Vascular smooth muscle cell dysfunction in patients with migraine
William N.Devor, MD, Kaiser Permanente San Diego, UCSD Neurosciences Department, Neurology Department, 4405 Vandever Avenue, San Diego, CA 92120wdevor@san.rr.com
Submitted September 02, 2009
The article by Napoli et al. describing experimental techniques to quantify vascular endothelial reactivity illuminates the presence of arterial endothelial acetylcholine receptors which are known to be coupled to the NO vasodilatory pathway. [1]
The endothelial cholinergic receptors are presumably associated with vascular cholinergic nerve terminals arising from nervi vasorum present in the arterial tunica adventia. Such cholinergic vascular nerve terminals have been demonstrated in skin biopsy specimens using stains for acetylcholinesterase. Cholinergic nerve terminals are the target of botulinum toxin raising the possibility that cholinergic denervation of the scalp arteries may underlie the benefit of botulinum toxin injections in the treatment of migraine.
Typical injection sites used for treatment of migraine in the areas of the temporalis, frontalis and occipitalis muscles are close to the temporal, supraorbital and occiptal arteries. Abundant data exist describing the role of vasodilation of the extracranial scalp arteries in a subset of migraine patients. Does cholinergic denervation of the scalp arteries reduce vasodilation and thereby ameliorate migraine? The findings of Napoli et al. suggest that this may not be the case as responsiveness to intravascular acetylcholine is reduced in migraine patients.
The hypothesis that cholinergic denervation of the scalp arteries may underlie the benefit of cranial botulinum toxin injections in the treatment of migraine should be explored.
Reference
1. Napoli R, Guardasole V, Zarra E et al. Vascular smooth muscle cell dysfunction in patients with migraine. Neurology 2009;72:2111-2114.
Dr. Devor received an honorarium from Plaza Research; and administers botulinum toxin for treatment of headache in a non-profit setting.
The article by Napoli et al. describing experimental techniques to quantify vascular endothelial reactivity illuminates the presence of arterial endothelial acetylcholine receptors which are known to be coupled to the NO vasodilatory pathway. [1]
The endothelial cholinergic receptors are presumably associated with vascular cholinergic nerve terminals arising from nervi vasorum present in the arterial tunica adventia. Such cholinergic vascular nerve terminals have been demonstrated in skin biopsy specimens using stains for acetylcholinesterase. Cholinergic nerve terminals are the target of botulinum toxin raising the possibility that cholinergic denervation of the scalp arteries may underlie the benefit of botulinum toxin injections in the treatment of migraine.
Typical injection sites used for treatment of migraine in the areas of the temporalis, frontalis and occipitalis muscles are close to the temporal, supraorbital and occiptal arteries. Abundant data exist describing the role of vasodilation of the extracranial scalp arteries in a subset of migraine patients. Does cholinergic denervation of the scalp arteries reduce vasodilation and thereby ameliorate migraine? The findings of Napoli et al. suggest that this may not be the case as responsiveness to intravascular acetylcholine is reduced in migraine patients.
The hypothesis that cholinergic denervation of the scalp arteries may underlie the benefit of cranial botulinum toxin injections in the treatment of migraine should be explored.
Reference
1. Napoli R, Guardasole V, Zarra E et al. Vascular smooth muscle cell dysfunction in patients with migraine. Neurology 2009;72:2111-2114.
Dr. Devor received an honorarium from Plaza Research; and administers botulinum toxin for treatment of headache in a non-profit setting.