Editorial Commentarv Spreading Depression Idio Athic Stabbing Hea (p Ache Neurovascular Disturbances in Head- Ache Patients. Clin Exp Neurol 4. Ekbom K. Some Observations on Pain in Cluster Headache. Headache Tension Headache

In a well-designed study, Piper et al. demonstrate that the induction of a cortical spreading depression (SD) by a stab wound to the cortex of the cat is dependent on the anesthetic employed. Isoflurane and halothane, commonly used volatile anesthetics in humans, inhibit SD. In contrast, a-chloralose, an injectable anesthetic, permits the induction of SD. The authors suggest that failure to observe SD in patients during neurosurgical procedures may be attributed to the use of volatile anesthetics. SD has been hypothesized as playing an important role in cerebrovascular pathophysiology. It is present in rat brain after focal cerebral ischemia, and the numbers of spreading depressions correlate with ischemic cell damage. SD has also been hypothesized as contributing to the pathogenesis of migraine. Although the literature contains provocative studies on the role of SD in cerebral pathophysiology, the lack of evidence supporting the presence of SD in the human dampens enthusiasm for these laboratory studies. The present work provides a possible explanation for the inability to document SD in neurosurgical patients by suggesting that anesthetic agents block SD, and thus keep alive the clinical relevance of SD as an important pathophysiological event. The results of the present study are also important for investigations of experimental cerebrovascular pathophysiology such as stroke and head trauma. If SD contributes to the cell damage in stroke and head trauma, the effect of anesthetic agents on SD in experimental models must be determined. A secondary benefit of the present study is that it provides insight into the mechanisms that facilitate the induction of SD. The authors discuss the effects of halothane and isoflurane on K + conductance and concentration, and the role of glial cells contributing to the induction of SD. In summary, this is an important study because it encourages further investigations into the role of SD in migraine and cerebrovascular injury, and provides opportunities to modify SD by mechanisms analogous to those provided by anesthetic agents.