Emotions, behavioral control, personality
5 MAJOR Lobes:
2. Parietal lobe
location of sensory somatic area
interpret impulses from sensory receptors
- Interpretation of taste, pain, touch, temperature, and
pressure
Perception, math spelling logic
Spatial perception
5 MAJOR Lobes:
3. Occipital lobe

special sense of vision

4. Temporal lobe

Auditory center

Wernicke’s area for comprehension of speech

● Memory
● Understanding language
5 MAJOR Lobes:

5. Limbic System
■ Emotional and visceral patterns for survival
■ Learning and memory
■ regulates sexual response
Diencephalon aka interbrain

Major structures: thalamus, hypothalamus, epithalamus

1. Thalamus
● relay station for sensory impulses passing upward to
sensory cortex
● Provides a pain gate
● Part of the reticular activating system
Diencephalon
2. Hypothalamus
Regulates autonomic responses of the sympathetic and
parasympathetic nervous systems
regulation of stress response, sleep, appetite, body
temperature, fluid balance, metabolism and emotions
center for thirst, appetite, sex, pain, pleasure
regulates pituitary gland to produce hormones
Diencephalon
3. Epithalamus
Important parts:
➢ pineal body (endocrine system)
◦ secretes melatonin
◦ controls sex drives, hunger, thirst, biological clock with
hypothalamus
Brain Stem
Major structures: midbrain, pons, medulla oblongata

1. MIDBRAIN
a. Responsible for motor coordination
b. Contains the visual reflex and auditory relay centers
PARTS:
➢ cerebral peduncles – convey ascending and descending impulses
➢ corpora quadrigemina – reflex centers involved with vision and
hearing
Brain Stem
2. PONS
➢ Contains the nuclei for respiratory centers and regulates breathing

3. MEDULLA
➢ contains many nuclei that regulate vital activities
➢ Contains all afferent and efferent tracts and cardiac, respiratory,
vomiting, and vasomotor centers
➢ Controls heartbeat, BP, breathing, swallowing, vomiting, sneezing
and coughing
Cerebellum

provides precise timing for skeletal muscle activity

controls our balance and equilibrium so that body
movements are smooth and coordinated
damaged of cerebellum, movements become
clumsy and disorganized
Protection of the CNS
1. Meninges
➢ dura mater
- double-layered membrane that surrounds the brain and spinal
cord
- - tough and fibrous membrane.
➢ arachnoid mater

- web-like meningeal layer with special structures, arachnoid villi

- a delicate membrane and contains CSF.
➢ pia mater

- a vascular membrane that clings tightly to the brain and spinal

cord
Protection of the CNS
2. Cerebrospinal Fluid (CSF)
clear, colorless fluid produced by the choroid plexus of the ventricles
Acts as a protective cushion; aids in the exchange of nutrients and
wastes
circulates in the subarachnoid space, through the ventricles to the
subarachnoid space of the meninges, where it is reabsorbed
it is produced at a rate of 500 ml/day
the ventricles and arachnoid space contain approximately 125- 150
ml of CSF
Normal pressure is 6 to 25 cm H2O.
Neurons

1. The neuron consists of the cell body, axon, and dendrites.

2. The cell body contains the nucleus.
3. sensory neurons - carrying impulses from the peripheral
nervous system to the CNS
4. motor neurons - carrying impulses away from the CNS
5. Synapse is the chemical transmission of impulses from one
neuron to another.
Axons and Dendrites
1. The axon conducts impulses from the cell body.
2. The dendrites receive stimuli from the body and
transmit them to the axon.
3. The neurons are protected and insulated by
Schwann cells.
4. The Schwann cell sheath is called the
neurolemma.
5. Neurons do not reproduce after the neonatal
period.
6. If an axon or dendrite is damaged, it will die and
be replaced slowly only if the neurolemma is intact
and the cell body has not died.
Spinal nerves

1. Afferent (sensory) nerve fibers and efferent

(motor) nerve fibers combine to form 31 pairs
of spinal nerves.
2. Mixed nerve fibers are formed by the
joining of the anterior motor and posterior
sensory roots.
Autonomic nervous system (involuntary functions)
1. Sympathetic (adrenergic) fibers
- dilate pupils, increase heart rate and rhythm, contract blood
vessels, and relax smooth muscles of the bronchi.
- Norepinephrine is a major neurotransmitter for the
sympathetic nervous system.

2. Parasympathetic (cholinergic) fibers

- contracts smooth muscles, dilates blood vessels, increases
bodily secretions, and slows heart rate.
- Acetylcholine is a major neurotransmitter for the
parasympathetic nervous system
Nervous System Assessment
Health History

Initial interview provides an opportunity to explore

the patient's current condition and related events

overall appearance, mental status, posture

movement, and affect

details about the COLDSPA, frequency of S/S, relieving factors

progression, remission and exacerbation
Nervous System Assessment
➢ Common Symptoms:
symptoms of neurologic disorders are varied
subtle or intense, fluctuating or permanent
inconvenient or devastating
1. Pain – multidimensional and entirely subjective

acute pain lasts for relatively short period time

and remits as the pathology resolves
Nervous System Assessment
acute pain in brain hemorrhage, spinal disk
disease, or trigeminal neuralgia

chronic pain or persistent pain extends for long

periods of time and represents a broader
pathology

in chronic and neurologic conditions

(e.g. multiple sclerosis)
Nervous System Assessment
2. Seizures

result of abnormal electrical discharges in the cerebral cortex

may manifest as an alteration in sensation, behavior, movement,
perception or consciousness

alteration may be short such as blank stare or longer such as tonic-clonic

grand mal seizure

can occur in isolated events, such as induced by fever, alcohol or drug

withdrawal, or hypoglycemia

may also be a first sign of brain lesion

Nervous System Assessment
3. Dizziness and Vertigo

an abnormal sensation of imbalance or movement

fairly common in older adults
variety of causes: e.g. viral syndromes, hot weather
roller-coaster rides, middle ear infection
Nervous System Assessment
about 50% of patients with dizziness have vertigo
vertigo usually a manifestation of vestibular
dysfunction, an illusion of movement in which the
individual or surroundings are sensed as moving,
usually rotation

can be severe that results in spatial disorientation

lightheadedness, loss of equilibrium, nausea and
vomiting
Nervous System Assessment
4. Visual Disturbances

may range from decreased visual acuity to sudden

blindness

nystagmus in multiple sclerosis

5. Muscle Weakness

common manifestation of neurologic disease

can be sudden and permanent as in stroke
can be progressive as in neuromuscular diseases
Nervous System Assessment
6. Abnormal sensation

a neurologic manifestation of both central and

peripheral nervous system disease

usually associated with weakness and pain

lack of sensation places a person risk for injury

Nervous System Assessment

➢ Past Health, Family, and Social History:

review of medical history and systems review
history of trauma or falls
use of medications, alcohol and illicit drugs
Physical Assessment
neurologic examination, a systematic process that includes a variety of
clinical test, observations, and assessments to evaluate neurologic status

the brain and spinal cord cannot be examined directly as the other
systems

indirect evaluation that assesses the function of specific body parts

controlled by the nervous system

divided into five components: consciousness and cognition, cranial

nerves, motor system, sensory system, and reflexes
Assessing Consciousness and Cognition
cerebral abnormalities may cause disturbances in mental status,
intellectual functioning, thought content, and emotional status

there may be alterations in language abilities, or lifestyle

overall level of consciousness

alterations should be described in specific and nonjudgmental terms

the term “inappropriate” or “demented” should be avoided because they

mean different things to different people
Assessing Consciousness and Cognition

1. Mental status

begin by observing the patient's appearance and behavior, noting dress,

grooming and personal hygiene

posture, gestures, movements and facial expression

assess orientation to time, place and person

assess for immediate and remote memory

Assessing Consciousness and Cognition

2. Intellectual function

a person with an average IQ can repeat seven digits without faltering

and can recite five digits backward

the capacity to interpret well-known proverbs “a stitch in time saves

nine”

questions that may assess the capacity to recognize similarities, “how

are pen and pencil alike”
Assessing Consciousness and Cognition
3. Thought content

are the patient's thought spontaneous, natural clear, relevant, and

coherent

illusions, preoccupations, morbid events, hallucinations, or paranoid

ideation
Assessing Consciousness and Cognition

4. Emotional status

is the patient's affect natural and even, or irritable and angry, anxious,
apathetic, flat or euphoric

mood swing
Assessing Consciousness and Cognition

5. Language ability

a person with normal neurologic function can understand and

communicate in spoken and written language

Aphasia

6. Impact on lifestyle

7. Level of Consciousness
Total Score: Best response 15
Comatose client 8 or less
Totally unresponsive 3
Examining the Cranial Nerves

Cranial nerves are assessed when level of consciousness is decreased,

with brain stem pathology, or in the presence of peripheral nervous system
disease

Equipment: tongue depressor, flashlight, sugar and salt samples, watch,

cotton-tipped swab, cotton swabs, Snellen chart, opthalmoscope, samples
of familiar odors, hot and cold water, tuning fork

Chart 65-3 Assessing Cranial Nerve Function Volume 2, page 1923

Examining the Motor System

- includes assessment of muscle size, tone, strength coordination and balance

1. Motor Ability

gait and posture

tremors

abnormalities in muscle tone: spasticity, rigidity, flaccidity

2. Muscle Strength

assessing the patient's ability to flex

or extend the extremities against
resistance
Examining the Motor System
3. Balance and Coordination

cerebellar and basal ganglia influence on the motor system is reflected in

balance control and coordination

4. Upper extremities:

1. pat thigh as fast as possible with each hand separately

2. alternately pronate and supinate hand rapidly

3. touch each fingers with thumb in consecutive motion

Examining the Motor System

5. Point-to-Point testing
- patient touch examiner's extended finger and own nose repeatedly

6. lower extremities
- having the patient run the heel down
- ataxia, incoordination of voluntary muscle action
- tremors

7. Romberg test
- screening test for balance
- can be done when the patient is seated or standing
Examining the Sensory System
sensory examination is largely subjective

involves tests for tactile sensation, superficial pain, temperature, vibration,

and position change

tactile sensation-lightly touching a cotton wisp or fingertip

pain and temperature. Pain is usually reserved for patient who do not
respond to touch

vibration with the use of tuning fork (Rinne and Weber test)
proprioception-position sense
Agnosia
Examining the Sensory System

Agnosia

the general loss of the ability to recognize objects

visual - occipital
auditory - temporal
tactile - parietal
body parts and relationships - parietal
Examining the Reflexes

involuntary contractions of muscle or muscle groups in response to a stimulus

deep tendon

superficial

pathologic
Examining the Reflexes
1. Superficial reflexes

corneal reflex

gag reflex

cremasteric reflex

2. Pathologic reflexes

Babinski reflex (sign)

 Diagnostic Evaluation
1. Skull and spinal radiography

- reveal the size and shape of the skull bones, suture separation in infants, fractures
or bony defects, erosion, and calcification.

- identify fractures, dislocation, compression, curvature, erosion, narrowed spinal

cord, and degenerative processes.

➢ Preprocedure interventions:

a. Provide nursing support for the confused, combative, or ventilator-dependent client.

b. Maintain immobilization of the neck if a spinal fracture is suspected.
c. Remove metal items from the client.
d. If the client has thick and heavy hair, this should be documented because it could
affect interpretation of the x-ray film.
Diagnostic Evaluation

2. CT Scan

▪ used to detect intracranial bleeding, space-occupying lesions, cerebral edema,

infarctions, hydrocephalus, cerebral atrophy and shifts of brain structures

▪ distinguish tissue densities of the skull, cortex subcortical structures and ventricles

▪ An informed consent is needed if an IV contrast agent may be used

Diagnostic Evaluation
➢ Nursing interventions:
Preprocedure:
1. Assess for allergies to iodine, contrast dyes, or shellfish if a dye is used.
2. Assess renal function
3. lie still and flat during the test
4. hold their breath when requested
5. Initiate an intravenous line with the appropriate gauge size (g18)
6. Remove objects from the head (e.g. wigs, earrings, hairpins)
7. Assess for claustrophobia.
8. Inform the client of possible mechanical noises as the scanning occurs
9. Inform about hot, flushed sensation and a metallic taste in the mouth when the
dye is injected.
10. withhold metformin on the day of the test if iodinated contrast dye is used
Diagnostic Evaluation
➢ Nursing interventions:

Postprocedure:

1. Provide replacement fluids, because diuresis from the dye is expected.

2. Monitor for an allergic reaction to the dye.
3. Assess the dye injection site for bleeding or hematoma, and monitor the
extremity for color, warmth, and the presence of distal pulses.
Diagnostic Evaluation
3. Magnetic Resonance Imaging (MRI)

▪ noninvasive procedure that identifies tissues, tumors, and vascular abnormalities

▪ can be done with or without contrast
▪ can identify cerebral abnormality earlier and more clearly
▪ provide information about chemical changes within cells, good to evaluate
treatment
▪ particularly useful in brain tumor, stroke or multiple sclerosis
 Diagnostic Evaluation
Nursing interventions
➢ Preprocedure interventions:
1. Education about the procedure
2. Remove all metal objects from the client
3. History on implants (e.g. pacemaker, implanted defibs, prosthesis)
4. Saline lock on all intravenous accesses prior to the procedure
5. Precautions for the client who is attached to a pulse oximeter
6. Assessment of the client with claustrophobia and administer
prescribed meds (for closed machines only)
7. Verify allergies and renal function prior to administration.
8. Remain still during the procedure
Diagnostic Evaluation

Nursing interventions

➢ Postprocedure interventions:
1. May resume normal activities.
2. Increase fluid intake and expect diuresis if a contrast
agent is used.
Diagnostic Evaluation

4. Positron Emission Tomography (PET)

▪ computer-based nuclear imaging technique that produces images of actual
organ functioning.
▪ patient inhales a radioactive gas or injected with radioactive substance that
emits positively charged particles.
▪ Single -Photon Emission Computed Tomography (SPECT) – provides a three-
dimensional images
▪ patient education
Diagnostic Evaluation

5. Cerebral angiography

▪ Injection of a contrast material, usually through the femoral artery (or

another artery) into the carotid arteries to visualize the cerebral
arteries and assess for lesions
▪ x-ray study of the cerebral circulation with contrast agent
▪ important tool in investigating vascular disease or anomalies
Diagnostic Evaluation (Nursing interventions)
➢ Pre-procedure:
1. Allergy to iodine and shellfish
2. BUN and creatinine levels
3. hydration for 2 days before the test(clear liquids)
4. NPO 4-6hrs prior test
5. void before the test
6. remain immobile during the test
7. expect a brief feeling of warmth in the face, behind the eyes, the tongue,
the lips and metallic taste
8. medication history of anticoagulation therapy
Diagnostic Evaluation (Nursing interventions)
➢ Post-procedure:
1. Monitor neurological status, vital signs, signs of bleeding,
2. Monitor for swelling in the neck and for difficulty swallowing
3. Maintain flat on bed for 6hrs and rest for 12 hours as prescribed (if
femoral is used)
4. Assess peripheral pulses.
5. Apply sandbags or another device to immobilize the limb and a
pressure dressing to the injection site.
6. Place ice on the puncture site as prescribed
7. Encourage fluid intake.
Diagnostic Evaluation

6. Myelography

x-ray with contrast of the spinal subarachnoid space

will show distortion of spinal cord by a tumor, herniated disks or other lesions
Nursing interventions:
1. lie in bed with HOB elevated at 30-45 degrees
2. should remain in the recommended position in bed for three hours to
minimize post-lumbar puncture headache
Diagnostic Evaluation

7. Non invasive carotid flow studies

● ultrasound imagery

● transcranial doppler
● helpful in assessing vasospasm, altered cerebral blood flow in occlusive
vascular diseases, other cerebral pathology and brain death
Diagnostic Evaluation
8. Electroencephalography

● represents a record of the electrical activity within the brain

● Noninvasive, graphic recording of the electrical activity of the

superficial layers of the cerebral cortex

● helpful in evaluating seizure disorders, coma or organic brain

syndrome
Diagnostic Evaluation (Nursing interventions)
Preprocedure:
1. Wash the client’s hair.
2. Inform the client that electrodes are attached to the head and
that electricity does not enter the head.
3. Withhold stimulants
4. Hold antidepressants; tranquilizers; and possibly antiseizure
medications for 24 to 48 hours before the test as prescribed
5. Allow the client to have breakfast if prescribed.
6. Premedicate for sedation as prescribed.
7. Deprive sleep night before the EEG
Diagnostic Evaluation (Nursing interventions)

Postprocedure:

1. Wash the client’s hair.

2. Maintain safety precautions if the client was
3. sedated.
Diagnostic Evaluation
9. Lumbar puncture and examination of CSF

● inserting a needle into the lumbar subarachnoid space at the level

between L3 and L4 or L4 and L5 to obtain CSF
● measure CSF fluid or pressure; or instill air, dye, or medications
● contraindicated in clients with increased intracranial pressure (ICP),
Diagnostic Evaluation (Nursing interventions)

Preprocedure:
1. Monitor for complications
2. Empty the bladder
3. Appropriate client education
4. Review coagulation studies/platelet count (risk of bleeding)
5. Increase fluid intake to decrease risk of post procedure
headache
Diagnostic Evaluation (Nursing interventions)

During procedure:
1. Position the client in a lateral recumbent position
2. Have the client draw the knees up to the abdomen
and the chin onto the chest
3. Assist with the collection of specimens (label the
specimens in sequence).
4. Maintain strict asepsis.
5. Assess for dizziness.
Diagnostic Evaluation (Nursing interventions)

Post procedure:
1. Monitor vital signs and neurological signs
2. Check for the presence of leakage of CSF
3. Monitor for headache
4. Position the client flat as prescribed.
5. Encourage fluids
6. Monitor intake and output.
Diagnostic Evaluation
Post-lumbar puncture headache

caused by CSF at the puncture site by way of needle tract from spinal canal

can be avoided by using small needle

may range from mild to severe

throbbing bifrontal or occipital headache

usually managed by bedrest, analgesics, hydration

Diagnostic Evaluation

Other complications:

herniation of cranial contents

spinal epidural abscess, hematoma

meningitis
To be continued...
02.
Altered Level of
Consciousness
and Increased
Intracranial Pressure
Axons and Dendrites
1. The axon conducts impulses from the cell body.
2. The dendrites receive stimuli from the body and
transmit them to the axon.
3. The neurons are protected and insulated by
Schwann cells.
4. The Schwann cell sheath is called the
neurolemma.
5. Neurons do not reproduce after the neonatal
period.
6. If an axon or dendrite is damaged, it will die and
be replaced slowly only if the neurolemma is intact
and the cell body has not died.
 Altered Level of Consciousness
● It is not a disorder itself, rather, it is a result of multiple pathophysiologic
phenomena.
● Altered LOC is present when the patient:

○ Is not oriented

○ Does not follow commands

○ Needs persistent stimuli to achieve a state of alertness

Altered Level of Consciousness
COMA (The Unconscious Client)
● Is a clinical state of unarousable, unresponsiveness in which there are no
purposeful responses to internal and external stimuli.

Akinetic Mutism
● Is a state of unresponsiveness to environment in which the patient makes
no voluntary movement.
Persistent Vegetative State
● The unresponsive patient resumes sleep-wake cycles after coma but
lacking of cognitive or affective mental function.
● also known as post-coma unresponsiveness (PCU)
Altered Level of Consciousness

A minimally conscious state

● Differs from persistent veg. state in that the patient has inconsistent but
reproducible signs of awareness.
Locked-in syndrome
● Results from a lesion affecting the pons and results in paralysis and the
inability to speak, but vertical eye movements and lid elevation remain
intact and are used to indicate responsiveness.
Pathophysiology of ALOC
● Not a disorder itself by a result of multiple pathophysiologic phenomena.
Causes:

● May be neurologic- head injury, stroke

● Toxicologic- drug overdose, or alcohol intoxication
● Metabolic- hepatic/renal failure, DKA
● The underlying causes of neurologic dysfunction is disruption of the cells of
the NS, neurotransmitter or brain anatomy.
● Disruption results from cellular edema or other mechanism like disruption
of chemical transmission.
 Clinical Manifestations of ALOC
● Depend on where the patient is on the continuum.
● As the patient’s state of alertness and consciousness decreases, changes
occur in the:
1. Pupillary response (contracts to light) – normal is PERRLA
2. Eyes opening response
3. Verbal response
4. Motor response
 Clinical Manifestations of ALOC
● Initial alterations in LOC may be reflected by subtle behavioral changes,
such as restlessness or increased anxiety.
● The pupils, normally round and quickly reactive to light, becomes sluggish
and as the patient becomes comatose, the pupils become fixed (no
response to light) → dilated pupil.
● The patient in coma does not:
1. Open eyes to voice/command
2. Respond verbally
3. Or move extremities to request/command
 Assessment
● Often starts with assessing verbal response
- By determining patient’s orientation to time, place, and person.

- Or where they are

- Who is the president?
- When is the next holiday?
● Alertness is measured by the patient’s ability to open the eyes
spontaneously or in response to vocal/noxious stimulus.
 Assessment
● Motor response includes spontaneous, purposeful movement.
- Awake patient can move all four extremities with equal strength in
command.
- Movement only in response to painful stimuli or abnormal posturing.
- If not responding to commands, the motor response is tested by applying
painful stimuli.
- If patient attempts to push/withdraw, the response is recorded as
purposeful or appropriate.
- An inappropriate response is random and aimless.
 Assessment
● Posturing (Decorticate/Decerebrate)

- Decerebrate- results from damage to the upper brain stem. Adducted arms
and extended. Wrist pronated and fingers flexed outward.

- Decorticate- result from damage to one or both corticospinal tract. Adducted

arms and flexed, wrist and fingers on the chest.
 Assessment
● CAUSES of decorticate posture include:
1. Bleeding in the brain from any cause.
2. Brain tumor
3. Stroke
4. Brain problem due to drugs poisoning or infection.
5. Head injury
6. Brain problem due to liver failure.
7. Increased pressure in the brain from any cause.
8. Primary brain tumor
 Assessment
● The most severe neurologic impairment results in flaccidity.
● The motor response cannot be elicited or assessed when the patient is
given pharmacologic paralyzing agents (i.e. neuromuscular blocking agents)
● In addition to LOC, the nurse monitors parameters such as respiratory
status, eye sign, and reflexes.
Management
● Maintaining a patent airway is the 1st priority of treatment.
- Placed on the ICU for constant monitoring (never leave unstable pts.)
- May be orally/nasally intubated Or tracheostomy may be performed.
- Mechanical ventilator to maintain adequate oxygenation and
ventilation.(increased CO2 increases ICP)
- Semi Fowler’s position (Avoid Trendelenburg’s)
● Monitor circulatory status (BP, HR) to ensure adequate perfusion to the
body and brain.
● Intravenous catheter to provide access or IV fluids and medications. (Use
SASH method)
Management

● Nutritional support via feeding tube/gastrostomy tube.

● Careful Turning q 2hrs (ensure intact skin integrity at all times)
● Strict I&O (positive and negative balance)
● instill artificial tears or cover the eyes with eye patches.
● Always assume that the client can hear
● Avoid restraints unless indicated
● Do Passive ROMs
● Use footboards (to avoid foot drop)
● Pharmacologic management
Nursing Interventions: Maintaining Airway
● Remove secretions to eliminate the danger of aspiration.
● Elevate HOB to 30 degrees to prevent aspiration.
● Position patient in a lateral/semiprone position to allow the jaw and
tongue to fall forward thus promoting drainage of secretions.
● Suctioning and oral hygiene to remove secretions from the posterior
pharynx and upper trachea. Adequate ventilation to prevent hypoxia.
● Chest physiotherapy and postural drainage to promote pulmonary hygiene.
● Auscultate chest at least every 8 hours to detect adventitious breath
sounds.
Nursing Diagnoses
● Ineffective Airway Clearance
● Risk for injury
● Deficient Fluid volume related to inability to take fluids by mouth.
● Impaired oral mucous membrane
● Impaired tissue integrity
● Ineffective thermoregulation related to damaged hypothalamic center.
● Impaired urinary elimination
● Bowel incontinence
● Ineffective health maintenance
Increased Intracranial Pressure
● Pushing of the brain against the skull
● may be caused by trauma, hemorrhage, growths or tumors, hydrocephalus,
edema, or inflammation
● can impede circulation to the brain, impede the absorption of CSF, affect the
functioning of nerve cells, and lead to brainstem compression and death.
● 20 mmHg and up – Increased ICP
Note:
- The rigid, cranial vault contains the: Brain tissue(1400 g), blood(75 ml), CSF(75 ml)
- The volume and pressure of these three components are usually in a state of equilibrium
and produce the ICP.
- The normal pressure to 0-10 mmHg, 15 mmHg is the upper limit
Increased Intracranial Pressure
CPP- Cerebral Perfusion Pressure
● The amount of blood flow from the systemic circulation required to provide
adequate glucose and oxygen for brain metabolism.
● net pressure gradient that drives oxygen delivery to cerebral tissue

● Normal is 70-100 mmHg ; CPP= MAP-ICP

MAP- Mean Arterial Pressure
● The average pressure during a cardiac cycle. Calculated by adding the
systolic pressure to twice the diastolic pressure divided 3.
● SBP+ (2 DBP)/ 3
● Should be MAP > 60mmHG (adult)
Pathophysiology of Increased ICP

Monro-Kellie Hypothesis/Doctrine
● States that because of the limited space for expansion within the skull, an
increase in any one of the components causes in the change of the volume
of the others.
● Because brain tissue has limited space to expand, compensation is typically
accomplished by displacing or shifting the CSF, increasing the absorption or
diminishing the production of CSF, or decreasing cerebral blood volume.
● Without such changes ICP begins to rise.
Pathophysiology of Increased ICP

Causes of Increased ICP

● Most commonly associated with head injury.
● Brain tumors
● Subarachnoid hemorrhage
● Toxic and viral encephalopathies
● Cerebral infarction
Pathophysiology of Increased ICP

Increased ICP from any cause will lead to:

● Decreased cerebral perfusion
● Stimulates further swelling
● Shift of brain tissue, resulting to herniation which is frequently a fatal
event.
Pathophysiology of Increased ICP
Decreased cerebral blood flow
● Decreased venous outflow → increases cerebral blood volume → ischemia
→ cell death
● Early stage of ischemia stimulates vasomotor centers resulting to changes
in BP, pulse, and respirations.
● These changes are important clinically, they suggest increased ICP.
● Carbon dioxide also plays a role in the regulation of cerebral blood flow.
● Increased PaCO2, causes vasodilation, increased cerebral blood flow and
increased ICP.
● Decreased PaO2, has vasoconstrictive effect. → decreased blood flow
Pathophysiology of Increased ICP

Cerebral Edema
● Can occur in the gray, white, or interstitial matter.
● As brain tissue swells, several mechanisms attempt to compensate for the
increasing ICP.
● Autoregulation to decrease production and flow of CSF.
● Mechanism is impaired when there is pathologic or sustained increase in
ICP.
Pathophysiology of Increased ICP
Cerebral Response to Increased ICP
● As ICP rises, compensatory mechanisms in the brain work to maintain blood flow
and prevent tissue damage.
● The brain can maintain a steady perfusion pressure if the arterial SBP is 50-100
mmHg and the ICP is less than 40 mmHg.
● CPP can increase to greater than 100 mmHg or decrease to less than 50 mmHg.
● A patient with less than 50 mmHg of CPP, experience irreversible neurologic
damage.
● Therefore, CPP must be maintained at 70-80 mmHg to ensure adequate blood flow
to the brain.
● If ICP is equal to MAP cerebral circulation stops.
Pathophysiology of
Increased ICP
Pathophysiology of Increased ICP

Compensatory Mechanism
● Compliance- Increased ICP but no signs and symptoms, cerebral circulation
is adapting.
● Autoregulation- to decreased size of lumen by vasoconstriction, decreased
cerebral blood flow.
● Displacement- shifting that will lead to herniation, compressed brain
tissues (most lethal)
Pathophysiology of Increased ICP
Cushing’s Response or Cushing’s Reflex
● A clinical phenomenon seen when the cerebral blood flow decreases.
● With ischemia, the vasomotor center triggers an increase in arterial
pressure to overcome the Increased ICP.
● A sympathetic medicated response causes an increase in SBP, widening of
pulse pressure, and reflex slowing of the heart.
● At certain point, the brain’s ability to autoregulate is effective and
decompensation begins (ischemia and infarction), resulting to changes in
mental status and vital signs.
● CUSHINGS’S TRIAD: Hypertension, bradycardia, bradypnea.
Clinical Manifestations

● initially by clinical changes in LOC (most sensitive and earliest indication )

● Headache and Vomiting
● abnormal respiratory and vasomotor responses.
● Pupil changes
Late Signs:
● Rise in blood pressure with widening pulse pressure, Slowing of pulse,
Elevated temperature changes in motor function from weakness to
hemiplegia, a positive Babinski’s reflex, decorticate or decerebrate
posturing, and seizures.
Clinical Manifestations
● Any sudden change such as restlessness without apparent cause,
confusion, or increasing drowsiness has neurologic significance.
● As ICP increases, the patient becomes stuporous. Reacting only to loud
and painful stimuli, this is serious impairment of cerebral circulation.
● Further, the patient becomes comatose with abnormal motor responses in
a form of decorticate and decerebrate or flaccidity.
● If coma is profound, with flexed and dilated pupil and impaired or absent
respirations, death is inevitable.
 Diagnostic Studies
● Most common diagnostic tests are CT Scan, and MRI.
● Cerebral angiography, PET, transcranial doppler.
● Lumbar Puncture is AVOIDED in increased ICP.
IMPORTANT:
-An informed consent is needed if an IV contrast agent may be used
-Patient education
-Thorough assessment is needed prior these procedures
Diagnostic Evaluation
➢ Nursing interventions:
Preprocedure:
1. Assess for allergies to iodine, contrast dyes, or shellfish if a dye is used.
2. Assess renal function
3. lie still and flat during the test
4. hold their breath when requested
5. Initiate an intravenous line with the appropriate gauge size (g18)
6. Remove objects from the head (e.g. wigs, earrings, hairpins)
7. Assess for claustrophobia.
8. Inform the client of possible mechanical noises as the scanning occurs
9. Inform about hot, flushed sensation and a metallic taste in the mouth when the
dye is injected.
10. withhold metformin on the day of the test if iodinated contrast dye is used
Diagnostic Evaluation
➢ Nursing interventions:

Postprocedure:

1. Provide replacement fluids, because diuresis from the dye is expected.

2. Monitor for an allergic reaction to the dye.
3. Assess the dye injection site for bleeding or hematoma, and monitor the
extremity for color, warmth, and the presence of distal pulses.

For cerebral angiogram:

1. Anticoagulation Medications history
2. Assess peripheral pulses
3. Apply sandbags or another device to immobilize the limb and a pressure dressing to
the injection site.
4. Place ice on the puncture site as prescribed
Complications
● Complications of Increased ICP include brain stem herniation, diabetes
insipidus, and SIADH.
● Brain Stem Herniation- increased pressure in the brain tissue results to
cessation of blood flow to the brain leading to irreversible anoxia and brain
death.
● Diabetes Insipidus- has excessive urine output, decreased urine osmolality
and serum hyperosmolality.
● SIADH- from increased secretion of ADH. Patient will suffer from volume
overload, decreased urine output and serum sodium becomes diluted.
Medical Management
● TREAT PROMPTLY!!! These goals are accomplished by:
GOALS: - Administering osmotic diuretics
- Decreasing cerebral edema - Restricting Fluids
- Lowering the volume of CSF - Draining CSF
- Decreasing cerebral blood volume - Controlling Fever
while maintaining cerebral
- Maintaining systemic BP and
perfusion.
oxygenation
- Reducing cellular metabolic
demands.
Medical Management

Maintaining Cerebral Perfusion

● Manipulating cardiac output to improve perfusion to the brain.
- Fluid volume
- Inotropic agents such as dobutamine (Dobutrex),
norepinephrine (Levophed)
- Effective cardiac output is reflected in the
CPP which is maintained at greater than 70 mmHg.
- Low CPP indicates insufficient cardiac output.
Medical Management

Decreasing Cerebral Edema

● Osmotic Diuretic such as mannitol
- To reduce cerebral edema
- Indwelling catheter to monitor urinary output
- Determine serum osmolality to assess hydration status
● Corticosteroids (Dexamethasone, Decadron)
- To reduce edema surrounding the tumor
● Fluid restriction
Medical Management

Reducing CSF and Intracranial Blood Volume

● Ventriculostomy drain can dramatically reduce ICP and restore CPP.

Controlling Fever

● Fever increases cerebral metabolism and the rate at which cerebral edema
forms.
Medical Management

Maintaining Oxygenation and Reducing Metabolic Demands

● Arterial Blood Gases and Pulse Oximetry monitoring to ensuring optimal
systemic oxygenation remains.
● High Doses of barbiturates reduced metabolic demands.
● Sedatives, the patient who receives this cannot move therefore decreases
the metabolic demands.
- Patients receiving barbiturates and sedatives should be
on cardiac monitoring.
- Pentobarbital (Nembutal), Thiopental (Pentothal)
Medical Management

Intracranial Pressure Monitoring

● Invasive monitoring is very important
● The purpose of ICP monitoring are:
- To identify increased ICP in its course.
- To quantify the degree of elevation.
- To initiate appropriate treatment.
- To provide CSF access for sampling and
drainage.
- To evaluate the effectiveness of
treatment.
Medical Management
Monitoring Devices
● Ventriculostomy or intraventricular catheter
- A fine-bore catheter is inserted into a lateral ventricle, preferably non-
dominant hemisphere used to drain CSF or blood from the ventricle.
- The catheter is connected to a fluid-filled system to a transducer to record
the pressure in a form of an electrical impulse.
- It has access for intraventricular administration of medications
- administration of contrast agent for ventriculography.
- Complications: infection, meningitis, ventricular collapse, occlusion drain
tissue or blood.
Medical Management

Monitoring Devices
● Subarachnoid screw or bolt
- A hollow device is inserted through the skull and dura matter into the
cranial subarachnoid space.
- It is attached to the pressure transducer and the output is recorded.
- complications: infection, blockage of screw by clot of brain tissue leading to
decrease reading accuracy.
Medical Management

Monitoring Devices
● Epidural Monitoring
- Uses a pneumatic flow sensor to detect ICP.
- Low incidence of infection and complications.
- Appears to read pressure accurately.
- One disadvantage is the inability to withdraw CSF for analysis.
Medical Management
Monitoring Devices
● Fiberoptic Monitor or Transducer-tipped Catheter
- The miniature transducer reflects pressure changes which are converted to
electrical signals in an amplifier and displayed on digital monitor.
- Can be inserted into the ventricle for drainage, the subarachnoid space or
subdural space under a bone flap.
- If inserted into the ventricle, can be used with CSF drainage device.
Medical Management

Interpreting Intracranial Pressure Waveforms

- Waveforms are captured and recorded on an Oscilloscope.
- The waves are classified as A waves, B waves, C waves.
● A waves (plateau waves)
- Transient, paroxysmal, recurring elevations of ICP that may last for 5 to 20
minutes in an amplitude of 50-100 mmHg.
- It indicates changes to compromise cerebral perfusion.
- It may increase amplitude and frequency reflecting cerebral ischemia and
damage before s/sx of increased ICP are seen clinically.
 Medical Management
Interpreting Intracranial Pressure Waveforms
● B waves
- shorter, 30 secs to 2 minutes
- Smaller amplitude, up to 50 mmHg
- Less clinical significance but if seen with patient with depressed
consciousness, may precede the appearance of A waves.
- Seen in patients with intracranial hypertension and decreased intracranial
compliance.
 Medical Management
Interpreting Intracranial Pressure Waveforms
● C waves
- Small, rhythmic oscillations with frequencies approximately six minutes
- Clinical significance is unknown
03.
INTRACRANIAL
SURGERY
 Intracranial Surgery
● A craniotomy involves opening the skull surgically to gain access to
intracranial structures.
● This procedure is performed to remove a tumor, relieve elevated ICP,
evacuate a blood clot, or control hemorrhage.
● Two approaches through the skull: supratentorial craniotomy, infratentorial
craniotomy.
● Transsphenoidal approach- third approach
Craniotomy
Complications:

● increased ICP from cerebral edema, hemorrhage, or

obstruction of the normal flow of CSF.

● hematomas, hypovolemic shock, hydrocephalus, respiratory

and neurogenic complications, pulmonary edema, and wound
infections.
● diabetes insipidus and inappropriate secretion of
antidiuretic hormone.
Nursing Care Following Craniotomy
● Monitor: ● Maintain:
- vital signs and neurological status - head of bed at least 30 degrees
- IICP - Suction on drain as prescribed and
- Decreased LOC record amount and color q8h
- Head dressing for drainage - Fluid restriction as prescribed
- Electrolyte levels - Maintain head on midline position
- Dysrhythmias (Due F/E imbalance) - Strict I&O
- Antiembolic stockings as prescribed
● Avoid:
- extreme hip or neck flexion ● Provide:
- Quiet environment
● Notify MDs - ROMs q8h
- For drainage for than 30-50ml q8h - Due Medications as prescribed
- For excessive drains or soaked
dressings
06.
Management of
Patients with Seizure
Disorders
 Seizure Disorders
● Seizures- are episodes of abnormal motor, sensory, autonomic, or psychic
activity (or a combination of these) that result from sudden, excessive
discharge from cerebral neurons.

- Part of all the brain may be involved.

 Classification of Seizures
● Generalized Seizures
- Tonic-clonic
- Myoclonic
- Atonic
● Focal seizures
● Unknown
 Classification of Seizures
● Generalized Seizures
- Often involved both hemispheres of the brain causing both body react.
- Intense rigidity of the body to occur, followed by: Alternating muscle
relaxation and concentration.
- The simultaneous contraction of the diaphragm and chest muscles
produced a characteristic epileptic cry.
- The tongue is often chewed.
- Incontinent of urine and feces.
- After 1 to 2 minutes, the convulsive movements begin to subside.
 Classification of Seizures
● Generalized Seizures
- Patient relaxes and lies in deep coma, breathing noisily.
- During the postictal, confused and difficult to arouse and may sleep for
hours.
- May report headache, sore muscles, depression.
● Tonic-clonic Seizure (grand mal seizure)
- Generalized seizure that affects the entire brain
- Most commonly associated with epilepsy.
 Classification of Seizures
● Tonic Seizure
- The tone is greatly increased, and the body, arms, or legs make sudden
stiffening movements.
- Consciousness usually preserved.
- Most often occur during sleep.
- Usually involved all/most of the brain.
● Clonic Seizure
- rare, common are tonic-clonic seizure
- Jerking is preceded by stiffening.
Classification of Seizures
● Myoclonic Seizure
- brief, shock-like jerks of a muscle/group of muscles.
- Person is usually awake and able to think clearly.
● Atonic seizure (drop seizure, akinetic seizure, drop attacks)
- Type of seizure that consists of brief lapse in muscle tone caused by
temporary alterations in brain function.
- Usually brief, usually less than 15 sec.
 Classification of Seizures
● Focal Seizure
- Also called partial and localized seizure
- Initially affect only one hemisphere of the brain
- No natural classification
- There may be impairment of awareness or consciousness
- Other dyscognitive features
- Progression of ictal events
 Pathophysiology
● Cause: - Allergies
- Cerebrovascular disease - CNS infection
- Hypoxemia of any cause - Metabolic and toxic conditions
(renal failure, hypoglycemia,
- Fever (childhood)
hyponatremia, hypocalcemia,
- Head injury pesticide exposure)
- Hypertension
- Brain tumor
- Drug and alcohol withdrawal
Pathophysiology
● The underlying cause is an electrical disturbance (dysrhythmia) in the nerve
cells in one section of the brain.
● The cells emit abnormal, recurring, uncontrolled electrical discharges
resulting to seizures.
● There is associated loss of consciousness.
● Excess movement or loss of muscle tone or movement.
● Disturbances of behavior, mood, sensation and perception.
● The specific causes of seizures are varied and can be categorized as
genetic, structural, or metabolic condition, or may be unknown.
Clinical Manifestations
● Depending on the location of discharging neurons.
● May range from simple staring to prolonged convulsive movements with loss of
consciousness.
● Initial pattern of seizure indicates the region in which the seizure originates.
● A hand or finger shake (frontal lobe)
● Mouth may jerk uncontrollably.
● May talk unintelligibly
● May be dizzy
● May experience unusual or unpleasant sights, odors, tastes, but without loss of
consciousness
Assessment
1. Seizure history
2. Type of seizure
3. Occurrences before, during, and after the seizure
4. Prodromal signs, such as mood changes, irritability, and insomnia
5. Aura: Sensation that warns the client of the impending seizure
6. Loss of motor activity or bowel and bladder function or loss of consciousness
during the seizure
7. Occurrences during the postictal state, such as headache, loss of
consciousness, sleepiness, and impaired speech or thinking
Diagnostic Findings
● Aimed at determining:
- The type of seizure
- Frequency and severity
- Precipitating Factors
● Developmental history, including events of pregnancy and childbirth
● Illnesses and head injuries
● EEG furnishes diagnostic evidence
Interventions
*** If the client is having a seizure, maintain a patent airway!!!
Do not force the jaws open or place anything in the client’s mouth.

1. Note the character, time and duration of the seizure.

2. Assess behavior at the onset of the seizure
3. If the client is standing or sitting, place the client on the floor and protect the
head and body.
4. Support airway, breathing, and circulation.
5. Administer oxygen.
6. Prepare to suction secretions.
7. Turn the client to the side to allow secretions to drain while maintaining the
airway.
8. Prevent injury during the seizure.
9. Remain with the client.
Interventions
10. Do not restrain the client.
11. Loosen restrictive clothing.
12. Administer intravenous medications as prescribed
13. Monitor behavior following the seizure, such as the state of consciousness,
motor ability, and speech ability.
14. Avoid alcohol, excessive stress, fatigue, and strobe lights.
Epilepsy
● Group of syndromes characterized by unprovoked, recurring seizures
● Classified by spectrum patterns of clinical features, age at onset, family
history, and seizure type.
CLASSIFICATION:
- Primary (idiopathic)
- Secondary (known cause- secondary to brain tumor)
Pathophysiology
● Message from the body are carried by the neurons of the brain by means of
discharges of electrochemical energy.
● These impulses occur in bursts wherever they perform a task.
● Sometimes, the cells continue firing even after the task is finished with
resultant dysfunction which may range from mild to incapacitating and
often causes loss of consciousness.
● If these uncontrolled, abnormal discharges occur repeatedly, the person
has epileptic syndrome.
Pathophysiology
● Epilepsy is not associated with intellectual level.
● Without other brain/ nervous system disabilities will have same
intelligence with the general population.
● Epilepsy is not synonymous with mental retardation or illness.
Medical Management
Pharmacologic Therapy:
● The exact mechanism of action is unknown.
● The goal is to control seizure with minimal side effects.
● Medication therapy controls, rather than cures seizures.
● If properly prescribed and taken, it controls 70% to 80% of seizure.
● 20-30% may not improve/ will not tolerate the side effects.
● Medications may need to be adjusted.
COMMONLY USED ORAL ANTI-EPILEPTICS
COMMONLY USED ORAL ANTI-EPILEPTICS
COMMONLY USED ORAL ANTI-EPILEPTICS
COMMONLY USED IV ANTI-EPILEPTICS
COMMONLY USED IV ANTI-EPILEPTICS
Surgical Management
● Indicated for patient with intracranial tumors, abscesses, cysts/ vascular
anomalies.
● In focal atrophic process, a well-circumscribed area of the brain may be
excised without producing significant neurologic deficits.
Status Epilepticus
● A medical emergency as it produces cumulative effect.
● Acute prolonged seizure activity, series of generalized seizures that occur
without full recovery of consciousness between attacks.
● Continuous clinical/electrical seizures (on EEG) lasting at least 30 minutes
even without impairment of consciousness.
● Vigorous muscular contractions impose a heavy metabolic demand and can
interfere with respirations.
● Some respiratory arrest at the height of each seizure produces venous
congestion and hypoxia of the brain.
● Repeated episodes of anoxia and edema to the brain may lead to
irreversible and fatal brain damage.
Status Epilepticus
Precipitating Factors:
● Withdrawal of antiseizure medication
● Fever
● Concurrent infection/other illness
Medical Management:
● Goal: to stop the seizure as quickly as possible, to ensure adequate
cerebral oxygenation, and to maintain the patient in a seizure-free state.
Status Epilepticus
Medical Management:
● Establish an airway and adequate oxygenation.
● ET if patient remains unconscious and unresponsive.
● Pharmacologic Management: IV diazepam (Valium), Lorazepam (Ativan),
Phenytoin, phenobarbital administered later to maintain a seizure free
state.
Status Epilepticus
Nursing Management:
● Initiate ongoing assessment and monitoring of respirations and cardiac function
due to the delay of depression of respiration and BP secondary to administration
of anti-seizure medication and sedatives.
● Monitoring and documenting seizure activity and the patient’s responsiveness.
● Turn to sides to assist in draining pharyngeal secretions.
● Suction equipment due to risk of aspiration.
● Side effects of long-term seizure medication: Puts the person at risk for fractures
resulting from bone disease (osteoporosis, osteomalacia, hyperthyroidism)
● Person should be protected from injury during seizure.
Break! CVD next
04.
Traumatic Brain Injury
 Traumatic Brain Injury
● Any alteration in brain function caused by an external force that can be
mild, moderate or severe

● Happens when a bump, blow, jolt or other injury causes brain damage.

● Important consideration!!! IS THE BRAIN INJURED??

● Even seemingly a minor injury can cause significant brain damage

secondary to obstructed blood flow.

● Immediate complications include cerebral bleeding, hematomas,

uncontrolled increased ICP, infections, and seizures.
Traumatic Brain Injury
Types of Injury:
1. Open 3. Fractures
a. Scalp lacerations a. Open
b. Fractures in the skull b. Closed
c. Interruption of the dura mater c. Basilar
2. Closed 4. Bleeds
a. Concussions a. Epidural
b. Contusions b. Subdural
- Coup c. Intracerebral
- Countercoup
Traumatic Brain Injury (Types of Injury)
Traumatic Brain Injury (Concussion)
● Concussion
- A temporary loss of neurologic function with no apparent structural
damage to the brain.
- May or may not produce a brief loss of consciousness
- Also referred as mild TBI
- CAUSES: blunt trauma, direct blow/blast injury
- Frontal lobe: temporary amnesia or disorientation.
Traumatic Brain Injury (Concussion)
Three Grades of Concussion by the American Academy of Neurology
A. Grade 1
- Has transient confusion, no loss of consciousness, mental status
abnormalities that last for 15 minutes.
B. Grade 2
- Also has symptoms of transient confusion and no loss of consciousness
but mental status abnormalities last more than 15 minutes.
C. Grade 3
- There is loss of consciousness lasting from seconds to minutes.
Traumatic Brain Injury (Concussion)

Management:
● Monitor for decrease level of consciousness, worsening headache,
dizziness, seizures, abnormal pupil response, vomiting, irritability, slurred
speech, and numbness/weakness in the arms and legs.
● The occurrence of these symptoms need further evaluation.
● Recovery may appear complete but long-term sequelae are possible and
repeat injuries are common.
● May result to problem in interpersonal relationship.
Traumatic Brain Injury (Contusion)
● Contusion (Bruise on the brain)
- Coup or countercoup
- a moderate to severe head injury, the brain tissue is bruised and damaged
in specific areas.
- CAUSE: severe acceleration-deceleration forces/blunt trauma.
- The impact of the brain against the skull leads to a contusion.
- Common in the anterior portion of frontal and temporal lobe.
- The effects of injury (hemorrhage and edema) peak after 18-36 hours
- Patient outcome depends on the area and severity of the injury.
Traumatic Brain Injury (Contusion)

Clinical Manifestations:
- Loss of consciousness associated
with stupor and confusion.
- Temporal lobe contusions carry
greater risk of swelling, rapid
deterioration and herniation.
- Deep contusions are more often
associated with hemorrhage and
destruction of the reticular activating
fibers altering arousal.
Traumatic Brain Injury (Fracture)
Skull Fracture:
1. Open Fracture – Torn Dura
2. Closed Fracture – Dura is intact
3. Basilar Skull Fracture – fracture at the base of the
skull

Basilar fracture specific findings:

a. Battle’s Sign - bruising on the mastoid process
b. Raccoon eyes – Periorbital bruising
c. Cerebrospinal rhinorrhea (CLEAR ODORLESS FLUID
ON THE NOSE) - need to test drainage for CSF (halo
and glucose test)
● Otorrhea
● Cranial nerve palsy
● Hemotympanum
NEVER INSERT ANY TUBE IN A CLIENT’S NOSE WITH
BASILAR FRACTURE!!!
Traumatic Brain Injury (Diffuse Axonal Injury)
● Diffuse Axonal Injury
- Results from widespread shearing and rotational forces that produce
damage throughout the brain-to axons in the cerebral hemispheres, corpus
collosum and brain stem.
- Associated with prolonged traumatic coma.
- It is more serious and is associated with poor prognosis than a focal lesion
or ischemia.
Traumatic Brain Injury (Diffuse Axonal Injury)
Clinical Manifestations:
- No lucid interval
- Immediate coma
- Decorticate and decerebrate posturing
• Diagnosis made by clinical signs in conjunction with a CT Scan or MRI
• Recovery depends on the severity axonal injury.
Traumatic Brain Injury (Hematomas)
● Hematomas
- are collection of blood in the brain or Bleeding within the cranium

- Major symptoms are frequently delayed until the hematoma is large

enough to cause distortion of the brain and increased ICP.
TYPES:
● Epidural- above the dura
● Subdural- below the dura mater
● Intracerebral- within the brain tissue/anywhere
 Traumatic Brain Injury (Epidural Hematoma)
● Epidural Hematoma
- The most serious type of hematoma that forms rapidly and results from
arterial bleeding.
- considered a surgical emergency!!
- Blood collects in the space between the dura mater and the skull from a
tear in the meningeal artery .
- Is considered an extreme emergency as marked neurologic deficit or even
respiratory arrest occur within minutes.
Traumatic Brain Injury (Epidural Hematoma)
Symptoms: (“TALK AND DIE” SYNDROME)
- Depends on the expanding hematomas. WOF: Uncal herniation
- Often characterized by brief loss of consciousness followed by lucid
interval, awake and conversant, then rapidly progresses to coma
- Patient increasingly restless, agitated and confused due to increased ICP.
- Pupils from PERRLA are suddenly fixed and dilated
- GCS 14/15 going down. If GCS<8 – WOF the airway
- Airway and breathing pattern changes, Cushing’s triad(IICP).
- Headache, N/V, Seizure activity
- Weakness and paralysis, Reflex activity changes
Traumatic Brain Injury (Epidural Hematoma)
Medical Treatment:
- CT SCAN ASAP!!!
- A craniotomy (burr hole) may be required to Remove blood or clots and
control of bleeding.
- A drain usually inserted after craniotomy.
- Morphine sulfate or opioid medication with caution on respiratory
depression
 Traumatic Brain Injury (Epidural Hematoma)
Nsg Intervention:
1. Monitor Respiratory and neurological status;
2. Monitor VS and IICP; Initiate normothermia
3. maintain a patent airway and head elevation
4. Prevent neck flexion
5. Initiate seizure precautions
6. Do not attempt to clean the nose, suction, or allow the client to blow their
nose if drainage occurs.
7. Do not clean the ear if drainage is noted, but apply a loose, dry sterile
dressing.
8. Test drainage from nose or ear and inform MD if (+) CSF
Traumatic Brain Injury (Subdural Hematoma)
● Subdural Hematoma
- A occurs below the dura because of tears or ruptures in the small vessels
crossing the subdural space.
- forms slowly and results from a venous bleed
- The most common cause is trauma, but it can also occur from coagulopathies
and rupture of an aneurysm.
TYPES:
a. Acute
b. subacute
c. chronic
Traumatic Brain Injury (Subdural Hematoma)
● Acute
- associated with major head injury involving contusion or laceration.
- Clinical symptoms: develop over 24-48 hours.
- S/sx: changes in LOC, pupillary signs, hemiparesis
- Coma, Cushing’s triad are signs of rapidly expanding mass
● Subacute
- result of less severe contusions and head trauma.
- Clinical symptoms: develop between 48hrs to 2 weeks after injury.
- S/sx: similar to acute subdural hematoma.
Traumatic Brain Injury (Subdural Hematoma)
● Chronic
- from seemingly minor head injuries and seen frequently in older adults who are
prone to brain atrophy from aging.
- Clinical Symptoms: can be lengthy from 3 weeks to months.
- S/Sx: Severe headache that come and go.
- Focal neurologic signs.
- Personality changes, mental deterioration
- Focal seizure
TREATMENT:
● craniotomy to evacuate clot
Traumatic Brain Injury (Hemorrhage)
● Intracerebral hemorrhage
- occurs when a blood vessel within the brain ruptures, allowing blood to leak
inside the brain.
- Bleeding into the parenchyma of the brain
- Commonly seen in head injuries when force is exerted to the head over a small
area like bullet injuries/stab wounds.
- Onset may be insidious, starting with the development of neurologic deficits
followed by headache.
● Subarachnoid Hemorrhage
- bleeding into the subarachnoid space
- Due to head trauma or spontaneously, such as a ruptured cerebral aneurysm.
Traumatic Brain Injury (Hemorrhage)
CAUSES:
1. Systemic hypertension which causes degeneration and rupture of the vessel.
2. Vascular anomalies
3. Intracranial tumor (benign or malignant)
4. Bleeding disorders: leukemia, hemophilia
5. Complications from anticoagulant therapy

Management:
● Control of ICP
● Careful administration of fluids, electrolytes and antihypertensive medications.
● Surgical intervention by craniotomy or craniectomy for removal of blood clots
and control of hemorrhage.
Traumatic Brain Injury (Management)
Management of Brain Injuries
● Initial physical and neurologic examinations.
● CT and MRI scans are the main tools in evaluating brain structure, or PET for
assessing brain function.
● Any patient with brain injury is presumed to have cervical spine injury until proven
otherwise.
- Transported from the scene on a board with head and neck maintained in
alignment.
- Cervical collar applied and maintained until cervical x-ray is obtained and the
absence of injury.
Traumatic Brain Injury (Management)
● All therapy is directed toward preserving brain homeostasis and preventing
secondary brain injury.
● maintaining adequate cerebral oxygenation.
● Surgery is required for evacuation of blood clots, debridement and elevation of
depressed fractures of the skull.
● ICP is monitored closely.
● Elevating the head of the bed.
● Maintaining normal blood volume.
● Supportive measurements: ventilatory report, seizure prevention, fluid and
electrolyte maintenance, nutritional support, management of pain and anxiety,
comatose are intubated.
Traumatic Brain Injury (Brain Death)
● Brain Death
- 3 cardinal signs of brain death in clinical examination:
1. Coma
2. absence of brain stem reflexes
3. apnea
● Adjunctive tests: Cerebral flow studies, EEG, transcranial doppler and brain
stem auditory are used to confirm brain death.
● When a patient sustained severe head injury incompatible with life, the
patient is a potential organ donor.
05.
Spinal Cord Injury
Review of the Nervous System
Spinal Cord Injury
Spinal Cord Injury
● Damage to the spinal cord causes changes in its function, either temporary
or permanent.
● These changes translate into loss of muscle function, sensation and
autonomic functions in parts of the body served by the spinal cord below
the level of the lesion.
● Symptoms depend on the location of injury
● THE HIGHER THE INJURY, THE MORE FUNCTION IS LOST!!
● Injuries above T6: Monitor for AUTONOMIC DYSREFLEXIA
Spinal Cord Injury
● Most common causes: ● African-American (25%)
- Motor vehicular crashes (46%) ● Hispanic (8%)
- Falls (22%) ● All other racial groups (2%)
- Violence (16%) ● The predominant risk factors: young
age, male gender, alcohol and drug
- Sports (12%)
use (CDC, 2010)
● Males account for 80% of cases
● 15-35 years of age (50-70%)
● In the US: Caucasians (65%)
Spinal Cord Injury
● Damage in SCI ranges from:
- Transient concussion (from which patient fully recovers)
- Contusion
- Laceration
- Compression of spinal cord tissue (either alone or in a combination)
- Complete transection (severing) of the spinal cord which renders the patient
paralyzed below the level of the injury.
● The most common vertebrae involved: C5, C6, C7 T12, L1
● These vertebrae are most susceptible as there is a greater range of mobility in
these areas.
Spinal Cord Injury

● Paraplegia and Tetraplegia

can occur
- Incomplete tetraplegia- most
common
- Complete paraplegia
- Complete tetraplegia
- Incomplete paraplegia
Spinal Cord Injury
Two Categories of SCIs:
● Primary Injuries: the result of the initial insult or trauma and are usually
permanent.
● Secondary Injuries: usually the result of contusion or tear injury where the
nerve fibers begin to swell and disintegrate.
- A secondary chain of events produces ischemia, hypoxia, edema, and
hemorrhagic lesions that results to the destruction of myelin and axons.
- Experts believe that secondary injury is the principal cause of spinal cord
degeneration at the level of injury, that is reversible during the first 4-6
hours.
Spinal Cord Injury
Assessment and Diagnostic Findings
● Detailed neurologic examination
● Diagnostic x-rays (lateral cervical spine x-rays)
and CT Scan initially.
● MRI for further workup
● Myelogram to visualize the spinal axis if MRI is
contraindicated.
● Continuous electrocardiographic monitoring.
Spinal Cord Injury
Emergency Management:
● Any patient involved in motor vehicular crash, diving or contact sports
injury, a fall, or any direct trauma to the head and neck is considered to
have SCI until ruled out.
● Initial care must include:
- Rapid assessment
- Immobilization
- Extrication
- Stabilization and control of life-threatening injuries
- Transportation to most appropriate medical facility.
Spinal Cord Injury
● At the scene of injury
- Patient must be immobilized on a spinal board with the head and neck
maintained in a neutral position.
- Prevent flexion, rotation, or extension of the patient’s head.
- At least 4 people should slide patient carefully onto the board.
- Twisting movement may cause irreversible damage the spinal cord.
Spinal Cord Injury
Medical Management
● Resuscitation as necessary
● Oxygenation and cardiovascular stability are maintained.
- Oxygen is administered to maintain high partial pressure of arterial oxygen
(PaO2) as hypoxemia can create or worsen neurologic deficit.
- If ET inhalation is necessary, extreme care is taken to avoid flexion or
extension of patient’s neck.
Spinal Cord Injury
Skeletal Fracture Reduction and Traction
● Skeletal Traction is used to reduce cervical fractures or align cervical spine.
- Gardner-Wells Tong, crutchfield tong, or Vinke Calipers
- Halo device
- Halo device initially used with traction or after tong is removed, it provides
immobilization of cervical spine while allowing early ambulation.
● Traction is applied to the skeletal device by weights, depending on the size
or degree of fracture displacement.
● Reduction usually occurs after correct alignment has been restored
Spinal Cord Injury
Care of Traction
● Check the traction apparatus to see that the ropes are in wheel groves, ropes
not frayed, weights hang freely and knots are tied securely.
● Evaluates position- slipping down in bed may result in ineffective traction.
- Maintain position
- Position patient’s foot with a footboard to avoid footdrop.
● Prevent skin breakdown.
- Protect elbows and heels, inspect for pressure ulcers.
- Transparent film, hydrocolloid dressing, skin sealants may be applied to bony
prominences to decrease friction.
Spinal Cord Injury (Care of Traction)
● Assess for irritation and inflammation at least every 8 hours.
● Provide back care and keep the bed dry and free of crumbs and wrinkles.
● Provide overhead trapeze to help patient move about in bed and move on and
off the bedpan.
● 1st 48 hours after insertion- site is covered with sterile absorbent nonstick
dressing and a rolled gauze.
● Inspect the pin sites every 8 hours for reaction.
● Signs of reaction include redness, warmth, and serosanguineous drainage at the
site.
● Prophylactic broad-spectrum IV antibiotics may be administered for 24-48 hours
postinsertion to prevent infection.
Spinal Cord Injury
Surgical Management
● GOAL: preserve neurologic function by removing pressure from the spinal cord
and provide stability.
● Surgery is indicated in any of the ff. situations:
- Compression of the cord is evident.
- Injury results in fragmented or unstable vertebral body.
- The injury involves a wound that penetrates the cord.
- Body fragments are in the spinal canal.
- The patient’s neurologic status is deteriorating.
Spinal Cord Injury
Acute Complications of SCI
● Spinal and neurogenic shock
● Spinal shock
- Reflects a sudden depression of reflex activity in the SC (areflexia) below the
level of injury.
- Without sensation, paralyzed, and flaccid, and the reflexes are absent.
- Bladder, and bowel functions are affected.
- Bowel distention and paralytic ileus is treated with intestinal decompression by
NGT insertion.
Spinal Cord Injury
Neurogenic Shock
● Develops as a result of the loss of autonomic NS functions below the level of the
lesion.
● Absence of perspiration on paralyzed portions of the body.
● With cervical and thoracic injuries, innervation of major accessory muscles of
respirations is lost.
● Decreased vital capacity, retention of secretions, increased PaCO2, decreased
oxygen levels, respiratory failure and pulmonary edema.
● Causing a decrease in BP, HR, and Cardiac output.
● Venous pooling in the extremities and peripheral vasodilation.
Spinal Cord Injury
Venous Thromboembolism
● Is a potential complication of immobility
● Formation of blood clots in the vein
● Patient with VTE are at risk of DVT, usually in the leg and PE.
● Homan’s sign- extend knee, leg is elevated, dorsiflex foot, patient complain of
pain in the calf. (+)
Management:
- Low dose anticoagulation therapy (to prevent PE)
- Anti-embolic stockings (to prevent stagnation of blood)
- Thrombolytic agents- “streptokinase”
Spinal Cord Injury
Other Complications
● Respiratory complications: respiratory failure and pneumonia
● Autonomic dysreflexia
● Pressure ulcers
● Infection: urinary, respiratory, traction pin sites
Spinal Cord Injury
Autonomic Dysreflexia (Hyperreflexia)
● Also known as “autonomic hyperreflexia” an acute life-threatening emergency
that occurs as a result of exaggerated autonomic responses to stimuli that are
harmless in normal people.
● It occurs after spinal shock is resolved
● This is characterized by:
- severe, pounding headache
- Paroxysmal hypertension
- Profuse diaphoresis, most often of the forehead
- Nausea, nasal congestion, bradycardia
Spinal Cord Injury (AUTONOMIC DYSREFLEXIA)

PATHOPHYSIOLOGY

Example: T1 injury with a full bladder

sacral nerve is affected >> no motor sensation below

the waist >> can’t empty full bladder >> Peripheral NS
can’t sense it >> sensory neurons can’t communicate to
the CNS >> bladder is irritated >> CNS senses it >>
vasoconstriction >> hypertensive crisis >> brain wonders
why the BP is so high >> sends signals to the alpha and
beta cardiac receptors for vasodilation >> signals are
blocked at the level of injury>>no vasodilation
Spinal Cord Injury (AUTONOMIC DYSREFLEXIA)

Thoracic & below injuries ONLY!!

Spinal Cord Injury
● The sudden increase of BP may cause rupture of one/more cerebral vessels or
may lead to increased ICP.
● Stimuli that may trigger this reflex:
- Distended bladder (most common cause)
- Distention or contraction of visceral organs specially the bowel from constipation
or impaction.
- Stimulation of the skin: tactile, pain, thermal or pressure ulcer.
Spinal Cord Injury
Management
● This is an emergency situation, and the goal is to remove the triggering stimulus.
- Place patient immediately in a sitting position to lower the BP.
- Rapid assessment to identify and alleviate the cause.
- The bladder is emptied immediately via a urinary catheter.
Spinal Cord Injury
- The rectum is examined for fecal mass, then remove.
- The skin is examined for any areas of pressure irritation or broken skin.
- If these measures do not relieve hypertension and headache, Apresoline
(hydralazine hydrochloride) is administered via slow IV.
- The patient is instructed about prevention and management measures.
Rehabilitation
- Increasing mobility
- Promoting skin integrity
- Improving bladder management
- Establishing bowel control
END..
07.
Management of
Patients with
Cerebrovascular
Disorders
 Cerebrovascular Disorder
● An umbrella that refers to a functional abnormality of the CNS that occurs
when the blood supply to the brain is disrupted.
● Stroke is the primary cerebrovascular disorder in the US and 4th leading
cause of death after heart disease, cancer and lower respiratory disease.
● Approximately, 297,000 people experience stroke each year in the U.S.
 Cerebrovascular Disorder
Two Major Categories of Stroke:
● Ischemic- 87% of cases, vascular occlusion and significant hypoperfusion.
● Hemorrhagic- 13% of cases, there is extravasation of blood in the
brain/subarachnoid space.
● The two types differ in etiology, pathophysiology, medical management,
surgical management, and nursing care.
 Ischemic Stroke
● A.k.a. “Cerebrovascular Accident” CVA/”brain attack”
● Sudden loss of brain function resulting from disruption of blood supply to a
part of the brain.
● Subdivided into:
- Thrombotic
- Embolic
 Ischemic Stroke
Five Different Types Based on the Cause:
● Large artery thrombotic stroke- 20%
● Small penetrating artery thrombotic stroke- 25%
● Cardiogenic embolic strokes- 20%
● Cryptogenic stroke- 30%
● Others- 5%
 Ischemic Stroke
Large Artery Thrombotic Stroke
● By atherosclerotic plaques in the large blood vessel of the brain.
● Thrombus formation and occlusion at the site of atherosclerosis result in
ischemia and infarction.
Small Penetrating Artery Thrombotic Stroke
● Is the most common type of Ischemic Stroke.
● Also called lacunar stroke, because of the cavity created after the death of
infarcted brain tissue.
 Ischemic Stroke
Cardiogenic Embolic Stroke
● Associated with dysrhythmias, usually chronic atrial fibrillation.
● Also associated with valvular heart disease/thrombi in the left ventricle.
● Emboli originate from the heart and circulate in the cerebral vasculature,
usually the left middle cerebral artery.
● Can be prevented with anticoagulation therapy in patient with atrial
fibrillation.
Cryptogenic stroke– no known cause
 Ischemic Stroke
Strokes from other Causes
● Illicit drug use
● Coagulopathies
● Migraine
● Spontaneous Dissection of the carotid/vertebral arteries.
 Risk Factors of Stroke
Modifiable Non-Modifiable
● Hypertension ● Age
● Cardiovascular diseases and Atrial ● Gender
fibrillation
● Family History
● DM
● Race
● Prior stroke, history of TIA
(Transient Ischemic Attack)
● Other factors: Hyperlipidemia,
cigarette smoking, heavy alcohol
consumption.
Pathophysiology (board)
 Clinical Manifestations
● May cause a variety of neurologic deficits depending on the location of the
lesion.
● Thrombotic stroke may have warning signs, TIA.
● FAST (Facial Asymmetry, Arm weakness, Slurred speech, Time)
- May present with any of the ff signs and symptoms:
- Numbness/weakness of the face, arm /leg, especially on one side of the
body.
- Confusion or change in mental status
- Trouble speaking or understanding speech.
 Clinical Manifestations
- Visual disturbances
- Difficulty walking, dizziness/loss of balance or coordination.
- Sudden severe headache.
Motor Loss
● Hemiplegia
● Hemiparesis
● Dysphagia
 Clinical Manifestations
Communication Loss
● Aphasia- impaired speech
- Expressive aphasia (Broca’s)
- Receptive aphasia (Wernicke’s)
- Global aphasia
● Dysarthria- difficulty speaking due to muscle paralysis responsible for
producing speech.
● Apraxia- inability to perform previously learned reaction.
 Clinical Manifestations
Perceptual Disturbances
● Homonymous hemianopia- blindness in half of the visual field
● Diplopia
● Loss of peripheral vision
Sensory Loss
● Agnosia- deficits in the ability to recognize previously familiar objects
perceived by one/more of the senses.
● Paresthesia
 Clinical Manifestations
Cognitive Impairment and Psychological Effects
● Frontal Lobe- learning capacity, memory
● Reflected as short attention span, difficulties in comprehension,
forgetfulness, lack of motivation.
● Depression, emotional lability, hostility, lack of cooperation, frustration,
resentment.
Bowel and Bladder Incontinence
 Clinical Manifestations
Generalized Findings when Patient arrived in the ED
● Increased BP
● Headache
● Vomiting
● Seizures
● Changes in mental status
● Fever
● ECG changes
 Prevention
● Healthy Lifestyle
- Not smoking, maintaining a healthy weight.
- Maintaining a healthy diet, including modest alcohol consumption.
- Regular exercise
- DASH diet (Dietary Approaches to Stop Hypertension)
• High in fruits and vegetables, moderate low-fat dairy products, low in
animal protein, plant protein and legumes.
● Stroke Risk Screenings
 Medical Management
● Goals: early diagnosis and early identification of patients who can benefit
from thrombolytic therapy.
● Preserving cerebral oxygen
● Preventing complications and stroke recurrence.
● Rehabilitation
 Medical Management
● Patients who have TIA/stroke should have medical management for
secondary prevention.
- Coumadin
- Aspirin
- Clopidogrel
● Thrombolytic Therapy
- Window period of 3 hours (may be extended to 4.5 hrs)
- rt-PA (alteplase, reteplase, and tenecteplase)
- 0.9 mg/kg over one hour
- Maximum dose is 90 mg.
 Medical Management
● Eligibility criteria for rt-PA activator administration.
- 18 years old and above
- Clinical diagnosis of Ischemic Stroke
- Time of onset known and within guidelines.
- SBP less than 185 mmHg, DBP less than 110 mmHg.
- No seizure onset at stroke.
- Not taking warfarin
- Not receiving heparin within 48 hours, PTT not elevated.
- Platelet count above 100,000/mm3
 Medical Management
● Eligibility criteria for rt-PA activator administration.
- No prior intracranial hemorrhage.
- No major surgical procedure in 14 days.
- No GI/urinary bleeding within 21 days.
● Rehabilitation
- Physical Therapy
- Occupational Therapy
- Speech Therapy
- Classify ADL needs
 Hemorrhagic Stroke
● Primarily caused by intracranial or subarachnoid hemorrhage.
● Bleeding into the brain tissue, ventricles or subarachnoid space.
● Primary intracerebral hemorrhage
- From rupture of small vessels- 80%, chiefly caused by hypertension.
- Subarachnoid hemorrhage from ruptured intracranial aneurysm.
● Secondary intracerebral hemorrhage is associated with arteriovenous
malformation, intracranial aneurysm, intracranial neoplasm or medications
like anticoagulants.
● Symptoms produced when primary hemorrhage, aneurysm, or AVM press on
nearby cranial nerves, or brain tissue, or bleeding to the subarachnoid space.
Pathophysiology: board
 Assessment and Diagnostic Findings
● CT Scan
- to determine the type of stroke.
- Size and location of hematoma
- Presence or absence of ventricular blood
- Hydrocephalus
● MRI
● Lumbar puncture if no signs of increased ICP, as it can cause herniation on
the brain stem or rebleeding.
● Toxicology for patients below 40, due to illicit drug use.
 Assessment and Diagnostic Findings
● Cerebral angiography- to confirm diagnosis of intracranial aneurysm or AVM.
- Shows location and size of lesion
- Provide info about the affected arteries, veins, adjoining vessels and vascular
branches.
 Clinical Manifestations
● Hemorrhagic stroke presents a variety of neurologic deficits similar to patient with
ischemic stroke.
- headache, common complaint of conscious patient
- Some motor, sensory, cranial, cognitive and other functions that are disrupted.
- Rupture aneurysm and AVM
• sudden, unusually severe headache
• Loss of consciousness
• Nuchal rigidity
• Visual loss, diplopia, ptosis, tinnitus, dizziness, hemiparesis may occur.
• Severe bleeding will result in cerebral damage, followed rapidly by coma and death.
 Medical Management
● Goals:
- Allow the brain to recover from initial insult (bleeding).
- Prevent/minimize the risk of rebleeding.
- Prevent/treat complications.
● Bedrest with sedation to prevent agitation and stress.
● Manage vasospasm.
● If caused by warfarin, may be corrected with fresh frozen plasma and vitamin
K.
 Medical Management
● Prothrombin complex concentrates.
● Hemodialysis
● Antiseizure drug for seizure. (e.g. phenytoin)
● Sequential compression device or anti-embolism stocking to prevent DVT.
● If mobile for 1-4 days and bleeding ceases, DVT prevention medication like
unfractionated heparin may be prescribed.
● Analgesic for head and neck pain.
● Acetaminophen, cooling blanket for fever.
● After discharge, anti-hypertensive medication to decrease risk of another
intracerebral hemorrhage.
 Surgical Management
● Craniotomy- if showing signs of worsening neurologic deficit, increased ICP,
signs of brain stem compression.
 Prevention
● Managing hypertension and ameliorating other significant factors.
- Primary hypertension (essential hypertension), secondary hypertension
(disease)
- Malignant hypertension- persistent elevation of BP. Medication, diet exercise
cannot control the hypertension.
● Control of hypertension can reduce the risk of hemorrhagic stroke.
● Additional risk factors: increasing age, male gender, excessive alcohol intake.
● Health Education
● Stroke risk screening
 Potential Complications include:
● Cerebral hypoxia and decreased blood flow and extension of the area of the
injury.
- Immediate complications of hemorrhagic stroke
- Administering supplemental oxygen and maintaining the hemoglobin and
hematocrit at acceptable levels will assist in maintaining tissue oxygenation.
● Vasospasm- narrowing if the lumen
- Serious complication of subarachnoid hemorrhage, leading cause of
morbidity and mortality of those who survive the initial attack.
- 15%-20% with vasospasm die, frequently occurs 7-10 days after initial
hemorrhage.
 Potential Complications include:
- Based on theory, vasospasm is caused by an increased influx of calcium into
the cell.
- Nimodipine (Nimotop) antagonizes/ blocks this action and prevent or reverse
the action of vasospasm.
 Potential Complications include:
● Increased Intracranial Pressure
- Increased ICP can occur after either ischemic stroke or a hemorrhagic stroke
but almost always follows a subarachnoid hemorrhage due to disturbed
circulation of CSF by blood.
- CSF drainage may be instituted by ventricular catheter drainage.
- Mannitol
- Monitor fluid and electrolyte imbalance as this will be caused by long term
mannitol use.
Break! Next topic neuro trauma
08.
Management of
Patients with Cerebral
Infections
Meningitis
● An inflammation of the meninges(arachnoid and pia mater) of the brain and
spinal cord, which cover and protect the brain and spinal cord.
● THREE MAJOR CAUSES: virus, fungi and bacteria (more dangerous)
● Predisposing Factors: skull fractures, brain or spinal surgery, sinus or upper
respiratory infections, use of nasal sprays, compromised immunity
● Transmission: direct contact; droplet spread.
● Classified as:
a. Septic- caused by bacteria (Streptococcus pneumoniae, Neisseria Meningitidis)
b. Aseptic- caused by virus/ secondary to cancer/weak immune system
Meningitis (Pathophysiology)
● Originate in two ways:
1. Bloodstream - consequence of other infection
2. Direct spread after a traumatic injury of facial bones or secondary to invasive
procedures.

organism enters the bloodstream >> crosses the blood-brain

barrier >> proliferate in the CSF >> inflammation of the
subarachnoid and pia mater (s/sx: + Kernig’s & Brudzinski's Sign)
>> increased ICP
Meningitis (Clinical Manifestations)
● Headache and fever are frequently the initial symptoms that remains high
throughout the course of illness.
● Headache is steady or throbbing and severe as a result of meningeal irritation.
- nuchal rigidity (early sign)
- Positive Kernig’s sign
- Positive Brudzinski’s sign
- Photophobia- meniges covering the optic nerve is inflammed
- A rash can be a striking feature of N. meningitidis infection, occurring in about
half of patients with this type of meningitis.
Meningitis (Clinical Manifestations)
OTHER MANIFESTATIONS:
● Skin lesion ranging from petechial rash with purpuric lesions to large areas of
ecchymosis in 50% of patients.
● Disorientation and memory impairment are common in the early course of
the disease.
● Lethargy, unresponsiveness, and coma as the illness progresses.
● Seizure
● Increased ICP, herniation, brain stem compression
Meningitis (Assessment and Diagnosis)
● CT, MRI
● Lumbar puncture- to assess the CSF (cloudy/clear), check the presence of blood,
increased WBC
- Neurologic signs: ALOC, papilledema, neurologic deficits, new onset of seizure,
immunocompromised state.
● Prevention- infection control
- Meningococcal conjugated vaccine given to 11-12 years of age, booster at 16.
- Close contact with patient: antimicrobial prophylaxis [rifampin(Rifadin), ciprofloxacin
(Cipro), ceftriaxone (Rocephin)]
- Prophylaxis should be started 23 hours after
- Vaccination with pneumonia
Meningitis (Medical Management)
● Administration of antibiotic that crosses the blood-brain barrier into the
subarachnoid space to halt the multiplication of bacteria.
- Penicillin G in combination with one of the cephalosporins (ceftriaxone
sodium, cefotaxime sodium) intravenously
- Dexamethasone (Decadron) often use as adjunct in bacterial and
pneumococcal meningitis.
● IVF for shock and dehydration.
● Steroids
● Analgesics
● Antipyretics
Meningitis (Nursing Management)
● ISOLATION PRECAUTION!! (until 24 hours after initiation of antibiotic therapy )
● pain management due to overall body aches and neck pain
● Keep client rested in a quiet, darkened room
● Cooling blankets
● Encouraging the patient to stay hydrated either orally or peripherally
● Ensuring close neurologic and VS monitoring
● SAFETY PRECAUTION!! (protect from injury)
● Monitoring daily body weight
● Monitor for pressure ulcers and pneumonia due to immobility

PREVENTION:
- Hib vaccine
Brain Abscess
● Collection of infectious material within the tissue of the brain.
● Bacterial - most common causative organisms.
● Rare in people who are immunocompetent, may occur in people with otitis
media, rhinosinusitis.
● 50% of brain abscess is otogenic in origin (e.g. mastoiditis).
● May also result from intracranial surgery, penetrating head injury, tongue
piercing.
● Organisms causing brain abscess may reach the brain by hematologic spread
from the lungs, gums, tongue/heart, from a wound or intraabdominal
infection.
Brain Abscess(Clinical Manifestations)
● Headache - worse in the morning is the most prevalent.
● Fever may or may not be present.
● Vomiting
● weakness and decreasing vision that reflects the area of the brain involved.
● As the abscess expands: symptoms of IICP
● Frontal Lobe: Hemiparesis, expressive aphasia, seizure, frontal headache.
● Temporal Lobe: localized headache, changes in vision, facial weakness,
receptive aphasia.
● Cerebellar abscess: occipital headache, ataxia, nystagmus.
Brain Abscess (Diagnosis)
● CT Scan - identify the size and location of the abscess.
● Aspiration of abscess guided by CT scan or MRI for blood culture.
● MRI – most preferred because it detects smaller lesions such us
cerebritis
● EEG - help localize the lesion
● CXR - to rule out predisposing lung infections
Brain Abscess (Management)
Medical Management:

● Controlling increased ICP

● Draining the abscess using sterrotatic CT-guided aspiration

● Antimicrobial therapy based on the results of C/S.

● Ceftriaxone is usually started then adjusted with the results of C/S.

● Corticosteroids - help reduce the inflammatory cerebral edema

● Anticonvulsant

Nursing Management:

● Continue monitoring the neurologic status.

● Administer prescribed medication.

● Assessing the response to treatment.

● Providing supportive care.

Encephalitis
● inflammation of the brain parenchyma and often of the meninges causing
edema and necrosis.
● It affects the cerebrum, brainstem, and cerebellum
● Mostly viral in origin
● Herpes Simplex Virus (HSV) - most common cause in the US.
TYPES:
➢ Herpes Simplex Virus Encephalitis
➢ Arthropod- Borne Virus Encephalitis
➢ Fungal- Encephalitis
➢ Creutzfeldt-Jacob Disease
Encephalitis (Pathophysiology)

Causative agent >> inflammation of the brain tissue

>> local necrotizing hemorrhage >> cerebral edema
>> cerebral hypoperfusion >> progressive
deterioration of nerve cell bodies >> brain tissue
necrosis
Encephalitis (Assessment)
1. Changes in level of consciousness and mental status
2. Presence of cold sores, lesions, or ulcerations of the oral cavity
3. History of insect bites and swimming in fresh water
4. Exposure to infectious diseases
5. Travel to areas where the disease is prevalent
6. Fever
7. Nausea and vomiting
8. Nuchal rigidity
9. Signs of increased ICP
10. Motor dysfunction and focal neurological deficits
Encephalitis (Interventions)
1. Monitor vital and neurological signs.
2. Assess level of consciousness using the Glasgow Coma Scale.
3. Assess for mental status changes and personality and behavioral changes.
4. Assess for signs of increased ICP.
5. Assess for the presence of nuchal rigidity and a positive Kernig’s sign or Brudzinski’s
sign, indicating meningeal irritation (Fig. 59.3).
6. Assist the client to turn, cough, and deep- breathe frequently.
7. Elevate the head of the bed 30 to 45 degrees.
8. Assess for muscle and neurological deficits.
9. Administer acyclovir as prescribed (usually the medication of choice for herpes
encephalitis).
10. Initiate rehabilitation as needed for motor dysfunction or neurological deficits.
HSV Encephalitis

HSV Encephalitis
● Initial Manifestations
- Fever, headache, confusion, hallucination
● Focal Neurologic symptoms
- fever, headache, behavioral changes, focal seizures, dysphasia, hemiparesis,
and altered LOC.
HSV Encephalitis
Diagnostic Findings:
● MRI - neuroimaging of choice for early detection of changes.
● EEG - shows slowing or focal changes in the temporal lobe in majority of
patients.
● Lumbar puncture has high opening pressure with normal glucose and high
protein in CSF.
● Viral culture almost always negative.
● Polymerase chain reaction (PCR), it identifies DNA bands of HSV-1 in CSF
especially on the 3rd to 10th day.
HSV Encephalitis (Medical Management)
● Antiviral agents
- Acyclovir (Zovirax)
- Ganciclover (Cytorene)
- Treatment is up to 3 weeks, slow IV over an hour.
- Early administration is well tolerated and improves prognosis.
HSV Encephalitis (Nursing Management)

● Assessment of neurologic functions.

● Comfort measures to reduce headache.
- Dimming the light, limiting noise and visitors, grouping of nursing
interventions, administering analgesic, opioid analgesic.
- May mask neurologic symptoms.
HSV-1 Encephalitis
● Cause: necrotizing hemorrhage that becomes generalized, followed by
edema.
● S/SX: fever, headache, confusion, hallucination, hemiparesis, ALOC, dysphasia
● Assessment: EEG, CSF examination to diagnose.
● Management: Antiviral: Zovirax (Acyclovir)- choice
- Assess neurologic status
- Comfort measures to reduce headache, limiting noise, visitors, lights
- Promote safety- ALOC
- Monitor blood chemistry.
Arthropod-Borne Virus Encephalitis (Transmission)
● transmitted to human beings through the bite of an infected mosquito or
tick
● 5 main arboviral encephalitis
- Eastern equine encephalitis
- Western equine encephalitis
- St. Louis encephalitis
- La Crosse encephalitis
- West Nile Virus
 Arthropod-Borne Virus Encephalitis
Pathophysiology:

Viral replication >>> failed immune response >>>

viremia >>> gains access to the CNS (olfactory
tract) >>> encephalitis >>> IICP
 Arthropod-Borne Virus Encephalitis
Clinical Manifestations:
● Some cases have flu-like symptoms such as headache and fever.
● Unique to St. Louis is SIADH and hyponatremia.
● Incubation period of St. Louis is 4 to 12 days with abrupt onset of symptoms.
- fever, headache, nausea, dizziness, malaise.
- CNS: stiff neck, confusion, dizziness, and tremors.
- Coma can occur in severe cases, mortality increases with age.
- Seizures are indicator of poor prognosis, common to St. Louis.
 Arthropod-Borne Virus Encephalitis
Diagnostic Findings:
● Clinical presentation and location and dates of recent travel because certain
viruses are endemic in some geographical areas.
● MRI demonstrate inflammation of the:
- Basal ganglia in St. Louis
- Periventricular area in West Nile.
● IgM antibodies in West Nile virus.
● EEG can identify abnormal brain waves.
 Arthropod-Borne Virus Encephalitis
Medical Management:
● No specific medication, symptomatic management is the key, like controlling
seizures and increased ICP.
● Interferon is useful in St. Louis encephalitis but no specific drug is indicated.
Nursing Management:
● Carefully assess neurologic status and identifies improvement or
deterioration of patient’s condition.
● Public education addressing the prevention of arboviral encephalitis.
West Nile Virus Infection
● A potentially serious illness that affects the CNS
● The virus is contracted primarily by the bite of an infected
mosquito (mosquitoes become carriers when they feed on
infected birds).
● Symptoms typically develop between 3 and 14 days after
being bitten by the infected mosquito.
● Neurological effects can be permanent.
West Nile Virus Infection (Assessment)
● Usually no symptoms
● Mild symptoms: fever; headache and body aches; nausea;
vomiting; swollen glands; or a rash on the chest, stomach, or
back.
● Severe symptoms: high fever, headache, neck stiffness,
stupor, disorientation, tremors, muscle weakness, vision loss,
numbness, paralysis, seizures, or coma.
West Nile Virus Infection (Prevention)
● Use insect repellents containing DEET (diethyltoluamide) when outdoors
● wear long sleeves and pants and light-colored clothing.
● Stay indoors at dusk and dawn, when mosquitoes are most active.
● Ensure that breeding sites for mosquitoes, such as standing water and
water in bird baths, are eliminated. Keep wading pools empty and on their
sides when not in use.
Fungal Encephalitis
● Fungal infection of the CNS
● Example of Fungi:
- Cryptococcus neoformans
- Blastomyces dermatitidis
- Histoplasma capsulatum
- Aspergillus fumigatus
- Candida
- Coccidioides immitis
 Fungal Encephalitis (Pathophysiology)

inhalation of Fungal spores >>> infect the lungs (respi s/sx) >>>
fungi enters the bloodstream >>> fungemia >>> overwhelms the
immune response >>> fungus to CNS >>> meningitis, encephalitis,
brain abscess
Fungal Encephalitis (Clinical Manifestations)
● Fever, malaise, headache, meningeal signs
● Change of LOC, or cranial nerve dysfunction
● Increased ICP r/t hydrocephalus
● C. neoformans associated with skin lesions.
● H. capsulatum is associated with seizures.
● Aspergillus fumigatus may cause ischemic or hemorrhagic stroke.
Fungal Encephalitis (Diagnostic Findings)
Diagnostic Findings:
● History of immunosuppression like HIV
● History of travels
● CSF: elevated WBC and protein levels, decreased glucose
● Candida may be cultured.
Fungal Encephalitis (Management)
Medical Management:
● Antifungal Medications: fluconazole (Diflucan), flucytosine (Ancobon)
● Amphotericin B is used for progressive fungal infection that does not improve
with conventional therapy.
Nursing Management:
● Monitor ICP
● Administer diphenhydramine and paracetamol 30 minutes before giving
Amphotericin B to prevent flulike side effects.
Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob Disease
● degenerative infectious neurologic disorders called “transmissible
spongiform encephalopathies (TSE)”.
● Very rare and no identifiable cause.
● The human variation of bovine spongiform encephalopathy, commonly known
as mad cow disease.
● TSE is caused by prions.
● Prions are particles smaller than the virus that are resistant to standard
methods of sterilization.
● CJD and vCJD lack CNS stimulation.
● The incubation period of vCJD shorter (less than 10 years).
Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob Disease
Pathophysiology:
● The prions cross the blood-brain barrier.
● Deposited in the brain tissue and causes degeneration of the brain tissue.
● Cell death occurs and spongiform changes (spongy vacuole) are produced in
the brain surrounded by amyloid plaque.
Clinical Manifestation:
● Psychiatric symptoms: early in vCJD, late in CJD
● The mean age at onset: vCJD is 27, CJD is 65.
Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob Disease
VCJD:
● Affective symptoms, like behavioral changes
● Sensory disturbance
● Muscle spasm and rigidity
● Dysarthria, incoordination
● Cognitive impairment, sleep disturbance
Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob Disease
CJD:
● Memory loss
● Involuntary movement
● Paralysis
● Mutism as the disease progresses

● vCJD survive an average of 22 months.

● CJD less than one year.
Creutzfeldt-Jakob and Variant Creutzfeldt-Jakob Disease
Diagnostic Findings:
● CSF presence of kinase inhibitor which indicates neuronal death but not
specific of the disease.
● EEG reveals a characteristic pattern over the duration of the disease.
● MRI
Medical Management:
● No effective treatment.
● Symptomatic and palliative.
Trigeminal Neuralgia
 Trigeminal Neuralgia (former name: Tic Douloureux)
● A sensory disorder of the trigeminal (fifth cranial) nerve characterized by
paroxysms of sudden pain in the area innervated by any of the three branches
of the nerve.
● most common between the 5th and 6th decade of life
● common among women
● 5% in patients with MS
● The unilateral nature of the pain is an important feature.
● results in severe, recurrent, sharp facial pain along the trigeminal nerve.
Trigeminal Neuralgia
Causes:
● Blood vessel pressing the nerve as it exits the brain stem damaging the myelin
● Injury from sinus surgery or oral surgery
● Facial trauma or stroke
● MS
 Trigeminal Neuralgia (Symptoms)
● Pain varies depending on the type
● Type 1 (TN1): typical or classic form
- Causes extreme, sporadic, sudden burning or shock-like facial pain lasting for
seconds to minutes, in volleys lasting as long as 2 hours
● Type 2 (TN2): atypical
- Constant aching, burning or stabbing pain of lower intensity than type1
- Both pain can occur in same person or at same time
- Intensity of pain can be physically and mentally capacitating
Symptoms
Triggers
● Vibration or contact with
- Shaving, washing the face, applying make-up
- Brushing the teeth, eating, drinking, talking or being exposed to the wind
Medical Management
Pharmacologic Therapy
● Anticonvulsant agents- carbamazepine (Tegretol)- relieve pain
● Gabapentin and Baclofen- also used for pain control
● Phenytoin- if pain control is not achieved, this is used as adjunctive therapy.
Surgical Management
● Microvascular Decompression of the Trigeminal Nerve
● Radiofrequency Thermal Coagulation
● Percutaneous Balloon Microcompression
● Rhizotomy-Resection of the root of the nerve to relieve pain
● Glycerol injection: Destroys the myelinated fibers of the trigeminal nerve
 Nursing Management
● Preventing Pain
- Providing cotton pads and room temperature water for washing the face
- Instructing the patient to rinse with mouthwash after eating if toothbrushing
causes pain.
- Performing personal hygiene during pain-free intervals are all effective
strategies.
- The patient is instructed to take food and fluids at room temperature, to chew
on the unaffected side, and to ingest soft foods.
● Providing Postoperative Care
Interventions

● 1. Instruct the client to avoid hot or cold foods and fluids.

● 2. Provide small feedings of liquid and soft foods.
● 3. Instruct the client to chew food on the unaffected side.
● 4. Administer medications as prescribed (see Chapter 60).
Bell’s Palsy
 Bell palsy (facial paralysis)
● is caused by unilateral inflammation of the seventh cranial nerve, which results
in weakness or paralysis of the facial muscles on the affected side.
● Although the cause is unknown, theories include vascular ischemia, viral
disease (herpes simplex, herpes zoster), autoimmune disease, or a combination
of all of these factors.
● Most adults with Bell palsy are younger than 45 years.
● The inflamed, edematous nerve becomes compressed to the point of damage,
or its blood supply is occluded, producing ischemic necrosis of the nerve.
Clinical Manifestations
● The face is distorted from paralysis of the facial muscles.
● Decreased lacrimation (tearing) occurs.
● Painful sensations in the face, behind the ear, and in the eye.
● Experience speech difficulties
● May be unable to eat on the affected side because of weakness or paralysis of
the facial muscles.
● Flaccid facial muscles
● Upward movement of the eye when attempting to close the eyelid
● inability to raise the eyebrows, frown, smile, close the eyelids, or puff out the cheeks
● Loss of taste
Medical Management
● Objectives: maintain the muscle tone of the face and to prevent or minimize
denervation.
● Corticosteroid therapy (prednisone)- to reduce inflammation and edema
● Early administration of corticosteroid therapy appears to diminish the severity of the
disease, relieve the pain, and prevent or minimize denervation.
● Analgesics- for facial pain control
● Electrical stimulation may be applied to the face to prevent muscle atrophy.
 Nursing Management
● Protection of the eye from injury.
- To prevent injury, the eye should be covered with a protective shield at night.
- Moisturizing eye drops during the day and eye ointment at bedtime may help prevent injury.
- The patient can be educated to close the paralyzed eyelid manually before going to sleep.
- Wraparound sunglasses or goggles may be worn during the day to decrease evaporation from the
eye.
● Facial massage and exercises several times a day- to maintain muscle tone and prevent muscle
atrophy.
● Promote frequent oral care.
● Instruct the client to chew on the unaffected side.
Mononeuropathy
 Mononeuropathy
● is limited to a single peripheral nerve and its branches.
● trunk of the nerve is compressed or entrapped (as in carpal tunnel syndrome),
● traumatized (as when bruised by a blow),
● overstretched (as in joint dislocation),
● punctured by a needle used to inject a drug or damaged by the drugs thus
injected,
● or inflamed because an adjacent infectious process extends to the nerve trunk.
● Mononeuropathy is frequently seen in patients with diabetes.
 Mononeuropathy
● Pain is seldom a major symptom of mononeuropathy when the condition is due
to trauma.
● The skin in the areas supplied by nerves that are injured or diseased may
become reddened and glossy, the subcutaneous tissue may become edematous,
and the nails and hair in this area are altered.
● Chemical injuries to a nerve trunk, such as those caused by drugs injected into
or near it, are often permanent.
 Mononeuropathy
● The objective of treatment of mononeuropathy is to remove the cause, if
possible (e.g., freeing the compressed nerve).
● Local corticosteroid injections may reduce inflammation and the pressure on
the nerve.
● Aspirin or codeine may be used to relieve pain.
● Chronic pain can be treated with neuropathic pain medications such as
gabapentin.
● Nursing care involves protection of the affected limb or area from injury, as well
as appropriate patient education about mononeuropathy and its treatment.
END OF neuro
infection and
neuropathies
● Questions?
09.
Management of Patients
With Degenerative
Neurologic Disorders
 Degenerative Neurologic Disorders
● These disorders cause progressive decline in neurologic function
● Some progress quickly, over months to 1-2 years
● Some progress more gradually, sometimes over decades.
Alzheimer’s Disease
 Alzheimer's Disease (AD) and related Dementias
● Dementia- refers to the loss of memory, reasoning, judgment and language
skills
● Cognition- the act or process of thinking, perceiving and learning
● Cognitive activities that are impaired
➢ decision making, judgment, memory
➢ spatial orientation, thinking, reasoning, calculation
➢ personality and behavioral changes, verbal communication
Alzheimer's Disease
● is a progressive, irreversible, degenerative neurologic disease that begins
insidiously

● characterized by gradual losses of cognitive functions and disturbances in

behavior and affect.

● most common form of dementia among people over age 65.

● Estimates indicate that nearly half of people older than 85 have AD

● Brain quickly injured from hypoxia, reduced blood flow or drugs

Alzheimer's Disease
● MULTI-INFARCT (multiple strokes), is the second most common cause of
irreversible dementia

● Blood clots block small vessels in the brain and destroy brain tissue

● Typically occurs in men above 50

● Overtime leads to progressive decline in cognition

Alzheimer's Disease (Pathophysiology)
● Neurons are supported by microtubules and stabilized by protein tau to have normal
neuronal process

● AD disrupts the three neuronal processes that keeps neurons healthy:

[Link] - Receive signals (or information)

2. Metabolism - Integrate incoming signals and Communicate signals to target cells

3. repair

● Alois Alzheimer termed these changes as beta amyloid plaques and neurofibrillary
tangles
AD (Pathophysiology)

disruption of neuronal processes >>> Protein tau changed

chemically >>> formation of beta amyloid plaques and
neurofibrillary tangles >>> tubules degenerate >>> degenerate
neural cells they support >>> memory failure, personality changes,
problems carrying ADLs.
AD (Clinical Manifestations)
● Preclinical AD, begins near the hippocampus, a structure essential to the
formation of short and long term memories

● 10-20 years perhaps lead to memory loss

AD (Clinical Manifestations)
Mild Alzheimer's Disease
● the cerebral cortex begins to shrink
- memory disturbance
- poor judgment and problem solving skills
- careless in work habits and household chores
- may become confused
- agitation, apathy, dysphoria, aberrant motor behavior
AD (Clinical Manifestations)
Moderate Alzheimer's Disease
● demonstrate language disturbance characterized by impaired word finding
and circumlocution
● spontaneous speech becomes empty
● Paraphasias
● may repeat words and phrases spoken by themselves (palalia) or by others
(echolalia)
AD (Clinical Manifestations)
Moderate Alzheimer's Disease
● Apraxia- inability to perform purposeful movement, not related to paralysis
● restlessness with frequent pacing
● hyperorality
● swallowing may become difficult
● depression and irritability may worsen
● delusions and psychosis may appear
AD (Clinical Manifestations)
Severe Alzheimer's Disease
● Plaques and tangles are widespread throughout the brain
- cannot recognize family and friends
- Do not communicate in any way
- Voluntary movement is minimal
- Limbs become rigid with flexor posturing
- Urinary and fecal incontinence
- Aspiration and aspiration pneumonia are frequent
AD (Diagnostic Findings)
● No definitive test for AD,
● CT scan to identify ventricular dilation, sulcal enlargement and cerebral
atrophy
● MRI, PET to detect changes in brain function
● laboratory studies – CBC, urinalysis, BUN, creatinine, thyroid values, liver
function tests, syphilis serology, HIV testing
AD (Medical Management)
Pharmacologic: To control depression and agitation:
To maintain mental function: • Risperdal
- these drugs are used to maintain memory • Zyprexa
● donepezil (Aricept) • Seroquel
● rivastigmine (Exelon) • Zoloft
● memantine (Namenda)
● tacrine (Cognex)
● galanthamine (Reminyl)
AD (Nursing Diagnoses)
● Impaired verbal communication
● Impaired memory
● Risk for injury
● Self-care deficit
● Impaired nutrition: less than the body requirements
● Urinary and Fecal incontinence
● Caregiver role strain
Parkinson’s Disease
 Parkinson's Disease
● a chronic, progressive, neurologic disorder that results from the loss of
neurotransmitter DOPAMINE in a group of disorder that control movements

● Degeneration of dopamine neurons - interferes with the inhibition of excitatory

impulses, resulting in a dysfunction of the extrapyramidal system

● slow, progressive disease that results in a crippling disability.

● debilitation can result in falls, self-care deficits, failure of body systems,
and depression.

● Mental deterioration (late in the disease)

Parkinson's Disease
● Dopamine, a chemical substance that enables people to move normally and
smoothly.

● When PD occurs, degenerative changes are found in an area of the brain

known as substantia nigra, which produces dopamine.

● Once cell loss in substantia nigra reaches 50-80%, manifestations occur.

PD (Pathophysiology)
Stages of Parkinson's Disease
Stage I

● symptoms affect only one side of the body

● mild, patient may not be aware of symptoms

● typical motor symptoms: tremors and shaking limbs

● family may notice tremor, poor posture, mask face

Stages of Parkinson's Disease
Stage II

● symptoms begin affecting both sides of the body

● trouble walking and maintaining balance while standing

● increase difficulty performing once easy tasks: bathing, cleaning, dressing

● still some patients lead a normal life

● may begin taking medications

Stages of Parkinson's Disease
Stage III

● Symptoms are more pronounced but can still function without assistance

● obvious difficulty in standing, walking and other physical movements

● likely to fall, but some may perform independently

● Moderate stage
Stages of Parkinson's Disease

Stage IV

● symptoms are severe and disabling often needs assistance to walk, stand and
move

● motor symptoms: rigidity and bradykinesia are visible

● most cannot live alone

● Advanced stage
Stages of Parkinson's Disease
Stage V

● symptoms are most severe that require to be wheelchair-bound or bedridden

● may not be able to perform movement without assistance

● quality of life declines rapidly

● complications: infection, pneumonia, falls, choking

● with treatment may still live just like those without the disease
PD (Clinical Manifestations)

● Tremors at rest, pill rolling type, the first manifestation in 70% of the clients

● Rigidity, increased tone and stiffness of the muscle at rest

● Bradykinesia (slow movement), fine movements become clumsy

● Postural changes: flexed posture of the neck, trunk, limb

PD (Other Manifestations)
● slowing of ADLs, early of the disease tends to shuffle and exhibits decreased
arm swing
● as dexterity declines, micrographia develops
● stiff, mask-like without expression of the face during the advanced PD
● speech is low, monotonous tone and slow (dysphonia), words are poorly
articulated (dysarthria)
● saliva flow involuntarily
● fatigue is common
● sleep disturbance
● low gastric motility - constipation
PD (Other Manifestations)
● episodes of depression in 50% of clients
● usually does not affect intellectual ability
● dementia affects up to 70% of patients over the course of the disease
● the course is slowly, PROGRESSIVE, the person becomes more rigid, more
disabled, requiring a full assistance in ADLs
PD (Assessment and Diagnostic Findings)
● ongoing research with PET and CT scan has been helpful in understanding the
disease

● the disease is diagnosed from the patient's history and presence of two of
four cardinal manifestations:

1. Tremor
2. Rigidity
3. Bradykinesia
4. postural changes
PD (Medical Management)
● directed toward controlling symptoms and maintaining functional
independence
● no medical and surgical approaches currently use to prevent disease
progression
● antiparkinsonian medications act by increasing striatal dopaminergic activity
● Levodopa - most effective agent, it is converted to dopamine in the basal
ganglia, producing symptom relief
● Carbidopa is often added to avoid metabolism of levodopa before it can
reach the brain
● Sinemet (Levodopa/carbidopa)
PD (Medical Management)
● the beneficial effects levodopa are most pronounced in the first year to two
of treatment
● benefits begin to wane, and adverse effects become more severe over time
● confusion, hallucinations, depression, and sleep alterations are associated
with prolonged use
● in 5-10 years, dyskinesia (impaired ability to execute voluntary movements)
PD (Nursing Interventions)
● Stretching and Range of motion exercises to promote join flexibility.
● Warm baths and Massage to help relax muscles and relieve painful muscle
spams that accompany rigidity.
● Special walking techniques to offset the shuffling gait and the tendency to
lean forward.
● Perform breathing exercises while walking to help move ribcage and aerate
parts of the lungs.
● Frequent rest periods to aid in preventing frustrations and fatigue.
PD (Nursing Diagnoses)
● Impaired physical mobility related to muscle rigidity and postural impairment
● Self-care deficits related to tremor and muscle rigidity
● Constipation related to medication and reduced activity
● Impaired verbal communication related to decreased speech volume,
slowness of speech, inability to move facial muscles
● Ineffective coping related to depression and dysfunction due to disease
progression
Huntington’s Disease
 Huntington Disease
● is a chronic, progressive, hereditary disease of the nervous system that
results in progressive involuntary movement and dementia

● it is characterized by abnormal movements (chorea), intellectual decline, and

emotional disturbance.

● HD affects approximately 1 in 10,000 men or women of all races, at midlife

● usually begins in 30s and 40s

● it is transmitted as an autosomal dominant genetic disorder, therefore each

child of a parent with HD has 50% of inheriting the disorder.
Huntington Disease
● abnormal gene has been isolated in chromosome 4, the presence of a repeat
Huntington gene (HTT)

● HD does not skip generations

● lead to disability and death within 15-20 years, usually from respiratory tract
infection
HD (Pathophysiology)
● the basic pathology involves premature death of cells on the striatum
(caudate and putamen) of the basal ganglia involve in the control of
movement

● cells are also lost in the cortex, which are associated with thinking, memory,
perception, judgment and behavior. Also, in the cerebellum which
coordinates in voluntary muscle activity

● one theory about cell death is the glutamine abnormally collects in the cell
nucleus causing cell death
 HD (Pathophysiology)
● Regions of the brain affected by HD have:

➢ decreased GABA

➢ decreased Acetylcholine

➢ increased Dopamine
HD (Clinical Manifestations)
The most prominent clinical features of the disease:

● chorea – rapid, jerky, involuntary, purposeless movements

● impaired voluntary movement

● intellectual decline

● personality changes

● as disease progresses, a constant writhing, twisting, uncontrollable

movement of the entire body (athetosis)
HD (Clinical Manifestations)
● the person is constantly in motion devoid of purpose or rhythm

● attempts to perform voluntary movement can aggravate the abnormal

movement

● during sleep the movements diminish or disappear

● gait becomes disorganized to the point that ambulation eventually is

impossible

● eventually a person is confined to bed when chorea interferes with walking,

sitting and all other activities
HD (Clinical Manifestations)
● bowel and bladder control is lost
● cognitive function is altered, in the later stage marked dementia is present
● personality changes may result in nervous, irritable, or impatient behaviors
● uncontrollable anger, suicidal depression, apathy, anxiety, psychosis or
euphoria
● hallucinations, delusions, paranoid thinking may precede the appearance of
abnormal movements
● emotional and cognitive symptoms become less acute as the disease
progresses
HD (Assessment and Diagnostic Findings)
● diagnosis of HD is made on the basis of clinical manifestations and family
history, presence of genetic marker

● CT or MRI may show atrophy of the head of the caudate but not diagnostic of
HD

● the duration of HD ranges from 10-20 years

● the most common cause of death are infection, commonly pneumonia

HD (Medical Management)
● no medication that can reverse the underlying process, but medication may
reduce chorea

● tetrabenazine (Xenazine) is the only approved drug in the treatment of

chorea

● haloperidol decanoate, a dopamine blocker was use in the past, and may
control behavior manifestations

● selective serotonin reuptake inhibitors (SSRI) and tricyclic antidepressants

are used to control psychiatric manifestations
 HD (Nursing Diagnoses)
● Risk for injury related to falls

● Imbalanced nutrition: less than the body requirements related to inadequate

intake, disorders of swallowing, or choking

● Anxiety

● Impaired communication

● Confusion

● Impaired social interaction

HD (Nursing Interventions)
● Dysphagia, the most common and dangerous problems during the middle to
late stages.

● Communication difficulty from poor control of oral and respiratory muscles.

● Weight loss, physical injury from excessive movements.

Multiple Sclerosis
Multiple Sclerosis
● Damaged myelin sheaths that happens due to an autoimmune disorder that
attacks its own myelin sheath

● immune-mediated, chronic demyelinating disease that affects the myelin

sheath of neurons in the central nervous system

● patches of myelin deteriorate at irregular intervals along the nerve axons,

causing slowing of the transmission of impulses

● axonal destruction also occurs

● MS can occur in any age, but the peak of onset is between 25 and 35 years
MS
MS (Etiology and Risk Factors)
● the exact cause of MS is unknown

● most theories suggest that MS immunogenetic- viral disease

● viruses that trigger autoimmune response

Risk factors:

● genetic predisposition, but it has not been found to be genetically

transmitted

● smoking, lack of vitamin D exposure, and exposure to Epstein-Barr virus

MS (Pathophysiology)

● Normally, sensitized T and B lymphocytes cross the blood-brain barrier to check

CNS for antigen then leave

sensitized T cells remain in the CNS >>> infiltration of other agents >>> damage the
immune system >>> destruction of the myelin sheath >>> demyelination >>>
plaques form along the myelin sheath >>> scarring and destruction of myelin
sheath >>> interrupts flow of nerve impulses >>> degeneration of the axons >>>
permanent and irreversible damage
MS (Clinical Manifestations)
● may assume different patterns (relapsing-remitting)
● characterized by clearly acute attacks with full recovery or with residual deficit
upon recovery
● primary progressive – progression of disability from onset, without plateaus
and temporary minor improvements
● secondary progressive – begins with initial RR course, followed by progression
at variable rate, with occasional relapses and minor remissions
● progressive-relapsing – progression from onset but with clear acute relapses
with or without recovery
MS (Clinical Manifestations)
Charcot's Neurologic Triad:

● Dysarthria

● Nystagmus

● Intention tremor
MS (Clinical Manifestations)
● weakness or tingling sensations of one or more extremities due to involvement
of cerebrum and spinal cord
● vision loss from optic neuritis
● incoordination due to cerebellar involvement
● bowel and bladder dysfunction due to spinal cord Involvement
● fatigue is common, and one of the most disabling
● spasticity can reduce energy, inhibit motor control and interfere with self-care,
sexuality, vocational responsibilities and recreation
● pain
MS (Diagnostic Tests)
● CSF evaluation for oligoclonal banding (IgG), - presence of these proteins indicates
inflammation of the central nervous system.

● MRI of brain and spinal cord to determine presence of plaque

Medical Management
● no cure exists for MS
● the goal of treatment is to delay progression
● manage chronic symptoms and treat exacerbation
● PLASMAPHERESIS
Pharmacologic management
● treat relapses with IV or oral corticosteroids, with both anti-inflammatory and
immunosuppressive properties
● Methylprednisolone (should be tapered with oral prednisolone)
Medical Management
treat exacerbations:
● Interferon beta-1a (Rebif)
● Interferon beta-1b (Betaseron), administered subcutaneously
● Interferon beta-1a (Avonex) IM
symptomatic treatment:
● Baclofen for spasticity
● carbamazepine, phenytoin for trigeminal neuralgia
● Bisacodyl for constipation
 MS (Nursing Diagnoses)
● Impaired bed and physical mobility related to weakness, spasticity

● Risk for injury related to sensory and visual impairment

● Impaired verbal communication R/T cranial nerve involvement

● Risk for aspiration R/T cranial nerve involvement

● Ineffective individual coping related to uncertainty of the course of MS

Myasthenia Gravis
Myasthenia Gravis
● autoimmune disorder affecting the myoneural junction wherein the
Communication between the nerves and muscles are destroyed

● presents varying degree of muscular weakness and fatigue that worsens with
exercise and improves with rest

● the manifestations result from loss of acetylcholine receptors in the

postsynaptic neurons of the NMJ

● Blocks the acetylcholine and making the muscles really weak

MG (Pathophysiology)
● normally, a chemical impulse precipitates the release of acetylcholine from the
vesicles on the nerve terminal at the myoneural junction

antibodies attack the acetylcholine receptor sites >>> fewer available receptors for
stimulation >>> impair transmission of impulses across the myoneural junction >>>
voluntary muscle weakness that escalates with continued activity
MG (Clinical manifestations)
● Initial Manifestation: Involves ocular muscles: diplopia & ptosis are common (80%)

● weakness of the muscles of the face and throat (bulbar symptoms) that results in:

- bland facial expression

- dysphonia (voice impairment) from laryngeal involvement

- dysphagia that increases risk of choking and aspiration

MG (Clinical manifestations)
● PTOSIS - Drooping eyelids – key assessment finding

● generalized weakness affects all extremities

● weakness of intercostal muscles decreasing vital capacity and respiratory

failure

● a person may hold a hand under the jaw to keep it close

● purely a motor disorder with no effect on sensation and coordination

● with periods of remission and exacerbations

MG (Diagnostic Findings)
● Tensilon test - use to diagnose myasthenia gravis, an acetylcholinesterase
inhibitor test
● an acetylcholinesterase inhibitor stops the breakdown of acetylcholine
increasing availability at the NMJ
● Edrophonium chloride (Tensilon), a fast acting acetylcholinesterase inhibitor,
administered thru IV
● 30 seconds after injection, facial muscle weakness and ptosis should resolve for
about five minutes, (+) test, confirms the diagnosis
● atropine should be available to control side effects of edrophonium like
bradycardia, sweating and cramping
Tensilon test
MG (Assessment and Diagnostic Findings)
● ice test is indicated for patients with cardiac conditions or asthma that may
contraindicate edrophonium

● the test has comparable sensitivity to tensilon test the ice is applied over the
eyes for one minute, the ptosis should temporarily resolve in a patient with MG

● MRI scan for enlarged thymus

● acetylcholine receptor antibodies in the serum

MG (Medical Management)
● directed on improving function and removing circulating antibodies
Treatment modalities include:
● administration of acetylcholinesterase medications
● Cholinesterase inhibitor – enhance comm. Between nerves and muscles
● immunosuppressive therapy – stop making Ab that attack the nerve
● plasmapheresis
● thymectomy
● there is no cure for MG, treatments do not stop the production of acetylcholine
receptor antibodies
● Corticosteroids - reduce inflammation
MG (Pharmacologic Therapy)
● Pyridostigmine (Mestinon)
- Anticholinesterase - first line of defense
- inhibiting breakdown of acetylcholine and improving concentration at NMJ
- the dosage is gradually increased to a daily maximum in divided doses (usually
4X a day)
- tends to have fewer side effects compared to other anticholinesterase
medications: fasciculations, abdominal pain, diarrhea, increased oropharyngeal
secretions
● Neostigmine (Prostigmine)
MG (Immunosuppressive Therapy)
● to reduce production of the antibody
- corticosteroids - suppress the patient's immune response and decreasing amount
of antibody production
- prednisone is given for 1 to 2 months daily and the medication is tapered as
corticosteroid medications take effect
● Cytotoxic medication is used if there is inadequate response to steroids
- Azathioprine (Imuran) – to inhibit T lymphocytes and B cells proliferation reducing
acetylcholine receptor antibody level
MG (Management)
Plasmapheresis (plasma exchange)
● used to treat exacerbations
● the plasma and plasma components are removed
● the blood cells and antibody-containing plasma are separated, after which the
blood cells and plasma substitute are reinfused
● temporarily reduce circulating antibodies

Thymectomy
MG (Complications)
● myasthenic crisis
- a sudden worsening of their condition like dysphagia, dysarthria, eyelid ptosis,
diplopia, and prominent muscle weakness
● Cholinergic crisis
- overmedication: abdominal cramps, diarrhea, excessive pulmonary secretions
● Bronchial spasm
- requires intubation and mechanical ventilation
Guillain-Barre Syndrome
Guillain-Barre Syndrome
● Antibody and cell mediated immunologic reaction

● NOT AUTOIMMUNE because this occurs secondary to viral or bacterial illness

making the Body produce Ab to attack the NS

● the result is acute, rapid segmental demyelination of the peripheral nerves and
some cranial nerves

● producing ascending weakness and paralysis with dyskinesia (inability to

execute voluntary movement), hyporeflexia and paresthesia

● If ascends to the diaphragm – RESPIRATORY ARREST!!!

Guillain-Barre Syndrome (Cause)
● Recent illness or infection – “a GI bug”

- Campylobacter jejuni - organism responsible for GBS

● Cytomegalovirus

● EBV

● Mycoplasma pneumoniae

● H. influenzae

● HIV
GBS (Pathophysiology)
infectious agent >> mimics the peripheral nerve myelin sheath >>
immune system cannot distinguish the two proteins >> attacks them
both >> influx of macrophages and other immune-mediated agents
>> inflammation and destruction >> interruption of nerve conduction
>> axonal loss
GBS (Clinical Manifestations)
● ascending weakness
● the weakness evolves over hours to days with maximal deficit by 4 weeks in 90% of cases
● deep tendon reflexes are lost
● paresthesia or tingling
● deep aching muscle pain in the shoulder and thighs
● optic nerve demyelination with cranial nerve involvement
2 dangerous features:
- respiratory muscle weakness
- autonomic neuropathy: orthostatic hypotension, hypertension, cardiac dysrhythmia,
paralytic ileus, urinary retention
GBS (Assessment and Diagnostic Finding)
● patient presents with symmetric muscle weakness, diminished reflexes, and
upward progression of motor weakness

● history of viral illness in the previous few weeks

● serum laboratory are not useful, but elevated protein levels are detected in CSF
evaluation
GBS (Medical Management)
● it is a medical emergency!!! Admit to ICU
- respiratory therapy or mechanical ventilation, some may require elective
ventilation
● Plasmapheresis and Intravenous immunoglobulin (IVIG)
- reduce the amount of circulating antibody levels and reduce the amount of time
the patient is immobilized and dependent on mechanical ventilation
● ECG monitoring
● IV fluid for hypotension
GBS (Nursing Diagnoses)
● Ineffective breathing pattern and Impaired gas exchange R/T to rapidly
progressive weakness and impending respiratory failure
● Impaired bed and physical mobility R/T paralysis
● Imbalanced nutrition: less than the body requirements R/T inability to swallow
● Impaired verbal communication R/T cranial nerve dysfunction
● Fear and Anxiety R/T loss of control and paralysis
Thank you!
God Bless
☺