Transitory hearing impairment has been well documented in humans during basilar migraine attacks. Ischemia induced by activation of central nervous system adrenoreceptors by cAMP is one of the mechanisms that has been implicated, as well as calcium metabolism alterations. Propranolol-HCl has proven to be an effective treatment. Massive local adrenaline release is regarded as the primum movens mechanism triggering the liberation of other beta-receptor activators resulting in sterile edema and exudate. This exudate can be visualized (via ophthalmoscope) and is viewed as pathognomonic of a migraine attack. We investigated both the action of adrenaline and Propranolol-HCl on brainstem auditory potentials in 3 groups of young rats. The first group was perfused intra-arterially with adrenaline. The second group received the same treatment plus a prophylactic daily dose of Propranolol-HCl. The third group served as the control and received Propranolol-HCl, but was perfused with a Ringer solution. Alterations in blood flow and hearing sensitivity (BERA) following perfusion occurred in the first group only. Propranolol seems to exhibit a protective action during experimental attempts to induce migraine-like attacks in rats.
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