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VASCULAR SMOOTH MUSCLE CELL DYSFUNCTION IN PATIENTS WITH MIGRAINE

DYSFUNCTION IN PATIENTS WITH MIGRAINE To the Editor: The article by Napoli et al.1 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. The endothelial cholinergic receptors are presumably associated with vascular cholinergic nerve terminals arising from nervi vasorum present in the arterial tunica adventitia. 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 occipital arteries. Abundant data exist describing the role of vasodilation of the extracranial scalp arteries in a subset of patients with migraine. 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 patients with migraine. 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. William N. Devor, MD, San Diego, CA