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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.

Transient ischemia of the extremities was applied in compression or traumatic neuropathies affecting radial nerve (17 cases), ulnar nerve (3 cases), upper brachial plexus (4 cases) or peroneal nerve (10 cases). The limb opposite to that displaying paresis was submitted repeatedly to a 15-minute-period of ischemia every other day for two weeks. The procedure induced in most patients (27 out of 34 cases) a motor improvement of variable degree. In some patients (13 cases) the motor recovery occurred two days or more after starting the procedures, while in others (14 cases) during the very day in which the initial session of ischemia was made or even during the first hour of procedure application. The most beneficial effects of peripheral ischemia were noted in compression neuropathy of peroneal nerve palsy, 9 out of 10 patients with such a disorder being improved by the procedure. We suppose that the method of therapy proposed by us restores promptly the motility of patients with compression neuropathy by inducing a long-lasting activation of some central neural mechanisms.

The effects of centrophenoxine on catecholamine (CA) response to orthostasis and on postural blood pressure fall of 25 patients with orthostatic hypotension due to brainstem ischemia were studied. Before therapy, the patients responded to posture by a depression in norepinephrine (NE) excretion and a rise in epinephrine (E) excretion. After a 10-day treatment with centrophenoxine, 800 mg daily, the patients responded to posture like normals, i.e. by a rise in NE excretion and a reduction in E excretion. Although the orthostatic blood pressure fall was less marked after treatment, the favourable clinical effect of the drug could not be correlated significantly with the restoration of CA response to posture after treatment.

The influence of head down (HD) tilting on brain-stem auditory evoked responses (BAER) was studied in hypertensives with supine brain-stem disorders (occipital headache, vertigo, nausea, diplopia, blurred vision occurring after night recumbency), in hypertensives without such phenomena and in normotensives. In the latter two categories of subjects HD tilting had no effect on BAER. On the contrary, in hypertensives with supine brain-stem disorders the manoeuvre induced a constant prolongation of I-V and III-V intervals and a depression in the amplitude of wave V; the alterations of BAER produced by HD tilting reveal probably a dysfunction of the superior brain-stem area and might be due to the impaired cerebral venous draining subsequent to the manoeuvre. The study of BAER after HD tilting seems to be a proper means to attest the supine brain-stem disorders displayed by some hypertensives.

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

Hypertensives with (25 cases) or without (27 cases) cerebral hemorrhage (CH) and normotensives (25 cases) were exposed from 7 to 8.30 a.m. to a low light input and from 8.30 to 10 to a high light input (HLI), and urinary epinephrine (E) and norepinephrine (NE) were measured at the end of these periods. In normotensives HLI had no effect on E and NE excretion; in hypertensives with and without CH it increased E excretion and depressed NE excretion. Light activation of E release may be responsible for the daytime occurrence of CH in hypertensives.

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.

Urinary excretion of catecholamines under insulin hypoglycemia was studied in cerebral infarct patients as well as in patients with Parkinson’s disease and subjects with lumbar discopathy (control group). While in the last two categories of subjects a normal response to hypoglycemia, i.e., an increase in urinary excretion of epinephrine was noticed, no such increase was found in patients with cerebral infarction. The disorder is attributed to the unresponsiveness to hypoglycemia of the brain stem centers controlling epinephrine secretion.

The dynamics of blood coagulability and fibrinolysis (comparison of the initial values of the heparin clotting time, recalcified plasma clotting time and plasma fibrinolytic activity with those obtained 30 and 120 min after the application of an emotional stimulus) was studied in patients with cerebral vascular accidents one or several months after a stroke. Emotional stress induced a sustained hypercoagulability only in patients with occlusive cerebral softening (verified by angiography) and in those with peripheral atherosclerosis obliterans; concomitantly, in these patients an unresponsiveness of the fibrinolytic system to stress was observed. The prolonged hypercoagulability induced by emotion in patients with occlusive cerebral softening is interpreted as expressing an imbalance between the clotting and the anticlotting factors in favour of the former.