Seizure Disorder

Introduction

This is a disorder that involves a sudden episode of abnormal, uncontrolled dis-
charge of the electrical activity of the neurons within the brain. The patient may
experience a variety of symptoms depending on the type of seizure and the cause.


Seizures may be a symptom of another condition—such as a tumor or stroke
which has increased the intracranial pressure, a metabolic disorder, withdrawal
from alcohol or drugs—or may be due to a chronic seizure disorder such as
epilepsy. Prior to the seizure, the patient may experience an aura, a sensory alter-
ation involving sight, sound, or smell. After the seizure, the patient enters a
post-ictal stage where there may be confusion and the patient is often fatigued. The
patient may not recall any of the seizure or the time immediately surrounding
the seizure.

TREATMENT

If there is an underlying condition causing the disorder, removal of this condition
will often result in resolution of the disorder. The patient with a primary seizure
disorder will typically be managed with anticonvulsant medications. Some patients
will need multi-drug regimens to adequately control the seizure disorder. Patients
who do not respond to multiple antiepileptic drugs may be candidates for surgical
intervention.
• Administer antiepileptic medications:
• carbamazepine
• phenytoin
• phenobarbital
• clonazepam
• valproic acid
• lamotrigine
• gabapentin
• levetiracetam
• oxcarbazepine
• primidone
• tiagabine
• topiramate
• Seizure precautions per institution.
• Maintain IV access with saline lock if no intravenous fluids needed for hos-
pitalized patients.
• Surgery to remove seizure focal area or sever the connection between the cere-
bral hemispheres (corpus callostomy) to limit the amount of seizure activity
for patients who do not have adequate control of seizures with medications.
• Vagal nerve stimulation where there is implantation of an electrical device
that provides a predetermined pattern of vagal stimulation. This is used to
decrease the frequency of seizures.

NURSING DIAGNOSES

• Risk for ineffective breathing pattern or airway clearance
• Risk for fall
• Anxiety

NURSING INTERVENTION

• Monitor patient during the seizure for breathing, skin color (cyanosis)—
patient may have diminished oxygenation during seizure.
• May need supplemental oxygen post-seizure.
• Keep oxygen equipment and suction equipment and emergency airway man-
agement equipment at bedside (intubation may be performed by anesthesi-
ologist, nurse anesthetist, or respiratory therapist).
• Monitor duration of seizure and progression of symptoms.
• Monitor for incontinence of bladder or bowel.
• Monitor for status epilepticus—prolonged seizures or repeated seizures,
considered a medical emergency.
• Position patient to decrease risk of injury:
• remove objects that may injure patient.
• turn patient on side to reduce risk of aspiration.
• do not insert anything in patient’s mouth during seizure.
• Assess the patient post-seizure.
• Explain to the patient:
• Medication use, side effects, and interactions.
• Importance of taking medications on time, not skipping doses.
• Importance of checking with prescriber before taking any new medica-
tions or over-the-counter (OTC) medications or supplements.
• Have lab tests for drug level of antiepileptic drugs checked as directed.

Stroke

Introduction:

Astroke is also known as a cerebrovascular accident (CVA) or a brain attack. Blood
supply is interrupted to part of the brain, causing brain cells to die; this results in the
patient losing brain function in the affected area. Interruption is usually caused by
an obstruction of arterial blood flow (ischemic stroke), such as formation of a blood
clot, but can also be caused by a leaking or ruptured blood vessel (hemorrhagic
stroke). A blood clot may develop from a piece of unstable plaque lining a vessel
wall that breaks free, or an embolus that travels from elsewhere in the body and
lodges within the vessel. The bleeding may occur as a result of trauma or sponta-
neously, as in the setting of uncontrolled hypertension. Ischemia occurs when insuf-
ficient blood is getting to the brain tissue. This leads to lack of available oxygen
(hypoxia) and glucose (hypoglycemia) for the brain. When these nutrients are not
available for a sustained period, the brain cells die, causing an area of infarction.
Permanent deficits result from infarction. There is increased risk for stroke in
patients with a history of hypertension, diabetes mellitus, high cholesterol, atrial
fibrillation, obesity, smoking, or oral contraceptive use.
Patients may also experience a transient ischemic attack (TIA) in which the
symptoms result from a temporary problem with blood flow to a specific area of
the brain. The symptoms have a duration between a few minutes and 24 hours.

PROGNOSIS

The degree of damage and location of the stroke will determine the outcome for the
patient. Strokes occur suddenly and patients should seek immediate treatment for
the best possible outcome. The majority of strokes are ischemic. Rapid entry into
the healthcare system and treatment with thrombolytic agents (unless there are con-
traindications to this treatment) to break up a clot that has caused the ischemia gives
the patient the best chance for recovery without permanent disability. Patients
with hemorrhagic stroke may need surgery to relieve intracranial pressure or stop
the bleeding. A large area of damage may lead to significant permanent disability
or death.

SIGNS AND SYMPTOMS

• Mental impairment
• Disorientation, confusion
• Emotional changes, personality changes
• Aphasia (difficulty with speech; may be receptive, expressive)
• Slurring of words
• Sensory changes (paresthesia, visual changes, hearing changes)
• Unilateral numbness or weakness in face or limbs
• Seizure
• Severe headache due to increased intracranial pressure from hemorrhage
• TIA symptoms are similar but have a shorter duration and resolve

TREATMENT

It is most important to determine whether the patient has suffered an ischemic or
hemorrhagic stroke as the treatment is different. Giving a thrombolytic agent to the
the brain. Caution is also recommended in patients with head trauma, uncontrolled
hypertension, hemorrhagic retinopathy, gastrointestinal bleeding, recent surgery,
recent MI, or pregnancy.
• Administer TPA (thromoblytic agent) within 3 hours of onset of symptoms,
unless contraindicated.
• Administer anticoagulants for patients with ischemic stroke after use of TPA:
• heparin, warfarin, low-molecular weight heparin, aspirin
• Administer antiplatelet medications to decrease platelet adhesiveness; used
to prevent recurrent stroke:
• clopidogrel, ticlopidine hydrochloride, dipyridamole
• Administer corticosteroid to decrease swelling:
• dexamethasone (Decadron)
• Physical therapy to help maintain muscle tone or return function.
• Speech therapy to help with speech and swallowing.
• Occupational therapy to help regain function.
• Bed rest to reduce chance of injury.
• Adequate nutrition in appropriate food type for patient.
• Carotid artery endarterectomy to remove plaque from within the carotid artery
if stenosis is present.
• Stenting of carotid artery to maintain bloodflow.
• Surgical correction of arteriovenous malformation, aneurysm, intracranial
bleeding.

NURSING DIAGNOSES

• Risk for injury
• Ineffective tissue perfusion

NURSING INTERVENTION

• Monitor vital signs for changes.
patient who has had a hemorrhagic stroke will only cause further bleeding into
• Monitor for signs of increased intracranial pressure—diminished level of con-
sciousness, headaches, restlessness, confusion, nausea and vomiting, speech
changes, or seizures.
• Notify healthcare provider of changes in neurologic status.
• Develop a means of communication with the patient—aphasia may compro-
mise use of call bell system or intercom.
• Assess for neglect syndrome—patient may act as if unaware of the side
affected by paralysis due to the stroke.
• Need for rehabilitation to return to prior functional ability.
• Explain to the patient:
• Home care needs.
• Proper technique to transfer from bed to chair.
• Use of ambulatory assist devices: cane, crutch, walker.
• Special dietary needs; use of Thick-it® for liquids.
• Medication schedule, use, side effects, and interactions.

Spinal Cord Injury

Introduction:

Injury to the spinal cord results in compression, twisting, severing, or pulling on the
spinal cord. The damage to the cord may involve the entire thickness of the cord
(complete), or only a partial area of the spinal cord (incomplete). The most com-
mon cause of spinal cord injury is trauma. Any level of the spinal cord may have
been affected by the injury. Loss of sensation, motor control, or reflexes may occur
below the level of injury or within 1 to 2 vertebrae or spinal nerves above the level
of injury. The loss may be unilateral or bilateral. Damage to the vertebrae may
have occurred at the same time as the spinal cord injury. Swelling due to the ini-
tial trauma may make the injury seem more severe than it actually is. When the
initial swelling resolves, the actual degree of permanent injury can be more accu-
rately assessed.


PROGNOSIS
The level of injury will determine the degree of disability the patient is likely to sus-
tain.Ahigh-level injury, such as a cervical injury, will more likely result in quadra-
plegia (paralysis of all four extremities) and compromise of the respiratory drive.
A complete spinal cord injury will result in greater disability than an incomplete
injury. Spinal cord tissue does not regenerate after an injury. Swelling that occurs
immediately following an injury may be controlled with medications and some
clinical improvement may occur, but the damage to the cord cannot be undone.

SIGNS AND SYMPTOMS

• Loss of motor control due to damage to the anterior horn of the spinal cord
• Loss of reflexes due to damage of the spinal cord, the point of synaptic trans-
mission of sensory impulse to motor response
• Flaccid paralysis
• Lack of bowel and bladder control
• Altered sensation (tingling—paresthesia; diminished—hypoesthesia; in-
creased—hyperesthesia)
• Bradycardia, hypotension, hypothermia due to problems with the autonomic
nervous system

TREATMENT

• Immobilize the affected area of the spinal cord to decrease chance of further
irritation.
• Place the patient in a flat position to avoid flexion or misalignment of the
spine.
• Monitor traction or collar to prevent skin irritation.
• Administer corticosteroid to decrease inflammation at point of injury:
• methylprednisolone
• prednisone
• dexamethasone
• Administer dextran, a plasma expander, which increases blood flow in the
spinal cord, increasing oxygenation to the tissue.
• Assist respirations if indicated.
• Administer H2 receptor antagonists to protect stomach from stress ulcer formation:
• cimetidine, ranitidine, famotidine, nizatidine
• Administer gastric mucosal protective agent to coat stomach lining:
• sucralfate
• Place patient in a rotation bed for repositioning to prevent pressure on skin.
• Surgical repair of vertebral fracture or decompression may be necessary.


NURSING DIAGNOSES

• Impaired physical mobility
• Powerlessness

NURSING INTERVENTION

• Monitor respiratory status—assess for changes in rate, effort, use of acces-
sory muscles, cyanosis, altered mental status, and pulse oximetry reading.
• Monitor neurologic status for changes—assess sensation, temperature, touch,
position sense, comparing right to left.
• Monitor for spinal shock:
• Flaccid paralysis, loss of reflexes below the level of injury, hypotension,
bradycardia, possible paralytic ileus.
• Monitor pulse and blood pressure for changes—change in heart rate, hypo-
tension, or hypertension.
• Assess skin for signs of pressure (redness) or breakdown.
• Assess abdomen and listen for bowel sounds.
• Explain to the patient:
• Importance of regular bowel and bladder function to avoid autonomic
dysreflexia due to distension: severe headache, hypertension, bradycardia,
flushing, nasal congestion, sweating, nausea.
• Use of incentive spirometer.
• Need for turning and positioning or special rotating bed to decrease pressure.
• Monitor intake and output.
• Home care needs—accessibility, equipment needs.
• Proper way to transfer from bed to wheelchair.
• Care of pin sites for cervical traction devices (e.g. halo traction).

Parkinson’s Disease

Introduction:

There is a gradual degeneration of the midbrain area known as the substantia nigra.
The neurons use the neurotransmitter dopamine to send their signals from cell to
cell. The loss of neurons within the substantia nigra continues and results in dimin-
ished voluntary fine motor skills due to dopamine loss. There is also development
of sympathetic noradrenergic lesions, causing norepinephrine loss within the sym-
pathetic nervous system. There is excess effect of the excitatory neurotransmitter
acetylcholine on the neurons; this causes increased muscle tone, leading to rigid-
ity and tremors. There seems to be a genetic tendency towards development of
Parkinson’s disease. Environmental factors such as exposure to airborne contami-
nants, occupational chemicals, toxins, or a virus have been implicated in the devel-
opment of the disease. Typical age of onset is after the fifth decade of life.

PROGNOSIS

Parkinson’s disease is a progressive disorder and does not have a cure. The symp-
toms can be managed with medications, but will return as the medications wear off.
The dosages will need to be adjusted periodically, and additional medications may
be needed to address the side effects of the medications used. Some patients
develop mental status changes or dementia in conjunction with Parkinson’s disease.

SIGNS AND SYMPTOMS

• Mask-like facial expressions
• Slow, shuffling gait
• Pill-rolling movements of hands
• Stooping posture
• Tremor at rest
• Change in handwriting—gets progressively smaller over time
• Bradykinesia (slow movement)
• Trouble chewing or swallowing
• Drooling
• Inability to control voluntary movement (dyskinesia) and fine-skilled move-
ment, or to initiate movement—due to loss of dopamine which has an
inhibitory effect and helps refine movements while acetylcholine retains the
excitatory effect on the neurons
• Rigidity of limbs:
• Cogwheeling—there is a rhythmic stopping or interruption of the move-
ment of the extremity
• Lead pipe—no bending; resists movement completely
• Orthostatic hypotension due to lack of norepinephrine within the sympa-
thetic nervous system, affecting the cardiovascular system

TREATMENT

• Administer antiparkinsonian agents which are able to cross the blood-brain
barrier. These drugs absorb better on an empty stomach:
• levodopa
• carbidopa-levodopa
• Administer dopamine receptor agonists to act directly on the dopamine
receptor sites:
• pergolide
• bromocriptine
• pramipexole
• ropinirole
• Administer selegiline, a selective monoamine oxidase B inhibitor that slows
the breakdown of dopamine and allows lower doses of levodopa to be used
because it prolongs its effect.
• Administer catechol O-methyltransferase (COMT) inhibitors which help block
the breakdown of levodopa:
• entacapone
• tolcapone
• Administer acetylcholine blocking drugs to decrease tremor and rigidity in
patients:
• biperiden
• benztropine mesylate
• procyclidine
• orphenadrine
• trihexyphenidyl
• Diet high in protein and calories.
• Soft food diet.
• Physical therapy.


NURSING DIAGNOSES

• Activity intolerance
• Impaired mobility
• Risk for injury

NURSING INTERVENTION

• Monitor neurological status for changes.
• Monitor respiratory status for changes.
• Encourage self-care, allow patient extra time.
• Encourage exercise; assist with passive ROM if necessary.
• Weigh patient.
• Record food intake.
• Explain to the patient:
• Importance of following medication time schedule as well as effects of
medication wearing off.
• Reduce risk of falls at home.

Myasthenia Gravis

Introduction:

This is a disorder of the peripheral nervous system involving antibodies that have
been produced by the body; they bind to receptor sites that normally bind acetyl-
choline. This prevents the acetylcholine from binding to the receptor sites on the
skeletal muscle, inhibiting normal muscle contraction in the affected area. The
areas of the body most commonly affected by the autoimmune disease include the
muscles in the eyes, face, lips, tongue, throat, and neck, resulting in weakness and
fatigue of these areas. The disease does not seem to be hereditary, but does have
a family tendency toward autoimmune disorders. The majority of the patients
have a hyperplasia (excessive growth of normal cells) of the thymus gland.
Myasthenia gravis is more likely to develop in young adults and is more common
in women.

PROGNOSIS

The disease can take a variety of forms from mild weakness and drooping of the
eye muscles to generalized, progressive weakness that ultimately affects respira-
tory function. Progression of symptoms will vary from patient to patient. There are
typically episodes of exacerbations and remissions. The more aggressive form of
the disease progresses more rapidly, resulting in death from respiratory failure.

SIGNS AND SYMPTOMS

• Ptosis (drooping of the eyelid) due to muscular weakness
• Diplopia (double vision) due to inability to keep both eyes focused on the
same object
• Trouble closing eyes completely; dry eyes due to muscle weakness
• Difficulty swallowing (dysphagia) due to muscle weakness
• Muscle weakness later in the day due to fatigue
• Proximal muscle weakness
• Fatigue
• In advanced disease—loss of bowel and bladder control; difficulty with res-
piratory function
• Myasthenic crisis is an exacerbation of symptoms due to insufficient
medication:
• Tachycardia
• Tachypnea
• Elevated blood pressure
• Cyanosis
• Decrease in urinary output
• Incontinence of bowel and bladder
• Loss of gag reflex
• Cholinergic crisis is an exacerbation of weakness due to too much choliner-
gic medication:
• Blurred vision
• Nausea, vomiting, diarrhea
• Abdominal cramping
• Paleness
• Twitching of facial muscles
• Small pupils (miosis)
• Low blood pressure

TREATMENT

• Administer immunosuppressants to induce remission and help control
symptoms:
• prednisone or dexamethasone initially to improve symptoms
• azathioprine and cyclophosphamide in the long term to help control
symptoms
• Administer cholinesterase inhibitors for long-term control of symptoms. These
drugs have short duration of action, therefore have to be dosed several times
during the day:
• neostigmine

NURSING DIAGNOSES

• Impaired physical mobility
• Impaired verbal communication
• Ineffective air exchange
• Self-care deficit

NURSING INTERVENTION

• Encourage frequent rest periods.
• Monitor vital signs.
• Monitor nutritional intake.
• Monitor weight.
• Monitor neurologic status for changes in pupil reaction, extraocular move-
ments, eyelid movement, facial symmetry, hand grip strength, coordination,
fine motor skills, and gait.
• Monitor respiratory status for changes in rate, effort, skin color, use of acces-
sory muscles, or change in mental status.
• Monitor gag reflex.
• Arrange for appropriate communication with staff if patient is unable to use
call bell system or unable to be heard over intercom from room.
• Explain to the patient:
• Home care needs.
• Medication use; need to maintain time schedule for medications.
• Time meals one hour after medications to decrease chance of aspiration.
• Teach use of oral-pharyngeal suctioning catheter to clear secretions.
• Avoid heat extremes (hot tubs, saunas).
• pyridostigmine
• ambenonium
• Administer natural tears or other lubricant to keep eyes moist:
• patch eyes if unable to close
• High-calorie diet of appropriate food type—patient may have difficulty
swallowing.
• Removing antibodies from plasma (plasmapheresis) may be beneficial.
• BiPAP or CPAP for enhanced air movement and oxygenation.
• Thymectomy (surgical removal of thymus gland) for patients with thymoma.
• Avoid aminoglycoside antibiotics which may exacerbate symptoms.
• Alcohol may exacerbate symptoms.

Multiple Sclerosis (MS)

Introduction:

This is an autoimmune disease that results in demyelination of the white matter of
the nervous system. Nerve impulses travel along the myelin coating on the outside
of the nerve cells. With the disruption in the myelin on the outside of the nerve
cells, the transmission of information from cell to cell within the nervous system is
altered. The patient’s sensations, movements, or mental function may be affected.
A patient with relapsing-remitting disease will have episodes of exacerbation when
symptoms occur and then months or years of symptom-free episodes. A portion of
these patients will progress to enter a disease state that has a steady pattern of dete-
rioration without relation to the periodic exacerbations; this is referred to as a sec-
ondary progressive disease. Other patients have a primary progressive disease and
develop the steady deterioration from the onset of the disease.

PROGNOSIS

The actual cause of the disease is unknown, although it is thought to be autoim-
mune. The disease is progressive. Stress may be noted to aggravate symptoms.
When damage is done to the nerve cells, it is not repairable, even when symptoms
resolve in between periods of exacerbation. The pattern of symptoms will vary
from one patient to the next. The time frame between exacerbations will also vary.
As the disease progresses, the patient will lose more functional ability and will
ultimately need assistance with basic self-care needs.

SIGNS AND SYMPTOMS

Symptoms have periods of exacerbation and remission. Symptoms typically
resolve completely in between exacerbations early in the disease process.
• Double vision (diplopia)
• Blurred vision
• Fatigue
• Muscle weakness or unsteadiness
• Unsteady gait due to muscle weakness and general unsteadiness
• Intolerance of temperature changes
• Ataxia (decrease in motor coordination, gross motor movements)
• Increased deep tendon reflexes
• Slurred speech
• Burning tingling on the skin (paresthesia)
• Paralysis later in disease state
• Memory loss; loss of attention or mental focus
• Urinary urgency or hesitancy due to changes in sphincter control


TREATMENT

• Use one of the following Biologic Response Modifiers on a continuous
basis, not just during periods of exacerbation:
• interferon beta-1a
• interferon beta-1b
• glatiramer acetate
• Administer immunosuppressants—may be helpful for secondary progres-
sive MS:
• cyclophosphamide
• azathioprine
• methotrexate
• cladribine
• mitoxantrone
TREATMENT
• Use one of the following Biologic Response Modifiers on a continuous
basis, not just during periods of exacerbation:
• interferon beta-1a
• interferon beta-1b
• glatiramer acetate
• Administer immunosuppressants—may be helpful for secondary progres-
sive MS:
• cyclophosphamide
• azathioprine
• methotrexate
• cladribine
• mitoxantrone
thesia
• Administer medications to help with altered bladder function:
• oxybutynin
• hyoscyamine sulfate
• darifenacin
• solifenacin
• tolterodine
• Remove antibodies by removing plasma (plasmapheresis).

NURSING DIAGNOSES

• Impaired physical mobility
• Fatigue
• Self-care deficit

NURSING INTERVENTION

• Monitor motor movements for interference with ADLs.
• Encourage activity balanced with rest periods.
• Assess cognitive function for changes, or deterioration.
• Explain to the patient:
• Bladder training.
• Teach self-catheterization if necessary (for patients with flexic bladder).
• Increase fluid intake unless other medical problems contraindicate.
• Importance of positioning.
• Avoid temperature extremes.
• Medication compliance.

Meningitis

Introduction:

Meningitis is the inflammation of the meningeal coverings of the brain and spinal
cord, most commonly due to bacteria or viral cause, although it can also be caused
by fungus, protozoa, or toxic exposure. Bacterial meningitis is the most common
and is typically due to Streptococcus pneumoniae (pneumococcal), Neisseria menin-
gitides (meningococcal), or Haemophilus influenzae. The incidence of H. influenzae
meningitis infections has decreased since the vaccine against H. influenzae began
to be used routinely in infants in the early 1990s. Other organisms that can cause
bacterial meningitis include Staphylococcus aureus, Escherichia coli, and Pseudo-
monas. Organisms typically travel either through the bloodstream to the central
nervous system or enter by direct contamination (skull fracture or extension from
sinus infections). Bacterial meningitis is more common in colder months when
upper respiratory tract infections are more common. People in close living con-
ditions, such as prisons, military barracks, or college dorms are at greater risk for
outbreaks of bacterial meningitis due to likelihood of transmission.
Viral meningitis may follow other viral infections, such as mumps, herpes sim-
plex or zoster, enterovirus, and measles. Viral meningitis is often a self-limiting
illness.
Patients who are immunocompromised have an increased risk for contracting a
fungal meningitis. This may travel from the bloodstream to the central nervous
system or by direct contamination. Cryptococcus neoformans may be the causative
organism in these patients.

PROGNOSIS

Identification of meningitis and the causative organism is important in order to
adequately treat the patient. Bacterial meningitis still has a significant mortality rate
and these patients need to be managed in the hospital. Some patients will have per-
manent neurologic effects following the acute episode. Viral meningitis is typically
self-limiting. Fungal meningitis often occurs in patients who are immunocompro-
mised. Patients who have comorbidities or are elderly have greater difficulty with
the symptoms of meningitis.

SIGNS AND SYMPTOMS

• Stiff neck due to meningeal irritation and irritation of the spinal nerves
• Nuchal rigidity (pain when flexing chin toward chest) due to meningeal irri-
tation and irritation of the spinal nerves
• Headache due to increased intracranial pressure
• Nausea and vomiting due to increased intracranial pressure
• Photophobia (sensitivity to light) due to irritation of the cranial nerves
• Fever due to infection
• Malaise and fatigue due to infection
• Myalgia (muscle aches) due to viral infection
• Petechial rash on skin and mucous membranes with meningococcal infection
• Seizures due to irritation of brain from increased intracranial pressure

TREATMENT

• Administer antibiotics as soon as possible to improve outcome for bacterial
meningitis:
• penicillin G
• ceftriaxone
• cefotaxime
• vancomycin plus ceftriaxone or cefotaxime
• ceftazidime
• Fungal infections are typically treated with:
• amphotericin B
• fluconazole
• flucytosine
• Administer corticosteroid to decrease inflammation in pneumococcal
infection:
• dexamethasone
• Administer osmotic diuretic for cerebral edema:
• mannitol
• Administer analgesics for headache if needed:
• acetaminophen
• Administer anticonvulsant if necessary:
• phenytoin, phenobarbital
• Bed rest until neurologic irritation improves.

NURSING DIAGNOSES

• Risk for injury
• Powerlessness

NURSING INTERVENTION

• Monitor intake and output to check fluid balance.
• Keep room darkened due to photophobia.
• Monitor neurologic function at least every 2 to 4 hours, changes in mental
status, level of consciousness, pupil reactions, speech, facial movement sym-
metry, and signs of increased intracranial pressure.
• Seizure precautions per institution policy.
• Isolation per policy depending on organism.
• Explain to the patient:
• Why restrictions (bed rest) are necessary.
• Vaccine available for meningococcal meningitis—the 2 different types
are meningococcal polysaccharide vaccine (MPSV4) and conjugate vac-
cine (MCV4).

Huntington’s Disease (Chorea)

Introduction:

This is a degenerative disease that presents with a gradual onset of involuntary,
jerking movements (chorea) and a progressive decline in mental ability, resulting
in behavioral changes and dementia. The disease is transmitted genetically, as an
autosomal dominant trait located on chromosome 4. Family members of patients
can have genetic testing done to identify presence of the gene. The symptoms typ-
ically appear between the ages of 30 and 50 years.

PROGNOSIS

The patient may present with either abnormalities of movements or changes in
intellectual function. In time, both will be present. The mental status changes will
progress to dementia. The disease will prove to be fatal within 10 to 20 years from
the time of onset.

SIGNS AND SYMPTOMS

• Personality changes
• Irritability or moodiness
• Psychiatric disturbance
• Progressive dementia as disease causes further neurologic degeneration
• Restlessness or fidgeting due to dyskinesia
• Abnormal, jerking movements (chorea)
• Depression

TREATMENT

Huntington’s disease is progressive and while there is no cure for it, medications
can be used to control symptoms.
• Genetic counseling.
• Control dyskinesia and behavior with medication to block dopamine receptors:
• phenothiazines
• haloperidol
• reserpine.

NURSING DIAGNOSES

• Risk for injury
• Impaired physical mobility
• Ineffective health maintenance

NURSING INTERVENTION

• Provide basic needs for the patient, assist with ADLs as needed.
• Protect the patient from suicide attempts due to depression.
• Assist the patient with positioning for safety and comfort.
• Explain to the patient:
• Nature of disease.
• Genetic counseling available for family members of patients.

Encephalitis

Introduction:

Encephalitis is the inflammation of the brain tissue, most often caused by a virus,
although it can also be due to bacteria, fungus, or protozoa. In the case of viral
encephalitis, the patient typically will have had viral symptoms prior to the current
illness. The virus enters the central nervous system via the bloodstream and begins
to reproduce. Inflammation in the area follows, causing damage to the neurons.
Demyelination of the nerve fibers in the affected area and hemorrhage, edema, and
necrosis occur, which create small cavities within the brain tissue. Herpes simplex
virus 1, cytomegalovirus, echovirus, Coxsackie virus, and herpes zoster can all
cause encephalitis. Some forms of encephalitis can be transmitted by insects (such
as mosquitoes or ticks) to humans, such as West Nile virus, St. Louis encephalitis,
or equine encephalitis.

PROGNOSIS

Identification of the organism is important in order to individualize the treatment
for the patient. The earlier that symptoms are recognized and the earlier the patient
enters the healthcare system the better. Some patients will incur permanent dis-
ability from the irreversible damage that occurs to the brain. These patients may
be in need of long-term custodial care.

SIGNS AND SYMPTOMS

• Fever due to infection
• Nausea and vomiting due to increased intracranial pressure
• Stiff neck due to meningeal irritation
• Drowsiness, lethargy, or stupor due to increased intracranial pressure
• Altered mental status—irritability, confusion, disorientation, personality change
• Headache due to increased intracranial pressure
• Seizure activity possible due to irritation of brain tissue


TREATMENT

• Monitor respiratory status for compromise.
• Monitor vital signs for widened pulse pressure and bradycardia—signs of
increased intracranial pressure.
• Monitor neurologic function for change.
• Administer corticosteroid to decrease inflammation:
• dexamethasone
• Administer antipyretics to reduce fever:
• acetaminophen
• Administer anticonvulsants to decrease chance of seizure activity:
• phenytoin, phenobarbital
• furosemide
• mannitol

NURSING DIAGNOSES

• Impaired physical mobility
• Disturbed thought processes

NURSING INTERVENTION

• Range of motion exercises—active or passive.
• Turn and position patient.
• Administer diuretics to decrease cerebral edema, if indicated:
• Provide a quiet environment to decrease unnecessary stimulation.
• Monitor fluid input and output.
• Explain to the patient and family:
• Home care needs.
• Necessity of turning and positioning.
• Medication actions, side effects, and interactions.

Brain Tumor

Introduction:

A brain tumor is a growth of abnormal cells within the brain tissue. The tumor may
be a primary site that originated in the brain or a secondary site that has metastasized
from a cancer site elsewhere in the body. Because the tumor is growing within the
confined space of the skull, the patient will eventually develop signs of increased
intracranial pressure. Some cell types grow faster than others; the patients with the
more aggressive, fast-growing cancers will develop symptoms more quickly.

PROGNOSIS

Meningiomas are typically benign tumors that begin from the meninges (covering
the brain). They are more common in women and in people as they age. Treatment
is surgical removal, but the growth tends to recur.
Gliomas are malignant brain tumors of the neuroglial cells that tend to be fast-
growing. Patients have nonspecific symptoms of increased intracranial pressure.
Treatment typically includes surgical debulking of the tumor; complete removal is
often not possible at the time of diagnosis. Surgery is followed by radiation and
chemotherapy. Astrocytoma is the most common glioma and has a variable progno-
sis. Oligodendroglioma is more slow-growing and may be calcified. Glioblastoma is
a poorly differentiated glioma with a poor prognosis.

SIGNS AND SYMPTOMS

• Cerebellum or brain stem:
• Lack of coordination—cerebellum helps coordinate gross movements
• Hypotonia of limbs
• Ataxia
• Frontal lobe:
• Inability to speak (expressive aphasia)
• Slowing of mental activity
• Personality changes
• Anosmia (loss of sense of smell)
• Occipital lobe:
• Impaired vision—defect in visual fields; patient may deny or be unaware
of defect
• Prosopagnosia (patient is unable to recognize familiar faces)
• Change in color perception
• Parietal lobe:
• Seizures
• Sight disturbances result in visual field defect
• Sensory loss—unable to identify object placed in hand without looking
• Temporal lobe:
• Seizures
• Taste or smell hallucinations
• Auditory hallucinations
• Depersonalization
• Emotional changes
• Visual field defects
• Receptive aphasia
• Altered perception of music

TREATMENT

• Chemotherapeutic agents alone or in combination with radiation and surgery.
May be given orally, intravenously or through an Ommaya reservoir. Drugs
are chosen based on cell type:
• carmustine, lomustine, procarbazine, vincristine, temozolomide, erlotinib,
gefitinib
• Irradiation of the area to decrease tumor size.
• Craniotomy to remove the tumor if appropriate; this depends on location,
size, primary site of cancer, and number of tumors. Some patients may have
several small, scattered tumors, making surgery impractical.
• Administer glucocorticoid to reduce swelling or inflammatory response
within confined space inside skull (no room to expand, bone does not give):
• dexamethasone
• Administer osmotic diuretic to reduce cerebral edema:
• mannitol
• Administer anticonvulsant to reduce chance of seizure activity:
• phenytoin, phenobarbital, carbamazepine, divalproex sodium, valproic
acid, levetiracetam, lamotrigine, clonazepam, topiramate, ethosuximide
• Administer mucosal barrier fortifier to reduce risk of gastric irritation:
• sucralfate
• Administer H2 receptor antagonists to reduce risk of gastric irritation:
• ranitidine, famotidine, nizatidine, cimetidine
• Administer proton pump inhibitors (PPIs) to reduce risk of gastric irritation:
• lansoprazole, omeprazole, esomeprazole, rabeprazole, pantoprazole


NURSING DIAGNOSES

• Disturbed sensory perception
• Risk for injury

NURSING INTERVENTION

• Monitor neurologic function.
• Check for side effects to medications.
• Seizure precautions per institution protocol.
• Assess for pain control.
• Explain to the patient:
• Home care needs.
• Possible need for hospice.

Brain Abscess

Introduction:

Collection of pus creates a space-occupying area within the brain. Symptoms are
similar to any other space-occupying lesion. The infection may be a primary site
within the brain or may have traveled from nearby sites such as the ear or sinuses
through bone erosion. It may also enter the brain via the systemic circulation from
any infected site in the body, such as the lungs in bronchiectasis. The organism
causes a local inflammatory reaction; there is pus and liquification of the affected
tissue. Cerebral edema of the surrounding tissue occurs. The area becomes en-capsulated within 10 to 14 days from the onset of the infection. The infections are
typically streptococci, staphylococci, anaerobes, or mixed-organism infections.
Immunocompromised patients may have fungal or yeast present in the abscess. Up
to 20 percent of the patients may have more than one abscess.

PROGNOSIS

Identification of the organism and appropriate treatment is imperative to resolution
of the infection. There is a significant mortality rate in these patients.

SIGNS AND SYMPTOMS

• Drowsiness due to increased intracranial pressure
• Headache due to increased intracranial pressure
• Confusion or inattention
• Seizures due to irritation of brain tissue
• Increasing intracranial pressure
• Widened pulse pressure and bradycardia due to increased intracranial pressure
• Focal neurologic deficit, depending on location of abscess
• Nystagmus with cerebral abscess
• Aphasia with frontal lobe abscess
• Loss of coordination (ataxia) with a cerebellar abscess

TREATMENT

• Surgically drain (aspiration or open) the abscess to relieve intracranial
pressure.
• Administer antibiotic intravenously, depending on organism:
• nafcillin sodium (penicillinase-resistant penicillin)
• penicillin G benzathine
• chloramphenicol
• metronidazole
• vancomycin
• Administer corticosteroids in divided doses to decrease inflammation:
• dexamethasone—taper dose down before stopping
• Administer anticonvulsants to reduce seizure risk; watch for drug interactions:
• phenytoin
• phenobarbital
• Administer osmotic diuretics to decrease cerebral edema:
• mannitol

NURSING DIAGNOSES

• Risk for disturbed thought process
• Risk for falls

NURSING INTERVENTION

• Assess the patient’s ability to think, reason, and remember.
• Assess the patient’s speech capabilities.
• Assess the patient’s movement and senses.
• Assess the patient’s cranial nerve function.
• Monitor vital signs.
• Monitor fluid intake and output.
• Monitor for signs of infection in post-operative patients.
• Monitor for side effects of medications.
• Explain to the patient:
• Need for continued antibiotic treatments.
• How to administer IV antibiotics at home, how to monitor IV access, and
when to call for problems.
• Need for follow up CT scan or MRI imaging for monitoring.

Bell’s Palsy

Introduction

This is an acute idiopathic facial paralysis of the seventh cranial nerve that affects
one side of the face. Often due to inflammation, the disorder is more common in
diabetic patients. One side of the face is paralyzed, making the patient unable to
close the eyelid, raise the eyebrow, or smile on the affected side of the face. Some
patients will experience pain around the ear on the affected side. The patient may
have an associated change in taste.

PROGNOSIS

The more severe the symptoms at the time of presentation, the poorer the progno-
sis. Some patients will have long-term persistence of symptoms, like facial disfig-
urement. The majority of patients will have complete resolution of symptoms.

SIGNS AND SYMPTOMS

• Unilateral facial paralysis—inability to close eye, wrinkle forehead, puff out
cheeks, or smile
• Pain near the ear and jaw
• Altered taste

TREATMENT
• Administer corticosteroids to decrease inflammation (unclear if there is a
definitive benefit):
• prednisone in divided doses for first few days, then taper down
• Administer artificial tears to maintain moisture within eyes.

NURSING DIAGNOSES

• Disturbed sensory perception
• Disturbed body image

NURSING INTERVENTION

• Monitor for pain control.
• Monitor for visual changes—dryness of eye can lead to irritation of cornea.
• Monitor patient for reaction to medications.
• Provide meals in private—patient may have difficulty keeping food in mouth
and may not feel food or liquid that is drooling out side of mouth.
• Explain to patient:
• How to properly instill artificial tear drops.
• How to use eye patch.

Amyotrophic Lateral Sclerosis (ALS)

Introduction:

ALS is commonly called Lou Gehrig’s disease and is a progressive, degenerative
disorder that involves both the upper and lower motor neurons. There is no change
in mental status or sensory function with the disease. The disease does result in
paralysis of the motor system, except the eyes. As the disease is more progressed,
families often can communicate with the patient through eye movements. Males
are affected more commonly than females. The disorder may present at any age,
but the age at onset is usually between 40 and late 60s. There is a familial form of
the disease that has been linked to an abnormality in chromosome 21.

PROGNOSIS
The disease is rapidly progressive and there is currently no known cure. As the
muscles weaken and atrophy, paralysis develops. Over time, the respiratory mus-
cles become involved. At first this results in poor air exchange, increasing the risk
for respiratory infections, such as pneumonia. Eventually, the respiratory compro-
mise leads to death from respiratory failure.

SIGNS AND SYMPTOMS

• Fatigue, especially with exertion
• Atrophy of muscles due to weakness
• Dysphagia (trouble swallowing) due to muscular weakness
• Weakness of muscles in the limbs
• Muscle twitching (fasciculation) due to changes within the muscles
• Slurred speech due to muscle weakness


TREATMENT
• Maintain adequate nutrition.
• Consult with speech pathologist for potential swallowing difficulties.
• Administer spasmolytic agent specific for amyotrophic lateral sclerosis, which
reduces the transmission of glutamine across the neural synapse. Use of this
drug appears to slow the progression of the disease:
• riluzole
• Administer medications to control symptoms.
• BIPAP (bi-level positive airway pressure) to assist respiration either at night-
time, intermittently as needed, or all day.
• Refer to hospice for end-of-life care.

NURSING DIAGNOSES
• Impaired physical mobility
• Ineffective airway clearance

NURSING INTERVENTION
• Develop a method of communication within the patient’s capabilities—ver-
bal communication may not be possible; patient may not be able to use call
bell system.
• Monitor vital signs—monitor respiratory function and cardiovascular status;
as muscular function decreases the respiratory muscles may be affected.
• Assess gag reflex—as muscular changes occur, normal protective gag reflex
will diminish.
• Explain to the patient:
• How to suction oral pharynx to remove secretions or food particles. As mus-
cle function decreases, the cough reflex will not be sufficient to remove these.
• How to tuck chin while drinking and eating to decrease chance of
aspiration.

• Monitor input and output.

Head Injury

Introduction:

The patient experiences a trauma to the head. The resulting injury may be a minor
scalp laceration or a major internal injury with or without a skull fracture. There
may be internal hemorrhage or cerebral edema resulting in hypoxia and a decrease
in cognitive and functional capabilities. There are a variety of injuries that may be
sustained. Open head injuries are typical of projectile wounds from gunshots or
knifes. Closed head injuries are typical of trauma from falls, motor vehicle acci-
dents, sports, or fights.
Concussion involves a blow to the head where there is a bruising-type injury as
the brain is thrust against the inside of skull. The point of injury where the brain
makes impact against the skull is referred to as a coup injury. There is also a con-
trecoup injury as the head recoils away from the point of impact and the brain is
thrust against the inside of the skull at the opposite point of the head, resulting in
injury there as well. Patients with concussion may experience a transient loss of
consciousness associated with bradycardia, or slowing of the heartrate; low blood
pressure; slow, shallow breathing; amnesia of the injury and the events immedi-
ately following the injury; headache; and temporary loss of mental focus. Cerebral
contusion is a more serious injury than concussion. Greater damage is done to the
brain; cerebral edema or hemorrhage may occur and lead to necrosis. Patients typ-
ically have longer loss of consciousness with a cerebral contusion.
Hemorrhages can occur at a variety of levels, between the skull and the outer
coverings (dura) of the brain, within the layers covering the brain, or within the
brain tissue. The bleeding may occur acutely, at the time of injury, or hours to weeks
later. An epidural hematoma happens at the time of injury from an arterial site. The
blood accumulates between the skull and the dura mater, or the outermost layer
covering the brain. The site is often in the temporal area. The patient is typically
awake and talking immediately after the blow to the head. Within a short time, the
patient becomes unstable and then unconscious. Emergency neurosurgery is neces-
sary to relieve the pressure and stop the bleeding. Subdural hematoma is typically
bleeding from a venous source into the area below the dura mater and above the
arachnoid mater. This may occur acutely in some patients, but can also occur as
a slow, chronic bleed, especially in the elderly patient. The elderly patient with a
chronic bleed may have a significant amount of blood accumulate before symptoms
occur due to age-related changes in volume of brain tissue. A subarachnoid hemor-
rhage causes blood to accumulate within the area below the arachnoid mater and
above the pia mater. The cerebrospinal fluid is found in this area. An intracerebral
bleed is an accumulation of blood within the tissues of the brain. This may be due
to a shearing force on the brain tissue from a twisting motion between the upper
part of the brain (cerebrum) and the brain stem or tearing of small vessels within
the brain. There will be associated edema and elevation of intracranial pressure.
Simple skull fractures are displaced and do not require specific intervention.
Depressed skull fractures have bone fragments that have been broken off from the
skull and pressed down toward the brain tissue. These fractures need to be cor-
rected surgically. A basilar skull fracture has classic signs that include periorbital
bruising (raccoon sign), blood behind the ear drum (Battle’s sign), and leaking of
cerebrospinal fluid from the nose or ear (check for glucose content to distinguish
from a runny nose).

PROGNOSIS
The prognosis following head injury varies greatly depending on the location of
the injury, the severity of the damage that occurred, and the treatment that was
received. Patients with loss of consciousness over 2 minutes have a more severe
injury and therefore worse prognosis. Patients who have loss of memory, either
about the incident or the events immediately following, also have a more severe
injury and worse prognosis. Some patients develop hemorrhage as a late effect of
head injury, occurring hours, or in some cases, days after the initial injury. Post-
traumatic seizure disorder can also occur as a late effect of head injury.

SIGNS AND SYMPTOMS

• Headache due to direct trauma and/or increasing intracranial pressure
• Disorientation or cognitive changes
• Changes in speech
• Changes in motor movements
• Nausea and vomiting due to increased intracranial pressure
• Unequal pupil size—important to determine if due to neurologic change or
if patient has always had unequal pupil size (small percentage of population
has unequal pupil size)
• Diminished or absent pupil reaction due to neurologic compromise
• Decreased level of consciousness or loss of consciousness
• Amnesia


TREATMENT

• Surgical interventions may be necessary (craniotomy):
• Removal of hematoma
• Ligation of bleeding vessel
• Burr holes (drilling holes) for decompression
• Debridement of foreign material and dead cells
• Administer antibiotics for open head injuries to prevent infection.
• Ventilatory assist if needed—intubation and mechanical ventilation.
• Administer low-dose opioids for restlessness, agitation, and pain in ventilator-
dependent patients:
• morphine sulfate or fentanyl citrate
• Administer osmotic diuretics to reduce cerebral edema:
• mannitol
• Administer loop diuretics to decrease edema and circulating blood volume:
• furosemide
• Administer analgesics:
• acetaminophen (Tylenol)
• High-protein, high-calorie, high-vitamin diet.
• Platelet and packed RBC transfusions—if blood counts warrant transfusion.

NURSING DIAGNOSES
• Risk for injury
• Ineffective tissue perfusion
• Decreased intracranial adaptive capacity
• Risk for disturbed thought processes


NURSING INTERVENTION
• Monitor intake and output.
• Monitor urine specific gravity, serum, and urine osmolarity.
• Collaborate with dietician for appropriate diet, if any swallowing or oral sen-
sory concerns.
• Seizure precautions per institution policy.
• Explain to the patient and family:
• Any dietary restrictions.
• Any activity restrictions.
• Medication actions, side effects, interactions.
• Avoid discussing the patient’s condition in the presence of the patient—
remember the patient can still hear you even though he or she is not con-
scious, and may recall the conversations after they regain consciousness.
• Monitor vital signs for stability—increased blood pressure with widening
pulse pressure and slow pulse, suggestive of increased intracranial pressure.
• Monitor neurologic status for changes—typically use Glasgow Coma Scale
or similar tool to grade response to stimuli (highest score 15):
• Eye-opening response spontaneous 4
to sound 3
to pain 2
none 1
• Motor responses obeys commands 6
localizes pain 5
withdrawal (normal) 4
abnormal flexion 3
extension 2
none 1
• Verbal responses oriented 5
confused conversation 4
inappropriate words 3
incomprehensible sounds 2
none 1

• What to do in case of a seizure, how to protect the patient from further
injury, time the seizure, monitor for breathing, when to call the doctor or
EMS.
• Call your physician at any signs of change in the level of consciousness—
drowsiness, lethargy, change in personality.

How the Nervous System Works

The nervous system is divided into the central and peripheral nervous systems.
The central nervous system is comprised of the brain and spinal cord. The periph-
eral nervous system contains the spinal nerves and peripheral nerves.
The basic component of the nervous system is the nerve cell or neuron. Aneuron
is composed of the nucleus (within the cell body), a dendrite, (which receives the sig-
nal), an axon (the extension of the cell that can pass on an impulse to the next nerve
cell), and the axon terminals (which can transmit the signals to other cells). The mes-
sages are sent from one nerve cell to another, crossing a synapse (or gap) between
cells. Neurotransmitters are chemicals released by the presynaptic neuron to enhance
the communication between nerve cells. There are specific receptor sites for the dif-
ferent neurotransmitters on the postsynaptic neuron. Electrically charged ions trans-
mit signals along the cell membranes of the nerve cells. A myelin coating on the
outer surface of the nerve cells helps to speed the transmission along the nerve cells.
This myelin coating also gives a white color to the nerve cells.
Some neurons are afferent neurons. They carry sensory information from the
peripheral areas of the body to the central nervous system. These neurons do not
have dendrites. Motor neurons that transmit information from the central nervous
system to the muscles or glands are efferent neurons.
The brain is protected within the skull. The outermost layer of the brain is the
cerebral cortex, made up primarily of neural cell bodies, giving a gray appearance.
The cerebral cortex is divided into right and left hemispheres and into frontal, pari-
etal, occipital, and temporal lobes. The frontal lobe has motor and pre-motor areas,
as well as Broca’s area, which controls speech articulation, behavior, moral decision-
making, and emotional outburst. The parietal area interprets sensory stimuli, pain,
and touch. The temporal lobe is involved in auditory processing, language interpreta-
tion (Wernicke’s area), and memory formation, and storage. The occipital lobe houses
the visual cortex. The diencephalon includes the thalamus, hypothalamus, and the basal
ganglia. The thalamus relays the sensory information from the body to the appropri-
ate part of the cerebral cortex. Descending messages from the cerebral cortex are
passed through the thalamus to the body. The hypothalamus controls neuroendocrine
function and maintains homeostasis, or constancy, within the body. The basal ganglia
control highly skilled movements that require precision without intentional thought.
The brainstem is comprised of the pons, medulla oblongata, and midbrain.
The spinal column is protected within the vertebral column. Both motor and
sensory fibers are found within the spinal column. Motor nerves are located along
the anterior horns and sensory nerves are located along the posterior horns of the
spinal column. The motor nerve fibers are more protected from traumatic injury
this way. If a patient sustains an external injury to the back that damages the spinal
column, the first area to be impacted will be the sensory nerves, hopefully main-
taining motor function. If enough damage has occurred, then both sensory and
motor function will be lost. Peripheral nerve fibers leave the spinal column to travel
to the rest of the body. Impulses travel from the central nervous system to muscle
fibers to control voluntary motion and involuntary function of organs. Impulses
are also sent from the body to the central nervous system for input.