Superior oblique myokymia as a migraine motor aura

Abstract

Abstract Purpose To do an epidemiological study of the proposal that superior oblique myokymia (SOM) is a migraine motor aura and propose a pathophysiological basis for the etiology of SOM. Migraine aura is a paroxysmal spreading depression of both excitatory and inhibitory neurons in the brain. These may be sensory neurons (numbness), motor neurons (dysarthria) and inhibitory neurons (chorea). Superior oblique myokymia is bursts of very rapid, jerky contrations of a superior oblique muscle causing shaking of one eye. Interfunctioning of the cortex and basal nuclei maintains stability of eye movements. Spreading depression of the cortex would cause inhibition of the inhibitory GABAergic fibres from basal ganglia to the midbrain which could result in paroxysmal firing of the 4th nerve neurons in SOM. A finely‐tuned homeostatic balance of GABAergic interneuron tone controls excitatory activation of CNS motorneurons. Small changes in GABAergic inhibition have profound effects on excitability. SOM, like auras, usually spontaneously disappears for years or permanently, which may account for the "success" of surgical treatments. The most effective treatment of SOM is gabapentin, a congener of GABA which enhances its activity. Methods Thirty seven patients with superior oblique myokymia had detailed questioning about a history of migraine headaches and auras. Results Every one of 37 patients with superior oblique myokymia had a history of migraine symptoms fulfilling all International Headache Society criteria. Every one had a history of migraine visual auras and many had also had sensory and dysphasic auras. Conclusion Epidemiological correlation and a pathophysiological explanation support the proposal that superior oblique myokymia is a migraine motor aura.