Cluster Headache: Origins and Treatment
Abstracts & commentary
Sources: May A, et al. Correlation between structural and functional changes in brain in an idiopathic headache syndrome. Nat Med 1999;5:836-838; Goadsby PJ, et al. Oral zolmitriptan is effective in the acute treatment of episodic cluster headache. Neurology 1999;52:A257, Abst S32.006.
Present dictum states that migraine mechanisms and symptoms originate in the central nervous system, either central, peripheral, or both. Most neurologists have considered cluster headaches as belonging to the migraine family. Until now, however, despite their 90% predilection in males, their agonizing pain, their short, 1-2 hour duration, their predictable cholinergic expressions of Horner syndrome, copious lachrymation, rhinorrhea, and facial sweating, their clock-like outbursts during cluster periods, and the long periods that sometimes separate their outbursts, little has been learned about the fundamental biology of cluster headaches or, much less, their relationships to migraine. Nor has any present-day expert on the disease attributed the pain of cluster headache to peripheral neural receptor systems. Three recent communications, however, have now begun to identify unique changes that appear during and between times of active cluster headaches. The first two report on functional and anatomical changes that are apparently unique within the brains of patients suffering from cluster headache. In the third, Goadsby and colleagues comment that zolmitriptan, a variant anti-migraine drug, relieves about 40% of patients with episodic, but not chronic, cluster headaches.
A little more than a year ago, May and associates (May A, et al. Lancet 1998;351:275-278) published the first report to identify specific, functional brain regions associated with cluster headaches. (Neurology Alert apologizes for letting this go by.) Headaches identical to the spontaneous cluster head pains, including the cholinergic side effects, were induced by inhaled nitroglycerin (this maneuver produces no headache in normals). In response, the susceptible men developed not only the usual expected functional areas creating or reacting from pain, but also revealed unpredicted, high, specific diencephalic activity in the posterior hypothalmus ipsilateral to the headache. For the first time, a specific relation of vascular headache to a functional area of the brain had been discovered.
As emphasized in the Nature Medicine report, further experimentation identified increased functional brain activity in both hypothalamic areas, but remained greater on the headache side both during headaches and in their absence. The explanation of such "neuronal increase," its duration and its durability remains to be evaluated. Furthermore, May et al have identified significant anatomic increases in bilateral gray matter density surrounding the hypothalamic zones of the headache cluster patients. May et al infer that these areas contain increased neurons packed tightly in the two regions, creating a specific "previously unrecognized abnormality in the hypothalamic region." Age did not affect the consistent findings but, as is well known, males expressed at least 90% of the total cases. This lack of difference implies a consistent, continuous functional change in the hypothalamus of patients with cluster headache.
Commentary
This important and ingenious study leaves both patient and doctor wondering about the exact neurologic functions that pull the hypothalamic trigger in the cluster-susceptible brain. May et al emphasize, somewhat tangentially, that the sleep/wake pattern reminds one of the hypothalamic regulation of normal circadian sleep/ wake cycles. It is hard to overlook the clock-like repetitions of these headache patterns as they come relatively regularly both night and day. Nevertheless, one cannot immediately associate them with consistent patterned activity generated by hypothalamic circadian functions. For one thing, and fortunately for cluster patients, what in the basal hypothalamic supra-optic time-clock would generously permit the headache signal to turn off for months at a time? Only circadian sleep or hormonal studies may presently more greatly relate the expressions of active cluster to other hypothalamic activities. One can’t help thinking of the seasonal and daily periods of clusters that characterize peripherally generated, classic trigeminal neuralgia (TN), with or without the putative trauma of possible cerebellar artery pulsations beating on the peripheral branches. TN also has a tendency to appear day or night in spring or fall, but the epidemiology of onset and times of the clock have not been abundantly analyzed. Also, TN more frequently affects persons older than 55 years of age and may suddenly, spontaneously cease for as much as years between episodes. And so it goes for clinical neuroscience: we’ll never solve all its questions, we only can try. —fp
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