NEUROLOGICAL

DISORDERS
Multiple Sclerosis
• A chronic, progressive, noncontagious, degenerative
disease of the CNS characterized by demyelinization
of the neurons.
• neurodegenerative disease in which axonal loss is
the major cause of irreversible neurological disability
• It usually occurs between the ages of 20 and 40
years and consists of periods of remissions and
exacerbations.
Four main types of MS
• 1. Relapsing-remitting MS
• Symptoms in this type come in the form of
attacks. In between attacks, people recover or
return to their usual level of disability. When
symptoms occur in this form of MS, it is called
an attack, a relapse, or exacerbation.
• The periods of disease inactivity between MS
attacks are referred to as remission.
Four main types of MS
•2. Secondary-progressive MS
• People with this form of MS usually have
had a previous history of MS attacks but
then start to develop gradual and steady
symptoms and deterioration in their
function over time.
Four main types of MS
• 3. Primary-progressive MS
• less common and is characterized by
progressively worsening symptoms from
the beginning with no noticeable
relapses or exacerbations of the disease,
although there may be temporary or
minor relief from symptoms.
Four main types of MS
•4. Progressive-relapsing MS
• The rarest form of MS is characterized by
a steady worsening of symptoms from
the beginning with acute relapses that
can occur over time during the disease
course.
Causes

• unknown, but the disease is thought to be

the result of an autoimmune response or
viral infection.
Laboratory Findings
• The changes in brain electrical activity in EEG may detect
deteriorations of cerebral neurons in the form of slowing
in the background activity
• MRI scans of the brain and spinal cord to look for the
characteristic lesions of MS.
• Assessment of a lumbar puncture indicates an increased
gamma globulin level, but the serum globulin level is
normal.
Assessment
• Fatigue and weakness
• Ataxia and vertigo
• Tremors and spasticity of the lower extremities
• Paresthesias
• Blurred vision, diplopia, and transient blindness
• Nystagmus
Assessment
• Dysphasia
• Decreased perception to pain, touch, and temperature
• Bladder and bowel disturbances, including urgency,
frequency, retention, and incontinence
• Abnormal reflexes, including hyperreflexia, absent reflexes,
and a positive Babinski reflex
• Emotional changes such as apathy, euphoria, irritability, and
depression
• Memory changes and confusion
Interventions
• 1.Provide energy conservation measures during
exacerbation.
• 2.Protect the client from injury by providing safety
measures
• 3.Place an eye patch on the eye for diplopia.
• 4.Promote regular elimination by bladder and bowel
training.
• 5.Assist the client to establish a regular exercise and
rest program and to balance moderate activity with
rest periods.
Interventions
• 6.Instruct the client to avoid fatigue, stress, infection,
overheating, and chilling.
• 7.Instruct the client to increase fluid intake and eat balanced
diet, including low-fat, high-fiber foods and foods high in
potassium.
• 8.Instruct the client in safety measures related to sensory loss,
such as regulating the temperature of bath water and avoiding
heating pads.
• 9.Instruct the client in safety measures related to motor loss,
such as avoiding the use of scatter rugs and using assistive
devices.
Myasthenia Gravis
• A neuromuscular disease characterized by
considerable weakness and abnormal
fatigue of the voluntary muscles
• A defect in the transmission of nerve
impulses at the myoneural junction occurs.
Causes
•Insufficient secretion of acetylcholine
•Excessive secretion of cholinesterase
•Unresponsiveness of the muscle
fibers to acetylcholine.
Assessment
• Weakness and fatigue
• Difficulty chewing and swallowing
• Dysphagia
• Ptosis
• Diplopia
Assessment

• Weak, hoarse voice

• Difficulty breathing
• Diminished breath sounds
• Respiratory paralysis and failure
Interventions
• 1.Monitor respiratory status and ability to
cough and deep-breathe adequately.
• 2.Maintain suctioning and emergency
equipment at the bedside.
• 3.Monitor vital signs
• 4.Prevent aspiration
• 5.Encourage the client to sit up when eating.
Interventions
• 6.Plan short activities that coincide with times
of maximal muscle strength.
• 7.Monitor for myasthenic and cholinergic
crises.
• 8.Administer anticholinesterase medications as
prescribed.
• 9.Instruct the client to avoid stress, infection,
fatigue, and over-the-counter medications.
To diagnose myasthenia gravis
• Edrophonium injection is administered to the client.
• Positive for myasthenia gravis:
• Client shows improvement in muscle strength after the
administration of edrophonium.
• Negative for myasthenia gravis:
• Client shows no improvement in muscle strength, and
strength may even deteriorate after injection of
edrophonium.
Edrophonium (Tensilon) test
• *Have atropine sulfate available when performing the
edrophonium test.*
• This test is performed by the neurologist to diagnose
myasthenia gravis and to differentiate between
myasthenic crisis and cholinergic crisis.
• The test places the client at risk for ventricular
fibrillation and cardiac arrest; emergency equipment
needs to be available.
To differentiate crisis
• Myasthenic crisis:
• Edrophonium is administered and, if strength
improves, the client needs more medication.
• Cholinergic crisis:
• Edrophonium is administered and, if weakness is
more severe, the client is overmedicated; prepare
to administer atropine sulfate, the antidote, as
prescribed.
A.Myasthenic crisis

• An acute exacerbation of the disease

• The crisis is caused by a rapid,
unrecognized progression of the disease,
inadequate amount of medication,
infection, fatigue, or stress.
Assessment
• Increased pulse, respirations, and blood
pressure
• Dyspnea, anoxia, and cyanosis
• Bowel and bladder incontinence
• Decreased urine output
• Absent cough and swallow reflex
Interventions

•1.Assess for signs of myasthenic

crisis.
•2.Increase anticholinesterase
medication, as prescribed
B. Cholinergic crisis

• Results in depolarization of the motor

end plates
• The crisis is caused by overmedication
with anticholinesterase.
Assessment
• Abdominal cramps
• Nausea, vomiting, and diarrhea
• Blurred vision
• Pallor
• Facial muscle twitching
• Hypotension
• Pupillary miosis
Interventions
• 1.Withhold anticholinesterase
medication.
• 2.Prepare to administer the antidote,
atropine sulfate, if prescribed.
Medications
• Cholinesterase inhibitors.
• pyridostigmine (Mestinon, Regonal) enhance communication
between nerves and muscles.
• Corticosteroids
• prednisone (Rayos) inhibit the immune system, limiting antibody
production.
• Immunosuppressants
• azathioprine (Azasan, Imuran), mycophenolate mofetil (Cellcept),
cyclosporine (Sandimmune, Gengraf, others), methotrexate
(Trexall) or tacrolimus (Astrograf XL, Prograf, others).
Parkinson’s Disease
• A degenerative disease caused by the depletion of
dopamine, which interferes with the inhibition of excitatory
impulses, resulting in a dysfunction of the extrapyramidal
system.
• It is a slow, progressive disease that results in a crippling
disability.
• The debilitation can result in falls, self-care deficits, failure of
body systems, and depression.
• Mental deterioration occurs late in the disease.
Assessment
• Bradykinesia
• Akinesia
• Monotonous speech
• Handwriting that becomes progressively smaller
• Tremors in hands and fingers at rest (pillrolling)
• Tremors increasing when fatigued and decreasing with
purposeful activity or sleep
• Rigidity with jerky movements
Assessment
• Restlessness and pacing
• Blank facial expression; masklike faces
• Drooling
• Difficulty swallowing and speaking
• Loss of coordination and balance
Interventions
• 1.Assess neurological status.
• 2.Provide high-calorie, high-protein, high-fiber
soft diet with small, frequent feedings.
• 3.Assist with ambulation and provide assistive
devices
• 4.Encourage the client to lift the feet when
walking and to avoid prolonged sitting.
Interventions
• 5.Instruct in proper posture by teaching the
client to hold the hands behind the back to keep
the spine and neck erect.
• 6.Administer antiparkinsonian medications to
increase the level of dopamine in the CNS.
• 7.Instruct the client to avoid foods high in
vitaminB6
Medication
• Medication can be used to improve the main
symptoms of Parkinson's disease, such as shaking
(tremors) and movement problems.
• But not all the medications available are useful for
everyone, and the short- and long-term effects of each
are different.
• Three main types of medication are commonly used:
• levodopa
• dopamine agonists
• monoamine oxidase-B inhibitors
Medication
• Levodopa
• absorbed by the nerve cells in your brain and
turned into the chemical dopamine, which is
used to transmit messages between the parts
of the brain and nerves that control
movement.
• administered with carbidopa.
Medication
• Monoamine oxidase-B (MAO-B) inhibitors
• selegiline and rasagiline, are another
alternative to levodopa for treating early
Parkinson's disease.
• They block the effects of an enzyme or brain
substance that breaks down dopamine
(monoamine oxidase-B), increasing dopamine
levels.
Medication
• Catechol-O-methyltransferase inhibitors
• Catechol-O-methyltransferase (COMT)
inhibitors are prescribed for people in later
stages of Parkinson's disease.
• They prevent levodopa being broken down
by the enzyme COMT.
Guillain-Barŕe Syndrome
• An acute infectious neuronitis of the cranial
and peripheral nerves.
• The immune system overreacts to the infection
and destroys the myelin sheath.
• The syndrome usually is preceded by a mild
upper respiratory infection or gastroenteritis.
• The recovery is as low process and can take
years.
Assessment
• People with GBS usually first feel these symptoms in
both legs. Some people then have weakness and
tingling in their arms and upper body.
• Paresthesias
• Pain and/or hypersensitivity such as with the weight of
bed sheets or other items touching the body
• Weakness of lower extremities
• Gradual progressive weakness of the upper extremities
and facial muscles
Assessment

• Possible progression to respiratory

failure
• Cardiac dysrhythmias
• CSF that reveals an elevated protein
level
• Abnormal electroencephalogram
Causes

• Diarrhea or a respiratory illness

(Infection with Campylobacter jejuni)
• Viral infections: Some people with
GBS had the flu or infections with
cytomegalovirus, Epstein Barr virus,
Zika virus, or other viruses.
Treatment

• Plasma exchange
• High-dose immunoglobulin therapy
(an infusion of antibodies)
Interventions
• 1.Care is directed toward the treatment of
symptoms, including pain management.
• 2.Monitor respiratory status closely.
• 3.Prepare to initiate respiratory support.
• 4.Monitor cardiac status.
• 5.Assess for complications of immobility.
• 6.Provide the client and family with support.
Amyotrophic Lateral Sclerosis
• Also known as Lou Gehrig’s disease
• It is a progressive degenerative disease involving the
motor system.
• The sensory and autonomic systems are not involved,
and mental status changes do not result from the
disease.
• The cause of the disease may be related to an excess of
glutamate, a chemical responsible for relaying messages
between the motor neurons.
Amyotrophic Lateral Sclerosis
• As the disease progresses, muscle weakness
and atrophy develop until a flaccid tetraplegia
develops.
• Eventually, the respiratory muscles become
affected, leading to respiratory compromise,
pneumonia, and death.
• No cure is known, and the treatment is
symptomatic.
Risk factors
• Heredity. Five to 10 percent of the people with ALS
inherited it (familial ALS).
• Age- most common between the ages of 40 and the
mid-60s.
• Sex. Before the age of 65, slightly more men than
women develop ALS. This sex difference disappears
after age 70.
• Genetics
Risk factors
• Smoking. Smoking is the only likely
environmental risk factor for ALS. The risk
seems to be greatest for women, particularly
after menopause.
• Environmental toxin exposure. Some evidence
suggests that exposure to lead or other
substances in the workplace or at home might
be linked to ALS.
Assessment

•Respiratory difficulty
•Fatigue while talking
•Muscle weakness and atrophy
•Tongue atrophy
Assessment

• Dysphagia
• Weakness of the hands and arms
• Fasciculations of the face
• Nasal quality of speech
• Dysarthria
Interventions

• 1.Care is directed toward the treatment

of symptoms.
• 2.Monitor respiratory status and
institute measures to prevent
aspiration.
• 3.Provide respiratory treatments.
Interventions
• 4.Prepare to initiate respiratory support.
• 5.Assess for complications of immobility.
• 6.Address advance directives as
appropriate.
• 7.Provide the client and family with
psychosocial support.
Medications
• Riluzole (Rilutek) is an oral medication believed to
reduce damage to motor neurons by decreasing
levels of glutamate, which transports messages
between nerve cells and motor neurons.
• Edaravone (Radicava) is given intravenously and
has been shown to slow the decline in clinical
assessment of daily functioning in people with
ALS.