Digiulio M., Keogh J. Medical-Surgical Nursing Demystified
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CHAPTER 5 Nervous System
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Administer corticosteroids:
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methylprednisolone intravenously
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prednisone 60 to 80 mg daily the first week, then tapered over the next
couple of weeks
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dexamethasone
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Administer one of the following for muscle relaxation:
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dantrolene
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baclofen
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carisoprodol
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metaxalone
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tizanidine
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diazepam
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Use of the following medications may help with fatigue symptoms:
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modafinil
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methylphenidate
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Administer antidepressants if indicated:
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fluoxetine (selective serotonin reuptake inhibitor—SSRI)
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sertraline (SSRI)
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paroxetine (SSRI)
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citalopram (SSRI)
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escitalopram (SSRI)
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venlafaxine (inhibits norepinephrine, serotonin, and dopamine reuptake)
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bupropion (inhibits norepinephrine and dopamine reuptake)
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duloxetine (inhibits norepinephrine and serotonin reuptake)
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amitriptyline (tricyclic) may help with discomfort associated with pares-
thesia
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Administer medications to help with altered bladder function:
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oxybutynin
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hyoscyamine sulfate
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darifenacin
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solifenacin
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tolterodine
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Remove antibodies by removing plasma (plasmapheresis).
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NURSING DIAGNOSES
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Impaired physical mobility
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Fatigue
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Self-care deficit
NURSING INTERVENTION
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Monitor motor movements for interference with ADLs.
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Encourage activity balanced with rest periods.
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Assess cognitive function for changes, or deterioration.
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Explain to the patient:
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Bladder training.
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Teach self-catheterization if necessary (for patients with flexic bladder).
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Increase fluid intake unless other medical problems contraindicate.
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Importance of positioning.
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Avoid temperature extremes.
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Medication compliance.
Myasthenia Gravis
WHAT WENT WRONG?
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.
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CHAPTER 5 Nervous System
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.
HALLMARK SIGNS AND SYMPTOMS
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Ptosis (drooping of the eyelid) due to muscular weakness
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Diplopia (double vision) due to inability to keep both eyes focused on the
same object
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Trouble closing eyes completely; dry eyes due to muscle weakness
•
Difficulty swallowing (dysphagia) due to muscle weakness
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Muscle weakness later in the day due to fatigue
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Proximal muscle weakness
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Fatigue
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In advanced disease—loss of bowel and bladder control; difficulty with res-
piratory function
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Myasthenic crisis is an exacerbation of symptoms due to insufficient
medication:
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Tachycardia
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Tachypnea
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Elevated blood pressure
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Cyanosis
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Decrease in urinary output
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Incontinence of bowel and bladder
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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
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Twitching of facial muscles
•
Small pupils (miosis)
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Low blood pressure
INTERPRETING TEST RESULTS
Symptoms are relieved temporarily after administering endrophonium (Tensilon)
or neostigmine bromide (Prostigmin) because the drug will allow the acetylcholine to
bind at the post-synaptic receptor site on the muscle at which it should normally bind.
•
Acetylcholine receptor antibodies are present in greater than 80 percent of
patients with myasthenia gravis.
•
Electromyography (EMG) shows reduced muscle response to repeated
stimulations.
•
CT scan to rule out thymoma.
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
•
pyridostigmine
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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.
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CHAPTER 5 Nervous System
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).
•
Alcohol may exacerbate symptoms.
Parkinson’s Disease
WHAT WENT WRONG?
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
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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.
HALLMARK 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
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CHAPTER 5 Nervous System
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Orthostatic hypotension due to lack of norepinephrine within the sympa-
thetic nervous system, affecting the cardiovascular system
INTERPRETING TEST RESULTS
•
Cerebrospinal fluid levels may show low levels of dopamine.
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.
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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.
Spinal Cord Injury
WHAT WENT WRONG?
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.
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PROGNOSIS
The level of injury will determine the degree of disability the patient is likely to sus-
tain. A high-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.
HALLMARK 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
INTERPRETING TEST RESULTS
•
MRI shows vertebral or spinal cord injury and edema.
•
CT scan shows vertebral or spinal cord injury and edema.
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
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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.