Abstract
In recent years there has been a popular tendency in medicine to make sweeping and unwarranted generalizations regarding the activity of the sympathetic nervous system in a number of clinical conditions of obscure etiology. Terms such as sympathicotonia, vagotonia, autonomic dysfunction and the like are commonly used in the literature as a cloak for ignorance of the actual mechanism of the condition in question. These remarks are particularly applicable to the problem of migraine, in which so many investigators recently have implicated the sympathetic nervous system in theories regarding the etiology of the disease.1These theories have been especially difficult to evaluate on account of the almost complete absence of evidence either for or against them. In spite of this situation, perhaps because of it, the theory of sympathetic dysfunction in migraine is becoming more widely accepted.2 The recent successful use of ergotamine in the relief of the
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