NCLEX: Neurologic disorders

Neurologic disorders: Cerebral aneurysm

Focus topic: Neurologic disorders

Cerebral aneurysm, a localized dilation of a cerebral artery, results from a weakness in the arterial wall. (See Common sites of cerebral aneurysm, page 134.) The incidence is slightly higher in women than in men, especially those in their late 40s to mid-50s, but cerebral aneurysm may occur at any age. Prognosis is uncertain because cerebral aneurysms can rupture and cause subarachnoid hemorrhage; one-half of all patients suffering subarachnoid hemorrhages die immediately. However, with new and better treatment, the prognosis is improving.

What causes it

Cerebral aneurysm results from congenital vascular disease, infection, or atherosclerosis.

Pathophysiology

Blood flow exerts pressure against a congenitally weak area of arterial wall, causing it to stretch and thin, somewhat like an overblown balloon. At this point, the risk of rupture is high. A rupture is followed by a subarachnoid hemorrhage, in which blood spills into the space normally occupied by CSF. In some cases, blood also spills into brain tissue, where a clot can damage brain tissue or cause a life-threatening increase in ICP.

Neurologic disorders

What to look for
Most patients are asymptomatic until the time of bleeding. Premonitory symptoms resulting from oozing of blood into the subarachnoid space include:

  • headache, intermittent nausea
  • nuchal rigidity
  • stiff back and legs.

Rupture usually occurs abruptly and may cause:

  • sudden severe headache
  • nausea and projectile vomiting
  • altered LOC, including deep coma
  • meningeal irritation, resulting in nuchal rigidity, back and leg pain, fever, restlessness, irritability, seizures, photophobia, and blurred vision
  • hemiparesis, hemisensory defects, dysphagia, and visual defects
  • diplopia, ptosis, dilated pupils, and an inability to rotate the eye.

What tests tell you

  • Angiography can confirm an unruptured cerebral aneurysm. Unfortunately, diagnosis usually follows the rupture.
  • A CT scan may help detect subarachnoid hemorrhage.
  • MRI may detect vasospasm.

How it’s treated
To reduce the risk of rebleeding, the surgeon may attempt to repair the aneurysm. Usually, surgical repair (by clipping, ligating, wrapping the aneurysm neck with muscle, or using electrothrombosis) takes place within several days after the initial bleed.

Neurologic disorders: More conservative

Focus topic: Neurologic disorders

The patient may receive conservative treatment if surgical correction poses too great a risk (common with elderly patients and those with heart, lung, or other serious diseases), the aneurysm is in a particularly dangerous location, or vasospasm necessitates a delay in surgery.
Commonly, treatment for the patient who isn’t a good candidate for surgery includes bed rest in a quiet, darkened room for as long as 4 to 6 weeks. The patient must avoid stimulants (including caffeine) and aspirin. He may receive codeine or another analgesic, hydralazine or another antihypertensive (if he’s hypertensive), cortico steroids to reduce edema, and phenobarbital or another sedative. Nimo dipine may be prescribed to limit possible neurologic deficits. If the patient is hypotensive, he may receive dopamine to ensure adequate brain perfusion.
An accurate neurologic assessment, good patient care, patient and family teaching, and psychological support can speed recovery and reduce complications. The medical-surgical nurse assumes care for the patient recovering from an aneurysm repair when he’s transferred from the ICU.

What to do

  • Assess neurologic status to screen for changes in the patient’s condition.
  • Administer medications, as ordered.
  • Maintain adequate nutrition.
  • Promote activity based on the patient’s ability.
  • Provide support to the patient and his family, especially if neurologic deficits have occurred.
  • Refer the patient to appropriate health care team members, such as a social services representative and home care organization.
  • Check for a patent airway, normal breath sounds, consistent LOC with no additional neurologic deficits, and adequate hydration and nutrition.

Neurologic disorders: Guillain-Barré syndrome

Focus topic: Neurologic disorders

An acute, rapidly progressive, and potentially fatal form of polyneuritis, Guillain-Barré syndrome causes muscle weakness and mild distal sensory loss. About 95% of patients experience spontaneous and complete recovery, although mild motor or reflex deficits in the feet and legs may persist.

What causes it

The precise cause of this syndrome is unknown, but it may be a cell-mediated immunologic attack on peripheral nerves in response to a virus. Precipitating factors may include:

  • mild febrile or viral illness
  • surgery
  • rabies or swine influenza vaccination
  • Hodgkin’s disease or some other cancer
  • systemic lupus erythematosus.

Pathophysiology

The major pathologic manifestation of Guillain-Barré syndrome is segmental demyelination of the peripheral nerves, which prevents normal transmission of electrical impulses. Because this syndrome causes inflammation and degenerative changes in the posterior (sensory) and anterior (motor) nerve roots, signs of sensory and motor loss occur simultaneously. Additionally, autonomic nerve transmission may be impaired.

What to look for

Symmetrical muscle weakness usually appears in the legs first (ascending type) and then extends to the arms and facial nerves within 24 to 72 hours. Other signs and symptoms may include:

  • facial diplegia, possibly with ophthalmoplegia (ocular paralysis)
  • dysphagia, dysarthria
  • hypotonia, areflexia.

What tests tell you

  • Protein levels in CSF begin to rise several days after onset of signs and symptoms and peak in 4 to 6 weeks. White blood cell count in the CSF remains normal but, in severe disease, CSF pressure may rise above normal.
  • Complete blood count (CBC) shows leukocytosis and immature forms early in the illness, but blood studies soon return to normal.
  • Electromyography may show repeated firing of the same motor unit instead of widespread sectional stimulation. Nerve conduction velocities are slowed soon after paralysis develops.

How it’s treated

At the onset of symptoms, the patient should be hospitalized. Monitor respiratory function several times daily because the ascending pathology can lead to respiratory failure. Mechanical ventilation may be necessary. The other key treatment is plasmapheresis, which temporarily reduces circulating antibodies. Patients need less ventilator support if plasmapheresis begins within 2 weeks of onset. High-dose immune globulins and steroids are also used.

What to do

  • Watch for ascending motor loss. Commonly, sensation isn’t lost; in fact, the patient may be hypersensitive to pain and touch.
  • Monitor the patient’s vital signs and LOC.

Neurologic disorders: Take a deep breath

Focus topic: Neurologic disorders

  • Assess respiratory function. Watch for signs of increasing partial pressure of arterial carbon dioxide (PaCO2), such as confusion and tachypnea. Auscultate breath sounds, turn and position the patient, and encourage coughing and deep breathing. If respiratory failure becomes imminent, establish an emergency airway and assist with endotracheal intubation.
  • Provide meticulous skin care to prevent skin breakdown.

Neurologic disorders: Tanks, I needed that

Focus topic: Neurologic disorders

  • Perform passive ROM exercises within the patient’s pain limits, perhaps using a Hubbard tank to prevent contractures. When the patient’s condition stabilizes, change to gentle stretching and active assistance exercises.
  • Evaluate the patient’s gag reflex. If he has no gag reflex, administer NG feedings, as ordered. If it’s present, position the patient to prevent aspiration.
  • As the patient regains strength and can tolerate a vertical position, be alert for hypotension; prevent it with slow position changes.
  • Inspect the patient’s legs regularly for signs of thrombophlebitis, a common complication of Guillain-Barré syndrome. To prevent thrombophlebitis, apply antiembolism stockings and a sequential compression device and give prophylactic anticoagulants, as ordered.
  • Provide eye and mouth care every 4 hours if the patient has facial paralysis.
  • Watch for urine retention. Measure and record intake and output every 8 hours, and offer the bedpan every 3 to 4 hours. Encourage adequate fluid intake (2 qt [2 L]/day), unless contraindicated. If urine retention develops, the patient may need to use manual pressure over the bladder (Credé’s maneuver) to urinate. Use intermittent catheterization, if necessary.

Neurologic disorders: Bulking up

Focus topic: Neurologic disorders

  • To prevent or relieve constipation, offer prune juice and a high bulk diet. If necessary, give daily or alternate-day suppositories (docusate sodium [Colace] or bisacodyl [Dulcolax]), or enemas, as ordered.
  • Refer the patient for physical therapy, as needed.
  • Evaluate the patient for adequate respiratory function with a patent airway and clear lungs, adequate nutritional status, and optimal activity level.
  • Note whether the patient has expressed his feelings about his illness to members of the staff, his friends, or his family.

Neurologic disorders

Neurologic disorders: Headache

Focus topic: Neurologic disorders

Muscle contraction, tension, and vascular changes cause 90% of head aches. Occasionally, however, a headache indicates an underlying intracranial, systemic, or psychological disorder.
Throbbing, vascular headaches — migraine headaches — affect up to 10% of Americans. Migraines usually begin in childhood or adolescence and recur throughout adulthood. Migraine headaches tend to run in families and are more common in women than in men.

What causes it

Most chronic headaches result from muscle tension caused by:

  • emotional stress or fatigue
  • menstruation
  • environmental stimuli (noise, crowds, bright lights). Other possible causes include:
  • glaucoma
  • inflammation of the eyes or of the nasal or paranasal sinus mucosa
  • diseases of the scalp, teeth, extracranial arteries, or external or middle ear
  • vasodilators (nitrates, alcohol, histamine)
  • systemic disease
  • hypertension
  • head trauma or tumor
  • intracranial bleeding, abscess, or aneurysm.

Pathophysiology

Headache pain may emanate from the pain-sensitive structures of the skin, scalp, muscles, arteries, and veins; from cranial nerves V, VII, IX, and X; or from cervical nerves 1, 2, and 3. Intracranial mechanisms of headache include traction or displacement of arteries, venous sinuses, or venous tributaries and inflammation or direct pressure on the cranial nerves with afferent pain fibers.
The cause of migraine headaches isn’t known, but researchers associate the disorder with constriction and dilation of intracranial and extracranial arteries.

What to look for

Signs and symptoms depend on the type or cause of the headache: migraine headache, muscle contraction and traction-inflammatory vascular headache, intracranial bleeding, or tumor.

Neurologic disorders: Migraine headache

Focus topic: Neurologic disorders

  • Unilateral pulsating pain, which becomes more generalized over time, lasting up to 2 days
  • Premonitory aura of scintillating scotoma, hemianopsia, unilateral paresthesia, or a speech disorder
  • Irritability, anorexia, nausea, vomiting, photophobia

Neurologic disorders: Muscle contraction and traction-inflammatory
vascular headache

Focus topic: Neurologic disorders

  • Dull, persistent ache or severe, unrelenting pain
  • Tender spots on the head or neck
  • Feeling of tightness around the head with a characteristic “hatband” distribution

Neurologic disorders: Intracranial bleeding

Focus topic: Neurologic disorders

  • Neurologic deficits, such as paresthesia and muscle weakness
  • Pain unrelieved by opioids

Neurologic disorders: Tumor

Focus topic: Neurologic disorders

  • Pain that’s most severe when the patient wakes

What tests tell you

Skull X-rays (including cervical spine and sinus), EEG, MRI, CT scan (performed before lumbar puncture to rule out increased ICP), brain scan, and lumbar puncture may help determine the cause.

How it’s treated

Depending on the type of headache, analgesics ranging from aspirin to codeine or meperidine (Demerol) may provide symptomatic relief. A tranquilizer, such as diazepam, may help during acute attacks, as could identification and elimination of causative factors and, possibly, psychotherapy for headaches caused by emotional stress. Chronic tension headaches may require muscle relaxants.

Neurologic disorders: Taking a coffee break

Focus topic: Neurologic disorders

For migraine headache, ergotamine (Ergomar) alone or with caffeine provides the most effective treatment. Sumatriptan ( Imitrex), which binds with serotonin receptors, is also effective in aborting migraine head aches. These drugs and others, such as metoclopramide (Reglan) or na proxen (Naprosyn), work best when taken early in the course of an attack. Antiemetics, such as promethazine (Phenergan), may be prescribed to control nausea and vomiting. Drugs that can help prevent migraine head ache include propranolol (Inderal); calcium channel blockers, such as verapamil (Calan) and diltiazem (Cardizem); and antiseizure medications such as valproic acid.

What to do

Unless the headache is caused by a serious underlying disorder, hospitalization is rarely required. In these rare cases, direct your attention to treating the primary problem. The patient with migraine usually needs to be hospitalized only if nausea and vomiting are severe enough to induce dehydration and possible shock.

Neurologic disorders: Finding a sea of tranquility

Focus topic: Neurologic disorders

Evaluate the patient to determine the effectiveness of prescribed analgesics, tranquilizers, or muscle relaxants and document your findings. Help the patient understand the possible causes and remedies for the headaches.

Neurologic disorders: Huntington’s disease

Focus topic: Neurologic disorders

Huntington’s disease (Huntington’s chorea) is a hereditary disease that causes degeneration in the cerebral cortex and basal ganglia. This degeneration leads to chronic progressive chorea and mental
deterioration that ends in dementia.

Neurologic disorders

What causes it

The cause of Huntington’s disease isn’t known. However, it’s transmitted as an autosomal dominant trait.

Pathophysiology

Huntington’s disease involves a disturbance in neurotransmitter substances, primarily gamma aminobutyric acid (GABA) and dopamine. GABA neurons in the basal ganglia, frontal cortex, and cerebellum are destroyed and replaced with glial cells. The deficiency of GABA (an inhibitory neurotransmitter) causes an excess of dopamine and abnormal neurotransmission along the affected pathways.

What to look for

  • Severe choreic movements (involuntary, rapid, usually violent, and purposeless movements), initially unilateral and more prominent in the face and arms than in the legs
  • Dementia, typically mild at first and then growing more severe until it disrupts the personality
  • Loss of musculoskeletal control

What tests tell you

  • PET scan and deoxyribonucleic acid analysis can detect Huntington’s d isease.
  • CT scan and MRI reveal brain atrophy.

How it’s treated

Huntington’s disease has no known cure. Therefore, treatment focuses on supporting and protecting the patient, treating symptoms, and providing emotional support to the patient and his family. Tranquilizers and drugs, such as chlorpromazine, haloperidol, and imipramine (Tofranil), can help control choreic movement and alleviate discomfort and depression. However, they can’t stop mental deterioration. In addition, tranquilizers increase rigidity.

What to do

  • Attend to the patient’s basic needs, such as hygiene, skin care, bowel and bladder care, and nutrition. Increase support as his mental and physical deterioration becomes more pronounced.
  • Provide emotional support. The patient and his family can feel overwhelming despondency due to the degenerative and irreversible course of the disease. An extremely depressed patient may attempt suicide. Be alert for signs, and make sure the patient’s environment is free from instruments that could permit self-inflicted injury.

Neurologic disorders: Maintaining high levels

Focus topic: Neurologic disorders

  • Evaluate the patient’s mobility and level of function. Plan interventions that help him maintain the highest level of mobility and independence possible for as long as possible.
  • Keep the patient free from injury.
  • Help the family identify resources that can help them cope with the patient’s illness.

Neurologic disorders: Meningitis

Focus topic: Neurologic disorders

In meningitis, infection (bacterial or otherwise) causes inflammation of the brain and spinal meninges that can involve all three meningeal membranes: dura mater, arachnoid, and pia mater.

What causes it

  • Bacteremia, especially due to pneumonia, empyema, osteomyelitis, or endocarditis
  • Other infections, such as sinusitis, otitis media, encephalitis, or myelitis
  • Brain abscess, usually caused by Neisseria meningitidis, Haemophilus influenzae, Streptococcus pneumoniae, or Escherichia coli
  • Head injury, such as skull fracture, penetrating head wound, or neurosurgery
  • Virus or other organism (aseptic meningitis)

What to look for

  • Fever, chills, malaise
  • Headache, vomiting
  • Signs of meningeal irritation, such as nuchal rigidity, positive Brudzinski’s and Kernig’s signs
  • Seizures
  • Delirium, deep stupor, and coma

Neurologic disorders

What tests tell you

Typically, CSF testing and positive Brudzinski’s and Kernig’s signs establish the diagnosis:

  • Look for elevated CSF pressure, high CSF protein levels and, possibly, low glucose levels.
  • CSF culture and sensitivity tests usually identify the infecting organism unless it’s a virus. The Xpert EV test identifies the enterovirus in CSF.

How it’s treated
Treatment includes antibiotic therapy (if the cause is bacterial) and vigorous supportive care. Usually, the patient receives I.V. antibiotics for 2 or more weeks, followed by oral antibiotics. Other prescribed drugs may include:

  • digoxin (Lanoxin) to control arrhythmias
  • mannitol (Osmitrol) to decrease cerebral edema
  • an anticonvulsant or a sedative to reduce restlessness
  • acetaminophen (Tylenol) to relieve headache and fever.

Neurologic disorders: Culture club

Focus topic: Neurologic disorders

Supportive measures include bed rest and measures to prevent dehydration. If nasal cultures are positive, isolation is necessary. Any coexisting conditions, such as endocarditis and pneumonia, are treated as well.

What to do

  • Assess the patient’s neurologic function often and watch for deterioration. Be especially alert for a temperature increase up to 102º F (38.9º C), deteriorating LOC, onset of seizures, and altered respirations, all of which may signal an impending crisis.

Neurologic disorders: Finding fluid equilibrium

Focus topic: Neurologic disorders

  • Monitor the patient’s fluid balance. Make sure he consumes enough fluids to prevent dehydration, but avoids fluid overload to decrease the risk of cerebral edema. Measure his central venous pressure, and record intake and output accurately.
  • Position the patient carefully to prevent joint stiffness and neck pain. Turn him often, according to a planned positioning schedule. Help with ROM exercises.
  • Maintain adequate nutrition and elimination.

Neurologic disorders: Keep it quiet…

Focus topic: Neurologic disorders

  • Maintain a quiet, comfortable environment. If necessary, darkening the room can help reduce photophobia.
  • Relieve headache with a nonopioid analgesic, such as acetaminophen, as ordered. (Opioids interfere with accurate neurologic assessment.)

Neurologic disorders: …and strictly aseptic

Focus topic: Neurologic disorders

  • Use strict aseptic technique when treating the patient with a head wound or skull fracture.
  • Provide reassurance and support. The patient may be frightened by his illness and the need for frequent lumbar punctures. If he’s disoriented or confused, calm and reorient him as often as needed. Reassure the family that the delirium and changes in behavior caused by meningitis usually disappear during recovery. However, if a severe neurologic deficit appears permanent, refer the patient to a rehabilitation program as soon as the acute phase of the illness has passed.
  • Evaluate the patient’s progress. If treatment is succeeding, the patient will be pain-free and his LOC will be normal. He’ll maintain adequate hydration and nutrition and his blood pressure, heart rate, and respiratory rate will remain within normal limits.

Neurologic disorders

Neurologic disorders

Neurologic disorders: Multiple sclerosis

Focus topic: Neurologic disorders

MS is a major cause of chronic disability in young adults. It results from progressive demyelination of the white matter of the brain and spinal cord and is characterized by exacerbations and remissions. The prognosis varies. MS may progress rapidly, disabling patients by early adulthood or causing death within months of onset. Fortunately, however, 70% of all patients lead active, productive lives with long periods of remission.

What causes it

The exact cause is unclear; however, current theories suggest that it may be caused by an autoimmune response to a slow-acting or latent viral infection or by environmental or genetic factors.

Pathophysiology

In MS, axon demyelination and nerve fiber loss occur in patches throughout the CNS, inducing widely disseminated and varied neurologic dysfunction.

What to look for

Accurate diagnosis requires evidence of multiple neurologic exacerbations and remissions. Signs and symptoms, which can vary considerably, include:

  • vision disturbances, such as optic neuritis, diplopia, ophthalmoplegia, and blurred vision
  • sensory impairment such as paresthesia
  • muscle dysfunction, such as weakness, paralysis ranging from monoplegia to quadriplegia, spasticity, hyperreflexia, intention tremor, and gait ataxia
  • urinary disturbances, such as incontinence, frequency, urgency, and frequent infections
  • emotional lability, such as mood swings, irritability, and euphoria
  • associated signs, such as poorly articulated speech and dysphagia.

What tests tell you

Because of the difficulty inherent in establishing a diagnosis, some patients may undergo years of periodic testing and close observation. These tests may help diagnose MS:

  • In one-third of all patients, EEG shows nonspecific abnormalities.
  • Lumbar puncture reveals CSF with elevated gamma globulin fraction of immunoglobulin G, but normal total protein levels. An elevated CSF gamma globulin level is significant only when serum gamma globulin levels are normal. It reflects hyperactivity of the immune system due to chronic demyelination. Oligoclonal bands of immunoglobulin can be detected when CSF gamma globulin is examined by electrophoresis.

Neurologic disorders: Evoking a reaction

Focus topic: Neurologic disorders

  • Evoked potential studies demonstrate slowed conduction of nerve impulses in 80% of patients.
  • A CT scan may reveal lesions within the brain’s white matter.

Neurologic disorders: Legions with lesions

Focus topic: Neurologic disorders

  • MRI is the most sensitive method of detecting lesions and is also used to evaluate disease progression. Lesions are present in more than 90% of all patients undergoing this test.

How it’s treated

The aim of treatment is to shorten exacerbations and relieve neurologic deficits to help the patient maintain as normal a lifestyle as possible. Drug therapy and other measures can achieve these goals.

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Neurologic disorders: Medicate, don’t exacerbate

Focus topic: Neurologic disorders

Methylprednisolone (Medrol) is commonly prescribed during acute exacerbations to reduce CNS inflammation. Other typically used corticosteroids include dexamethasone, prednisone, betamethasone (Celestone), and prednisolone (Prelone). For relapsing MS, glatiramer acetate (Copaxone) may be prescribed to reduce the frequency of attacks. Interferon beta-1a (Avonex) or interferon beta-1b (Betaseron) are effective in reducing disability progression and in decreasing the frequency of exacerbations.
In conjunction with corticosteroids, the practitioner may prescribe:

  • fluoxetine to combat depression
  • baclofen (Lioresal) or dantrolene (Dantrium) to relieve spasticity
  • oxybutynin (Ditropan) to relieve urine retention and minimize frequency and urgency.

Neurologic disorders: Support to cut short

Focus topic: Neurologic disorders

During acute exacerbation, treatment routinely calls for:

  • bed rest
  • physical therapy and massages
  • measures to prevent fatigue
  • meticulous skin care to prevent pressure ulcers
  • bowel and bladder training (if necessary)
  • antibiotic treatment of bladder infection
  • counseling.

What to do

  • Nursing interventions focus on maintaining mobility, ensuring proper nutrition, and controlling pain during exacerbations.
  • Form a care plan based on the patient’s abilities and symptoms.
  • Help with physical therapy and provide massages, relaxing baths, and other measures that promote comfort.
  • Assist with active, resistive, and stretching exercises to maintain muscle tone and joint mobility, reduce spasticity, improve coordination, and boost morale.
  • Encourage emotional stability by helping the patient establish a daily routine that maintains optimal functioning. Let the patient’s tolerance regulate the level of daily activity. Encourage daily physical exercise and regular rest periods to prevent fatigue.
  • Watch for drug therapy adverse effects.

Neurologic disorders

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