CHAPTER 5 Neurologic Disorders
Section One Inflammatory Disorders of the Nervous System
Multiple Sclerosis
Assessment
Signs and symptoms/physical findings
Damage to motor and sensory control centers
Urinary frequency, urgency, or retention; urinary and fecal incontinence; constipation.
Diagnostic Tests
MRI
Reveals presence of plaques and demyelinization in the CNS. This is the test of choice when MS is suspected, although it is not a definitive measure of MS. MRI technology is capable of identifying current sites of inflammation and demyelinization and showing changes associated with disease progression. T1-weighted MRI sequences may show hypointense lesions (black holes), a finding that correlates with axonal loss and indicates old lesions. T2-weighted MRI sequences can show old and new lesions and is used to document response to treatment. Gadolinium (Gd) enhancement shows areas of active demyelinization. MRI diffusion tensor imaging and MR spectroscopy often reveal involvement of otherwise normal-appearing white matter. Magnetization transfer imaging may show indirect evidence of axonal loss. MR spectroscopy can measure decline in a brain chemical called N-acetylaspartate (NAA) as a marker of axonal damage and appears to predict disease severity. Functional MRI (fMRI) can show new lesions. Fluid-attenuated inversion recovery (FLAIR) is also used for detecting cerebral lesions, and short tau inversion recovery (STIR) is useful in detecting demyelinization.
Collaborative Management
Pharmacotherapy
Steroidal antiinflammatory agents (e.g., methylprednisolone)
For an exacerbation and for optic neuritis to reduce symptoms by decreasing inflammation and associated edema of the myelin and thereby hastening onset of remission. Antacids, histamine H2-receptor blockers, insulin coverage, K+ supplements, diuretics, BP medications, and psychotropic agents may be given to combat side effects of steroids.
Antispasmodics and muscle relaxants (e.g., baclofen, tizanidine, dantrolene sodium, and methocarbamol)
Antidepressants (e.g., fluoxetine, nortriptyline, and sertraline)
For depression related to cerebral lesions. These agents also may reduce complaints of paresthesias.
Tranquilizers (e.g., diazepam)
For anxiety reducing and muscle relaxant effects, which may help with spasms and tremors.
Proton pump inhibitor (e.g., pantoprazole), histamine H2-receptor blockers (e.g., famotidine), and sucralfate
Analgesics (e.g., acetaminophen), neuropathic pain medications (e.g., anticonvulsants such as carbamazepine, topiramate, and lamotrigine; tricyclic antidepressants such as amitriptyline and imipramine), and medications used for facial trigeminal pain or limb burning (e.g., amantadine, topical capsaicin, misoprostol, mexiletine, perphenazine)
Dextromethorphan-quinidine combination
To reduce inappropriate emotional episodes (e.g., laughing and crying).
Speech therapy
Improves speech deficits using accessory respiratory muscles, tongue, and facial muscles.
Nursing Diagnoses and Interventions
Deficient knowledge
related to factors that aggravate and exacerbate MS symptoms
Nursing Interventions
Nursing Interventions
Nursing Interventions
Patient-Family Teaching and Discharge Planning
Guillain-Barré Syndrome
Assessment
Collaborative Management
Pharmacotherapy
Stool softeners (e.g., docusate), laxatives (e.g., bisacodyl), and suppositories
May be prescribed to prevent fecal impaction and minimize incontinence.
Proton pump inhibitor (e.g., pantoprazole), histamine H2-receptor blockers (e.g., famotidine), and sucralfate
Exercise and activity
Passive ROM exercise during acute phase with a goal of preventing contractures, dislocations, or subluxations. Turning and meticulous skin care to prevent skin breakdown are important interventions. After patient stabilizes, active ROM or active-assistive ROM is implemented, and PT and a rehabilitation program are initiated with a goal of early mobilization. OT and assistive devices or braces are employed so that patient can maintain mobility and independence with activities of daily living (ADL). Muscle strengthening exercises, conditioning exercises, and gait training are commonly prescribed.
Management of acute autonomic dysfunction
Short-acting antihypertensive agents for hypertension; intravascular volume expanders or vasopressors for hypotension; cardiac monitoring of dysrhythmias; gastric suction, nutrition, and parenteral fluids for adynamic ileus; and catheterization and medications for urinary retention. Phenoxybenzamine may be used to help with paroxysmal hypertension, headache, sweating, anxiety, and fever. Diabetes insipidus (DI) (see p. 404) and SIADH (see p. 409) have been reported; therefore urine output, state of hydration, and serum and urine electrolytes are monitored.
Nursing Diagnoses and Interventions
Ineffective breathing pattern
related to neuromuscular weakness or paralysis of the facial, throat, and respiratory muscles
Nursing Interventions
Nursing Interventions
Nursing Interventions
Nursing Interventions
Nursing Interventions
Nursing Interventions
Patient-Family Teaching and Discharge Planning
Bacterial Meningitis
Overview/Pathophysiology
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.
Assessment
Signs and symptoms/physical findings
Cardinal signs include headache, fever, stiff neck, change in mental status.
IICP and herniation
Decreased level of consciousness (LOC) (irritability, drowsiness, stupor, coma), nausea and vomiting, decreasing Glasgow Coma Scale (GCS) score (see p. 307), VS changes (increased BP, decreased heart rate [HR], widening pulse pressure), changes in respiratory pattern, decreased pupillary reaction to light, pupillary dilation or inequality, and severe headache.