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BRIEF COMMUNICATIONS: Eduard Linetsky, Ronen R. Leker, and Tamir Ben-Hur Headache characteristics in patients after migrainous stroke Neurology 2001; 57: 130-132 [Abstract] [Full text] [PDF]

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Reply to Allaryari et al.

T Ben-Hur, "R R Leker, E Linetsky"   (6 November 2001)

Headache characteristics in patients after migrainous stroke

P Allaryari, "GN McAbee, L Mueller, R White"   (6 November 2001)

Reply to Allaryari et al. 6 November 2001
T Ben-Hur Hadassah-Hebrew University Hospital Jerusalem Israel, "R R Leker, E Linetsky" Send Correspondence to journal: Re: Reply to Allaryari et al. tamir{at}hadassah.org.il T Ben-Hur, et al.	Allaryari et al describes a patient in whom migraine attacks disappeared after a major left hemispheric infarction. They suggest that the cessation of migraine headaches after the stroke may be related to a reduced cortical excitability secondary to the brain injury. This patient would not have entered our series since he did not meet the strictly defined criteria of migrainous cerebral infarction: Headache at presentation of stroke was different from his typical migraine attacks, and the neurologic deficit did not correspond to his aura. The development of a major stroke in association with unilateral headache, presence of ptosis (possibly due to a partial Horner syndrome) and complete occlusion of the ICA in a relatively young patient may suggest that he suffered from arterial dissection. Dissection of the ICA has been related to migraine. [1, 2] The suggestion that pain is no longer perceived after stroke due to impaired central processing does not seem a likely mechanism in our cases of migainous infarction, as most patients had a mild stroke with excellent recovery. Moreover, subcortical function (i.e. thalamus) is sufficient to perceive pain, although without accurate localization. An apparent association between loss of vasoreactivity and improvement in migraine headaches was observed in two of our patients as well as in the general population of migraineurs. [3] This may suggest that reduced responses of the arterial wall to vasoactive substances may be associated with reduced pain transmission, according to current evidence on trigemino-vascular mechanisms in the initiation of pain independently from cortical excitability. [4] One could speculate that if, indeed, the patient of Allaryari et al had a dissection, it may have also involved the proximal middle cerebral artery and reduced its nociceptive-transmitting capabilities. In view of their interesting case, it would be interesting to study whether headache patterns change in-patients after strokes of various causes. References: 1. D'Anglejan-Chatillon J, Ribeiro V, Mas JL, Youl BD, Bousser MG. Migraine--a risk factor for dissection of cervical arteries. Headache 1989;29:560-561. 2. Biousse V, D'Anglejan-Chatillon J, Massiou H, Bousser MG. Head pain in non-traumatic carotid artery dissection: a series of 65 patients. Cephalalgia 1994;14:33-36. 3. Meyer JS, Terayama Y, Konno S et al. Age-related cerebrovascular disease alters the symptomatic course of migraine. Cephalalgia 1998;18:202 -208. 4. Goadsby PJ, Edvinsson L. The trigeminovascular system and migraine: studies characterizing cerebrovascular and neuropeptide changes seen in humans and cats. Ann Neurol 1993;33:48-56.
Headache characteristics in patients after migrainous stroke 6 November 2001
P Allaryari UMDNJ-SOM Stratford, NJ, "GN McAbee, L Mueller, R White" Send Correspondence to journal: Re: Headache characteristics in patients after migrainous stroke sandi_moriarity{at}urmc.rochester.edu P Allaryari, et al.	Linetsky et al. report an interesting observation regarding six patients with migrainous stroke whose headache severity and frequency improved following stroke. [1] The putative mechanism was a loss of vasoreactivity of the affected cerebral blood vessel ( to vasodilator substances), as determined by breath holding index (BHI), resulting in reduced nocipetive transmission. The significance of reduced blood flow measured by BHI is unclear in migraine, as it has been reported with carotid stenosis (without apparent headache), in migraineurs between attacks, and also as generalized phenomenon during attacks of unilateral migraine without aura. [2, 3] We report a similar patient and propose that these patients provide support for a direct affect on cortex as the reason for improvement in migraine. A 53-year-old man had a 20-year history of bilateral migraine headaches lasting 6-8 hours at a frequency of 2-3 months. A prodrome of sudden fatigue and generalized non-specific discomfort preceded the headaches. His father died of a stroke at age 58. Family history for migraine was present in his mother, oldest brother (and his children), and his younger sister. The patient had no prior history of coronary artery disease, diabetes, hypercholesteremia or hypertension. He was diagnosed with unilateral loss of vision with ptosis, eye pain and subsequent headache, which was unrelieved with subcutaneous sumatriptan and oral naratriptan (administered over several days). On the third day he developed global aphasia and right hemiplegia/hemisensory deficits. Initial CT was negative; follow-up 36 hours later demonstrated a large, acute, left middle cerebral artery infarction. MRI/MRA demonstrated a large area of left hemisphere infarction involving middle cerebral artery which primarily involved frontal and temporal lobes, especially operculum, extending medially to involve deep gray as well as internal and external capsules. There was complete occlusion of the left internal carotid artery from its origin off of the common carotid. Echocardiogram and coagulations studies were negative. Follow-up 28 months later showed the patient has an expressive aphasia, right hemiparesis/mild hemisensory loss, but has remained headache free. Three of Linetsky’s patients, as well as ours, had infarction/ischemia in major cortex regions. Two others had involvement of frontoparietal subcortical region and cerebellum, which can directly affect cortical function. [4] The reduction in migraine might simply be attributed to the damaged cortex’s reduction in excitability to external stimuli, and the effect on spreading cortical depression. [5] Could the authors comment on the possibility that migraine pathophysiology may still be occurring in these patients, but pain is not being perceived due to impaired central processing of pain? Can they correlate infarct size and specific neuroanatomical regions affected to possible damaged neurotransmitter/neuropeptide systems? Could the proposed reduction in nociceptive transmission be explained by decreased sensory input from areas with sensory loss? References: 1)Linetsky E, Leker R R, Ben-Hur T. Headache characteristics in patients after migrainous stroke. Neurology 2001;57:130-132. 2)Markus H S, Harrison M J G. Estimation of cerebrovascular reactivity using transcranial Doppler, including the use of breathholding as the vasodilatory stimulus. Stroke 1992;23:668-673. 3)Silestrini M, Cupini L M, Troisi E, et al. Estimation of cerebrovascular reactivity in migraine without aura. Stroke 1995;26:81-83. 4)Newburg, A B, Alavi A, Alavi J. Contralateral cortical diaschisis in a patient with cerebellar astrocytoma after radiation therapy. Clin Nucl Med 2000;25:431-433. 5)Woods R P, Iacoboni M, Mazziotta J C. Bilateral spreading cerebral hypoperfusion during spontaneous migraine headache. N Engl J Med 1994;331:1689-1692.