Posted by Bob P (188.8.131.52) on August 14, 2000 at 10:24:53:
In Reply to: Cant read it. Password protected nt. posted by Doug L on August 14, 2000 at 10:08:09:
Deals with neurotransmitters and nerve stimulation in pain, etc. I'll try to difest it after work but looks interesting.
Here are the quick sections on migraine & cluster.
The results of trigeminal ganglion stimulation in man led my colleagues and me to examine the levels of various neuropeptides in patients during migraine attacks.
Blood samples were drawn from the external jugular vein during the headache. The patients were assessed using markers for the sympathetic (NPY), the
parasympathetic (VIP) and the trigeminovascular systems (CGRP and substance P). We observed no changes in the peripheral blood levels of the peptides studied,
or in NPY, VIP, or substance P in the external jugular venous blood; however, we noted a marked increase in CGRP during migraine headache. Two patients with
symptoms similar to those seen in cluster headache (eg, nasal congestion and rhinorrhea) had increases in VIP, but these changes were not significant for the group
as a whole. The changes in VIP suggest that some reflexive, parasympathetically mediated event was occurring. There was no difference between migraine with aura
or without aura; both resulted in substantial elevations in CGRP levels as recorded in the jugular venous outflow blood. There were also no differences in substance
P, VIP, or NPY levels in jugular or peripheral venous blood in patients with aura vs those without aura.
We postulated that the selective release of CGRP might be due to the fact that the cerebral circulation is preferentially innervated by CGRP from the trigeminal
ganglion. These observations have been confirmed in further studies.[17,18] We also found that following sumatriptan administration, CGRP returned to control
levels with successful amelioration of the headache.
Cluster headache is an ideal condition to examine in that it is a well-described, clear-cut clinical syndrome. Thus, we examined patients with episodic cluster
headache, upon fulfilling the criteria of the International Headache Society (IHS), during acute spontaneous attacks of headache to determine the local cranial release
of neuropeptides. During the attacks, the levels of CGRP and VIP were markedly raised, while there were no changes in NPY or substance P. Treatment with
oxygen or subcutaneous sumatriptan reduced the CGRP levels to normal, while opiate administration did not alter the peptide levels.
These data demonstrate activation of the trigeminovascular system and the cranial parasympathetic nervous system in an acute attack of cluster headache. It is
particularly noteworthy that all subjects had release of VIP. This is in concert with the facial symptoms well known to the symptomatology of this disorder.
Furthermore, it was shown that both oxygen and sumatriptan, while aborting the attacks, terminated the activity in the trigeminovascular system.
This agrees well with the results of others demonstrating release of CGRP in nitroglycerine-elicited attacks of cluster headache. Calcitonin gene-related peptide
was found to be augmented in the external jugular vein ipsilateral to the pain side in cluster headache patients during the active period and was further elevated at the
peak of the provoked attack. Complete reversal occurred during both the spontaneous and the sumatriptan-induced remission. Interestingly, nitroglycerine neither
provoked a cluster headache attack nor altered CGRP levels in patients outside of their cluster bout. In addition, there were no alterations in substance P levels.
Thus, CGRP, which marks the trigeminovascular system, and VIP, which marks parasympathetic activity, are both elevated in the cranial venous blood of patients
with an acute spontaneous attack of cluster headache. The termination of the attack with either sumatriptan or oxygen causes normalization of the CGRP levels,
reflecting cessation of activity in the trigeminovascular system, whereas pain relief after administration of an opiate agonist apparently terminates the pain of the attack
but does not immediately end the trigeminovascular activity. The finding of both CGRP and VIP in the cranial venous blood suggests that there is activation of a brain
stem reflex, the afferent arc of which is the trigeminal nerve, and the efferent arc, the cranial parasympathetic outflow from cranial nerve VII (Figure 2).
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