Chapter 45 B: MS and ALS Flashcards
Manifestations of multiple sclerosis
Muscle weakness and spasticity
Fatigue
Intention tremors
Dysmetria: inability to direct or limit movement
Hypalgesia: decreased sensitivity to pain
Ataxia: decreased motor coordination
Dysarthia: slurred speech
Dysphasia
Diplopia, nystagmus, scotomas: Changes in peripheral vision, decreased visual and hearing acuity, tinnitus, vertigo
Bowel and bladder dysfunction
Alterations in sexual function and impotence
Cognitive changes such as memory loss, impaired judgment, decreased problem-solving, calculations
Pathophysiology of multiple sclerosis
Chronic autoimmune disease that affects the myelin sheath in the conduction pathway of the central nervous system. It has periods of remission and exacerbation. There is an inflammatory response that results in patchy areas of plaque in the white matter of theCNS. The myelin sheath is damaged and thickness is reduced, altering impulses between the brain and the spinal cord. They are still transmitted but not as effective.
Areas usually affected include optic nerve, pyramid all tracks, posterior columns, brainstem nuclei, and that periventricular region of the brain.
Nursing assessment of multiple sclerosis
Perform a complete neurological assessment. Assess the patient’s ability to move, fatigue and stiffness of the extremities. Along with fatigue is associated continuous sensitivity to temperature. Flexor spasms at night may wake and the patient from sleep. There maybe hyperactive deep tendon reflexes, clonus, positive Babinski’s reflex, absent abdominal reflexes. Motor movements are often clumsy.
Always get a thorough history. Often symptoms were vague and nonspecific but they went away several years ago and no treatment was sought. Now symptoms are progressing.
Laboratory assessment for multiple sclerosis
No test is Definitive for MS. CSF may have an elevated protein and slight increase in wbc’s. There may be presence of immunoglobulin bands.
MRI shows the presence of plaques and can be diagnostic for MS. Evoked potential studies are abnormal and EMGs. Diagnosis is made by excluding other neurological diseases.
Drug of choice for MS acute exacerbations
Solu-Medrol/methylprednisolone is used to reduce edema and the inflammatory response in acute exacerbations. One gram given IV daily for 3 to 14 days. They course of oral prednisone 60 mg a day for 5 to 7 days may be used.
The client should be taught to avoid individuals with any type of upper respiratory illness because this medication is immunosuppressive.
Monitor for hyperglycemia and hypokalemia
mitoxantrone / Novatrone
Is a chemotherapeutic drug that has been shown to be effective in reducing neurological disability. It decreases the frequency of clinical relapses in patients with secondary progressive, progressive relapsing or relapsing remitting MS.
Long-term use has a risk of developing cardiotoxicity when used for long periods. Adverse effects are congestive heart failure and dysrhythmias
Cytoxan/cyclophosphamide and Solu-Medrol/methylprednisolone
Used to stabilize the disease process. It is immunosuppressive and the client should avoid people with upper respiratory illness.
Treatment for MS
In addition to medication therapy promote mobility and manage symptoms. Physical therapy and occupational therapy. Avoid rigorous activities that increase body temperature and lead to fatigue.
Assist with orientation, use a calendar, encourage lists and messages. Referred to a speech language pathologist. Discuss sexual intimacy. Manage bladder problems and increase fluids. Use an eyepatch to treat diplopia alternated every few minutes.
Alter the home environment to make it safe. Avoid overexertion, stress, extreme temperatures, humidity, and people with upper respiratory tract infections. Obtain adequate rest.
Pathophysiology of amyotrophic lateral sclerosis
Also known as Lou Gehrig’s disease. Adult-onset upper and lower motor neuron disease. Progressive weakness, muscle wasting, specificity eventually leading to paralysis. The entire body becomes involved including the ability to talk swallow and breathe. Death usually occurs in three years. There is no known cause, cure, treatment, prevention. The sensory and autonomic nervous system’s are not involved. Usually between 40 and 70 years of age. It is more common in men than women.
Assessment inALS
Early manifestations include tongue atrophy, weakness at the hands and arms, atrophy of the arms, fasciculations or twitching of the face, nasal quality of speech, dysarthria, dysphasia, fatigue while talking
As the disease progresses muscle atrophy particularly of the trapezius and sternocleidomastoid muscles develop. Eventually respiratory muscles become involved leading to respiratory compromise, pneumonia, and death.
There are no diagnostic test but there is often an elevated creatinine kinase, abnormal EMG, muscle biopsy can be done, pulmonary function tests showed decreased vital capacity
Interventions for ALS
Riluzole/rilutek May extend survival time. The usual dose is 50 mg twice a day on an empty stomach. Monitoring the patient for liver toxicity. Medications may be given for pain, fatigue, spacticity, excessive secretions, sleep disturbances, and complications.
Develop a communication plan for when the patient can no longer verbalize. A nutrition plan it needs to be made to determine if the patient wants enteral feedings or not. These should be included in the advanced directives along with whether or not to use a ventilator.
