Biotech Values

[biomaven0]

> Migraine prevention and suvorexant

I did a bit of digging, and this is all I could come up with on the basis for this:

We have showed that the level of plasma orexin-A in the migraine patients during headache free period is lower than that of control. From the animal experiments, we also showed that intracerebroventricular injection of orexin induces the increase in the cerebral cortical blood flow, and that the intraarterial application of orexin cannot increase the cerebral blood flow. We consider that orexinegic neurons in the lateral hypothalamus may be a generator of migraine.

Versus this perhaps contradictory finding:

Cephalalgia. 2008 Jul;28(7):714-22. Epub 2008 May 13.
Involvement of corticotrophin-releasing factor and orexin-A in chronic migraine and medication-overuse headache: findings from cerebrospinal fluid.
Sarchielli P, Rainero I, Coppola F, Rossi C, Mancini M, Pinessi L, Calabresi P.
Source
Neurologic Clinic, University of Perugia, Perugia, Italy. [e-mail]
Abstract
The study set out to investigate the role of corticotrophin-releasing factor (CRF) and orexin-A in chronic migraine (CM) and medication-overuse headache (MOH). Twenty-seven patients affected by CM and 30 with MOH were enrolled. Control CSF specimens were obtained from 20 age-matched subjects who underwent lumbar puncture for diagnostic purposes, and in all of them CSF and blood tests excluded central nervous system or systemic diseases. Orexin-A and CRF were determined by radioimmunoassay methods. Significantly higher levels of orexin-A and CRF were found in the CSF of MOH and to a lesser extent in patients with CM compared with control subjects (orexin-A: P < 0.001 and P < 0.02; CRF: P < 0.002 and P < 0.0003). A significant positive correlation was also found between CSF orexin-A values and those of CRF (R = 0.71; P < 0.0008), monthly drug intake group (R = 0.39; P < 0.03) and scores of a self-completion 10-item instrument to measure dependence upon a variety of substances, the Leeds Dependence Questionnaire (LDQ) in the MOH group (R = 0.68; P < 0.0003). The significantly higher orexin-A levels found in CM and MOH can be interpreted as a compensatory response to chronic head pain or, alternatively, as an expression of hypothalamic response to stress due to chronic pain. A potential role for orexin-A in driving drug seeking in MOH patients through activation of stress pathways in the brain can also be hypothesized.

So unclear if an antagonist would help here, but who knows. The hypothalamus has often been suspected as a possible instigator of migraine.

Peter