Cocaine use and stroke.

Stroke is the third most common cause of death in developed countries. In England and Wales, 1000 people under the age of 30 have a stroke each year. Cocaine is the most commonly used class A drug, and the first report of cocaine-induced stroke was in 1977. Since the development of alkaloidal "crack" cocaine in the 1980s, there has been a significant rise in the number of case reports describing both ischaemic and haemorrhagic stroke associated with cocaine use. Cocaine is a potent central nervous system stimulant, and acts by binding to specific receptors at pre-synaptic sites preventing the reuptake of neurotransmitters. The exact mechanism of cocaine-induced stroke remains unclear and there are likely to be a number of factors involved including vasospasm, cerebral vasculitis, enhanced platelet aggregation, cardioembolism, and hypertensive surges associated with altered cerebral autoregulation. The evidence surrounding each of these factors will be considered here.

Diseases and impairments as risk factors for onset of disability in the older population in England and Wales: findings from the Medical Research Council Cognitive Function and Ageing Study.

BACKGROUND: This paper reports the association between self-reported diseases and impairments and 2-year onset of disability in a prospective study of people aged 65 years or older in five urban and rural centers in England and Wales (Medical Research Council Cognitive Function and Ageing Study; MRC-CFAS). METHODS: We initially reviewed risk factors for onset of disability in 35 prospective studies of functional decline in older people published in 1998-2001. In the present study, disability was defined as requiring help from another person at least several times a week and was assessed by dependency in activities of daily living. Polytomous and bivariate logistic regression models were fitted for onset of disability and mortality among those nondisabled at baseline (n=7913), adjusting for age, sex, and sociodemography. RESULTS: Among prevalent conditions, arthritis (population-attributable risk 11.4%) and cognitive impairment indicated by a Mini-Mental State Examination score of

Current status of statin therapy for stroke prevention.

Stroke is a leading cause of mortality and long-term disability in the Western world. Lipid abnormalities are a key risk factor for stroke, elevated LDL-cholesterol being the most common abnormality. No clear association has been demonstrated between elevated LDL-cholesterol and stroke incidence, possibly due to the lack of appropriate etiopathophysiological classification of stroke in most studies. Nonetheless, statin therapy is associated with significant reduction in first and recurrent stroke, and there remains a net benefit despite a significant but small increase in hemorrhagic stroke. Following a stroke, indirect evidence supports continuation of prestroke statin therapy while the impact of de novo statin therapy in acute stroke remains uncertain. International guidelines advise an objective assessment of cardiovascular risk to determine the appropriateness of statins for primary prevention and near universal use of statins for secondary prevention after the acute phase of ischemic stroke. There is lack of consensus with regard to the choice of agent, timing of initiation, dose and duration of therapy. Some guidelines advocate high-dose atorvastatin while others suggest the use of simvastatin owing to generic availability and low cost. While the benefits of preventive interventions for stroke are well established and clearly outlined in international guidelines, there is poor application of such measures in clinical practice. This article summarizes the current understanding of the role of statins in stroke prevention and early studies of potential interventions to overcome the barriers to effective statin therapy for secondary prevention. There is a clear need for further research into identifying deficiencies in long-term management, barriers to optimal secondary prevention and novel interventions to overcome these barriers.

Measurement of cerebral blood flow responses to the thigh cuff maneuver: a comparison of TCD with a novel MRI method.

Cerebral autoregulation (CA) describes the mechanism responsible for maintaining cerebral blood flow (CBF) relatively constant, despite changes in mean arterial blood pressure (ABP). This paper introduces a novel method for assessing CA using magnetic resonance imaging (MRI). Images are rapidly and repeatedly acquired using a gradient-echo echo-planar imaging pulse sequence for a period of 4 minutes, during which a transient decrease in ABP is induced by rapid release of bilateral thigh cuffs. The method was validated by comparing the observed MRI signal intensity change with the CBF velocity change in the middle cerebral arteries, as measured by transcranial Doppler (TCD) ultrasound, using a standardized thigh cuff maneuver in both cases. Cross-correlation analysis of the response profiles from the left and right hemispheres showed a greater consistency for MRI measures than for TCD, both for interhemisphere comparisons and for repeated measures. The new MRI method may provide opportunities for assessing regional autoregulatory changes following acute stroke, and in other conditions in which poor autoregulation is implicated.