Sixty patients admitted to hospital for hemispherical ischemic stroke causing severe disabilities were enrolled in the study. The patients were divided in two groups: A and B. The patients in group A were given intensive rehabilitative treatment; those in group B were given ordinary rehabilitative treatment. Both treatments lasted 14 days. At the end of that period, the patients of both groups were sent to the same rehabilitation center to continue treatment, using the same methods for all. The patients were evaluated by means of the modified N. I. H. Stroke Scale and the Barthel-Index on the day of enrollment, on the 14(th) and 180(th) day. The results obtained from intensive treatment were no better than those obtained from ordinary treatment. This study shows that there is no point in adopting an intensive rehabilitative treatment for an ischemic stroke in its acute phase: a more expensive and time-consuming effort does not in any way lead to a better outcome.

Glutamate dehydrogenase (GDH) activity was studied in 17 regions of six human brains. Duration and conditions of the postmortem period did not affect enzyme activity. Specific activity ranged between 103 and 377 nmoles/min/mg protein at 25 degrees C and it was 10-fold higher than that found in leukocytes. Apart from exclusively white matter regions (corpus callosum and centrum ovale), there was a moderate regional distribution (2.5-fold variation), with highest values in the inferior olive and hypothalamus, and lowest in the cerebellum and lenticular nucleus. With alpha-ketoglutarate (alpha-KG), NADH, or NH4+ as variable substrate, the apparent Km values in human brain were Km alpha-KG = 1.9 X 10(-3) M, KmNADH = 0.21 X 10(-3) M, and KmNH4+ = 28 X 10(-3) M, and in leukocytes they were Km alpha-KG = 1.7 X 10(-3) M, KmNADH = 0.24 X 10(-3) M, and KmNH4+ = 28 X 10(-3) M. The effects of cofactors, inhibitor, and pH were similar in brain and leukocyte GDH.

The binding of L-[3H]aspartate was investigated in washed membranes prepared from whole rat brain. We were able to differentiate two separate binding sites differing in their Na dependence. The Na-independent binding was saturable, reversible, and optimal at 20 degrees C and at pHs in the neutral range. The dissociation constant (Kd) at 20 degrees C was about 200 nM. This binding site seemed to be modulated by magnesium and calcium at physiological concentrations. None of the amino acids tested was a potent competitor for Na-independent L-[3H]aspartate binding. This binding site was unevenly distributed in the rat central nervous system: cerebellum = cerebral cortex greater than pons-medulla greater than spinal cord. Destruction of the intrinsic neurons of the cerebellum by injecting kainic acid 30 days before sacrifice resulted in a 53% reduction in Na-independent binding in this region. The Na-dependent binding of L-[3H]-aspartate (Kd = 4894 nM) was strongly inhibited by D-aspartate, L-glutamate, D,L-aspartate beta-hydroxamate; was unaffected by calcium and magnesium; and showed a different pattern of distribution: cerebral cortex greater than cerebellum = pons-medulla = spinal cord. This binding in cerebellum was unaffected by injections of kainic acid.

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