Stroke is an emergency.

Stroke is an emergency. Ischemic stroke is similar to myocardial infarction in that the pathogenesis is loss of blood supply to the tissue, which can result in irreversible damage if blood flow is not restored quickly. Public education is needed to emphasize the warning signs of stroke. Patients should seek medical help immediately, using emergency transport systems. Therapy geared toward minimizing the damage from an acute stroke should be started without delay in the emergency room. This includes measures to protect brain tissue, support perfusion pressure, and minimize cerebral edema. Strategies for improving recovery should also begin immediately. All major medical centers need stroke teams and stroke units. Stroke prevention should be given high priority as a public health strategy. Risk factor management should be part of general health care and should begin in childhood, with emphasis on nutrition, exercise, weight control, and avoidance of tobacco. Health screening and early treatment of hypertension and hypercholesterolemia has decreased the incidence of stroke and heart disease, but these efforts need to be expanded to reach all segments of the population. Basic research has opened the door to new therapies aimed at re-establishing blood flow and limiting tissue damage. Clinical trials have already led to changes in stroke prevention, including studies of carotid endarterectomy and ticlopidine and warfarin therapy (for patients with atrial fibrillation). Trials in progress are testing the usefulness of ancrod, neuroprotective agents, antioxidant agents, anti-inflammatory agents, low-molecular-weight heparin, thrombolytic drugs, and angioplasty. Any delay starting therapy after an acute stroke will result in progressive, irreversible loss of brain tissue. Clinicians should remember that for a stroke patient, time is brain tissue.

Anticoagulation for prevention of cerebral infarcts following subarachnoid hemorrhage.

BACKGROUND: Late neurologic deterioration following subarachnoid hemorrhage is often due to vasospasm and rebleeding. Although the sudden onset of a focal neurologic deficit can actually be the result of thromboembolism, anticoagulation has rarely been used in such cases. METHODS: We report a case of a 55-year-old woman who developed recurrent transient focal neurologic deficits 13 days after having a subarachnoid hemorrhage, with multiple cerebral infarcts by CT. Two cerebral angiograms showed no aneurysm. Her symptoms and clinical temporal profile were consistent with thromboembolic phenomenon. We elected to treat her with systemic anticoagulation. RESULTS: The patient had no recurrent events after systemic anticoagulation, but had episodic sensory changes and a new infarct on MRI once the anticoagulation was discontinued. CONCLUSIONS: Anticoagulant was safely administered after subarachnoid hemorrhage (SAH) in this patient and may have been effective in preventing further cerebral ischemic infarction following her SAH. Our patient's clinical profile of sudden (rather than gradual) onset of a transient focal neurologic deficit and resolution of blood on CT indicates one setting in which the use of heparin may be considered.

Neurologic disorders of pregnancy. Connective tissue disorders.

Although neurological manifestations are well described in patients with connective tissue diseases, there is no evidence of increased frequency during pregnancy. Treatment varies with the neurological disorder and the nature of pathogenetic process, with modifications of usual therapies sometimes required during pregnancy. Termination of pregnancy is a consideration only with the more serious vasculitic diseases (i.e., PAN or WG), in patients with cardiac or renal failure, or in patients with severe exacerbations of their systemic disease that is refractory to therapy.

Central nervous system disease in patients with systemic lupus erythematosus.

Central nervous system (CNS) dysfunction in patients with systemic lupus erythematosus (SLE) is highly variable, although it is often described under a single heading of "neuropsychiatric" or "CNS" SLE. To clarify these CNS abnormalities, we studied 91 lupus patients, 63 of whom had CNS symptoms or signs, over 599 patient years. By placing patients in relatively homogeneous clinical groups (stroke, seizure, suicide attempt, hallucination, confusion, decreased alertness) we detected significant (but variable among groups) correlations with other manifestations of SLE, suggesting separate mechanisms for each CNS disorder. These correlations were lost if all "CNS-SLE" was considered as a single group. Patients with decreased alertness often had undetected systemic infections and had a high death rate from infection, rather than from CNS-SLE. The understanding of the pathogenesis and potential treatment of CNS disorders in lupus will depend on classifying the patients into homogeneous groups.