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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 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.

Catecholamine (CA) response to exercise was studied in patients with common (16 cases) or classic (7 cases) migraine as well as in subjects with lumbar disc disease (20 control cases). In migrainous patients exercise induced constantly a rise in epinephrine (E) urinary excretion and a depression in norepinephrine (NE) excretion; the post-exercise E excretion represented the double or the treble of basal E excretion. In controls the pattern of CA response to exercise was opposite to that noted in migraineurs: the exercise induced in almost all controls an augmentation in NE excretion and a depression in E excretion. The pattern of CA response to exercise of migrainous patients is similar to that noted in them after light exposure. As such patients responded by an E discharge to both exercise and light exposure, two conditions preceding quite often the onset of migraine attack, the data suggest the participation of this biochemical abnormality in the pathogeny of migraine. The interpretation is also supported by our previous data demonstrating that the antimigraine drugs are able to prevent the E discharge induced in migrainous patients by light exposure.

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 effect of amitriptyline on catecholamine (CA) response to light of 20 migrainous patients was studied. The drug was given orally, 36 mg daily (12 mg x 3), for ten days. Before therapy, the migraineurs responded to light by an increase in epinephrine (E) excretion and not by the rise in norepinephrine (NE) excretion, noticed in controls. The NE excretion of migrainous subjects underwent very often a depression after photostimulation. Amitriptyline therapy prevented the post-photic rise in E excretion of migraineurs, without influencing significantly the variation in NE excretion produced in them by light. In other 8 migrainous subjects the effect of flunarizine, a selective calcium channel blocker, on CA response to light was tested. The dosage was of 5 mg daily, for ten days. Flunarizine had similar effects to those displayed by amitriptyline; the drug prevented the rise in E excretion produced by light without normalizing the NE response to light of migrainous subjects. The results suggest that the efficiency of these two drugs in migraine prophylaxis is connected with the ability of these substances to block the E discharge produced in migraineurs by light or by other stimuli. The interpretation is all the more likely as propranolol, another drug applied in migraine prophylaxis also blocks the post-photic E discharge of migraineurs.

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.