Effect of Reserpine on Regional Cerebral Glucose Metabolism jjss in Control and Migraine Subjects

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Abstract
• The regional cerebral metabolic rate of glucose metabolism (RCMRGIu) in five headache and six control subjects was measured with positron emission tomography (PET) using the tracer 2-deoxy-D-[1-11C] glucose before and after the administration of reserpine. The short half-life of the carbon 11 tracer made possible a test-retest paradigm wherein each subject served as his own control in assessing the effect of reserpine on RCMRGIu. Thus, measurements were first performed with subjects at rest and subsequently at 1 1/2 hours after the parenteral administration of reserpine (rest-reserpine). In control subjects without history of migraine, reserpine did not induce headache, and, furthermore, PET measurements 11/2 hours after drug administration consistently showed a global increase in RCMRGIu over resting values similar to that observed in a normal control (rest-rest) group not receiving reserpine. By contrast, four of the five subjects with migraine began to experience a mild unilateral headache or visual disturbances 11/2 hours after reserpine, at which time PET scanning showed a 5% to 30% decline in RCMRGlu below the values that had been measured before reserpine injection, all well outside of the 99% confidence limits of normal variation separately determined on 25 control subjects (rest-rest). There was no apparent laterality, and subjects with a history of either common or classic migraine responded in a similar manner. The difference in percent change in RCMRGIu following administration of reserpine observed in these four subjects with migraine headaches was significantly different over all regions of interest as compared with all six control subjects receiving the drug. In one subject with migraine headaches, RCMRGIu was determined through the headache phase (31/2 hours after administration of reserpine); RCMRGIu at this time was greater than the values measured at 11/2 hours after the administration of reserpine, but still well below the resting levels. From this study, it would appear that cerebral glucose hypometabolism is an initial and persistent event in the migrainous headache induced by reserpine in susceptible subjects. Although this result supports the model of deranged cerebral function as being part of the migraine headache, it does not rule out the involvement of other or additional mechanisms in the spontaneous attack.

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