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Howard Sachs, MD, PhD; Alfred Wolf, PhD; Jerome A. G. Russell, PhD; David R. Christman, DSc

Arch Neurol. 1986;43(11):1117-1123.

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.

Author Affiliations
From the Department of Chemistry, Brookhaven National Laboratory, Upton, NY (Drs Sachs, Wolf, Russell, and Christman), the Department of Neurology, State University at Stony Brook (NY) (Dr Sachs), and Northport (NY) Veterans Administration Medical Center (Dr Sachs).

Footnotes
Accepted for publication July 10, 1986.

Presented at the Second International Headache Congress, Copenhagen, June 21, 1985, and at the 26th annual Scientific Meeting of the American Association for the Study of Headache, San Francisco, June 22, 1984.

Reprint requests to the Department of Chemistry, Brookhaven National Laboratory, Upton, NY 11973 (Dr Sachs).

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