Brain oxidative metabolism has been studied in nine patients with classical migraine at the Neurological Institute, University of Bologna, Italy. An increase in plasma lactate was found after standardized muscular effort and deficits of various mitochondrial respiratory chain enzymes in muscle biopsies occurred in 7. Two patients had 72% and 60% depression of cytochrome C oxidase activity; 1 also showed ragged red fibers and subsarcolemmal clusters of giant mitochondria with paracrystalline inclusions. The findings indicated a dysfunction of mitochondrial energy metabolism and suggested that migraine is the result of a defect of brain oxidative metabolism. The authors conclude that neural energetic lability, especially if coupled with vascular metabolic dysfunction, could result - particularly under stressful conditions - in the neurological deficits of classical migraine. It was their hypothesis that a metabolic oxidative defect involving brain cells and possibly brain vessels represents the critical factor predisposing migraineurs to transient or persistent neurological deficits. [1]

COMMENT. The neurological deficits of migraine have been attributed to brain ischemia or a primary derangement of brain metabolism. The progression of the aura and the prodromal symptoms are difficult to reconcile with a purely vascular problem and changes in platelet function suggest a diffuse extracerebral metabolic disturbance. Migraine attacks sometimes occur as complications of mitochondrial encephalomyopathies which reinforces the suggestion that migraine is the result of a defect of brain oxidative metabolism.