A stroke interrupts the blood flow to the brain, often leading to damage to some functions of the brain. This can cause persisting paralysis of some parts of the body or other difficulties with various physical functions. Experiments in animals have shown that amphetamines (stimulants) might be able to improve recovery from stroke. The mechanisms behind the faster recovery seen after stroke in animals are not clearly understood. This review identified 10 small randomized trials of amphetamines in patients with stroke. There was no evidence that amphetamines did more good than harm. There is not enough evidence to support the routine use of amphetamines to promote recovery after stroke. Further controlled trials are needed.
At present, too few patients have been studied to draw any definite conclusions about the effects of amphetamine treatment on recovery from stroke. The suggested benefits on motor function and the non-significant trend towards increased risk of death could be related to imbalances in prognostic variables or other bias in the studies. Further research is therefore justified.
Animal research shows that treatment with amphetamines improves recovery after focal cerebral ischaemia. If the effects are similar in humans, amphetamine treatment could have a major impact on recovery from stroke.
To assess the effects of amphetamine treatment in patients with stroke.
We searched the Cochrane Stroke Group Trials Register (last searched January 2006), the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2006), MEDLINE (1966 to January 2006), EMBASE (1980 to January 2006), CINAHL (1982 to January 2006), CINAHL (1982 to January 2006), Science Citation Index (1992 to March 2005) and registers of ongoing trials. We also checked the reference lists of all relevant articles and reviews, and contacted researchers in the field.
Randomized unconfounded trials comparing amphetamine with placebo.
Two review authors independently selected trials for inclusion and assessed trial quality; one extracted the data.
Ten studies involving 287 patients were included, but not all trials contributed data to each outcome examined in this review. The quality of the trials varied but was generally high. Based on three trials (106 patients) there was no evidence that amphetamine treatment reduced death or dependence (Peto's odds ratio (Peto OR) 1.5, 95% confidence interval (CI) 0.6 to 3.3). Imbalances at baseline with more serious stroke allocated to amphetamine may account for the trend for more deaths at the end of follow up among amphetamine-allocated patients (Peto OR 2.8, 95% CI 0.9 to 8.6). Based on two trials (73 patients) systolic (weighted mean difference (WMD) 8.4 mm Hg, 95% CI 1.6 to 15.2) and diastolic (WMD 4.9 mm Hg, 95% CI 1.1 to 8.8) blood pressure, as well as heart rate, increased (WMD 10.6 bpm, 95% CI 3.3 to 17.8) in amphetamine-allocated patients. Based on six studies (176 patients) there was evidence of a better relative change from baseline to last follow up in motor function (WMD -6.1 points; 95% CI -10.4 to -1.9) Different results with different analysis approaches emphasize caution in the interpretation of the results.