MULTIPLE SCLEROSIS AND PARKINSONS DISEASE

MULTIPLE SCLEROSIS
PATHOPHYSIOLOGY
Chronic progressive, degenerative neuromuscular disease that is
characterized by inflammation of the white matter of the CNS.
Usually affects young to middle aged adults, with onset between 15 -10 years
of age
Women are more affected than men
Cause is unknown, however it may be related to infectious, immunological,
dietary deficiencies (Vitamin D), and genetic factors.
Possible precipitating factors include:
o Infection
o Physical injury
o Emotional stress
o Excessive language
o Pregnancy
o Poor state of health
Disease process consists of loss of myelin, disappearance of
oligodendrocytes, and proliferation of astrocytes.
Changes result in plaque formation, with plaques scattered throughout the
CNS.
Client may complain of noticeable impairment of function.
Nerve impulse slows down without myelin. With the destruction of axons,
impulses are totally blocked, resulting in permanent loss of nerve function.
CLINICAL MANIFESTATION
Symptoms are characterized by chronic, progressive deterioration in some
clients, with remission and exacerbations in others.
Common sign and symptoms of MS include the following:
o Motor manifestations, which may include:
Weakness or feelings of heaviness in the legs
Paralysis of limbs
Diplopia
Hyper-reflexia
Spasticity of muscles and sensory
Cerebellar and neurobehavioural problems
o Sensory manifestations which may include:
Numbness and tingling
Blurred vision
Vertigo
Tinnitus
o Cerebellar manifestations which may include:
Nystagmus
Ataxia

 Dysarthria
Dysphagia
o Other symptoms may include optic neuritis, and fatigue. Sexual
dysfunction can also occur with MS.
o Bladder control is the major problem for many clients with MSalthough anticholinergic drugs is beneficial to decrease spasticity,
other clients may need to be taught catheterization.
o Bowel problems, particularly constipation, occur frequently in clients
with MS- increasing dietary fibre intake may help clients achieve
regularity in bowel habits.
DIAGNOSTIC
Based on history and clinical manifestations and the presence of multiple
lesions over time as measured by MRI and CT scan
Laboratory test will show an increase in activated T4 lymphocytes and IgG
content
THERAPEUTIC AND NURSING CONSIDERATIONS
The goal of treatment is to maintain the clients independence for as long as
possible. Drug therapy for the treatment of MS includes:
o Corticosteroids, which are used to treat acute exacerbations by
reducing edema and inflammation at the site of demyelination
o Immunosuppressive therapy, secondary-progressive, and primaryprogressive type of MS
o Immunomodulators include interferon-beta 1b (Betaseron),
interferon-beta-1a (Avonex), glatiramer (Copaxone), natalizumab
(Antagren) and mitoxantrone (Novantrone).
o Antispasmodics, CNS stimulants, anticholinergics, tricyslic
antidepressants, and antiseizure medications may also be prescribed.
o Muscle relaxants
Surgical interventions such as:
o Neurectomy
o Rhizotomy or cordotomy, or dorsal column electrical stimulation may
be required of spasticity is not controlled with antispasmodics
Neurological dysfunction sometimes improves with physical therapy and
speech therapy
Nutritional therapy prescribed high protein diet with supplementary
vitamins
Clients will be encouraged to balance rest with activities and maintain
optimal nutrition
As condition progresses, symptomatic treatment and assistance will be
needed.
Support group for MS has been very beneficial for clients and their families.
PLANNING
1. Maximize neuromuscular function

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3.
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Maintain independence in activities of daily living for as possible

Manage disabling fatigue
Optimize psychological well-being
Adjust to the illness
Reduce factors that precipitate exacerbations.

SKELETAL MUSCLE RELAXANTS

Depress the CNS by blocking nerve impulse that cause muscle tone and
contraction.
Primary use is for muscle spasm
o Baclofen (lioresal) is used to treat the spasticity of MS and spinal cord
injury
o Dantrolene (Dantrium) inhibits muscle contraction relieving the
muscle spasticity and malignant hypertension. (the safety of these
drugs for children 12 years and under has not been established)
o Diazepam (Valium) is used for muscle spasms and inflammation
o Methocarbamol (Robaxin) is used for muscle spasm and inflammation
Nursing consideration relating to Muscle relaxants
o Use all safety precautions relating to drugs that produce CNS
depression
o Teach client about avoiding dangerous activities that require
alertness and quick reflexes.
PARKINSONS DISEASE
PATHOPHYSIOLOGY
Disease of the basal ganglia characterized by slowing down in the initiation
and execution of movement (bradykinesia), increased muscle tone (rigidity),
tremor at rest, and impaired postural reflexes.
Diagnosis of Parkinsons increases postural reflexes.
More common in men than in women and is caused by the following
conditions:
o Onset of parkinsons before age 50 is usually due to a genetic defect
o In many cases, the cause of parkinsons is unknown
o Some cases are caused by exposure to toxins from drugs and
chemicals that destroy the cells in the substantial nigra of the brain.
o Other causes of Parkinsons include hydrocephalus, hypoxia,
infectious, stroke, tumour, and trauma.
Affects extrapyramidal system, which influences movement.
A dopamine deficiency occurs in the basal ganglia. Reduction of dopamine in
the corpus striatum upsets the normal balance between the dopamine
(inhibitor) and acetylcholine (excitatory) neurotransmitters.
Symptoms occur when affected brain cells can no longer perform their
normal inhibitory function within the CNS.

CLINICAL MANIFESTATION
Symptoms of the diseases do not occur until 80% of neurons in the
substantia nigra are lost. The classic triad manifestations includes, tremor,
rigidity, and bradykinesia
o Insidious tremor begins in the fingers (unilateral pillroll tremor). The
tremor is more prominent at rest and is aggravated by emotional
stress or increased concentration.
o Rigidity is caused by sustained muscle contraction and consequently
elicits complaints of soreness and feeling tired and achy. Rigidity
inhibits the alternating contraction and relaxation in opposing muscle
groups, slowing movement. The rigidity may be uniform or jerky
(cogwheel rigidity). The client may have difficulty walking with the
gait lacking normal parallel motion. Bradykinesia (slow and retarded
movement) is particularly evident.
o Other symptoms include a high-pitched, monotone voice, drooling, a
masklike facial expression, slow, slurred speech, and dysphagia.
Complications of Parkinsons are caused by progressive deterioration and
the negative impact this deterioration may have on the client. For example,
dysphagia can lead to malnutrition. Dementia occurs in up to 40% of clients
with Parkinsons.
DIAGNOSTIC
History and physical examination
Tremor
Rigidity
Bradykinesia
Positive response to antiparkinsonian drugs
Rule out the side effects pf phenothiazines, reserpine, benzodiazepines,
haloperidol.
There are no specific tests for diagnosing Parkinsons Diagnosis based solely
on the history and clinical features.
THERAPEUTICS AND NURSING CONSIDERATIONS
There is no cure for PD, collaborative management is focused on relieving the
symptoms.
The drug is aim at correcting imbalances of neurotransmitters within the
CNS. These drugs either enhance the release or supply of dopamine or
antagonize or block the effects of acetylcholine. The drug treatment are listed
below:
o Levodopa with carbidopa (Sinemet) is often the first drug used.
Levodopa is a precursor of dopamine and can cross the blood-brain
brarrier. It is converted to dopamine in the basal ganglia. Carbidopa
inhibits an enzyme that breaks down levodopa before it reaches the

brain. The effect of Sinemet could wear off after a few years of
therapy.
o Anticholinergics may be used in the management of Parkinsons.
o Antihistamines and antiviral agents are also used.
o As parkinsons progresses, a combination therapy is ofthen required.
Surgical therapy are aimed at relieving symptoms in client who are usually
unresponsivene to drug therapy. Ablation therapy has a large been replaced
by deep brain stimulation, which involves placing electrodes in the thalamus,
globus pallidus, or subthalamic nucleus. Both ablation and deep brain
stimulation procedures work by reducing the increased neuronal activity
produced by the dopamine depletion. Transplantation of fetal neural tissue
into the basal ganglia provides dopamine-producing cells in the brains of
client with parkinsons. This type of therapy is still experimenting.
Since malnutrition and constipation can cause serious consequences,
adequate nutrition is essential.
Clients with dysphagia and bradykenisia need food that is easily chewed and
swallowed. The clients need roughage. Small, frequent meals are best to
prevent fatigue. Ample time must be allowed for the client to eat and not
become frustrated.
Levodopa can be impaired by protein ingestion

PLANNING
Experience a lower intensity and frequency od distressing symptoms
Maximize neurological function
Maintain independence in activities of daily living for as long as possible
Optimize psychosocial well being.
ANTI-PARKINSONS DISEASE AGENTS
Aimed at increasing or enhancing the action of dopamine in the brain (using
dopaminergic agents) and inhibiting the action of (Ach with anticholinergic
agent) for the purpose of restoring the balance between dopamine and Ach.
DOPAMINERGIC AGENTS
These drugs increase the effects of dopamine at receptor sites in the
substantia nigra. Since dopamine cannot cross the blood-brain barrier, drugs
that act like dopamine or increase dopamine concentration are used.
o Levodopa (l-dopa) crosses the BBB where it is converted to dopamine.
Large amounts are broken down to dopamine prior to passing
through the BBB into the CNS. Levodopa given requires a high dosage
to produce the desired effects.
o Carbidopa inhibits the breakdown of levodopa outside the CNS,
allowing greater amounts of levodopa to enter the CNS. This effect
results in a lower-dosage requirement. Commonly, a levodopacarbidopa combination drugs is administered.

o Amantadine (Symmetrel) increase dopamine release and blocks the

reuptake of dopamine into the presynaptic neuron.
o Selegiline decrease the breakdown of dopamine by monoamine
oxidase B (MAO-B) inhibitors. Monoamine oxidase is an enzyme that
breaks down neurotransmitter.
o Entacapone decreased the breakdown of dopamine by COMT
(catechol-O-methytransferase, the enzyme that breaks down
levodopa).
Adverse effect:
o Nausea and vomiting
o Orthostatic hypotension
o Palpitations
o Dizziness
o Nervousness and agitation
o Muscle irritability
Beneficial effect is not seen until a few weeks after treatment begins.
Vitamin B6 facilitates the breakdown of levodopa, reducing levels outside the
CNS and limiting the amount of dopamine reaching the brain.

ANTICHOLINERGIC DRUGS
Oppose effect of Ach at the receptor sites in the substantia nigra and corpus
striatum, thus helping restore chemical balance in the area.
They also alleviate the tremors and rigidity associated with Parkinsons
disease. Examples include benztropine (Congentin) and trihexyphenidyl.
Adverse effects:
o Drowsiness
o Confusion
o Constipation
o Dry mouth
o Urinary retention
o Pupillary dilation
NURSING CONSIDERATIONS RELATING ANTIPARKINSONS DRUGS
Prior to administration, perform an assessment of health history for CNS, GI,
and urinary functioning and psychological state, such as swallowing, voiding
patterns, constipation, peptic ulcer disease, prostate enlargement,
depression, and so on, to identify possible contraindications or cautions.
Administer following meals and at bedtime with a full glass of water
Encourage regular mouth care due to drying effects
Tell clients to avoid foods high in vitamin B6 (such as spinach, bananas, liver
and sweet potato)
Teach importance of ingesting foods high in fibre to maintain regular GI
functioning and avoid constipation
Teach client that Entacapone will produce a brownish discoloration of the
urine that is normal

Observe for and chart desired and adverse effects experienced by clients
Encourage clients to report any undesirable effects that are experienced.