Posted by Bob P (129.65.106.155) on November 13, 2000 at 22:31:30:
In Reply to: Called em vascular headaches..some smart person wanna jump in here(NT) posted by Dennis O'C on November 13, 2000 at 18:15:05:
This is copied from the OUCH Library.
J Cereb Blood Flow Metab 1999 Feb;19(2):115-27
The trigeminovascular system in humans: pathophysiologic implications for
primary headache syndromes of the neural influences on the cerebral
circulation.
May A, Goadsby PJ
University Department of Clinical Neurology, Institute of Neurology, The
National Hospital for Neurology and Neurosurgery, London, UK.
Primary headache syndromes, such as cluster headache and migraine, are
widely described as vascular headaches, although considerable clinical
evidence suggests that both are primarily driven from the brain. The shared
anatomical and physiologic substrate for both of these clinical problems is
the neural innervation of the cranial circulation. Functional imaging with
positron emission tomography has shed light on the genesis of both
syndromes, documenting activation in the midbrain and pons in migraine and
in the hypothalamic gray in cluster headache. These areas are involved in
the pain process in a permissive or triggering manner rather than as a
response to first-division nociceptive pain impulses. In a positron
emission tomography study in cluster headache, however, activation in the
region of the major basal arteries was observed. This is likely to result
from vasodilation of these vessels during the acute pain attack as opposed
to the rest state in cluster headache, and represents the first convincing
activation of neural vasodilator mechanisms in humans. The observation of
vasodilation was also made in an experimental trigeminal pain study, which
concluded that the observed dilation of these vessels in trigeminal pain is
not inherent to a specific headache syndrome, but rather is a feature of
the trigeminal neural innervation of the cranial circulation. Clinical and
animal data suggest that the observed vasodilation is, in part, an effect
of a trigeminoparasympathetic reflex. The data presented here review these
developments in the physiology of the trigeminovascular system, which
demand renewed consideration of the neural influences at work in many
primary headaches and, thus, further consideration of the physiology of the
neural innervation of the cranial circulation. We take the view that the
known physiologic and pathophysiologic mechanisms of the systems involved
dictate that these disorders should be collectively regarded as
neurovascular headaches to emphasize the interaction between nerves and
vessels, which is the underlying characteristic of these syndromes.
Moreover, the syndromes can be understood only by a detailed study of the
cerebrovascular physiologic mechanisms that underpin their expression.
Publication Types:
* Review
* Review, tutorial
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