Juvenile Head Trauma Syndromes and Their Relationship to Migraine

Abstract

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.

Post–traumatic headache from moderate head injury

“…Also, in 1975 Haas [7] suggested that the same pathogenic mechanism existed in PTH and migraine in young patients, however, that the trauma was only a triggering momentum. In 1993, the same author did not find any relation between the severity of a trauma and the onset of chronic headache, and confirmed this in 1997 [8].…”

Delayed, Transient Neurological Deterioration After Mild Head Injury. Case Report.

“…in previously reported cases of JHTS in which the delay between head injury and the onset of the neurological episodes varied from several seconds, minutes, and hours up to 2 days, 7,8,25,27,29) and the episodes lasted from several minutes to several days. Presumably, the majority of the acute type of JHTS, especially those at intervals of several seconds or minutes, involve electrical and/or neuronal reflex phenomena such as cortical spreading depression 25,29) or a trigeminovascular response, because these phenomena appear immediately after the input of stimuli.…”

“…8) Cerebral angiography found no abnormalities in six of 37 patients with JHTS. 25) In contrast, investigation of migraine suggested that vasodilation and hyperemia are the underlying causes of JHTS, but there was no radiological evidence.…”

“…10) This finding suggests that hyperemia is involved in mild head injury, although the majority of patients regain normal autoregulation. 7,8,25,27,29) Post-traumatic hyperemia can be divided into malignant and benign types depending on the association with intracranial hypertension. 4,[12][13][14][15]19,23,26,27) Analysis of intracranial pressure and cerebral blood flow in 59 patients with moderate or severe head injuries showed that the median duration of hyperemia associated with intracranial hypertension was longer (median 6 days, range 1-14 days) than that of hyperemia without intracranial hypertension (median 2.5 days, range 0-5 days).…”

“…7,8,25,27,29) Almost all of the symptoms characteristically appear within 48 hours, usually within several hours, after craniofacial injury. 7,8,25,27,29) JHTS has recently been classified into acute and delayed types on the basis of whether symptoms appear before or after 48 hours. 27) However, any difference in the pathophysiologies for these types has not been identified.…”