Neuro Study Guide

Multiple Sclerosis (MS)

Etiology Chronic, immune-mediated, progressive, degenerative disorder
of the CNS.

Chronic inflammation, demyelinization nerve fibers of brain and

spinal cord, and scarring (gliosis) in the CNS

Increased incidence in northern Europe, northern U.S., southern

Canada, southern Australia, and New Zealand

Primarily in young adults aged 20-40 years of age, women

more frequently than men

May have genetic predisposition: cluster of HLA on cell wall is

present

T-lymphocytes/B lymphocytes are activated and travel to the

CNS crossing the blood brain barrier and causing an antigen-
antibody response that causes inflammation of axons and
progressive loss of myelin, the disappearance of
oligodendrocytes, and > in astrocytes; causes > plaque
formation (sclerosis) and plaques scattered throughout
multiple sites of the CNS

Early in the disease:

myelin of the brain and spinal cord are attacked
myelin sheath is damaged
nerve fiber not affected  impulses still transmitted.
Pt. c/o weakness, but myelin regenerates and s/s
disappear and remission occurs

If glial scar tissue formed:

hard sclerotic plaques found in multiple regions
myelin loss  slowed nerve impulses, destruction of axons, and
total impulse blocking=permanent loss of function

Signs/Symptom Vague S/S that occur intermittently over months/years

s
Progressive deterioration or others have remissions and
exacerbations. With each exacerbation there is > scarring,
 resulting in > neurological deficits

S/S depend on areas involved=motor, sensory, cerebellar,

emotional problems

Motor
fatigue, weakness/numbness, paralysis of limbs, trunk,
head, loss of balance, difficulty in co-ordination, spasticity
Sensory
numbness, tingling, paresthesias, dysesthesia(abnormal
sensations) vertigo, blurring of vision, diplopia,scotoma
(patchy blindness)/total blindness, tinnitus, < hearing,
neuropathic pain
Cognitive/Pychosocial
memory loss, decreased concentration
Bowel/bladder elimination
may be constipation; urinary problems=spastic bladder,
or flaccid bladder

Spastic: lesion above the 2nd sacral vertebrae, which cuts

inhibiting influences on bladder contraction; =urgency
and frequency=dribbling/incontinence
Flaccid: lesion in reflex arc controlling bladder function;
no sensation to void and no pressure, no pain; urinary
retention results

Sexual dysfunction
Spinal cord involved <libido for women, <orgasmic
response, painful intercourse, < vaginal lubrication

Pregnancy can result in remission/exacerbation

Intellectual functioning intact

Emotional stability
anger, depression, or euphoria; aggravated by emotional,
physical trauma; fatigue; infection

Tests No definitive diagnostic test

Dx based on history, clinical S/S.

& Presence of lesions over time as seen in MRI

In the CSF:
increased oligoclonal IgG
increased lymphocytes
 increased monocytes

Evoked potential studies=delayed in persons with MS d/t <

nerve conduction form eye/ear to brain

Urodynamic studies to assess bladder dysfunction

Nursing Exacerbations may =worsening of disease

implications
Triggers=infections like UTI, URI; trauma; immunization,
pregnancy, stress, climate change(heat/cold)

Usually enter hospital with acute exacerbation=CBR and focus is

on preventing problems of immobility
Speech therapy for cranial nerve involvement
Visual problems=patch the eye, large print, etc.
Family counseling often needed

Physical Immobility Interventions

Relaxation and coordination exercises

Progressive resistive exercises to strengthen weak

muscles

Warm packs to relieve adductor spasms of hips and

knees; avoiding cold

Hot baths > risk of injury d/t loss of sensation

Promote a daily exercise routine(swimming , stationery

bicycle)

No extreme exercise and plan rest periods

Monitor skin closely for breakdown/ Encourage deep

breathing exercises

Prevention of injury
Walk with feet apart to widen base of support

Watch feet while walking

Assistive devices (walker, cane, braces, crutches)

Wheelchair/motorized scooter
 Refer to occupational therapist

Bowel and Bladder Control

Inability to store urine or inability to empty urine or both
issues

If urgency, client needs to have bedpan/urinal available

(female urinal) ; external condom catheter

Voiding schedule(read p. 1961)

Intermittent self-catheterization

Bowel issues=adequate fluids (at least 2000 ml/day),

dietary fiber, bowel training program

Communication
If slurring of speech, low volume of speech, and difficulty
in phonation occur, and/or dysphagia, contact speech
therapist .

Reinforce the speech therapist’s plan

Sensory/ Cognitive Function

Vision=Eye patch or covered eye lens for diplopia

Prism glasses for bedridden client to read in supine

position

Large print books

Talking books
Emotional Responses
Some clients are forgetful and easily distracted

Some have emotional liability

Family is affected and needs support to understand the

emotional changes.

Hobbies to assist outlook of the client

Memory aids (lists, a routine)

The unpredictability of the disease is stressful for clients

and families
 Sexual Function
Many issues=fatigue, erectile disorder,ejaculatory
problems for the male, and adductor spasms of the thigh
muscles for the female interfere with normal sexual
function

Bowel/bladder incontinence/UTI add to the problems

If needed, referral to a sexual counselor for enhancing

communication between spouses can help.

Teaching
Avoid extremes of heat and cold
Avoid fatigue
Avoid others with infection
Nutritious diet
Measures to increase mobility(assistive devices)
Medications, administration of SQ, and what to look for as
far as side effects, or OTC interactions
Self catheterization; >roughage for bowel elimination
Check homecare checklist, chart 64-4, p. 1963

Treatments & Providing symptomatic relief with drugs

Medications
Corticosteroids=shorten duration of relapse

Immunomodulators
interferon beta 1a(Rebif) given
interferon beta-1b(Betaseron)administered SQ
interferon beta 1a (Avonex) given IM once /week

Side effects of the immune drugs are flulike.

Rx with Tylenol, motrin and SE end after a few months,
potential liver damage, fetal abnormalities, depression;
Immunosuppressant copaxone < no. of plaques noted on
MRI;IV prednilosone IV and then tapered.

Spasticity treated with

Baclofen(Lioresal): a gamma-aminobutyric acid (GABA)
Benzodiazepines (Valium)
tizanidine(Zanaflex)
Dantrolene(Dantrium)
 Fatigue treated with
Amantadine(Symmetrol)

Ataxia treated with

beta-adrenergic blockers(Inderal)
and antiseizure drugs (Neurontin, Klonopin)

UTI protection treated with

Ascorbic acid

Nursing Dx Impaired physical mobility r/t muscle weakness , muscle paresis,

spasticity

Risk for injury r/t sensory and visual impairment

Impaired urinary and bowel elimination r/t nervous system

dysfunction

Impaired verbal communication and risk for aspiration r/t

cranial nerve involvement

Disturbed thought processes r/t cerebral dysfunction

Ineffective coping r/t uncertainty of course of MS

Impaired home maintenance management r/t physical,

psychological, and social limits imposed by MS

Potential for sexual dysfunction r/t lesions or psychological

reaction to MS

Myasthenia Gravis
Etiology autoimmune disease of the neuromuscular junction
characterized by fluctuating weakness of certain voluntary
muscle groups
 Approximately 60,000 people in the US

Occurs ages 10-65; the peak age is for women aged 20-40; it is
three times more common in women
Antibodies attack acetylcholine (Ach) receptors and this results
in a decreased number of Ach receptors at the neuromuscular
junction site

Ach doesn’t attach to receptor sites on the motor endplate to

then stimulate muscle contraction

Anti-Ach receptor antibodies are found in 80-90% of clients with

generalized MG and 50% of clients with ocular MG; 80% have
thymic hyperplasia or thymic tumors

Signs & Fluctuating weakness of skeletal muscle strength which is

Symptoms restored after a period of rest

Muscles moving the eyes are affected causing:

diplopia,
ptosis (eye lids dropping)
swallowing and chewing can be affected
dysphonia (speaking becomes weak, muffled, and has a nasal
quality)
breathing can be affected
90% of the eyelid muscles affected and extra-ocular muscles
affected; facial mobility and expression affected; the smile
becomes a snarl

Muscles of the trunk and limbs are less affected and more often
the muscles of the neck, shoulder, and hip are affected

No sensory losses, reflexes are normal, and muscle atrophy

is rare

The course of the disease is variable=for some clients it’s a short

term problem and others severe, progressive involvement

Exacerbations occur due to stress, pregnancy, menses,

illness, trauma, extremes in temperature, loss of K+

The drugs a client is taking can increase the s/s.

Examples are:
aminoglycosides(ie.amikacin, gentamycin )
beta-adrenergic blocking agents(ie. dobutamine
 [dobutrex], terbutaline [brethine] )
procainamide(procanbid)
quinidine(quinidex)
dilantin

Tests Tensilon test

IV Tensilon is administered and the client will experience
improved contractility.

This Anticholinesterase (acetylcholinesterase

inhibitor)drug blocks the enzyme acetylcholinesterase
which breaks down acetylcholine .

This increases the amount of acetylcholine that is

available to enter receptor sites.

Then contraction improves and resolves facial weakness

and ptosis for about 5 minutes .

This represents a positive test and confirms myasthenia

gravis.

Tensilon Test verifies myasthenic crisis versus

cholinergic crisis (Atropine will improve a cholinergic
crisis)

They keep atropine available to reverse side effects

of bradycardia, sweating, and cramping.

Presence of acetylcholine receptor antibodies

MRI shows enlarged thymus gland

EMG detects a delay or failure of neuromuscular transmission

and 99% effective in confirming diagnosis

Nursing Tensilon Test verifies myasthenic crisis versus cholinergic crisis

Implications (Atropine will improve a cholinergic crisis)

They keep atropine available to reverse side effects of

bradycardia, sweating, and cramping.

Myasthenic Crisis:
An acute exacerbation of muscle weakness triggered by
 infection, surgery, emotional stress, or overdose or
underdose of drug therapy

Major concern=Swallowing and breathing=aspiration,

respiratory insufficiency, respiratory infection

S/S=tachycardia, tachypnea, severe respiratory

distress, dysphagia, restlessness, impaired speech,
and anxiety
—Assess for fatigue of muscle groups=face, limbs

—Assess swallowing, cough, and gag reflexes

—Monitor respiratory rate, depth, O2 saturation level

—Assess speech (volume and clarity)

—Often seen in the hospital for myasthenic
crisis=triggered by respiratory infection

—Key is adequate ventilation, may require intubation

and mechanical ventilation, do plasmapheresis or IVIG at
this time

—Do chest physiotherapy

—May require nutritional support=NG tube

—Avoid sedatives and tranquilizers as they aggravate

hypoxia, hypercapnia, and can cause respiratory and
cardiac depression

Cholinergic Crisis
—Due to overdose of anticholinesterase (cholinergic)
medications

—S/S=GI symptoms, severe muscle weakness, vertigo,

respiratory distress

—If Atropine is given and S/S diminish, it is a cholinergic

crisis

NURSING CARE:

—Assess response to therapies

—Teach that to manage the disease the maintenence of

 stable blood levels of anticholinesterase medications is
imperative to stabilize muscle strength; strict schedule to
be maintained so client doesn’t become too weak to take
med. orally

—Diet=in myasthenic crisis may need aspiration

precautions, and alternate feeding approaches ; if able to
swallow have foods that are easily swallowed; should rest
before meals, sit upright with neck slightly flexed, have
suction available; eat at peak of medication’s effect

—Visual interventions=eye patch, artificial tears, taping

—Teach to conserve energy; assess living arrangements

—Avoidance of activities that add stress=emotional
stress, exposure to infections, vigorous physical exercise,
increased temperature

—Offer Myasthenia Gravis Foundation support group

Treatments & Anticholinesterase medications

Medication neostigmine (Prostigmin)

Pyridostigmine(Mestinon)
dose gradually increased to a daily maximum and
administered in divided doses (usually 4 times/day)
Many adverse side effects:

CNS=irritability, anxiety, insomnia, headache, dysarthria,

syncope, seizures, coma, diaphoresis

Respiratory=bronchial relaxation, > bronchial

secretions; cardiovascular=tachycardia, <BP

GI=abdominal cramps, nausea, vomiting, diarrhea,

anorexia, > salivation

skeletal muscles= fasciculations, spasms, weakness;

Genitourinary=frequency, urgency;
Integumentary=rash, flushing
 Steroids
prednisone(initial dose daily then tapered, and possibly a
maintainence dose)

Azathioprine (Imuran) (inhibits T lymphocytes and <

acetylcholine receptor site antibodies) 3-12months to be
effective; check leukopenia, hepatotoxicity

Extreme care when giving medications due to respiratory issues.

Alert when giving anesthetics, anti-arrhythmics, antibiotics,
quinine, barbiturates, sedative-hypnotics

Intravenous immune globulin (IVIG) for exacerbations

Consult with dr. with new medication orders as can exacerbate

symptoms of Myasthenia Gravis ie. Antibiotics, antiseizure
meds., morphine, quinine, beta-blockers, procaine(notify
dentist)

Surgery:
Thymus gland increases release of Ach receptor antibodies and
can do thymectomy surgery

Thymectomy for tumors, p. 1965

Plasmapheresis(plasma exchange)=< of circulating antibodies

Nursing Ineffective breathing pattern r/t intercostal muscle weakness

Diagnosis
Ineffective airway clearance r/t intercostal muscle weakness
and impaired cough and gag reflex

Impaired verbal communication r/t weakness of the larynx, lips,

mouth, pharynx, and jaw

Imbalanced nutrition: less than body requirements r/t impaired

swallowing

Disturbed sensory perception(visual) r/t ptosis, decreased eye

movements, disconjugate gaze

Activity intolerance r/t muscle weakness and fatigability

 Disturbed body image r/t inability to maintain usual lifestyle
and role responsibilities

Anxiety r/t body changes and loss of control

Guillain-Barre Syndrome
Etiology is an autoimmune attack on peripheral nerve myelin. It affects
peripheral nerves and cranial nerves.

It results in the loss of myelin, edema and inflammation of the

affected nerves, and causes a loss of nuerotransmission to the
periphery.

1 to 2 cases per 100,000

More frequent in males between 16-25 years of age and 45-60

years of age

60-75% recover completely; residual deficits in 20-25% of

patients

Immune cells become sensitized and destroy myelin;

demyelination occurs and muscles innervated by damaged
peripheral nerves atrophy; recovery can take place and nerves
remyelinate; occurs from proximal to distal

Signs & ascending weakness,

Symptoms dyskinesia(inability to execute voluntary movements);
hyporeflexia( diminished reflexes)
paresthesias(numbness).
Tests CSF can elevated protein levels

Normal protein initially and then in 7-10 days elevates to a

protein level of 700 mg/dl (normal protein is 15-45mg/dl)

EMG abnormal=< nerve conduction

Changes of vital capacity

Nursing Triggering events:

Implications Viral infection with Campylobacter jejuni,
cytomegalovirus, EpsteinBarr , Mycoplasma pneunoniae,
H. influenzae, and HIV

—Begins with muscle weakness and < reflexes of the lower

extremities and progresses upward

—If demyelination of nerves that innervate the diaphragm

occurs, then respiratory failure can take place

—Sensory symptoms of paresthesias of hands and feet

—Pain d/t demyelination

—Cranial nerve 1=optic nerve demyelination=can result in

blindness

—Glossopharngeal/Vagus nerve involvement=inability to

swallow or clear secretions; cardiac instability

—No change in alertness or LOC

—History of viral illness in previous few weeks

Treatments & ACUTE CARE:

Medication —Ventilator in ICU=close respiratory assessment; ABG’s;
suctioning, chest physio, incentive spirometer

—Check gag reflex, corneal reflex, swallowing reflex,

suctioning

—Plasma exchange(Plasmapheresis) in first 2 weeks

—IV immunoglobulin(Sandoglobulin)IVIG

—Care with feeding d/t dyphagia=upright with flexed

head or tube feeding; paralytic ileus use TPN; get
nutritional assessment data=weight, serum albumin,
calorie count, IV replacement

—Prevent immobility complications:

anticoagulants/anti-embolism stockings, monitor for
DVT, passive ROM
 EKG Monitoring

Communication system with patient

Monitor for infection and give antibiotics

Urinary retention=intermittent catheterization

Physical therapy for immobility; ROM

Facial nerve involvement=eye care

Bowel elimination assessment

Monitor vital signs=risk for tachycardia, bradycardia;

check <BP & use IV fluid to correct; check for>BP,
arrhythmias=use of alpha adrenergic blocking agents for
tachycardia/HPN

HOME CARE:
—Check Chart 64-6, p. 1969
—Rehabilitation in a center or plans for this at home often are
required
—Family members need to be a part of the plan

Nursing Ineffective breathing pattern and impaired gas exchange related

Diagnosis to rapidly progressive weakness and impending respiratory
failure

Impaired bed and physical mobility related to paralysis

Imbalanced nutrition, less than body requirements, related to

inability to swallow

Impaired verbal communication r/t intubation or cranial nerve

dysfunction

Fear and anxiety r/t loss of control and paralysis

 Self-care deficits r/t inability to use muscles to accomplish
activities of daily living

Parkinson’s Disease
Etiology Parkinson’s disease (PD) is a slowly progressing neurologic
movement disorder. Associated with < levels of dopamine
resulting form destruction of pigmented neuronal cells in the
substantia nigra to the corpus striatum

Through the neurotransmiters acetylcholine(excitatory) and

dopamine(inhibitory)striatal neurons relay messages to higher
motor centers that control motor movements

Signs &
Symptoms
Tests
Nursing
Implications
Treatments &
Medication
Nursing
Diagnosis

Amyotrophic Lateral Sclerosis

Etiology ALS (Lou Gehrig’s Disease) is a disease of unknown cause.

A loss of motor neurons in the anterior horns of the spinal cord

and motor nuclei of the lower brain stem occurs. With the death
of motor neurons, muscles undergo atrophic changes.

Signs & Depends on the affected motor neuron

Symptoms Chief symptoms:
Fatigue, progressive muscle weakness, cramps,
fasciculations (twitching) and incoordination

With loss of motor neurons in the anterior horns of the spinal

cord, progressive weakness of the muscles of the arms, trunk, or
legs occurs.

Deep tendon reflexes become brisk and overactive

No bladder/bowel loss of control

 25% of clients have weakness start in the muscles supplied by
the cranial nerves difficulty talking, swallowing, breathing .

This results in regurgitation of fluids through the nose,

inability to laugh, cough or blow the nose, problems with
speaking, swallowing. Some experience cognitive
problems.

Death due to compromised respiratory function resulting in

infection, respiratory failure, or aspiration.

Tests
Nursing The diagnosis is made based on the signs and symptoms.
Implications
Electromyography and muscle biopsy studies of affected
muscles show < in the no. of functioning motor units

MRI scan shows high signal intensity in the corticospinal tracts

The average survival time is 3-5 years

Focus is on maintaining function, promoting well-being, and

quality of life

Riluzole(Rilutek) a glutamate antagonist is the only medication

apporoved by the FDA . How it works is unclear ,but it is
suggested that it has neuroprotective quality in early stages of
ALS.

Common hospital admissions include:

Dehydration
Malnutrition
Pneumonia
Respiratory Failure

At advanced stage, family/client face end-of-life issues=pain

management, mechanical ventilation, enteral feeding

Speak about advance directive=“living will”

Make Amyotrophic Lateral Sclerosis Association available as a

resource to families
Treatments & Riluzole (Rilutek) a glutamate antagonist is the only
Medication medication apporoved by the FDA .
How it works is unclear, but it is suggested that it has
neuroprotective quality in early stages of ALS.

Used for Spasticity and relieves pain associated with this:

Bacolfen (Lioresal)
dantrolene sodium (Dantrium)
diazepam(Valium)

Home management for the majority of clients but hospitalized

for acute problems

Nursing
Diagnosis

Bell’s Palsy
Etiology cranial nerve disorder characterized by facial paralysis.

Peripheral involvement of the 7th cranial nerve (facial nerve)

produces weakness or paralysis of the facial muscles.

The cause of this condition is unknown, but the majority of

patient's have experienced a viral upper respiratory infection 1
to 3 weeks prior to the onset of symptoms.

Complications associated with Bell's palsy include facial

weakness, facial spasm with contracture, corneal ulceration, and
blindness.
Signs & Distortion of face.
Symptoms
Numbness of face and tongue.

Overflow of tears down the cheek from keratitis caused by

drying of cornea and lack of blink reflex.

Tests
Nursing Decreased tear production that may predispose to infection.
Implications Speech difficulty secondary to facial paralysis.

Maintain muscle tone of the face.

Prevent or minimize denervation.
Protect the involved eye.
 If blink reflex is absent, eye is vulnerable to dust and foreign
particles
Instill artificial tears (methylcellulose) to protect the cornea.
Increase environmental humidity.
Instruct patient to close affected eye frequently using accessory
facial muscles
Instruct patient to wear a protective patch at night. (Keep in
mind
that patch may eventually abrade cornea as paralyzed eyelids
are difficult to keep closed.)

Instruct patient to wear protective glasses to further protect eye

and decrease normal evaporation of moisture from eye.
 
Administer steroid therapy, as ordered. (May reduce
inflammation and edema and restore normal blood circulation to
the nerve.)
Provide for pain relief with analgesics and local application of
heat.
Facial massage may be prescribed to help maintain muscle tone.
Surgical intervention may be necessary: Decompression of facial
nerve, Surgical correction of eyelid deformities.

Treatments &
Medication
Nursing
Diagnosis

Trigeminal Neuralgia
Etiology also known as Tic Douloureux, is a disorder of the 5th cranial
nerve (trigeminal nerve). It is characterized by sudden
paroxysms of burning pain along one or more of the branches of
the trigeminal nerve. The pain alternates with periods of
complete comfort.

Signs & Sudden, severe pain appearing without warning. (Along

Symptoms one or more branches of trigeminal nerve.)

Numerous individual flashes of pain, ending abruptly and

usually on one side of the face only.

Attacks provoked by pressure on a "trigger point" (the

terminals of the affected branches of the trigeminal
nerve). Such triggers include:
 (a) Shaving.
(b) Talking.
(c) Yawning.
(d) Chewing gum.
(e) Cold wind.

Tests

Nursing Instruct patient to avoid exposing affected cheek to

Implications sudden cold if this is known to trigger the nerve. For
example, avoid:
(a) Iced drinks.
(b) Cold wind.
(c) Swimming in cold water.
Administer drug therapy, as ordered.
(a) Tegretol or Dilantin--relieves and
prevents pain in some patients.
(b) Serum blood levels of drug are
monitored in long term use.
Surgical procedures to sever the affected nerve provide
optimum pain relief with minimum impairment.

Instruct patient in methods to prevent environmental

stimulation of pain.
(a) Eat foods that are easily chewed and are
served at room temperature.
(b) Avoids drafts and breezes.

Treatments &
Medication
Nursing
Diagnosis