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The catecholamine (CA) response to light before and after propranolol therapy was studied in 25 migrainous subjects. Before therapy an abnormal CA response to light consisting of a rise in epinephrine excretion and a depression in norepinephrine (NE) excretion was noticed in migrainous patients. After propranolol administration (60 mg daily for 10 days) the post-photic augmentation in epinephrine excretion and the post-photic depression in NE excretion no longer occurred. As epinephrine discharge may be pathogenetic for migraine attack, the favorable effect of propranolol in migraine therapy could be due to its ability to prevent the epinephrine release induced by light or other stimuli.

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.