Neurologic Disorders

CHAPTER 5 Neurologic Disorders


Section One Inflammatory Disorders of the Nervous System



imageMultiple Sclerosis



Overview/Pathophysiology


Multiple sclerosis (MS) is an inflammatory autoimmune disorder causing scattered and sporadic demyelinization of the central nervous system (CNS). Myelin permits nerve impulses to travel quickly through the nerve pathways of the CNS. In response to the inflammation, the myelin nerve sheaths scar, degenerate, or separate from the axon cylinders. This demyelinization interrupts electrical nerve transmission and causes the wide variety of symptoms associated with MS. As less severe inflammation resolves, myelin function may regenerate, thereby enabling electrical nerve impulse transmission to be restored. When the inflammation is severe and causes irreversible destruction of myelin or axon degeneration, involved areas are replaced by dense glial scar tissue that forms patchy areas of sclerotic plaque that permanently damage conductive pathways of the CNS. Axon nerve fibers may degenerate. Deficits present after 3 mo usually are permanent.


The course of MS is highly variable, with several general categories of progression. Motor or coordination symptoms at onset and/or frequent attacks during the first 2 yr of the disease usually indicate a poor outlook. In the benign form of MS (10% of patients), attacks are few and mild. Complete or nearly complete clearing of symptoms occurs with little or no disability. At least initially, most patients (70%-80%) have the relapsing-remitting form characterized by episodes of neurologic impairment (“attacks,” exacerbations), followed by complete or nearly complete recovery and stability with no disease progression (remission). Typically, increasing numbers of symptoms occur with each exacerbation, with less complete clearing of symptoms and with deficits becoming cumulative. Over time the relapsing-remitting form usually undergoes transition to the secondary progressive form, in which neurologic impairment progresses continuously with or without superimposed relapses. A small proportion of patients (10%-20%) will initially begin with the primary progressive form, characterized by gradual ongoing accumulation of symptoms and deficits, with absence of clear-cut exacerbations and remissions. The progressive relapsing form (5%) is characterized by a progressive disease course from onset, with clear acute exacerbations. Progression continues during the periods between disease exacerbations. In the most severe cases of acute MS, significant disability may occur in weeks or months.



Assessment



Signs and symptoms/physical findings


Onset of MS can be extremely rapid, or it can be insidious with exacerbations and remissions. Signs and symptoms vary widely, depending on site and extent of demyelinization, and can change from day to day. Usually early symptoms are mild, including fatigue, weakness, heaviness, clumsiness, numbness, and tingling. Optic neuritis and visual problems often are the first symptoms. Lhermitte’s sign may be present, in which an electrical sensation runs down the back and legs during neck flexion. Ophthalmoscopic inspection may reveal temporal pallor of optic disks. Reflex assessment may show increased deep tendon reflexes (DTRs) and diminished abdominal skin and cremasteric reflexes.










Diagnostic Tests


MS is sometimes called the “great masquerader.” Diagnosis of MS usually is made after other neurologic disorders with similar symptoms have been ruled out (when the patient has experienced two or more exacerbations of neurologic symptoms) and when the patient has two or more areas of demyelinization or plaque formation throughout the CNS, as demonstrated by diagnostic tests such as magnetic resonance imaging (MRI) and evoked potential (EP) studies or by the patient’s clinical symptoms.









Collaborative Management


Generally, treatment is symptomatic and supportive. Various treatments slow the rate of exacerbation or hasten recovery from an exacerbation, but the general course of the disease process has not been positively affected.




Pharmacotherapy


































Nursing Diagnoses and Interventions



Deficient knowledge


related to factors that aggravate and exacerbate MS symptoms




Nursing Interventions















Nursing Interventions







Give patients taking antispasmotics/muscle relaxants (e.g., baclofen or dantrolene) these additional instructions:














imagePatient-Family Teaching and Discharge Planning


The patient with MS may have a wide variety of symptoms that cause disability, ranging from mild to severe. Include verbal and written information about the following:













imageGuillain-Barré Syndrome



Overview/Pathophysiology


Guillain-Barré syndrome (GBS) is a rapidly progressing acute idiopathic polyneuritis. It is an autoimmune disease triggered by a preceding infection that is commonly caused by Campylobacter jejuni, Mycoplasma pneumoniae, cytomegalovirus (CMV), or Epstein-Barr virus (EBV). An inflammatory process enables lymphocytes to enter perivascular spaces and destroy the myelin sheath covering peripheral or cranial nerves. Posterior (sensory) and anterior (motor) nerve roots can be affected because of this segmental demyelinization, and individuals may experience both sensory and motor losses. There is relative sparing of the axon, except in one form of the disease. Respiratory insufficiency may occur in as many as half of affected individuals. Life-threatening respiratory muscle weakness can develop as rapidly as 24-72 hr after onset of initial symptoms. In about 25% of cases, motor weakness progresses to total paralysis.


Peak severity of symptoms usually occurs within days to 3 wk after onset of symptoms. A plateau stage follows that usually lasts 1-2 wk. The recovery stage starts with a return of function as remyelinization occurs, but it may take months to years for a full recovery. Eighty to ninety percent of patients recover completely or have only minor residual weakness or abnormal sensations, such as numbness or tingling. Of patients with GBS, 5%-10% may have permanent severe disability. Deficits are the result of axonal nerve degeneration.


GBS has several variants defined by the symptoms, preceding infection, and severity. Variants of GBS include those with a rapid progressive phase (e.g., acute inflammatory demyelinating polyneuropathy, Miller-Fisher syndrome) and those with a slow progressive phase (e.g., recurrent GBS, multifocal motor neuropathy).



Assessment



Signs and symptoms/physical findings


Progressive weakness and areflexia are the most common indicators. Typically, numbness and weakness begin in the legs and ascend symmetrically upward, progressing to the arms and facial nerves. Ascending GBS is most common, but descending GBS, in which cranial nerves are affected first and weakness progresses downward with rapid respiratory involvement, also can occur. GBS does not affect level of consciousness (LOC), cognitive function, or pupillary function. Assess for symmetric motor weakness, impaired position and vibration sense, hypoactive or absent deep tendon reflexes (DTRs), hypotonia in affected muscles, and decreased ventilatory capacity.








Collaborative Management


Patients are likely to be in the ICU when the neurologic deficit is progressing and are at risk for respiratory failure and autonomic dysfunction. Treatment is focused on ventilatory support and administration of immunomodulating agents to shorten the course of the diseaase. Only plasma exchange therapy and IV immune serum globulin have proved to be effective.













Nursing Diagnoses and Interventions



Ineffective breathing pattern


related to neuromuscular weakness or paralysis of the facial, throat, and respiratory muscles




Nursing Interventions


























Nursing Interventions




















imagePatient-Family Teaching and Discharge Planning


Most patients with GBS eventually recover fully, but because the recovery period can be prolonged, the patient often goes home with some degree of neurologic deficit. Discharge planning and teaching will vary according to the degree of disability. Include verbal and written information about the following:











imageBacterial Meningitis



Overview/Pathophysiology


Bacterial meningitis is an infection that results in inflammation of the meningeal membranes covering the brain and spinal cord. Bacteria in the subarachnoid space multiply and cause an inflammatory reaction of the pia and arachnoid meninges. Purulent exudate is produced, and inflammation and infection spread quickly through the cerebrospinal fluid (CSF) that circulates around the brain and spinal cord. Bacteria and exudate can create vascular congestion, plugging the arachnoid villi. This obstruction of CSF flow and decreased reabsorption of CSF can lead to hydrocephalus, increased intracranial pressure (IICP), brain herniation, and death.


Meningitis generally is transmitted in one of four ways: (1) via airborne droplets or contact with oral secretions from infected individuals; (2) from direct contamination (e.g., from a penetrating skull wound; a skull fracture, often basilar, causing a tear in the dura; lumbar puncture (LP); ventricular shunt; or surgical procedure); (3) via the bloodstream (e.g., pneumonia, endocarditis); or (4) from direct contact with an infectious process that invades the meningeal membranes, as can occur with osteomyelitis, sinusitis, otitis media, mastoiditis, or brain abscess. In adults, pneumococcal meningitis, caused by Streptococcus pneumoniae, is the most common bacterial meningitis. Meningococcal meningitis, caused by Neisseria meningitidis, is next. Infection with Haemophilus influenzae type b has decreased significantly with the immunization of infants. Listeria monocytogenes infection is on the rise, especially in the immunocompromised or the extremely young or old. Outbreaks have been associated with consumption of contaminated dairy or undercooked fish, chicken, and meat. Any bacterium can cause meningitis, and some forms of meningitis, such as one caused by Staphylococcus aureus, can be difficult to treat because of their resistance to important antibiotics. Adhesions and fibrotic changes in the arachnoid layer and subspace may cause obstruction or reabsorption problems with CSF that result in hydrocephalus. Although the mortality rate is still high among untreated or delayed-treatment cases, prognosis for most patients with bacterial meningitis is generally good. Complete neurologic recovery is possible if the disorder is recognized early and antibiotic treatment is initiated promptly.


Sep 1, 2016 | Posted by in NURSING | Comments Off on Neurologic Disorders

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