Functional imaging in migraine
Migraine is a common disabling condition likely to be associated with dysfunction of brain pathways involved in pain and other sensory modalities. Functional brain imaging in acute migraine has proved challenging due to the logistic problems associated with an episodic condition although it has provided us with important insights into the pathophysiology of the condition. Since the seminal observation of brainstem activation in migraine there has only been a single case substantiating this finding. Our objectives were, first, to test the hypothesis that brainstem activation could be detected in migraine and to refine the anatomical localisation with higher resolution positron emission tomography (PET) and more advanced analysis techniques. Secondly, we wanted to explore the glyceryl trinitrate (GTN) model of migraine further to determine reliability and reproducibility. Finally, using this model we wished to explore the issue of laterality in migraine and, in particular, how it relates to brainstem activation. H2150-labelled PET was used to study acute migraine attacks occurring spontaneously in five migraineurs. Using GTN-triggered migraine twenty-four migraineurs (divided into three groups according to the site of their headache: right/ left/ bilateral) and eight controls were scanned. The data was analysed using statistical parametric mapping (SPM99). Significant brainstem activation was seen in the dorsolateral pons (P < 0.05 after small volume correction) during the migraine state versus the pain-free state in both spontaneous and induced migraine groups. When the induced group was analysed separately, to investigate laterality, it was found that the dorsal pontine activation was ipsilateral in the right-sided and left-sided groups and bilateral in the bilateral headache group with a left-sided preponderance. Looking at the GTN model, thirty-three of the forty-four patients administered GTN had a migraine attack fulfilling International Headache Society criteria. Twelve patients described typical premonitory symptoms, which have not been previously documented with GTN-induced migraine. A repeat attack was triggered in all subjects but one and laterality was also remarkably reproducible. In one case a visual aura was also triggered both times. Our study shows that GTN-induced triggering is common in our patients, and remarkably reproducible. Overall, our findings provide clear evidence for dorsal pontine activation in migraine, and reinforce the view that migraine is a subcortical disorder involving modulation of afferent neural traffic. The results also suggest that lateralisation of pain in migraine is due to lateralised brain dysfunction.