Abstract
There is considerable evidence that the headache phase of migraine is associated with dilatation of the external carotid circulation [1, 4, 6,19]. Vasodilatation per se does not seem to be painful, as it may occur before the headache to the same extent as during it [1,19], and it may be bilateral during unilateral headache [4]. Thus, additional factors are required to mediate the pain. During the headache phase of classical migraine there are increases in both the intracranial blood flow and, especially, the extracranial blood flow [18]. The suggestion of Harold Wolff that the aura symptoms in classical migraine patients are due to cerebral ischaemia, which received some support from the blood flow studies of Sakai and Meyer [18], has led to the assumption that the headache is due to reactive hyperaemia following the reduction in cerebral blood flow, and that this reduction is not great enought to cause focal symptoms in attacks of common migraine. If this is the case, the headache should always occur on the side contralateral to the aura symptoms in classical migraine patients. With this in mind we have reviewed the lateralisation of the symptoms in classical migraine patients attending the Princess Margaret Migraine Clinic at Charing Cross Hospital [16].
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