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Barbanti and Fabbrini draw attention to reported evidence linking the pathophysiological features of migraine with the extrapyramidal system and suggest that the high frequency of migraine in TS, reported by us, may be attributed to the aberrant basal ganglia–thalamocortical circuitry underlying TS. They previously proposed a role of the basal ganglia in migraine based on their observation that the substantia nigra and red nucleus are activated during migraine attack, as demonstrated with functional magnetic resonance imaging.¹

Dysfunction of the basal ganglia–thalamocortical neural circuitry in TS has been suggested by several physiological and imaging studies.^2-3 On the basis of various functional imaging and neurophysiological studies, failure to inhibit unwanted or noxious stimuli, which may be relevant in TS migraines, has been associated with hypometabolism and physiological abnormalities in particular areas in the basal ganglia and temporolimbic pathway, specifically the anterior cingulate and parahippocampal and insular cortices. Although the underlying . . . [Full Text of this Article]

Joseph Jankovic, MD; Carolyn Kwak, PA
Houston, Tex