Neurology of Other Systemic Diseases
CASE
A 57-year-old woman complains of weakness when getting out of a chair, and a hoarse voice. She has been losing hair and gaining weight, and friends tell her she is “slowing down.” On examination, her reflexes are hypoactive, and her muscles feel doughy to the touch.
Many systemic diseases exhibit neurologic manifestations. This has been described in preceding chapters regarding the neurology of diabetes, malignancy, uremia, and alcohol, as well as in the stroke chapter. The physician must recognize the many neurologic complications that accompany systemic disorders and treat them accordingly.
CARDIAC DISEASE
Cardiac abnormalities can cause reduced cerebral perfusion, or emboli that lead to neurologic sequelae. The severity of neurologic manifestations of reduced cardiac output varies with the rate and extent of decreased cerebral perfusion.
Ischemic brain injury can lead to seizures, cerebral edema, loss of consciousness, amnesia, and dementia.
Emboli from the heart are the cause of 15% of ischemic strokes. Thrombi, from which emboli emerge, may develop from a left atrial or ventricular mural thrombus, an intracardiac tumor, bacterial and nonbacterial endocarditis, or the systemic and right heart circulation via intracardiac shunts (paradoxic emboli).
Conditions that predispose the patient to develop such emboli include:
Atrial fibrillation.
Acute and chronic ischemic heart disease.
Valvular heart diseases (rheumatic and prosthetic).
Patent foramen ovale and atrial septal aneurysm also can cause cerebral emboli. The role of closure of patent foramen ovale is still being reevaluated at the present time.
Patients with recurrent emboli who have no other cause of embolism other than PFO are candidates for catheter closure of PFO. Some of these patients have associated coagulation disorders and should be evaluated for such disorders.
Young patients with strokes, but without evidence of cerebrovascular disease, should still be suspected of having a cardiac cause of stroke.
Electrocardiogram (ECG), echocardiography, prolonged ECG monitoring to identify arrhythmias, and transesophageal echocardiography are helpful tests for detecting the cause of cardiogenic stroke. Transthoracic echocardiography has a low yield in showing cardiac sources of embolism, and is not an effective “screening tool” for embolic sources of stroke.
Anticoagulation therapy reduces the risk of embolism in atrial fibrillation, rheumatic mitral stenosis, and cardiomyopathy with ventricular thrombi.
After a myocardial infarction (MI), patients are at risk for stroke, especially with anterior wall infarction. If echocardiography detects a developing thrombus, anticoagulation reduces the risk of post-MI stroke by at least 60%.
Anoxic encephalopathy, lack of oxygen to the brain, often occurs in the setting of cardiac arrest. Mild degrees of hypoxemia cause inattention, drowsiness, and impaired judgment. In patients with prior deficits, hypoxemia may make symptoms worse.
Anoxic injury may cause a variety of symptoms that can occur individually or in combination and include the following:
Memory impairment caused by injury to the mesial thalamus and hippocampus.
Choreoathetosis or a parkinsonian syndrome.
“Man in the barrel” syndrome; with weakness of shoulder girdle muscles sparing the hands, so the affected person cannot abduct the arms. This pattern results from infarction affecting the shoulder region in the cortex, which lies between anterior and middle cerebral territories in the watershed zone.
Coma, stupor, or persistent vegetative state may occur with severe diffuse injury.
Recently cooling of body temperature, beginning within 6 hours of an anoxic event, has been shown to significantly improve
functional outcome and survival. This should be considered in any patient who is not immediately awakening after an anoxic event.
functional outcome and survival. This should be considered in any patient who is not immediately awakening after an anoxic event.
Cardiac complications of open heart surgery are a major source of morbidity in the postoperative state. These include both central nervous system complications and peripheral nervous system disorders. The four following disorders are the most common neurologic problems after open heart surgery:
Encephalopathy: A generalized encephalopathy occurs in about 6% of patients after open heart surgery. This is more common with elderly patients, prolonged surgery, a patient with preexisting cognitive dysfunction, and patients with major underlying medical morbidities, such as renal failure. This usually improves. When measured, however, many patients post open heart surgery have some level of cognitive decline.
Stroke: Stroke syndromes are a major source of morbidity after open heart surgery and occur in about 3% to 5% of open heart surgery patients. Most of these are due to emboli from the arch, microemboli from cardiac bypass, or due to atrial fibrillation, and are not usually related to carotid atherosclerosis. Stroke is more common in patients undergoing valvular surgery than patients having coronary artery bypass grafting. It is unclear whether surgery or stenting for severe carotid stenosis prior to open heart surgery is beneficial, as there are no randomized trials of these treatments.
Anoxic encephalopathy: Anoxic encephalopathy can occur with open heart surgery, and is usually associated with documented severe hypotension, or cessation of circulation other than the usual bypass transitions.
Brachial plexopathy: Between 2% and 10% of post open heart patients will develop a brachial plexopathy. This appears to be due to injury to the brachial plexus by compression from the dorsal ribs, rather than from stretch injury (anatomic studies). It may cause burning pain in an arm; usually in a lower trunk distribution causing tingling and burning in the fifth digits, and weakness of intrinsic hand muscles. It may improve slowly if at all.
ENDOCRINE DISEASE
Thyroid disease: Hyperthyroid patients often complain of anxiety, fatigue, and irritability. They may have seizures, tremor, chorea, and usually have brisk tendon reflexes. They also may develop ophthalmopathy, including proptosis and
ophthalmoplegia. A myopathy with proximal muscle weakness and wasting is not uncommon. On physical examination, hypoactive reflexes with a delayed relaxation time usually can be demonstrated. Reflexes may be pendular (i.e., the leg swings to and fro more often than normal if allowed to swing freely). Encephalopathy may occur with Hashimoto thyroiditis. In this syndrome patients may have confusion, altered consciousness, and seizures associated with increased anti-thyroid antibodies, and may respond to steroid therapy. Myxedema coma is rare and carries a high mortality rate. Some myxedematous patients may develop seizures, obstructive sleep apnea, ataxia, or sensorineural hearing loss.
Note: Check for hyperthyroidism in patients with action tremor; check for hypothyroidism in patients with carpal tunnel syndrome.
Parathyroid: Patients with hyperparathyroidism often display psychiatric symptoms, such as those associated with mania, schizophrenia, or depression. Myopathy is common. Patients with hypoparathyroidism may have psychiatric symptoms similar to those seen in hyperparathyroidism. Seizures can occur from hypocalcemia; particularly in hyperparathyroid patients after adenoma removal. Hypocalcemia and hypomagnesemia can cause tetany. To elicit latent tetany, have the patient hyperventilate and tap the facial nerve, causing facial muscle contraction (Chvostek sign), or occlude venous return from an arm, resulting in carpopedal spasm (Trousseau sign). Laryngeal spasm also may occur in this setting.
Glucocorticoids: Myopathy is common with corticosteroid therapy, and myalgia may accompany the weakness. Treatment involves tapering or use of alternate-day steroids, alternate forms of immunosuppression, or nonfluorinated steroids. Patients with Cushing syndrome may experience psychiatric symptoms, and occasionally frank psychosis. Patients on exogenous steroids may also experience such symptoms, as well as insomnia. Patients with Addison disease, and patients after withdrawal from steroids, may experience acute confusional states or psychosis. Seizures can occur from hyponatremia.
FLUID AND ELECTROLYTE DISTURBANCES
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