UNIT 2: UROLOGY
UNIT 3: NEUROLOGY
1. INTRACRANIAL PRESSURE Evidence
Base
ICP is the pressure exerted by the contents
inside the cranial vault—the brain tissue (gray
and white matter), Cerebrospinal Fluid (CSF),
and the blood volume. Increased ICP is
defined as CSF pressure greater than 15 mm
Hg.
Pathophysiology and Etiology
1. ICP is comprised of the following
components and volume ratio: brain tissue,
80%; CSF, 10%; blood volume, 10%.
2. The Monroe-Kellie doctrine states that the
intracranial vault is a closed structure with a
fixed intracranial volume.
3. The brain attempts to compensate for rises
in ICP by:
a. Displacement/shunting of CSF from the
intracranial compartment to the lumbar
subarachnoid space (SAS.
b. Increased CSF absorption.
c. Decreased cerebral blood volume by
displacement of cerebral venous blood into
the venous sinuses.
4. Intracranial compliance is “tightness” of the
brain. Compliance is the relationship between
intracranial volume and ICP.
5. Factors that influence the ability of the
body to achieve this steady state include:
a. Systemic BP.
b. Ventilation and oxygenation.
c. Metabolic rate and oxygen consumption
(fever, shivering, physical activity).
d. Regional cerebral vasospasm.
e. Oxygen saturation and hematocrit.
6. Inability to maintain a steady state results
in increased ICP. Traumatic brain injury,
cerebral edema, intracerebral hemorrhage,
ischemic stroke, abscess and infection,
lesions, intracranial surgery, and radiation
therapy can be potential etiologies of
increased ICP.
7. Increased ICP constitutes an emergency
and requires prompt treatment. ICP can be
monitored using an intraventricular catheter,
a subarachnoid screw or bolt, or an epidural
pressure-recording device.
8. Alterations or compromise in cerebral
blood flow can be measured noninvasively by
a transcranial Doppler (TCD.
Nursing Assessment
Change in LOC Caused by increased cerebral
pressure. Assess for:
1. Change in LOC (awareness): drowsiness,
lethargy
2. Early behavioral changes: restlessness,
irritability, contusion, and apathy
3. Falling score on the GCS (see page 488) a.
Change in orientation: disorientation to time,
place, or person
b. Difficulty or inability to follow commands
c. Difficulty or inability in verbalization or in
responsiveness to auditory stimuli
d. Change in response to painful stimuli (eg,
purposeful to inappropriate or absent
responses)
e. Posturing (abnormal flexion or extension)
Changes in Vital Signs
Caused by pressure on brain stem.
Assess for: 1. Rising BP or widening pulse
pressure (the difference between systolic and
diastolic BP). This may be followed by
hypotension and labile vital signs, indicating
further brain stem compromise.
2. Pulse changes with bradycardia changing to
tachycardia as ICP rises.
3. Respiratory irregularities: tachypnea (early
sign of increased ICP); slowing of rate with
lengthening periods of apnea;
Nursing Diagnosis
Decreased Intracranial
Nursing Interventions
Decreasing Intracranial Pressure
NURSING ALERT Increased ICP is a true life-
threatening medical emergency that requires
immediate recognition and prompt
therapeutic intervention.
1. Establish and maintain airway, breathing,
and circulation.
2. Promote normal PCO2. Hyperventilation is
not recommended for prophylactic treatment
of increased ICP as cerebral circulation is
reduced by 50% the first 24 hours after injury.
3. Avoid hypoxia. Decreased PO2 (less than
60) causes cerebral vasodilation, thus
increasing ICP.
4. Maintain cerebral perfusion pressure (CPP)
greater than 60.
5. Administer mannitol (Osmitrol), an osmotic
diuretic, if ordered. Osmotic diuretics act by
establishing an osmotic gradient across the
blood-brain.
6. Administer hypertonic saline (2% or 3%), if
ordered. It creates an osmotic gradient that
pulls extra fluid from the brain with an intact
blood-brain barrier, lowers ICP, improves
cerebral blood flow by reducing viscosity, and
improves oxygen carrying capacity.
7. Insert an indwelling urinary catheter for
management of diuresis.
8. Administer corticosteroids, such as
dexamethasone (Decadron), as ordered, to
reduce vasogenic edema associated with
brain tumors.
9. Maintain balanced fluids and electrolytes.
Watch for increased or decreased serum
sodium due to the following conditions that
may occur with increased ICP.
10. Monitor effects of neuromuscular
paralyzing agents, such as pancuronium
(Pavulon); anesthetic agents, such as propofol
(Diprivan); and sedatives, such as midazolam
(Versed),
11. Avoid positions or activities that may
increase ICP. Keep head in alignment with
shoulders; neck flexion or rotation increases
ICP by impeding venous return.
12. Avoid hyperglycemia. Treat with sliding
scale insulin or insulin drip as ordered.
13. Initiate treatment modalities, as ordered,
for sustained increased ICP (above 20 mm Hg
persisting 15 minutes or more or if there is a
significant shift in pressure).
14. Pretreat prior to known activities that
raise ICP, and avoid taking pressure readings
immediately after a procedure. Allow patient
to rest for approximately 5 minutes.
15. Record ICP readings every hour, and
correlate with significant clinical events or
treatments (suctioning, turning).
2. CEREBROVASCULAR ACCIDENT (STROKE,
BRAIN ATTACK)
Is the onset and persistence of neurologic
dysfunction lasting longer than 24 hours and
resulting from disruption of blood supply to
the brain and indicates infarction rather than
ischemia.
Pathophysiology and Etiology
Types of stroke
1. Ischemic Stroke
1. Partial or complete occlusion of a cerebral
blood flow to an area of the brain due to: a.
Thrombus (most common)—due to
arteriosclerotic plaque in a cerebral artery,
usually at the bifurcation of larger arteries;
occurs over several days.
 b. Embolus—a moving clot of cardiac origin
(frequently due to atrial fibrillation) or from a
carotid artery that travels quickly to the brain
and lodges in a small artery;
2. Area of brain affected is related to the
vascular territory that was occluded.
3. An area of injury includes edema, tissue
breakdown, and small arterial vessel damage.
4. Ischemic strokes are not activity
dependent; may occur at rest.
2. Hemorrhagic Stroke
1. Leakage of blood from a blood vessel and
hemorrhage into brain tissue, causing edema,
compression of brain tissue, and spasm of
adjacent blood vessels.
2. May occur outside the dura (extradural),
beneath the dura mater (subdural), in the
SAS, or within the brain substance
(intracerebral).
3. Causal mechanisms include:
a. Increased pressure due to hypertension.
b. Head trauma causing dissection or rupture
or vessel.
c. Deterioration of vessel wall from chronic
hypertension, diabetes mellitus, or cocaine
use.
d. Congenital weakening of blood vessel wall
with aneurysm or arteriovenous malformation
(AVM).
4. The intracranial haemorrhage becomes a
space occupying lesion within the skull and
compromises brain function.
5. Haemorrhage commonly occurs suddenly
while a person is active.
Clinical Manifestations
1. Clinical manifestations vary depending on
the vessel affected and the cerebral territories
it perfuses. Symptoms are usually multifocal.
2. Common clinical manifestations related to
vascular territory
a. Numbness (paresthesia), weakness
(paresis), or loss of motor ability (plegia) on
one side of the body.
b. Difficulty in swallowing (dysphagia). c.
Aphasia (nonfluent, fluent, global).
d. Visual difficulties of inattention or neglect
loss of half of a visual field (hemianopsia),
double vision, photophobia.
e. Altered cognitive abilities and psychological
affect.
f. Self-care deficits.
Diagnostic Evaluation
1. Carotid ultrasound—to detect carotid
stenosis in ischemic stroke.
2. CT scan—to determine cause and location
of stroke and type of stroke, ischemic versus
hemorrhagic.
3. MRA or CT angiogram—noninvasive
evaluation of cerebrovascular structures in
ischemic stroke.
4. Cerebral angiography—invasive evaluation
cerebrovasculature to determine the extent
of cerebrovascular injury/insufficiency and to
evaluate for structural abnormalities.
5. PET, MRI with DWIs—to localize ischemic
damage in ischemic stroke.
6. TCD—noninvasive method used to evaluate
cerebral perfusion.
Complications
1. Aspiration pneumonia
2. Dysphagia in 25% to 50% of patients after
stroke
3. Spasticity, contractures
4. Deep vein thrombosis, pulmonary
embolism
5. Brain stem herniation
6. Poststroke depression
Nursing Assessment
1. Maintain neurologic flow sheet (the
Modified Rankin scale or NIH Stroke Scale may
be used).
2. Assess for voluntary or involuntary
movements, tone of muscles, presence of
deep tendon reflexes
3. Also assess mental status, cranial nerve
function, sensation/proprioception.
4. Monitor bowel and bladder
function/control.
5. Monitor effectiveness of anticoagulation
therapy.
6. Frequently assess level of function and
psychosocial response to condition.
7. Assess for skin breakdown, contractures,
and other complications of immobility.
Nursing Diagnoses
 Risk for Injury related to neurologic
deficits
 Impaired Physical Mobility related to
motor deficits
 Disturbed Thought Processes related
to brain injury
 Impaired Verbal Communication
related to brain injury
 Self-Care Deficit: Bathing, Dressing,
Toileting related to
hemiparesis/paralysis
 Imbalanced Nutrition: Less Than Body
Requirements related to impaired
self-feeding, chewing, swallowing
 Impaired Urinary Elimination related
to motor/sensory deficits
 Disabled Family Coping related to
catastrophic illness, cognitive and
behavioral sequelae of stroke, and
caregiving burden.
Nursing Interventions
Preventing Falls and Other Injuries
1. Maintain bed rest during acute
phase with head of bed slightly
elevated and side rails in place.
2. Administer oxygen, as ordered,
during acute phase to maximize
cerebral oxygenation.
3. Frequently assess respiratory
status, vital signs, heart rate and
rhythm, and urine output to maintain
and support vital functions.
4. When patient becomes more alert
after acute phase, maintain frequent
vigilance and interactions aimed at
orienting, assessing, and meeting the
needs of the patient.
5. Try to allay confusion and agitation
with calm reassurance and presence.
6. Assess patient for risk for fall
status.
Preventing Complications of
Immobility
1. Maintain a functional position of all
extremities.
a. Apply a trochanter roll from the
crest of the ilium to the midthigh to
prevent external rotation of the hip.
b. Place a pillow in the axilla of the
affected side to keep arm away from
chest and prevent adduction of the
affected shoulder.
2. Apply splints and braces, as
indicated, to support flaccid
extremities
3. Exercise the affected extremities
passively through ROM four to five
times daily to maintain joint mobility
and enhance circulation
4. Teach patient to use unaffected
extremity to move affected one.
5. Assist with ambulation, as needed,
with help of physical therapy as
indicated.
Optimizing Cognitive Abilities
1. Be aware of the patient’s cognitive
alterations, and adjust interaction and
environment accordingly.
2. Participate in cognitive retraining
program—reality orientation, visual
imagery, cueing procedures—as
outlined by rehabilitation nurse or
therapist.
3. In patients with increased
awareness, use pictures of family
members
4. Focus on patient’s strengths, and
give positive feedback.
5. Be aware that depression is
common, and therapy should include
psychotherapy and early initation of
antidepressants.
Facilitating Communication
1. Speak slowly, using visual cues and
gestures; be consistent, and repeat as
necessary.
2. Speak directly to the patient while
facing him.
3. Give plenty of time for response,
and reinforce attempts as well as
correct responses.
4. Minimize distractions.
5. Use alternative methods of
communication other than verbal,
such as written words, gestures, or
pictures.
Fostering Independence
1. Teach the patient to use
nonaffected side for activities of daily
living.
2. Adjust the environment (eg, call
light, tray) to side of awareness
3. Teach the patient to scan
environment if visual deficits are
present.
4. Encourage the family to provide
clothing a size larger than patient
wears, with front closures and teach
the patient to dress while sitting to
maintain balance.
5. Make sure personal care items,
urinal, and commode are nearby.
Promoting Adequate Oral Intake
1. Perform a bedside swallow screen.
Follow institutional protocol. If any
coughing or difficulties are noted,
contact speech therapy for official
consult.
2. Initiate referral for a speech
therapist for individuals with
compromised LOC, dyspraxic speech,
or speech difficulties to evaluate
swallowing function at
3. Help the patient relearn swallowing
sequence using compensatory
techniques.
4. Encourage small, frequent meals,
and allow plenty of time to chew and
swallow.
5. Remind the patient to chew on
unaffected side.
6. Encourage the patient to drink
small sips from a straw with chin
tucked to the chest,
7. Inspect mouth for food collection
and pocketing before entry of each
new bolus of food.
8. Inspect oral buccosa for injury
from biting tongue or cheek.
9. Encourage frequent oral hygiene.
10. Teach the family how to assist the
patient with meals to facilitate
chewing and swallowing.
Attaining Bladder Control
1. Insert indwelling bladder
catheterization during acute stage for
accurate fluid management.
2. Establish regular voiding
schedule—every 2 to 3 hours.
3. Assist with standing or sitting to
void (especially males).
Strengthening Family Coping
1. Encourage the family to maintain
outside interests.
2. Teach stress management
techniques, such as relaxation
exercises.
 3. Encourage participation in support
group for family respite program for
caregivers.
4. Involve as many family and friends
in care as possible.
5. Provide information about stroke
and expected outcome.
6. Teach the family that stroke
survivors may show depression in the
first 3 months of recovery.
Patient Education and Health
Maintenance
1. Teach the patient and family to
adapt home environment for safety
and ease of use.
2. Instruct the patient of the need for
rest periods throughout day.
3. Reassure the family that it is
common for post stroke patients to
experience emotional lability and
depression; treatment can be given.
4. Encourage consistency in the
environment without distraction.
5. Assist the family to obtain self-help
aids for the patient.
6. Instruct the family in management
of aphasia
7. Educate those at risk for stroke
about lifestyle modifications and
medication therapy that can lower
risk
8. Refer the patient and family for
more information and support to such
agencies as The National Stroke
Association.
Evaluation: Expected Outcomes
 No falls, vital signs stable
 Maintains body alignment, no
contractures
 Oriented to person, place, and time
 Communicates appropriately
 Brushes teeth, puts on shirt and pants
independently
 Feeds self-two-thirds of meal
 Voids on commode at 2-hour intervals
 Family seeks help and assistance from
others
3. MENINGITIS
Is an inflammation of the pia mater and
arachnoid membranes that surround the
brain and the spinal cord.
Pathophysiology and Etiology
1. Viral meningitis is the most common form.
More than 10,000 cases are reported
annually, but the actual incidence may be as
high as 75,000.
2. In the United States, the incidence of acute,
bacterial meningitis is approximately three
cases per 100,000 per year.
3. Bacterial meningitis may cause damage to
the CNS from the inflammatory process rather
than the pathogen.
4. Fungal meningitis, particularly Cryptococcus
neoformans, affects immunosuppressed
patients through soil contaminated with
excrement from pigeons and chickens.
5. Parasitic meningitis is usually cause by
flukes, worms, or amoeba.
6. Hospital-acquired post craniotomy
meningitis, caused predominantly by gram-
negative bacilli, can result in mortalities of
30%; multiple craniotomy operations place
the patient at even higher risk.
7. Neoplastic meningitis affects approximately
3% to 8% of patients who have systemic
cancers.
8. Meningitis is the primary intracranial
complication of acute and chronic sinusitis
(sphenoid sinusitis most common
9. Listeria monocytogenes, a gram-positive
bacilli, may cause meningitis through
contaminated hot dogs, cold meats, and
unpasteurized dairy products.
10. The incidence of Haemophilus influenzae
meningitis has decreased due to the
haemophilus b conjugate vaccine.
Clinical Manifestations
1. Classic symptoms are fever, headache, and
nuchal rigidity. Constitutional symptoms of
vomiting, diarrhea, cough, and myalgias
appear in more than 50% of patients.
2. Altered mental status; confusion in older
patients.
3. Petechial (appears like “rug” burn) or
purpuric rash from coagulopathy, especially
with N. meningitidis.
4. Photophobia.
5. Neck tenderness or a bulging anterior
fontanel in infants.
6. Children may exhibit behavioral changes,
arching of the back and neck, a blank stare,
refusal to feed, and seizures. Viral meningitis
can cause a red, maculopapular rash in
children.
7. Positive Brudzinski’s and Kernig’s signs.
8. Neonates may exhibit poor feeding, altered
breathing patterns, or listlessness.
9. Onset may be over several hours or several
days depending on the infectious agent, the
patient’s age, immune status, comorbidities,
and other variables.
Diagnostic Evaluation
1. Complete blood count (CBC)
2. Blood cultures are obtained to indicate the
organism.
3. CSF evaluation for pressure, leukocytes,
protein,
3. A culture and smear
4. MRI/CT scan
5. Latex agglutination may be positive for
antigens in meningitis.
6. Low CD4 counts indicate
immunosuppression in HIVpositive patients
and other patients with immunosuppressive
disorders.
7. In patients with acquired immunodeficiency
syndrome (AIDS), MRI is used to detect
meningeal irritation,
Risk factors of meningitis
• Chronic medical disorder
Complications
1. Bacterial meningitis, particularly in children,
may result in deafness, learning difficulties,
spasticity, paresis, or cranial nerve disorders.
2. Increased ICP in AIDS patients with
cryptococcal meningitis can result in severe
visual losses.
3. Seizures occur in 20% to 30% of patients.
4. Increased ICP may result in cerebral edema,
decreased perfusion, and tissue damage.
5. Severe brain edema may result in
herniation or compression of the brain stem.
6. Purpura may be associated with
disseminated intravascular coagulation.
Nursing Assessment
1. Obtain a history of recent infections such as
upper respiratory infection and exposure to
causative agents.
2. Assess neurologic status and vital signs.
3. Evaluate for signs of meningeal irritation.
4. Assess sensorineural hearing loss (vision
and hearing), cranial nerve damage (eg, facial
nerve palsy), and diminished cognitive
function.
Nursing Diagnoses
 Hyperthermia related to the
infectious process and cerebral
edema
 Risk for Imbalanced Fluid Volume
related to fever and decreased intake
  Ineffective Tissue Perfusion (cerebral)
related to infectious process and
cerebral edema
 Acute Pain related to meningeal
irritation
 Impaired Physical Mobility related to
prolonged bed rest
Nursing Interventions
Reducing Fever
1. Administer antimicrobial agents on time to
maintain optimal blood levels. 2. Monitor
temperature frequently or continuously, and
administer antipyretics as ordered.
3. Institute other cooling measures, such as a
hypothermia blanket, as indicated.
Maintaining Fluid Balance
1. Prevent I.V. fluid overload, which may
worsen cerebral edema.
2. Monitor intake and output closely.
3. Monitor CVP frequently.
Enhancing Cerebral Perfusion
1. Assess LOC, vital signs, and neurologic
parameters frequently. Observe for signs and
symptoms of increased ICP (eg, decreased
LOC, dilated pupils, widening pulse pressure).
2. Maintain a quiet, calm environment to
prevent agitation, which may cause an
increased ICP.
3. Prepare patient for a lumbar puncture for
CSF evaluation, and repeat spinal tap, if
indicated.
4. Notify the health care provider of signs of
deterioration: increasing temperature,
decreasing LOC, seizure activity, or altered
respirations.
Reducing Pain
1. Administer analgesics as ordered; monitor
for response and adverse reactions.
2. Darken the room if photophobia is present.
3. Assist with position of comfort for neck
stiffness, and turn patient slowly and carefully
with head and neck in alignment.
4. Elevate the head of the bed to decrease ICP
and reduce pain.
Promoting Return to Optimal Level of
Functioning
1. Implement rehabilitation interventions
after admission (eg, turning, positioning).
2. Progress from passive to active exercises
based on the patient’s neurologic status.
Patient Education and Health Maintenance
1. Advise close contacts of the patient with
meningitis that prophylactic treatment may
be indicated; they should check with their
health care providers or the local public
health department.
2. Encourage the patient to follow medication
regimen as directed to fully eradicate the
infectious agent.
3. Encourage follow-up and prompt attention
to infections in future.
4. Encourage to eat healthy food and maintain
fluid intake.
5. Encourage to avoid activity that will worsen
the situation/condition.
6. Encourage the patient to seek for medical
assistance whenever they are experiencing
signs and symptoms.
7. Encourage the patient to have enough rest.
Evaluation
Expected Outcomes
 Afebrile
 Adequate urine output; CVP in normal
range
 Alert LOC; normal vital signs
 Pain controlled
 Optimal level of functioning after
resolution
4. EPILEPSY /SEIZURES/CONVULSION
DISORDERS
 Recurring/spontaneus
convulsions of unknown causes.
 Is the disturbances in the cells of
the brain, that cause the cells to
 give off abnormal, recurrent,
uncontrolled electrical discharges
 Sudden alteration in normal brain
activity that causes distinct
change in behaviours and body
function.
Causes/etiology
• unknown.
Can be due to one of the following factors:
• Trauma to the head or brain resulting
in scar tissue or cerebral atrophy.
• Trauma such as birth injuries.
• Tumours.
• Cranial surgery.
• Metabolic disorders
(hypocalmia,hypoglycemia/hyperglyc
emia/hyponatremia,anoxia).
• Drug toxicity, such as theophylline,
lidocaine, penicillin.
• CNS infection (e.g.meningitis and
encephalitis).
• Circulatory disorders.
• Drug withdrawal states: alcohol,
barbiturate.
• Congenital neuron degenerative
disorders.
• Non epileptogenic behaviour
• Vascular lesions e.g. arteriovenous
anomalies(AVM).
• Acidosis, hypoxia and electrolyte
imbalance.
• Hyperpyrexia, esp. in children(febrile
convulsions).
Pathophysiology
• Vascular lesions e.g. arteriovenous
anomalies(AVM).
• Acidosis, hypoxia and electrolyte
imbalance.
• Hyperpyrexia, especially in children
(febrile convulsions).
Types of epilepsy
1. Peptimal epilepsy - with sudden,
momentary blankness of
expression, or facial or limb
twitch.
 Patient does not fall nor does
he drop anything.
 incontinence of urine, and
faeces is unusual
2. Gland mal epilepsy -characterised
by generalised convulsions that
follow a defined pattern.
 Always an aura and tonic , the
clonic stages then convulsion
stage follows.
 The patient looses
consciousness, goes via
unconsciousness stage to
deep sleep.
 There maybe incontinence of
both urine and faeces during
the fit.
 The patient may injury
her/himself by biting his/her
tongue or hitting n object
when falling.
3. Partial seizeures- do not involve
the entire brain.
 Symptoms confined to one
part of the body.
 It include simple partial
seizures, which does cause
alteration of consciousness –
referred to as jacksonian
seizures.
 Fit is localised, may start in
hand and spread up to the
arm.
 Occasionally,may involve whole side
of the body (Mogtholane et
all,2014:882).
4. A complex partial seizure- characterised
by loss of consciousness.
Clinical manifestation
• Impaired consciousness.
• Disturbed muscles tones or
movement.
• Disturbances of behaviour, mood,
sensation,or perception.
• Disturbances of autonomic functions.
Diognostic evaluation
• EEG- to locate epileptic focus, spread,
intensity and duration and classify
seizure type.
• MRI, CT Scan-identity any lesion .
• Serum laboratory studies or lumbar
puncture –evaluate infection,
hormonal or metabolic etiology
Nursing diagnosis and
management/interventions
Management
• Pharmacotherpy- selected according
to seizure type(e.g.
phenytoin,barbiturates,carbamazepin
es,benzodiazepines etc.
• Biofeedback- useful with people with
reliable aura.
• Surgery-Temporal lobectomy, extra
temporal resection ,corpus
callosotomy(CC), hemispherectomy.
• Vagal nerve stimulation(VNS)
Complications
Status epilepticus –with recurrent
seizures, no intervals of normal
consciousness in between.
• Results in brain damage and death
from exhaustion and
• Hypoxia-in case of uncontrolled
convulsions.
• Injuries due to falls esp. head injuries
Hemispherectomy is a very rare surgical
procedure where one cerebral
hemisphere (half of the brain) is removed
or disabled.
Vagus nerve stimulation or vagal nerve
stimulation (VNS) is a medical treatment
that involves delivering electrical impulses
to the vagus nerve.
Anterior temporal lobectomy is the
complete removal of the anterior portion
of the temporal lobe of the brain.
5. BRAIN ABSCESS
Is the collection of infectious material/or pus
within the brain tissue.
Mostly occurs between:
• Dura and arachnoid linings-Subdural
abscess.
• Dura and skull -epidural.
• in the epidural region-Spinal abscess .
Pathophysiology and aetiology
1. Intracranial subdural abscess- due to
streptococcus.
• Caused by purulent drainage between
dura and arachnoid, meninges ,middle
ear/mastoid, sinuses, septicaemia or
skull fracture.
1. Intracranial epidural abscesses-
involving an infection of the cranium.
• Occurs due to chronic
mastoiditis or sinusitis ,head
trauma, or craniotomy.
• Abscess may related to
empyema(collection of
purulent drainage originating
from nasal sinuses,
meningitis, or
intraparenchyma abscess.
2. Spinal epidural abscess- occurs in the
spinal canal ,external to the dura.
• Result from :infected adjacent tissue
e.g infected pressure ulcer,
• infected site e.g .skin.
• contamination from spinal surgery,
spinal instrumentation e.g. lumbar
puncture- causative organism S
.aureus
3. Intra medullar abscess
• Common in paediatric population.
• Associated with lumbosacral dermal
sinuses.
• No obvious infectious causes.
4. Fungal brain abscess
• Common in HIV positive patients and
other immune compromised
populations.
• Commonly caused by candida species
5. M.tuberculosis
• Causes abscess containing Acid Fast
Bacilli(AFB).
• Found in HIV- positive patients and
other immunosuppressive diseases.
6. Organism invades the brain
parenchyma cause local
inflammation, edema, cerebritis leads
to necrotic lesion.
Clinical manifestations
• Headache-dull, poorly localised.
• Increased intracranial pressure.
• Nausea and vomiting.
• Fever-in less than 50% of cases.
• Hemi sensory and paresis deficits.
• Aphasia and ataxia may be present.
• Dental abscess, sinusitis and otitis
media may be present
• Severe headache, fever, nuchal
rigidity-if cerebral subdural empyema.
• Meningeal irritation(kerning and
brudzinski s sign-if cerebral subdural
empyema.
• Fever, lethargy and severe headache-
if intra cranial abscess.
• Severe backache, fever ,headache,
lower extremities weakness or
paralysis, nuchal rigidity, Kernig sign,
and local tenderness- in spinal
epidural abscess
Diognostic evaluation
• CT scan and MRI-to locate the site.
• Blood cultures-identify the causative
organism.
• Needle aspiration-for culture and
sensitivity.
• EEG-detect seizure disorders.
Management
• Craniotomy-drain the pus.
• Closed stereostatic needle biopsy-to
drain/evacuate pus.( under guidance
of CT scan).
• Laminectomy and surgical drainage (if
spinal epidural abscess).
• Antibiotics.
• Antifungal therapy.
• Anti tuberculosis therapy.
• Corticosteroids and diuretics.
• Anticonvulsants(Sandra :2014:519).
Complications
• Rupture of an abscess into ventricular
space
• Severe headache and death.
• Papilledema.
 • Permanent seizure disorders, visual
deficit, hemiparesis and CN palsies.
• Flaccid paraplegia.
Nursing diagnosis
• Acute pain related to cerebral
abscess.
• Risk for injury related to neurologic
deficity.
• Anxiety related to surgery
Nursing intervention
• Relieving pain
• Promoting thought process.
• Monitoring neurologic deficits.
• Reducing anxiety.
An electroencephalogram (EEG) is a test that
detects electrical activity in the brain using
small, flat metal discs (electrodes) attached to
the scalp.
Hemiparesis is weakness of the entire left or
right side of the body.
Microvascular cranial nerve palsy (MCNP) is a
neurological condition involving the small
blood vessels that affects the muscles that
move the eyes.
Papilledema (or papilloedema) is optic disc
swelling that is caused by increased
intracranial pressure.
Facial paralysis is a condition defined by the
total lack of voluntary muscle movement on
one side of the face.
Facial paralysis is caused by Bell’s Palsy,
Bell’s Palsy, a condition that causes the
nerves in the face to become inflamed.
Other common causes of facial paralysis
include:
• Stroke
• Brain Tumor
• Sarcoidosis
• Lyme disease
• Infection
• Birth trauma in newborns
Aphasia is a communication disorder that
results from damage to the parts of the
brain that contain language OR
Aphasia is an impairment of language,
affecting the production or
comprehension of speech and the ability
to read or write.
Ataxia-
Amnesia-
6. ENCEPHALITIS
Is an inflammation of cerebral tissue, typically
accompanied by meningeal inflammation.
Pathophysiology and Etiology
Types of encephalitis
1. In primary encephalitis, the brain or
spinal cord is the predominant foci of
the toxin or pathogen.
2. Secondary encephalitis is a less
serious form of encephalitis; it is
caused by an infection that is spread
from another part of the body.
3. Acute viral encephalitis, accounting
for the vast majority of cases, is
caused by a direct infection of the
gray matter containing neural cells.
4. Brainstem encephalitis targets the
basal ganglia or cranial nerves.
5. Postischemic inflammatory
encephalitis occurs due to brain
inflammation following a CVA.
6. West Nile Virus (WNV) is an arthropod
virus (arbovirus). The mosquito is the
primary vector, and birds are the
primary hosts.
7. Herpes simplex encephalitis may
result from reactivation of the virus
 that has been dormant in the cranial
and other ganglia or to reinfection.
Herpes simplex virus type 1, which is
responsible for almost all cases of
herpes simplex encephalitis in
children and adults.
Herpes simplex type 2 is more
common in neonates who are born to
mothers with this infection during
pregnancy.
8. Postinfectious encephalomyelitis
follows a viral or bacterial infectious
process, but organisms do not directly
affect the neural tissue in the white
matter.
9. Cytomegalovirus encephalitis should
be considered in patients who have
advanced HIV infection.
10. Toxoplasma encephalitis is also
common in patients with AIDS.
Clinical Manifestations
1. Signs and symptoms may develop hours or
weeks after exposure.
2. Classic symptoms include fever, headache,
and brain aberration (eg, disorientation,
neurologic deficits, seizures).
3. Increased ICP may result in alteration in
consciousness, nausea, and vomiting.
4. Motor weakness, such as hemiparesis
5. Increased deep tendon
6. Bizarre behavior and personality changes
may present at onset.
7. Hypothalamic-pituitary involvement may
result in hypothermia, diabetes insipidus,
8. Neurologic symptoms may include superior
quadrant visual field defects, aphasia,
dysphagia, ataxia, and paresthesias.
9. The patient with brainstem encephalitis
may present with nystagmus, decreased
extraocular movements, hearing loss,
dysphagia, dysarthria, respiratory
abnormalities, and motor involvement.
10. Limbic encephalitis may cause mood and
personality changes that progress to severe
memory loss and delirium.
Complications
1. Sequelae of the herpes simplex virus may
cause temporal lobe swelling, which can
result in compression of the brain stem
2. Relapse of encephalitis may be seen after
initial improvement and completion of
antiviral therapy.
3. Mortality and morbidity depend on the
infectious agent, host status, and other
considerations.
Nursing Assessment
1. Obtain patient history of recent infection,
animal exposure, tick or mosquito bite, recent
travel, exposure to ill contacts.
2. Perform a complete clinical assessment.
3. Before delivery, women should be
questioned regarding a history of congenital
herpes simplex virus and examined for
evidence of this virus; a cesarean delivery
should be explored with the physician.
4. Strict standard precautions should be
adhered to in order to contain drainage from
herpetic lesions.
5. Vesicular lesions or rashes on neonates
should be reported immediately because
these could indicate active herpes simplex
infection.
Nursing Diagnoses and Nursing interventions
• Risk for Injury related to seizures and
cerebral edema
1. Maintain a quiet environment to
allow the patient to rest.
2. Provide care gently, avoiding
overactivity and agitation, which
may cause increased ICP.
3. Maintain seizure precautions
with side rails padded to prevent
the patient from falling.
 4. Keep suction equipment at
bedside to help suction the
patient in order to maintain the
airways.
5. Administer medications as
ordered; monitor response and
adverse reactions.
• Ineffective Tissue Perfusion
(cerebral) related to disease process
1. Monitor neurologic status closely.
Observe for subtle changes, such as
behavior or personality changes,
weakness, and notify the health care
provider.
2. Restrict fluids to passively
dehydrate the brain.
3. Reorient the patient frequently.
4. Provide supportive care if coma
develops; may last several weeks.
5. Encourage significant others to
interact with the patient, and
participate in the patient’s
rehabilitation, even while the patient
is in a coma
• Hyperthermia related to infectious
process
1. Monitor temperature and vital
signs frequently.
2. Administer antipyretics and other
cooling measures as indicated.
3. Monitor fluid intake and output,
and provide fluid replacement
through I.V. lines as needed.
4. Ensure enough bed rest.
5. Maintain a quiet environment.
6. Keep doors and window close to
help keep the patient warm.
• Disturbed Thought Processes due to
personality changes
1. Orient to person, place, time.
2. Maintain memory book, and
provide cues to perform required
activities
• Risk of Infection related to
transmittal
1. Maintain strict standard
precautions.
2. Initiate and maintain isolation per
your facility’s policy
Patient Education and Health Maintenance
1. Explain the effects of the disease process
and the rationale for care.
2. Reassure significant others based on
patient’s prognosis.
3. Encourage follow-up for evaluation of
deficits and rehabilitation progress.
4. Educate others about the signs and
symptoms of encephalitis if epidemic is
suspected.
5. To prevent WNV, advise the use of
repellants when outdoors and removal of
standing water that acts as a breeding ground
for mosquitoes.
Evaluation: Expected Outcomes
• No seizures or signs of increased ICP
• Alert with no neurologic deficits
• Afebrile Oriented, memory intact
• No transmission of infection
Headache/Migraine/Vertigo
It divides headaches into two categories:
-primary headache disorders, which include:
migraine, tension type headache, and cluster
headache;
-and secondary headache disorders
Pathophysiology and Etiology
Primary Headaches
Diagnosis is generally based on the
characteristic clinical history and elimination
of other pathology such as stroke, or brain
tumor.
1. Migraine headache—consists of initial
vasospasm followed by dilation of
intracranial and extracranial arteries;
 occurs in about 10% of the
population.
-It consis of five phases of attack:
prodrome, aura, headache,
resolution, and postdrome.
2. Tension headache—due to irritation of
sensitive nerve endings in the head, jaw, and
neck from prolonged muscle contraction in
the face, head, and neck; Precipitating factors
include fatigue, stress, poor posture.
3. Cluster headache—release of increased
histamine results in vasodilation. Occurs more
often in men.
Secondary Headaches
Headache due to a neurologic or systemic
disease. It is caused bt the following:
1. Mass lesion (tumor, abscess).
2. Intracranial infection (meningitis or
encephalitis).
3. Inflammation (giant cell arteritis, vasculitis).
4. Cerebrovascular disease (subarachnoid
hemorrhage, intracranial hemorrhage).
5. Increased intracranial pressure.
6. Low-pressure headache (postlumbar
puncture, trauma induced).
7. Sinus infection, viral infection such as
influenza, systemic illness.
Clinical Manifestations
Diagnostic Evaluation
1. Skull/sinus films to rule out lesions,
sinusitis
2. CT scan/MRI to rule out lesions,
hemorrhage, chronic sinusitis
3. Erythrocyte sedimentation rate
Nonpharmacologic Management of
headache
1. Relaxation techniques,
2. Biofeedback, cognitive therapy.
3. Trigger identification and control of
such factors as intake of alcohol
4. To prevent migraine: avoidance of
monosodium glutamate, mixed spices
such as “seasoned salt,”
5. Rest in a quiet, dark room at onset of
headache.
6. If caffeine user, spread caffeine intake
evenly over the day.
7. Routine exercise program
Nursing Assessment
1. Obtain a history of related symptoms,
triggering factors, degree of pain, and
medications used
2. Perform a complete neurologic
examination to detect any focal deficits or
signs of increased ICP
3. Assess coping mechanisms and
emotional status.
Nursing Diagnoses
-Acute Pain related to headache
-Ineffective Coping related to chronic
and/or disabling pain
Nursing interventions
Controlling Pain
1. Reduce environmental stimuli: light,
noise, to decrease severity of pain.
2. Suggest light massage to tight muscles
in neck and headaches.
3. Apply warm, moist heat to areas of
muscle tension.
4. Encourage the patient to lie down and
attempt to sleep.
5. Teach progressive muscle relaxation to
treat and prevent tension headaches.
6. Teach patient the cause of headache
and proper use of medication.
 7. Encourage adequate rest once a
headache is relieved to recover from
fatigue of the pain.
Promoting Positive Coping
1. Encourage patient to become aware of
triggering factors and early symptoms of
headache,
2. Encourage adequate nutrition,
relaxation, and avoidance of stress to
better cope with headaches.
3. Implement problem-solving to help
patients manage problems that arise in
social situations related to headaches.
4. Review coping mechanisms, and
strengthen positive ones.
Patient Education and Health
Maintenance
1. Teach proper administration of
medication.
2. Teach about adverse effects of
medications such as gastritis, chest pain,
wheezing
3. Advise avoidance of alcohol, which can
worsen headaches.
4. Teach about foods that are high in
tyramine, which may trigger migraines—
such as liver.
5. Teach patient how to perform
relaxation techniques to reduce stress and
promote inner well-being.
6. Refer patient for more information to
the International Headache Society.
7. Encourage patient to drink enough
water to keep their body hydrated.
TRAUMATIC CONDITIONS: 541
Traumatic brain injury
also known as head injury, is the disruption of
normal brain function due to trauma-related
injury.
TBI produces compromised neurologic
function, resulting in focal or diffuse
symptoms. Falls are the most common
etiology of injury, followed by motor vehicle
accidents.
Pathophysiology and Etiology
Types of Traumatic Brain Injury
1. Cerebral concussion—transient
interruption in brain activity; no
structural injury noted on
radiographics.
2. Cerebral contusion—bruising of the
brain with associated swelling.
Temporal and frontal lobes are
common sites.
3. Intracerebral hematoma—bleeding
into the brain tissue commonly
associated with edema.
4. Epidural hematoma—blood between
the inner table of the skull and dura.
Frequently associated with injury or
laceration of the middle meningeal
artery secondary to a temporal bone
fracture.
5. Subdural hematoma—blood between
the dura and arachnoid caused by
venous bleeding; commonly
associated with contusion, or
intracerebral hematoma.
6. Diffuse axonal injury (DAI) or shear
injury —axonal tears within the white
matter of the brain.
CEREBRAL CONTUSION
• Cerebral contusion is a more severe
injury in which the brain is bruised,
with possible surface hemorrhage.
• It is a form of traumatic brain injury, a
bruise of the brain tissue.
• Like bruises in other tissues, cerebral
contusion can be caused by multiple
microhemorrhages, small blood vessel
leaks into brain tissue.
• The patient is unconscious for more
than a few seconds or minutes
 • Head CT scans of unconscious
patients reveal that 20% have
hemorrhagic contusion
Causes of cerebral contusion
Most common Focal brain Injury
Sites  Impact site/ under skull #
Anteroinferior frontal
Anterior Temporal
Occipital Regions
Petechial hemorrhages  coalesce 
Intracerebral Hematomas later on.
Clinical manifestation
• Clinical signs and symptoms depend
on the size of the contusion and the
amount of associated cerebral edema.
• The patient may lie motionless, with
a faint pulse, shallow respirations, and
cool, pale skin.
• Often there is involuntary emptying
of the bowels and the bladder.
• The patient may be aroused with
effort but soon slips back into
unconsciousness.
• The blood pressure and the
temperature are subnormal, and the
picture is somewhat similar to that of
shock
CEREBRAL LACERATION
Involves actual tearing of the brain tissue.
Intracerebral hemorrhage is generally
associated with a cerebral laceration.
Can cause
-Massive destruction of brain tissue
-Bleeding into the cranial cavity with
increased intracranial pressure.
CEREBRAL COMPRESSION
• Cerebral compression occurs when
there is a build-up of pressure on the
brain due to an accumulation of blood
within the skull or swelling of injured
brain tissues.
OR
• Compression of the brain is a
condition in which something
increases the amount of pressure
pushing on the brain, which can
damage brain tissue.
Causes of compression
• The brain is housed in the skull, where
it is cushioned by a protective fluid
called cerebrospinal fluid (CSF).
• The pressure inside the skull that
pushes on the brain and cerebrospinal
fluid is called intracranial pressure.
• Since the skull isn't flexible, if
something causes intracranial
pressure to increase, the brain gets
compressed.
• This is most commonly the result of
a head injury that causes bleeding or
swelling in the brain,
• Can be due trauma, neoplasms,
hematomas, abscess, hernia in one or
more intervertebral or increase in
CSF.
Clinical manifestation
Symptoms of brain compression,
which can show up immediately
following a head injury or weeks later,
include:
• headaches
• vomiting
• drowsiness
• dizziness
• confusion,
• progressive loss of consciousness
• Sensory and motor deficits in the
affected areas.
• Blood pressure abnormality
Treatment
• Surgical decompression
• Procedures may involve draining
blood from the brain,
• Removing a tumor or abscess, or
removing a section of the skull to
decrease intracranial pressure
• Physiotherapy
• Analgesics and corticosteroid
Complication
Compression of the brain can lead to:
• the destruction of brain tissue
• even death
CEREBRAL OEDEMA
is the excess accumulation of water in the
intra-and/or extracellular spaces of the
brain
• A swelling in the brain caused by the
presence of excessive fluid
• Causes increased intracranial pressure
 Fatal if left untreated
 Generalised in hypoxia, brain injury
 Surrounding other lesions eg tumour,
abscess
 Cerebral oedema is a life-threatening
condition that develops as a result of
an inflammatory reaction.
Pathophysiology
• Cerebral oedema at cellular level is
complex
• Damaged cells swell, injured blood
vessels leak and blocked absorption
pathways force fluid to enter brain
tissues.
• Cellular and blood vessel damage
follows activation of an injury
cascade.
• The cascade begins with glutamate
release into the extracellular space.
• Calcium and sodium entry channels
on cell membranes are opened by
glutamate stimulation.
• Membrane ATPase pumps calcium
ion exchange for 3 sodium ions.
• Sodium builds up within the cell
creating an osmotic gradient and
increasing cell volume by entry of
water.
• Increase in water causes dysfunction
but not necessarily permanent
damage.
• Finally, hypoxia depletes, the cells’
energy stores disabling the sodium -
potassium ATPase and reducing
calcium exchange
• Failure of the energy-dependent
sodium pump in the cellular
membrane, sodium accumulates
intracellularly and water moves from
the extracellular to the intracellular
space to maintain osmotic equilibrium
Type of cerebral oedema Etiology/causes cont…..

1. Vasogenic cerebral oedema refers to Non-neurological conditions

the influx of fluid and solutes into the
• Diabetic ketoacidosis,
brain through an incompetent blood
brain-barrier (BBB) • lactic acidotic coma
• Breakdown in the blood-brain barrier • Malignant hypertension,
allows movement of proteins from
the intravascular space through the • hypertensive encephalopathy
capillary wall into the extracellular • Fulminant viral hepatitis,
space.
• hepatic encephalopathy,
2. Cellular (cytotoxic) cerebral oedema
refers to a cellular swelling • Reye’s syndrome

• It is seen in conditions like head • Systemic poisoning (carbon monoxide

injury and hypoxia. and lead)

• It results from the swelling of brain • Hyponatraemia,

cells, most likely due to the release of • Opioid drug abuse dependence
toxic factors from neutrophils and
/bacteria. • Bites of certain reptiles and marine
animals
• Cytotoxic oedema is caused by
swelling of glia, neurons, endothelial • High altitude cerebral oedema
cells and begins within minutes after (HACO)
an insult.
Clinical manifestation
• 3. Interstitial oedema is seen in
• ICP reaches a level that produces local
hydrocephalus when outflow of CSF is
ischaemia,
obstructed and intraventricular
pressure increases. • Cerebral oedema alone will not
produce clinical neurological
Etiology/causes
abnormalities
• Cerebral oedema is seen in the
• Alteration in level of consciousness,
following neurological and non-
neurological conditions: • appearance of bradycardia,

Neurological conditions : • rise in blood pressure,

• Ischaemic stroke • abnormal breathing patterns evidence

of extra ocular movement
• intracerebral haemorrhage
abnormalities,
• Brain tumours
• alteration and inequality of pupillary
• Meningitis and encephalitis of all size
etiologies
• neurological deterioration
• Other brain infections like
• death during acute ischaemic
cysticercosis, tuberculosis and
toxoplasma
SURGICAL TREATMENT
• Temporary ventriculostomy or
craniectomy may prevent
deterioration and may be lifesaving.
• Decompressive craniectomy in the
setting of acute brain swelling from
cerebral infarction is a life saving
procedure and should be considered
in younger patients who have a
rapidly deteriorating neurological
status
• The surgical removal of lesions
responsible for cerebral oedema
results in resolution of cerebral
oedema.
• In cases of severe hydrocephalus VP
shunt is very helpful .
COMPLICATIONS
• Stroke
• Herniation
• visual loss
• cerebral atrophy
• Ischemia
• diabetic ketoacidosis but is rare
• Death
Classification
1. Mild (GCS 13 to 15, with loss of
consciousness to 15 minutes) 2
2. Moderate (GCS 9 to 12, with loss of
consciousness for up to 6 hours)
3. Severe (GCS 3 to 8, with loss of
consciousness greater than 6 hours)
Clinical Manifestations
1. Disturbances in consciousness: confusion to
coma
2. Headache, vertigo
3. Agitation, restlessness
4. Respiratory irregularities
5. Cognitive deficits (confusion, aphasia,
reading difficulties, writing difficulties,
memory
6. Pupillary abnormalities
7. Sudden onset of neurologic deficit
8. Coma and coma syndromes; persistent
vegetative state
9. Episodes of altered LOC, tachycardia,
tachypnea, hyperthermia,
10. Abnormal bleeding due to coagulopathy
11. Cardiac arrhythmias due to increased
release of catecholamines in stress response
Diagnostic Evaluation
1. CT scan
2. Skull and cervical spine films
3. Neuropsychological tests
4. MRI
5. CBC, coagulation profile, electrolyte levels,
serum osmolarity, ABG values.
6. ICP monotoring
Complications
1. Infections: systemic (respiratory, urinary),
neurologic
2. Increased ICP, hydrocephalus, brain
herniation
3. Posttraumatic seizure disorder
4. Permanent neurologic deficits: cognitive,
motor, sensory, speech
5. Neurobehavioral alterations
6. Persistent sympathetic storming
7. Death
Nursing Assessment
1. Monitor for signs of increased ICP—
altered LOC, abnormal pupil
responses, vomiting,.
2. Monitor for signs of sympathetic
storming—altered LOC, diaphoresis,
tachycardia, tachypnea, hypertension,
3. Monitor cardiac status for
hypotension and arrhythmias
4. Be alert for DI—excessive urine
output, dilute urine, hypernatremia
5. Be alert for hyponatremia and assess
etiology
6. Monitor laboratory findings and
report abnormal values
7. 7. Perform cranial nerve, motor,
sensory, and reflex assessment.
8. 8. Assess for behavior that warrants
potential for injury to self or others.
Nursing Interventions Maintaining
Adequate Cerebral Perfusin
1. Maintain a patent airway.
2. Monitor ICP, as ordered
3. Monitor cerebral oxygenation,
temperature, or neurochemicals, as
ordered.
4. Monitor response to pharmacologic
therapy, including antiepileptic drugs
(levels, as directed.
8. Monitor laboratory data, CSF cultures,
and Gram stains,
9. Monitor for hypernatremia and
administer fluid replacement as directed.
10. Monitor for hyponatremia and
administer oral or I.V. salt replacement as
directed.
11. Monitor respiratory rate, depth, and
pattern of respirations; report any
abnormal pattern,
12. Turn patient every 2 hours, and assist
with coughing and deep breathing.
13. Suction patient as needed; however,
hyperventilate the patient before
suctioning to prevent hypoxia.
14. Begin nutritional support as soon as
possible after a head injury;
15. Consult with dietitian to provide the
increased calories and nitrogen
requirement
16. Consult speech therapist for bedside
or radiographic swallow study before
initiation of oral foods.
17. Reassure the patient and family during
periods of agitation and irrational
behavior.
18. Pad side rails, and wrap hands in mitts
if patient is agitated.
19. Consult with social worker or
psychologist to assist the family in
adjusting to patient’s permanent
neurologic deficits.
20. Help the family assist the patient to
recognize current progress and not focus
on limit
Patient Education and Health
Maintenance
1. Review the signs of increased ICP with
the family.
2. Reinforce the lability of cognitive,
language, and physical functioning of the
person with brain injury and the lengthy
recovery period.
3. Teach the family techniques to calm the
agitated patient
TRAUMATIC INTRACRANIAL HAEMORRHAGE:
1. SUBDURAL
2. EPIDURAL
3. INTRACEREBRAL
FRACTURES OF THE SKULL
1. LINEAR SKULL FRACTURE
2. BASAL SKULL FRACTURE
3. DEPRESSED SKULL FRACTURE
DEGENERATIVE CONDITIONS
1. MULTIPLE SCLEROSIS
MS is a chronic, frequently progressive
neurologic disease of the CNS of unknown
etiology and uncertain trajectory.
MS is characterized by the occurrence of
small patches of demyelination of the white
matter of the optic nerve, brain, and spinal
cord.
MS is distinguished by exacerbations and
remissions of symptoms over the course of
the illness.
Pathophysiology and Etiology
1. Demyelination refers to the destruction of
the myelin, the fatty and protein material that
covers certain nerve fibers in the brain and
spinal cord.
2. Demyelination results in disordered
transmission of nerve impulses.
3. Inflammatory changes lead to scarring of
the affected nerve fibers.
4. Cause is unknown but may possibly be
related to autoimmune dysfunction, genetic
susceptibility, or an infectious process.
5. More prevalent in the northern latitudes
and among whites.
Classification
1. Relapsing remitting (RR)—clearly defined
acute attacks evolve over days to weeks.
2. Secondary progressive (SP)—always begins
as RR but clinical course changes with
increasing relapse rate, with a steady
deterioration in neurologic function unrelated
3. Primary progressive (PP)—characterized by
steady progression of disability from onset
without exacerbations and remissions.
4. Progressive relapsing (PR)—the same as PP
except that patients experience acute
exacerbations along with a steadily
progressive course (rarest form).
Clinical Manifestations
1. Fatigue and weakness. 2. Abnormal reflexes
3. Vision disturbances 4. Motor dysfunction
5. Sensory disturbances 6. Impaired speech
7. Urinary dysfunction
8. Neurobehavioral syndromes
Diagnostic Evaluation
1. Serial brain MRI studies
2. Magnetic resonance spectroscopy
3. Electrophoresis study
4. Visual, auditory, and somatosensory
Complications
1. Respiratory dysfunction
2. Infections: bladder, respiratory, sepsis
3. Complications from immobility
4. Speech, voice, and language disorders such
as dysarthria
Nursing Assessment
1. Observe motor strength, coordination, and
gait.
2. Perform cranial nerve assessment.
3. Evaluate elimination function.
4. Explore coping, effect on activity and sexual
function, emotional adjustment.
5. Assess patient and family coping, support
systems, available resources.
Nursing Diagnoses • Plan ahead, and prioritize activities.
Take brief rest periods throughout the
 Impaired Physical Mobility related to
day.
muscle weakness, spasticity, and
incoordination • Avoid overheating, overexertion, and
 Fatigue related to disease process and infection.
stress of coping
• Help patient develop healthy lifestyle
 Disturbed Sensory Perception (tactile,
with balanced diet, rest, exercise, and
kinesthetic, visual) related to disease
relaxation
process
 Impaired Urinary Elimination related • Encourage ophthalmologic
to the disease process consultation to maximize vision.
 Interrupted Family Processes related
• Provide a safe environment for
to inability to fulfill expected roles
patient with any sensory alteration
 Sexual Dysfunction related to disease
process • Ensure adequate fluid intake to help
prevent infection and stone
Nursing interventions
formation.
• Perform muscle stretching and
• Assess for urine retention, and
strengthening exercises daily, or teach
catheterize for residual urine as
patient or family to perform exercise
indicated.
at home.
• Teach patient to report signs of UTI
• Apply ice packs before stretching to
immediately.
reduce spasticity.
• Set up bladder training program to
• Allow patient to take frequent rest
reduce incontinence by encourage
period.
fluids every 2 hours.
• Encourage the patient to avoid
• Encourage verbalization of feelings of
muscle fatigue by minimising activity
each family member.
• Encourage ambulation and activity,
• Encourage counseling and use of
and teach patient how to use such
church or community resources.
devices as braces, canes, and walkers
when necessary. Surgical procedures

• Inform the patient to avoid sudden • Baclofen is a medication that acts on

changes in position, which may cause
falls due to loss of position sense, and
to walk with a wide-based gait.
• Encourage frequent change in
position while immobilized to prevent
contractures; sleeping prone will
minimize flexor spasm of hips and
knees.
• Help patient and family understand
that fatigue is an integral part of MS.
the central nervous system to relieve
spasms, cramping, and muscle
tightness caused by spasticity in MS. It
also improves muscle movement and
relieves spasticity-related pain
• Deep brain stimulation is a surgical
procedure where electrodes are
placed in the brain to correct damage
that has led to abnormal neurological
activity, such as tremors
 • Rhizotomy is a surgical procedure
that is recommended by the doctors
when patient is having a chronic pain
that cannot be controlled by
medication
Patient Education and Health Maintenance
1. Encourage the patient to maintain previous
activities, although at a lowered level of
intensity.
2. Teach the patient to respect fatigue and
avoid physical overexertion and emotional
stress; remind patient that activity tolerance
may vary from day to day.
3. Advise the patient to avoid exposure to
heat and cold or infectious agents.
4. Encourage a nutritious diet that is high in
fiber to promote health and good bowel
elimination.
5. Advise the patient that some medications
may accentuate weakness, such as some
antibiotics, muscle relaxants,
6. Instruct the patient receiving interferon
beta-1a and interferon beta-1b in self-
injection technique.
8. Try to include children in the education of
MS and the relationship of fatigue and
functional status.
9. Refer the patient/family for more
information and support to such agencies a
2. MYASTHENIA GRAVIS 538
3. RHEUMATIC CHOREA
4. PARKINSON’S DISEASE
Is a chronic, progressive neurologic disease
affecting the brain centers responsible for
control and regulation of movement.
5. ALZHEIMER DISEASE
6. GUILIAN BARRE SYNDROME SYNCOPE
Is an acute, rapidly progressing, ascending
inflammatory demyelinating polyneuropathy
of the peripheral sensory and motor nerves
and nerve roots.
Pathophysiology and Etiology
1. Believed to be an autoimmune disorder
that causes acute neuromuscular paralysis
due to destruction of the myelin sheath
surrounding peripheral nerve axons and
subsequent slowing of transmission.
2. Viral infection, immunization, or other
event may trigger the autoimmune response.
3. About 30% to 40% of cases are preceded by
Campylobacter infection, an acute infectious
diarrheal illness.
4. Cell-mediated immune reaction is aimed at
peripheral nerves, causing demyelination and,
possibly, axonal degeneration.
Clinical Manifestations
1. Paresthesias and, possibly, dysthesias.
2. Acute onset of symmetric progressive
muscle weakness;.
3. Difficulty with swallowing, speech, and
chewing due to cranial nerve involvement.
4. Decreased or absent deep tendon reflexes,
position and vibratory perception.
5. Autonomic dysfunction (increased heart
rate and postural hypotension).
6. Decreased vital capacity, depth of
respirations, and breath sounds.
7. Occasionally spasm and fasciculations of
muscles.
Diagnostic Evaluation
1. History and neurologic exam.
2. Lumbar puncture for CSF examination
3. Electrophysiologic studies
Management
1. Plasmapheresis produces temporary
reduction of circulating antibodies to reduce
the severity and duration of the GBS episode.
2. High-dose immunoglobulin therapy is used
to reduce the severity of the episode.
3. ECG monitoring and treatment of cardiac
dysrhythmias.
4. Analgesics and muscle relaxants as needed.
5. Intubation and mechanical ventilation if
respiratory paralysis develops.
Complications
1. Respiratory failure
2. Cardiac dysrhythmias
3. Complications of immobility and paralysis
4. Anxiety and depression
Nursing Assessment
1. Assess pain level due to muscle spasms and
dysthesias.
2. Assess cardiac function including
orthostatic BPs.
3. Assess respiratory status closely to
determine hypoventilation due to weakness.
4. Perform cranial nerve assessment,
especially ninth cranial nerve for gag reflex.
5. Assess motor strength.
Nursing Diagnoses
 Ineffective Breathing Pattern related
to weakness/paralysis of respiratory
muscles
 Impaired Physical Mobility related to
paralysis
 Imbalanced Nutrition: Less Than Body
Requirements, related to cranial
nerve dysfunction
 Impaired Verbal Communication
related to intubation, cranial nerve
dysfunction
 Chronic Pain related to disease
pathology
 Anxiety related to communication
difficulties and deteriorating physical
condition
Nursing Interventions
Maintaining Respiration
1. Monitor respiratory status through vital
capacity measurements, rate and depth of
respirations, breath sounds. 2. Monitor
level of weakness as it ascends toward
respiratory muscles. 3. Watch for
breathlessness while talking, a sign of
respiratory fatigue.
4. Maintain calm environment, and
position the patient with head of bed
elevated to provide for maximum chest
excursion.
5. As much as possible, avoid opioids and
sedatives that may depress respirations.
6. Monitor the patient for signs of
impending respiratory failure
Avoiding Complications of Immobility 1.
Position the patient correctly, and provide
ROM exercises
2. Encourage physical and occupational
therapy exercises to regain strength
during the rehabilitative period.
3. Assess for complications, such as
contractures, pressure ulcers, edema of
lower extremities, and constipation.
4. Provide assistive devices, as needed,
such as cane or wheelchair, for patient to
take home.
5. Recommend referral to rehabilitation
services or physical therapy for evaluation
and treatment.
Promoting Adequate Nutrition
1. Auscultate for bowel sounds; hold
enteral feedings if bowel sounds are
absent to prevent gastric distention.
2. Assess chewing and swallowing ability
by testing CN V, IX and X; if function is
inadequate, provide alternate feeding.
 3. During rehabilitation period, encourage
a well-balanced, nutritious diet in small,
frequent feedings with vitamin
supplement if indicated.
4. Recommend referral to dietitian for
evaluation and proper diet therapy.
Maintaining Communication
1. Develop a communication system with
the patient who cannot speak.
2. Have frequent contact with the patient,
and provide explanation and reassurance,
remembering that the patient is fully
conscious.
3. Provide some type of patient call
system.
4. Recommend referral to speech therapy
for evaluation and treatment. 5. Refer to
counselor, social workers, or psychologist
to develop/enhance coping skills and
regain sense of control.
Relieving Pain
1. Administer analgesics as required;
monitor for adverse reactions, such as
hypotension, nausea and vomiting, and
respiratory depression.
2. Provide adjunct pain management
therapies, such as therapeutic touch,
massage.
3. Provide explanations to relieve anxiety,
which augments pain.
4. Turn the patient frequently to relieve
painful pressure areas.
Reducing Anxiety
1. Get to know the patient, and build a
trusting relationship.
2. Discuss fears and concerns while verbal
communication is possible.
3. Reassure the patient that recovery is
probable.
4. Use relaxation techniques such as listening
to soft music.
5. Provide choices in care, and give the patient
a sense of control.
6. Enlist the support of significant others.
Patient Education and Health Maintenance
1. Advise the patient and family that acute
phase lasts 1 to 4 weeks, then the patient
stabilizes and rehabilitation can begin;
however, convalescence may be lengthy, from
3 months to 2 years.
2. Instruct the patient in breathing exercises
to reestablish normal patterns.
3. Teach the patient to wear good supportive
and protective shoes while out of bed to
prevent injuries due to weakness and
paresthesia.
4. Instruct the patient to check feet routinely
for injuries because trauma may go unnoticed
due to sensory changes.
5. Reinforce maintenance of normal weight;
additional weight will further stress the motor
abilities.
6. Encourage the use of scheduled rest
periods to avoid overfatigue.
7. Refer the patient/family for more
information and support .
INFECTIVE CONDITIONS
1. Herpes Zoster
TRAUMATIC CONDITIONS OF THE SPINAL
VERTEBRAE AND SPINAL CORD
1. INJURY TO SPINAL CORD
2. INJURY TO SPINAL NERVES
3. PARALYSIS
4. LUMBAGO
5. SCIATICA
SURGICAL INTERVENTIONS
1. SURGERY TO THE SKULL
2. INTERNAL FIXATION OF THE VERTEBRAE