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The effect of forearm or calf ischemia on computerized EEG was studied in five patients with peripheral nervous system affections and five patients with cerebral infarction. Spatial analysis of power spectra in various frequency bands was performed in two 8-sec epochs, the former before ischemia and the latter after 5-min from the cessation of circulatory arrest which lasted 15 min. Transient peripheral ischemia resulted in consistent augmentation of alpha activity involving both the anterior and the posterior hemispheric areas, bilaterally. On the other hand, the slower frequency bands (theta, delta) underwent minor, nonsignificant alterations after ischemic stress. The rise of alpha amplitude induced by ischemic stress was ascribed to the activation of nonspecific thalamic system. The activation of this system might also be involved in the favourable effects exerted by ischemic stress on motor recovery of paretic limbs.

The catecholamine (CA) response to upright posture was studied in 30 brainstem infarct patients with orthostatic arterial hypotension; the investigation was made before and after 10 days propranolol therapy (in 15 cases) and before and after 10 days metoclopramide therapy (in other 15 cases). Before treatment almost all patients responded to posture by a rise in adrenaline (A) excretion and by a depression in noradrenaline (NA) excretion. Propranolol therapy prevented the excessive A release produced by standing and normalized their NA response to posture. Metoclopramide administration also prevented the post-orthostatic A discharge but had no significant influence on NA response to posture. Both drugs exerted a favourable influence on postural hypotension of investigated patients. As post-orthostatic A discharge observed in patients with postural hypotension is involved in the pathogeny of this syndrome and both metoclopramide and propranolol are able to correct this disorder one may maintain that the clinical favourable results obtained with these drugs are ascribable at least partly to their blocking effect on A release.

The reactivity of the higher autonomic centers to hypoglycemia prior to and after the treatment with pyrithioxin or caffeine in patients with cerebral infarct was studied. Before treatment a hyporeact

A method of treatment consisting in administration of a neurodynamic drug, pyrithioxin, combined with a short period of hyperventilation (HV) was applied in cerebral infarct patients with hemiplegia. The combination was superior to pyrithioxin alone for the motor recovery of these patients. In some cases, it induced immediately a partial restoration of motility. The combination constantly brought about an increase in urinary excretion of norepinephrine and vanilmandelic acid, which failed to occur after pyrithioxin or HV alone. HV appears to facilitate the neural effects of the drug by promoting its transfer into the CNS.

The oral erythrodiapedesis was studied by estimating the number of erythrocytes in the sediment of oral washing fluid. The investigation was performed in the acute period of cerebrovascular accidents. Most of the patients with cerebral infarct (84%) displayed a low oral erythrodiapedesis similar to that noticed in controls. On the contrary more than half of the cerebral hemorrhage patients exhibited a high oral erythrodiapedesis. The authors assume that the cerebral hemorrhages associated with enhanced oral erythrodiapedesis are caused by some general humoral disturbances with repercussion both on cerebral and other capillaries. They feel that the investigation of oral erythrodiapedesis is a reliable test for differentiation between hemorrhagic and ischemic cerebral accidents.