We report a severe acute headache that occurred in conjunction with a solitary fresh lesion of multiple sclerosis in the periaqueductal gray region of a 16-year-old girl. This unique natural event supports the recent proposition, based on observations of patients with implanted electrodes, that perturbations of the periaqueductal gray region can produce headache. It also suggests that headaches accompanying attacks of multiple sclerosis are due to disturbances in particular regions of the brain.

This paper reviews the literature on complex temporary disturbances of brain function triggered by mild blows to the head in children, adolescents, and young adults. It consolidates the evidence by which these attacks have been identified as classical or complicated migraines, and provides a historical account of the descriptions and proffered explanations of these attacks. The clinical features and the electroencephalography, angiography, computerized tomography, and cerebrospinal fluid findings of trauma-induced migraine are presented and compared to those of spontaneous migraine. Ideas about the pathogenesis of this condition are related to current thinking on the neurological phenomena of migraine in general.

The clinical spectrum of juvenile head trauma syndromes was derived from an analysis of 50 attacks in 25 patients. Attacks were grouped into four clinical types: (1) hemiparesis; (2) somnolence, irritability, and vomiting; (3) blindness; and (4) brain stem signs. Our evidence shows that these four types are different manifestations of a common underlying process. All attacks followed mild head trauma after a latent interval, generally of one to ten minutes. Forty of the 50 attacks occurred in patients under 14 years of age. Full recovery occurred after a variable time in all but one instance. This patient, and one other, had an angiographically demonstrable occlusion of a branch of the middle cerebral artery. In clinical and laboratory features, these attacks resemble classical migraine and presumably have a similar underlying mechanism.

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Some patients with cerebral arteriovenous malformations (AVMs) suffer recurrent migrainous attacks which meet the official criteria for migraine. The relationship of these attacks to the malformations has been poorly substantiated. Instances where attacks disappeared following surgical extirpation of an AVM support a relationship, but several other reported surgical outcomes do not. Both patients presented here had surgical results seemingly antithetical to a relationship: the attacks persisted in the first patient and began in the second after removal of the AVM. Nevertheless, data assembled from the literature attests to a causal role for AVMs in the production of migrainous attacks, by showing an overwhelming correlation between the side of the cranium with the AVM and the side afflicted by unilateral headache. An equally good correlation exists for lateralized auras. The correlative and surgical data together show that migrainous attacks develop in relation to AVMs, but not within the malformation itself. Instead, the neighboring brain is probably the generative site.