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Editorial Commentary
Migrainous stroke
Reports of migraine-associated stroke appear in the medical literature with regularity, but uncertainty persists as to themechanisms which may generate this uncommon complication of a common condition. In their article in this issue Drs Saninand Mathew describe a patient with migrainous stroke and arteriographic findings consistent with diffuse cerebral vasospasm.
In previous surveys of migrainous stroke, investigators have reported widely varying frequencies of abnormal cerebralangiography (1, 2). Arteriograms performed acutely appear to yield abnormal findings more often than those performed atlonger intervals following stroke onset. In many cases the abnormal findings reported have suggested vasospasm, and, in atleast one instance, serial arteriography demonstrated alternating and rapidly resolving internal carotid stenosis or occlusion(2).
While these data and the information now provided by Sanin and Mathew do not establish vasospasm as the causative mechanism in all cases of migraine-associated stroke, they do seem to establish a role for vasospasm in a proportion of suchcases. What implications this may have for acute treatment of migraine and migrainous stroke is unclear, but, as somepatients do exhibit hypersensitivity to circulating vasoactive amines during migraine attacks, administration of agents such asergotamine tartrate, dihydroergotamine or sumatriptan theoretically could produce or aggravate vasospasm in those patients.
Whether this presumed risk may outweigh the benefit of rapidly terminating the migraine attack with effective and relativelyspecific interventional therapy remains to be established.
Bogousslavsky J, Regli F, Van Melle G, Payot M, Uske A. Migraine stroke. Neurology 1988;38:223-7 Rothrock JF, Walicke P, Swenson MR, Leyden PD, Logan WR.
Migrainous stroke. Arch Neurol 1988;45:63-7 Charcot and Féré on migrainous infarction
The exemplary work on migraine by Charcot and his school has been forgotten since the 1940s, except in France.
Jean-Martin Charcot was the protagonist of French and international neurology in the last quarter of the 19th century. He wasthe first to propose that any transient neurological deficit in migraine could become permanent, and his disciple, Féré,published classic examples to illustrate Charcot's doctrine. Their work stands out at the beginning of a century of research onwhat the IHS classification of 1988 calls migrainous infarction, and it certainly deserves to be brought to the attention ofinternational readers in translation from the original French texts. Dr Ramadan is presenting Féré's observations as appliedhistory of medicine, comparing the ideas of these pioneers with current findings and theories, and he proposes the eponym ofCharcot-Féré syndrome for migrainous stroke. My own preference is to add yet another eponym, my reasoning for which Iprovide in greater depth in the Historical Section.
A gonadotropin-releasing hormone analog in chronic cluster headache
The circadian and circannual periodicity of cluster headache has been related to dysfunction of rhythm-regulating centers ofthe central nervous system (CNS). Several hormones have been studied (1), and, among others, low testosterone levels havebeen reported during active periods of cluster headache. The importance of this observation is at present somewhat unclear,however.
In this article, Nicolodi et al. have administered a gonadotropin-releasing hormone (Gn-RH) analog (leuprolide) to 30 male patients with chronic cluster headache in an attempt to modulate the activities of central neurons that might be of criticalimportance for the pain mechanisms in cluster headache. Leuprolide was found to induce a significant decrease of clusterheadache attacks, starting already after 10 days and becoming maximal after 20-30 days. Also, there was a marked decreaseof the mean duration of the attacks. Another 30 chronic sufferers of cluster headache received a saline injection and thusserved as controls. However, placebo had no effect on pain in this patient group.
Gn-RH represents a new concept for the prophylactic treatment of chronic cluster headache. The present patient material is impressively large and was recruited from a chronic patient group that was resistant to most kinds of medical treatment.
Thereby the authors have avoided such methodological errors as for instance spontaneous remissions of the disease. Fromthe pathogenetic point of view this investigation provides new information because the specific treatment affects neuronscontaining both opioids and serotonin, and thus in turn stimulates both endocrine and pain inhibitory systems that aregoverned by the same neurotransmitters.
Another interesting clue in the search for a pathogenetic model is the observation by Nicolodi et al. that chronic treatment with testosterone produced a marked increase of sexual excitability in chronic cluster headache sufferers. This alteration ofsexual behavior may represent a local hypothalamic hypersensitivity state and it further stresses the importance of the CNS incluster headache, notably opioidergic and serotonergic neuronal systems.
Waldenlind F. Cluster headache: studies on monoaminergic platelet functions and endocrine rhythms. AcademicDissertation, Stockholm 1987 Cervical headache
Watson and Trott's study is important to the growing literature on cervical headache because it brings with it arigor of measurement technique seldom seen in previous studies of this controversial entity. The authorshave painstakingly devised and validated methods of quantitating forward head position and isometricstrength and endurance of the upper cervical flexor muscles, and of assessing mobility in the upper cervicalspine (passive accessory intervertebral movement, PAIVM).
They applied these techniques to two groups of volunteers, one without headaches (i.e. less than one headache per month) and the other with headaches (two or more per month). Those in the headache groupwith normal PAIVMs were excluded from analysis, as were those with abnormal PAIVMs who, on asubsequent questionnaire, gave responses suggesting that their headache diagnosis was either migraine withaura or cluster headache. The objective of those exclusions was to ensure that the characteristics of theremaining patients were consistent with those of cervical headache.
The authors conclude that their findings indicate that cervical headache sufferers exhibit a forward head posture, and weakness and lack of endurance of the upper cervical flexor muscles. Quite sensibly, they statethat only more research will demonstrate whether or not this relation is causative, but that clinicians should beaware of the relationship between poor craniocervical posture and cervical headache, especially whenplanning therapy. They also suggest that patients with clinical features of migraine without aura, or oftension-type headache, should be screened for a cervical cause.
This publication encourages my belief that future studies which join the meticulous measurement techniques of this paper with exacting rigor of experimental design and interpretation will advance ourunderstanding of cervical headache.


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