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Biomedical subjects

L Martinsson

Publications and source records attributed to L Martinsson.

6 recordsLinked to original sources

Amphetamines for improving recovery after stroke.

BACKGROUND: Experimental animal research shows that treatment with amphetamines improves recovery after focal cerebral ischaemia. If the effect were similar in humans, amphetamine treatment could have a major impact on recovery from stroke. OBJECTIVES: The objective of this review was to assess the effects of amphetamine treatment in patients with stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched November 2002). In addition, we searched the Cochrane Controlled Trials Register (Cochrane Library, Issue 4 2002), MEDLINE (1966-September 2002), EMBASE (1980-November 2002), and Science Citation Index (1992-December 2002). The reference lists of all relevant articles and reviews were checked, and we contacted researchers in the field to identify further published and unpublished studies. SELECTION CRITERIA: Randomized unconfounded trials comparing amphetamine with placebo. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion, assessed trial quality and extracted the data. MAIN RESULTS: Seven studies involving 172 patients were included. The quality of the trials varied but was generally high. Based on two trials (85 patients) there was no evidence that amphetamine treatment reduced death or dependence (Peto's odds ratio, [Peto OR] 1.54; 95% Confidence Interval [CI] 0.64 to 3.73). In these two trials, there were imbalances at baseline, with more serious strokes allocated to amphetamine. This imbalance may account for the trend for more deaths at the end of follow-up among amphetamine allocated patients (Peto OR 3.33; 95% CI 0.99 to 11.24). Based on 4 studies (95 patients) there was evidence of a better relative change in motor function according to the Fugl-Meyer motor scale (Weighted Mean Difference, [WMD] -8.17 points; 95% CI -13.58 to -2.76) and based on 1 study (21 patients) there was evidence of a better change in language function as assessed by the Porch Index of Communicative Ability score (WMD -7.51 points; 95% CI -14.42 to -0.60) in amphetamine allocated patients. REVIEWER'S CONCLUSIONS: 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 and language function, and the non-significant trend towards increased risk of death, could be related to imbalances in prognostic variables or other bias in studies. Further research in this area is therefore justified.

Amphetamines↗

New concepts for drug therapy after stroke. Can we enhance recovery?

Neurologic functions improve in most patients days and weeks after onset of a stroke. This can not be explained by recovery of the early salvageable ischemia zone. The most likely mechanism is relearning, a process in which healthy brain takes over functions lost with the infarct. Experimental studies indicate that this recovery can be modulated by pharmacological agents. NMDA antagonists and GABA agonists found to reduce infarct size in stroke models may have a harmful effect on relearning and neurologic recovery. This should be considered when clinical trial protocols are designed.

Cerebrovascular Disorders↗

The blood-brain barrier in adrenaline-induced hypertension. Circadian variations and modification by beta-adrenoreceptor antagonists.

Rats were subjected to adrenaline-induced acute hypertension during either the day or night. Albumin leakage into the brain was studied with Evans blue and 125I labeled serum albumin. The leakage was significantly lower during the night than during the day (P less than 0.001). d,1-propranolol had a protective effect (P less than 0.001) during the day and a slight reduction of the radioactivity (P less than 0.05 in some parts of the brain) was obtained by metoprolol (10 mg/kg) but not by butoxamine (10 mg/kg). None of the drugs reduced the tracer leakage during the night. The results suggest that the degree of alertness is of importance for the function of the blood-brain barrier in acute hypertension. However, the present experimental situation does not allow a separation of the effect of alertness per se and dark/light cycles. The changed vulnerability during the night could be related to enhanced neuronal activity, altered beta-adrenoreceptor sensitivity or to hormonal factors.

Adrenergic beta-Agonists↗

Blood-brain barrier to albumin in awake rats in acute hypertension induced by adrenaline, noradrenaline or angiotensin.

Acute hypertension was induced by adrenaline, noradrenaline or angiotensin in awake unrestrained rats with chronic indwelling catheters in a jugular vein and in the aorta. The leakage of 125IHSA (human serum albumin) into the brains from rats given adrenaline was significantly larger than in the brains from rats given noradrenaline or angiotensin. It is likely that the enhanced vulnerability of the blood-brain barrier to an adrenaline-induced increase in blood pressure is due to the beta-adrenergic stimulating effect of adrenaline.

Acute Disease↗