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A pooled analysis of 3 European randomized trials has shown that in patients with space-occupying hemispheric infarction, surgical decompression initiated within 48 hours of stroke onset strongly reduces the risk of death and increases the chance of a favorable functional outcome at 1 year. However, this large reduction in case fatality comes at the expense of an increased risk of moderately severe or severe disability at 1 year, 1 and the majority of survivors have global cognitive impairment.2 Some authors have therefore expressed concerns about the effect of decompressive surgery on long-term quality of life.3 It is unknown whether the effects of surgery at 1 year are sustained over a longer follow-up period. We assessed outcomes 3 years after inclusion in the randomized Hemicraniectomy After Middle cerebral artery infarction with Life-threatening Edema Trial (HAMLET). MethodsThe design of HAMLET (ISRCTN94237756) has been reported previously.1 In brief, adult patients ≤60 years of age with space-occupying hemispheric infarction were randomly assigned to surgical decompression or to best medical treatment. The trial was approved by institutional review boards, and written informed consent was obtained for each patient.The primary outcome measure was functional outcome as measured with the modified Rankin Scale at 1 year, dichotomized between good (modified Rankin Scale, 0-3) and poor (modified Rankin Scale, 4, 5, or death). Predefined secondary outcome measures included functional outcome at 3 years, and case fatality, functional dependence assessed with the Barthel Index, quality of life assessed with the Medical Outcomes Study 36-item short-form health survey and a visual analogue scale, symptoms of depression measured by the Montgomery and Åsberg Depression Rating Scale, and caregiver strain assessed with the caregiver strain index at 1 and at 3 years.Background and Purpose-We assessed whether the effects of surgical decompression for space-occupying hemispheric infarction, observed at 1 year, are sustained at 3 years. Methods-Patients with space-occupying hemispheric infarction, who were enrolled in the Hemicraniectomy After Middle cerebral artery infarction with Life-threatening Edema Trial within 4 days after stroke onset, were followed up at 3 years. Outcome measures included functional outcome (modified Rankin Scale), death, quality of life, and place of residence. Poor functional outcome was defined as modified Rankin Scale >3. Results-Of 64 included patients, 32 were randomized to decompressive surgery and 32 to best medical treatment. Just as at 1 year, surgery had no effect on the risk of poor functional outcome at 3 years (absolute risk reduction, 1%; 95% confidence interval, −21 to 22), but it reduced case fatality (absolute risk reduction, 37%; 95% confidence interval, 14-60). Sixteen surgically treated patients and 8 controls lived at home (absolute risk reduction, 27%; 95% confidence interval, 4-50). Quality of life improved between 1 and 3 years in patients treated with surgery. Conclusions-...

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Creatine kinase (CK) release from male and female rat soleus muscles was studied for 4.5 h in vitro, under basal conditions and after electrical stimulation. Basal CK release was greater from male than from female muscles, and CK release from male muscles increased significantly when the muscle tension in the in-vitro set-up was increased. CK release after electrical stimulation was also more marked in male soleus muscles. Pretreatment of male rats and ovariectomized female rats with oestradiol for 3 weeks attenuated the enzyme efflux, but ovariectomy 24 h before in females, or oestradiol administration 24 h before in males, did not affect the release of CK in vitro. The data show that sex-linked differences in CK efflux are still present, under both basal and stimulated conditions, when muscles are isolated from the intact animal, and that hormone treatment of the intact animal affects these properties in the isolated muscle in vitro.

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Rats, fed a vitamin-E-deficient diet for 6 weeks, performed treadmill exercise for 2 h. Muscle damage was assessed by measuring the creatine kinase (CK) activity in plasma before and after exercise, and by studying semi-thin longitudinal sections of the soleus muscle 48 h after running. Vitamin-E-deficient male and female rats showed an increased post-exercise CK activity when compared to matched controls, but male rats showed a larger CK response than females. This rise in plasma CK activity was caused mainly by an increased activity of the muscle-specific CK-isoenzyme, CK-MM (males + 1238%; females + 540%, P less than 0.05). In a parallel histological study we observed in vitamin-E-deficient male rats a dramatic and significant disturbance of the normal cyto-architecture of the muscle fibres after exercise (focal necrosis, phagocytosis and cellular infiltrates), whereas in females only minor, non-significant, changes were seen. We conclude that vitamin E deficiency enhances the susceptibility to exercise-induced muscle damage in male rats more than in female rats. This difference between the sexes is attributed to the protective effect of oestradiol that remains operative in female rats when the vitamin E status is disturbed: male rats lack such hormonal protection.

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