PubMed · 491018
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K Uemura. 1979-06-29. [Cerebral regional circulation dynamics].. https://pubmed.ncbi.nlm.nih.gov/491018/
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Measurements of cerebral blood flow in man revealed that complex voluntary movements are associated with a blood flow increase in the supplementary motor area of the brain. This increase is additional to and similar in magnitude to the Rolandic sensorimotor area activation that occurs during all kinds of movement. When subjects counted silently there was no activation of any focal cortical area in the brain; when they counted aloud there was a marked increase in activity in the supplementary motor area. These results are consistent with the hypothesis that the supplementary motor area plays a major role in the initiation and control of at least some kinds of voluntary movement in man and is, therefore, a motor center of a higher order than the primary Rolandic areas.
The headache phase of migraine may develop as the result of an abnormal interaction (and perhaps an abnormal release) of vasoactive neurotransmitters from terminals of the trigeminal nerve with large intracranial and extracranial blood-vessels. These blood-vessels, which dilate during the headache phase of migraine, are thought to receive axonal projections from all three divisions of the trigeminal nerve. Substance P, a potent vasodilating peptide, seems to be released from trigeminal nerve endings in response to nervous stimulation and is involved in the transmission of painful stimuli within the periphery. The vasoactive molecule serotonin, implicated in the pathogenesis of migraine, coexists with substance P in some terminals of the central nervous system and is present within the trigeminal ganglia. Within this nerve serotonin may modulate the function of primary sensory neurons. The abnormal release of substance P or as yet unidentified peptides or other transmitters from the fifth cranial nerve may explain both the hemicranial pain and the vasodilation which are characteristic of the headache of migraine.