Rapid and sustained relief of migraine attacks with intranasal lidocaine: preliminary findings.

In a noncontrolled study, 23 migraine headache patients were treated with intranasal instillation of 0.4 mL of a 4% lidocaine solution during attacks of varying intensities. Evaluated were pretreatment and posttreatment changes in pain intensity, nausea, and side effects. Posttreatment intensity ratings significantly improved over pretreatment ratings, as determined by a Sandler A analysis (0.077; P < .0005). Migraine attacks were aborted in 12 of 23 patients, of which 8 were completely relieved within 5 minutes. In no case did an aborted attack return to more than a dull level within 24 hours, as determined by follow-up telephone calls. A successful response of migraine attacks to lidocaine treatment was more apt to occur in patients having migraine solely, when compared to migraine patients who also had daily dull headaches; the difference was not significant. Unilateral attacks, however, were significantly more treatment-responsive when compared to bilateral attacks (X2 = 3.85; P = .05). Nausea, associated with migraine attacks in 6 of 12 responders, was similarly aborted by lidocaine in 5 of 6 patients. Other side effects included mild nasal and eye burning of short duration (seconds), and oropharyngeal numbness of approximately 20 minutes' duration. Despite the abrupt and absolute relief of migraine attacks afforded by lidocaine in most of our study patients, its level of efficacy awaits results of double-blind, placebo-controlled studies. Our findings raise new questions regarding the differential pathogenesis of migraine and cluster headache attacks.(ABSTRACT TRUNCATED AT 250 WORDS)

Inheritance of cluster headache and its possible link to migraine.

We evaluated the possibility that cluster headache may be a transmitted disorder, influenced by migraine genetics. In the first part of a two part study, 24 female cluster headache probands having at least one first degree relative with cluster headache were evaluated for familial histories of cluster and migraine headache. Headache histories of most parents, siblings and children were satisfactorily documented by either direct interview or by information provided by knowledgeable relatives. In approximately a third of relatives, the headache history could not be properly ascertained. The second part of the study evaluated occurrence rates of cluster and migraine headaches among first degree relatives of 200 female and 100 male cluster headache patients, and the proportion of affected relatives. These data were compared to those of 200 women and 100 men with migraine headache; family history data were, for the most part, provided by headache patients. Twenty-four of two hundred cluster headache women (12%) had at least one first degree relative with cluster headache. Three generations of cluster headache were found in 7/24 kindreds (29.17%). Parental cluster headache was found in 19 of the 24 probands (79.17%); in 14/19 (73.68%), transmission was from father to proband. fifty percent of cluster probands also had migraine headaches, and almost 50% had a family history of migraine. Similarly, of the larger population of 300 cluster patients, approximately 45% had a positive family history of migraine. f 1652 relatives of all cluster patients, 3.45% had cluster headache (thirteen times the expected frequency of cluster headache in the general population) and 17.55% had migraine headaches.(ABSTRACT TRUNCATED AT 250 WORDS)

The pathogenesis of cluster headache.

Cluster headache is described here as having three distinct and contiguous clinical phases. Evidence of the pathophysiological changes associated with each phase is reviewed. The first phase, the cluster period, is characterized by chronobiological aberrations and impaired sympathetic nervous system activity. These changes may result in impaired autoregulatory chemoreceptor activity and susceptibility to attack provocation. An hypothesis that attempts to explain the second phase, cluster attack induction, is reviewed. Evidence for this model suggests that as a result of chemoreceptor dysfunction, a sustained hypoxemic event, as may result from altitude hypoxia, sleep apnea, or vasodilators, could provoke the cluster attack. Attack symptoms and signs, which constitute the third phase of cluster headache, are likely the result of parasympathetic and trigeminal nerve stimulation. Specifically, cluster headache pain is likely the consequence of neurovascular inflammation, as hypothesized in the trigeminovascular theory.

Handedness and headache.

A California handedness study involved 199 male and 74 female cluster headache sufferers as well as 477 migraineurs. Earlier reported data indicated that cluster headache patients had a left-handedness prevalence of over 15%. With the current data the prevalence in males was 11.0% and in females, 8.2%. The corresponding migraine figures were 11.8% and 8.1%. The cluster and migraine headache groups did not differ significantly from each other or from the expected 10% frequency of left-handedness in either sex.

Diagnosis and treatment of cluster headache.

This article classifies cluster headaches as distinct from other types of headaches and gives guidelines for diagnosis and treatment. Explanations of the pathophysiology and pathogenesis of cluster headaches are included also.

Association of sustained oxyhemoglobin desaturation and onset of cluster headache attacks.

Ten episodic cluster headache patients in their active cluster period, ten patients in remission and five control subjects were monitored for minute to minute changes in oxygen saturation (SaO2) and pulse rate before and after nitroglycerin (NTG) administration. A transient but significant decrease in SaO2 and increase in pulse rate of 25 minutes duration occurred following NTG in all groups. These changes may reflect physiologic hemodynamic effects of NTG as a smooth muscle relaxant. Subsequently, SaO2 levels and pulse rate recovered to baseline values in remission and control groups. In contrast, SaO2 values in the active cluster group decreased further and after an extended period culminated in cluster headache attacks in 10/10 patients. Three major changes, therefore, distinguished active cluster patients from remission and control groups. First, the magnitude of oxygen desaturation increased after the physiological effects of NTG ceased. Second, oxygen desaturation was sustained for an additional 9 to 30 minutes duration. Third, the hypoxemic state culminated in attacks in all cases. Our findings suggest that the active cluster period may be characterized by an impaired mechanism to autoregulate, and thus compensate, for hypoxemia. It is further proposed that persistence of hypoxemia and the cluster attack onset may share a common mechanism, coupling the two events. We suggest that abnormal central and/or peripheral chemoreceptor activity may be responsible for these events.

Successful aspirin prophylaxis in a child with chronic paroxysmal hemicrania.

It is generally recognized that indomethacin prophylaxis is the treatment of choice in adults with chronic paroxysmal hemicrania (CPH). Our case report is the first to demonstrate complete control of CPH in a 9 year-old child using small dose aspirin prophylaxis. This case also represents direct observation of the youngest patient with CPH having the earliest reported onset.

Episodic paroxysmal hemicrania?

Cyclic remissions in chronic paroxysmal hemicrania (CPH) have been considered to be transitory phenomena inevitably leading to the chronic stage. This conclusion has precluded the possibility of paroxysmal hemicrania having an episodic counterpart. Six case histories presented here establish the persistence of cyclic patterns for a mean of 23 years of illness, thus suggesting that the "pre-CPH" nomenclature may be presumptive, and, further, provide evidence for another classification: episodic paroxysmal hemicrania.

Sleep apnea in cluster headache.

The impetus to study sleep changes in a cluster population arose from a recent hypothesis that predicted the finding of sleep apnea in this disorder. It holds that cluster attacks may occur in response to oxygen desaturation. Proposed mechanisms involve impairment of carotid body activity secondary to hypothalamic-vasomotor regulatory dysfunction. Five chronic and five episodic cluster patients underwent nocturnal polysomnography, utilizing standard equipment for monitoring sleep status, cardiac activity, nasal and buccal air flow change, chest and abdominal breathing, muscle activity and oxygen saturation. All episodic patients and one of five chronic patients were found to have sleep apnea (60%). Mean apneas per hour during NREM sleep were similar to that of REM sleep; 26.7 and 28.2, respectively. Six patients with sleep apnea experienced 14 cluster headache attacks during the study period. Eight attacks (57%) followed episodes of oxygen desaturation ranging from 65% to 85%. In the sleep apnea group, 8 out of 14 attacks (57%) were associated with REM; three without, and five following oxygen desaturation. Of the non-apnea group, all of whom had chronic cluster headache, none of 5 attacks were associated with oxygen desaturation, and only 2/5 attacks occurred in relation to REM. Thus, our study showed that sleep apnea was a common finding in a randomly selected group of episodic cluster patients; and most nocturnal attacks were preceded by oxyhemoglobin desaturation and REM-related. These findings were uncommon in the chronic cluster group.

A possible role of the carotid body in the pathogenesis of cluster headache.

An hypothesis regarding the possible role of the carotid body in the pathogenesis of cluster headache is presented. It states: 1. The pathways concerned with cyclic cluster periods may begin centrally involving specific areas in the hypothalamus. The major influence of this physiological change is proposed to be an inhibition of the sympathetic and disinhibition of parasympathetic supplies to the carotid body. The result, whether due to increased vasomotor tonus or interruption of intrinsic sympathetic stimulation, is suggested to cause diminished peripheral chemoreceptor activity. 2. The pathway concerned with onset of spontaneous or induced attacks begins, as proposed, with oxygen desaturation--which, upon reaching threshold levels may induce a hyperactive chemoreceptor response, and stimulate through afferent pathways the nuclei of the 7th and 10th cranial nerves and respiratory centers, via the nucleus solitarius. 3. The consequence of this excitation may involve the third suggested pathway resulting in stimulation of peripheral secretory and other receptors innervated by the cranial nerves.