Stephen Marks

Central nervous system infarction related to cocaine abuse.

Background Cocaine use in the United States has reached epidemic proportions, and increased availability of “crack” since 1983 has noticeably increased the incidence of neurovascular complications. In this report, we examine the relationship between cocaine use and ischemic infarct. Summary of Comment This study reports 18 cases of ischemic cerebrovascular events, which occurred among 15 men and three women aged 21-47 years who were evaluated in a 2-year period. Clinical presentations include thirteen cases with hemispheric infarcts, two brain stem strokes, two anterior spinal artery infarcts, and one with both hemispheric and cerebellar infarcts. Nine patients smoked crack, four snorted cocaine, and three injected it intravenously. In two cases, the route of administration could not be determined. Two patients died, but the others survived with various degrees of neurological deficit. Conclusions Traditional risk factors for strokes were identified in only six patients, suggesting that these factors are not necessary for the occurrence of a cocaine-related infarct. Multiple overlapping mechanisms may be responsible, including vasospasm, sudden onset of hypertension, myocardial infarction with cardiac arrhythmias, increased platelet aggregation, and vasculitis.

Efficacy of 3‐Hydroxy‐3‐Methylglutaryl Coenzyme A Reductase Inhibitors for Prevention of Stroke

OBJECTIVE: To determine if 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are effective in preventing fatal and nonfatal strokes in patients at increased risk of coronary artery disease.DESIGN: Meta-analysis of randomized controlled trials. Clinical trials were identified by a computerized search of medline (1983 to June 1996), by an assessment of the bibliographies of published studies, meta-analyses and reviews, and by contacting pharmaceutical companies that manufacture statins. Trials were included in the analysis if their patients were randomly allocated to a statin or placebo group, and reported data on stroke events. Thirteen of 28 clinical trials were selected for review. Data were extracted for details of study design, patient characteristics, interventions, duration of therapy, cholesterol measurements, and the number of fatal and nonfatal stroke events in each arm of therapy. Missing data on stroke events were obtained by contacting the investigators of the clinical trials.MAIN RESULTS: Among 19,921 randomized patients, the rate of total stroke in the placebo group was 2.38% (90% nonfatal and 10% fatal). In contrast, patients who received statins had a 1.67% stroke rate. Using an exact stratified analysis, the pooled odds ratio (OR) for total stroke was 0.70 (95% confidence interval [CI] 0.57, 0.86; p=.0005). The pooled OR for nonfatal stroke was 0.64 (95% CI 0.51, 0.79; p=.00001), and the pooled OR for fatal stroke was 1.25 (95% CI 0.71, 2.24; p=.4973). In separate analyses, reductions in total and nonfatal stroke risk were found to be significant only for trials of secondary coronary disease prevention. Regression analysis showed no statistical association between the magnitude of cholesterol reduction and the relative risk for any stroke outcome.CONCLUSIONS: The available evidence clearly shows that HMG-CoA reductase inhibitors reduce the morbidity associated with strokes in patients at increased risk of cardiac events. Data from 13 placebo-controlled trials suggest that on average one stroke is prevented for every 143 patients treated with statins over a 4-year period.

Diagnostic challenges in Balamuthia mandrillaris infections

Balamuthia mandrillaris is an emerging cause of subacute granulomatous amebic encephalitis (GAE). The diagnosis of this infection has proven to be difficult and is usually made postmortem. Early recognition and treatment may offer some benefit. This report describes a previously healthy woman who died from GAE due to B. mandrillaris.

Estrogen replacement therapy for cognitive benefits: viable treatment or forgettable "senior moment"?

The perceived benefits of estrogen on cognitive function are one of the few remaining potential roles for estrogen replacement therapy. The justification for such a role has a strong biologic basis and is easily shown in animal models. Purported benefits for estrogen on cognitive function include neuroprotective, neurostimulating, and neurotrophic effects. The objective of this study was to review the literature and to evaluate the role of estrogen replacement therapy in improving cognition in Alzheimer disease, vascular dementia, premenopausal women, and postmenopausal women without dementia. Additionally, the authors separately looked at the neuroprotective effects of estrogen replacement therapy on the subsequent risk of dementia. The available data fail to show a therapeutic benefit of estrogen replacement therapy in Alzheimer disease. Surprisingly, limited data allow consideration of a possible role of estrogen in the management of vascular dementia. Additionally, younger females with low estrogen levels secondary to primary ovarian failure and Turner syndrome benefit from estrogen replacement therapy. Despite the limited role of estrogen replacement therapy in cognitive enhancement, neuroprotective properties are likely because several prospective studies indicate a reduced risk of Alzheimer disease. A critical window of opportunity seems to exist for this protective effect in Alzheimer disease because once established, the course of the disease is not affected by concomitant estrogen replacement therapy. The authors conclude that the use of estrogen replacement therapy is not substantiated for the treatment of patients with Alzheimer disease. Alternatively, because of the evidence for a possible neuroprotective effect, women at high risk for the development of Alzheimer disease may be appropriate candidates for estrogen replacement therapy. Such a decision should be made on a case-by-case basis, after careful consideration of the risks and benefits.

Recurring Strokes with Repeated Cocaine Use

Cerebral infarctions or subarachnoid hemorrhages have been described in association with cocaine use. We describe a patient who initially developed a subarachnoid hemorrhage following cocaine use, due