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Biology of Migraine and Other
Headaches |
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BY MAURY BREECHER
Contributing Writer |
SCOTTSDALE, ARIZ. (ECCC)—
The evidence for the role of cortical spreading depression (CSD)
as a cause of trigeminal activation which, in turn, causes
migraine pain and aura has gotten stronger, said Dr. Michael A.
Moskowitz on February 18 during a headache conference presented
by the Diamond Headache Clinic Research and Educational
Foundation.
“Experimental evidence supports a relationship between CSD as a
cause of migraine aura as well as CSD as a cause of trigeminal
activation,” explained Dr. Moskowitz, a professor of neurology
at Massachusetts General Hospital/Harvard Medical School,
Boston, in an interview following his presentation.
Dr. Moskowitz said the new evidence involved “knocking” human
mutations for Familial Hemiplegic migraine, a rare form of
migraine that causes paralysis, into laboratory mice.
As with migraineurs, the female mice were more susceptible than
males, and this susceptibility was linked to female hormones,
just like in humans, he said.
The data may have therapeutic implications in the development of
strategies to block trigeminal activation or its downstream
consequences that are key to the treatment of acute headache,
whereas strategies to block events lying upstream of trigeminal
activation “would be crucial in migraine prophylaxis,” said Dr.
Moskowitz.
He and his colleagues first demonstrated a link between a neural
mechanism now known as CSD with migraine aura and headache in
2002 (Nat Med. 2002;8(21):136-142). The researchers noted that
extracerebral cephalic blood blow activates trigeminovascular
meningeal afferents, evoking a series of cortical meningeal and
brainstem events consistent with the development of headache.
In 2005, Dr. Moskowitz demonstrated in the rat model that CSD
activated the trigeminovascular afferents and the development of
headache (J Headache Pain. 2005;6: (3)105-111).
“We speculated that visual, motor, or sensory aura might be
responsible for the generation of migraine pain and aura through
the mechanism we described,” said Dr. Moskowitz.
In one-fifth of all migraineurs, visual, sensory, or motor
neurological disturbance appears during or before the
development of the migraine aura.
Dr. Moskowitz and his fellow researchers have also learned that
susceptibility to CSD and to migraine “appears to be genetically
determined,” (Neurol Sci. 2006;27[suppl. 2]:S86-S90).
Overall, this research is helping build a better understanding
of migraine pathophysiology, he concluded.
“We believe it will eventually result in new insights into not
only migraine treatment, but also other neurological disorders
such as cerebral vascular disorders, transient global amnesia,
and traumatic brain injury.”
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