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Alcohol and Cluster Headaches
... Takođe, i u našem ispitivanju menstruacija i psihička napetost spadaju u najčešće okidače kod sve tri grupe ispitanika. Randolf W. Evans i Markus Schürks su u svom radu prikazali 50-godišnjeg pacijenta obolelog od GTT kome skoro svaki napad glavobolje uzrokuje konzumiranje alkoholnih pića [23]. U ispitivanju Tod D. Rozena i saradnika, u kojem je učestvovalo 1134 ispitanika, 52% ispitanika je navelo konzumiranje alkoholnih pića kao mogući okidač glavobolje. ...
... Other data suggested that heavy alcohol and coffee consumption is associated with a chronic CH unremitting from onset (CCHU), whereas heavy cigarette smoking seems to lead toward the chronic CH evolved from episodic (CCHE) [7]. Data about the use of alcohol in the CH population is conflicting [8]. CH patients drink 6.5 g of alcohol daily, less than the average 22.9 g in the general German population [9]. ...
Cluster headache patients seem to use more licit and illicit substances than the general population. The epidemiologic data supporting this is growing. We included the licit drugs in this review because their use seems to be driven by the same addiction mechanisms leading to illicit drug abuse. Some drugs may be used in an attempt to treat cluster headache, especially cocaine and hallucinogens. Drug exposure may also play a role in CH pathophysiology, as suggested by interesting data on tobacco use and second-hand smoke exposure. A common factor may contribute both to CH and drug use predisposition. Genetic factors may be at play, and the dopaminergic and orexinergic pathways could be targeted for future studies.
Objective
Headache disorders like migraine show geographic and ethnic differences between Asian and European/North American countries. In cluster headache, these differences are rarely mentioned and discussed. This article aimed to review the characteristics of cluster headache in Asian countries and compare the clinical features to those in European and North American populations.
Methods
We conducted a narrative literature review on the demographics, clinical presentations, and treatments of cluster headache in Asian countries.
Results
Patients with cluster headache in Asian populations showed a stronger male predominance compared to European and North American populations. Chronic cluster headache was rare in Asian countries. The clinical presentation of restlessness was not as common in Asian as it was in European and North American countries, and Asian patients with aura were extremely rare. Patients in Asian countries may have a lower circadian rhythmicity of cluster headache and a lower headache load, as demonstrated by lower attack frequencies per day, bout frequencies, and bout durations.
Conclusions
Regional differences in the presentation of cluster headache exist. Greater awareness for cluster headache should be raised in Asian regions, and further studies are warranted to elucidate the mechanisms behind observed differences.
Cluster headache is an excruciating, strictly one-sided pain syndrome with attacks that last between 15 minutes and 180 minutes and that are accompanied by marked ipsilateral cranial autonomic symptoms, such as lacrimation and conjunctival injection. The pain is so severe that female patients describe each attack as worse than childbirth. The past decade has seen remarkable progress in the understanding of the pathophysiological background of cluster headache and has implicated the brain, particularly the hypothalamus, as the generator of both the pain and the autonomic symptoms. Anatomical connections between the hypothalamus and the trigeminovascular system, as well as the parasympathetic nervous system, have also been implicated in cluster headache pathophysiology. The diagnosis of cluster headache involves excluding other primary headaches and secondary headaches and is based primarily on the patient's symptoms. Remarkable progress has been achieved in developing effective treatment options for single cluster attacks and in developing preventive measures, which include pharmacological therapies and neuromodulation.
Alcoholic drinks (ADs) have been reported as a migraine trigger in about one-third of the migraine patients in retrospective studies. Some studies found that ADs trigger also other primary headaches. The studies concerning the role of ADs in triggering various types of primary headaches published after the International Headache Society classification criteria of 1988 were reviewed, and the pathophysiological mechanisms were discussed. Many studies show that ADs are a trigger of migraine without aura (MO), migraine with aura (MA), cluster headache (CH), and tension-type headache (TH). While data on MO and CH are well delineated, those in MA and TH are discordant. There are sparse reports that ADs are also triggers of less frequent types of primary headache such as familial hemiplegic migraine, hemicrania continua, and paroxysmal hemicrania. However, in some countries, the occurrence of alcohol as headache trigger is negligible, perhaps determined by alcohol habits. The frequency estimates vary widely based on the study approach and population. In fact, prospective studies report a limited importance of ADs as migraine trigger. If ADs are capable of triggering practically all primary headaches, they should act at a common pathogenetic level. The mechanisms of alcohol-provoking headache were discussed in relationship to the principal pathogenetic theories of primary headaches. The conclusion was that vasodilatation is hardly compatible with ADs trigger activity of all primary headaches and a common pathogenetic mechanism at cortical, or more likely at subcortical/brainstem, level is more plausible.
The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders characterized by paroxysmal unilateral head pain that occurs in association with ipsilateral cranial autonomic features. The TACs comprises cluster headache, paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT), and short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA).
The TACs differ in attack duration and frequency as well as the response to therapy. However, there are considerable clinical and therapeutic overlaps among the TACs and it has been hypothesized that all TACs may have a common pathophysiology. Both peripheral and central mechanisms are involved in generation of attacks and trigeminovascular-nociceptive pathways, including trigeminal autonomic reflex are the final pathways for the manifestations of these disorders. The periodicity of TAC attacks, endocrinal abnormalities, and hypothalamic activation suggest that the hypothalamus may play a key role in the pathogenesis of TACs. A number of hypothalamic nuclei and circuits have been suggested for the abnormalities of nociceptive, autonomic, and neuroendocrine functions of TACs, including orexinergic, somatostatinergic, serotoninergic, and opioidergic pathways. The interrelations of these circuits and their relations with the trigeminal autonomic reflex are still to be determined. Dysfunctions in the hypothalamus and its circuits may facilitate inputs on the trigeminovascular system and lead to the various TAC symptoms. Secondary TACs may result from a range of other disorders.
The influence of prenatal events on the development of headaches at childhood has not been investigated and is the scope of our study. Of 2,173 children identified as the target sample, consents and analyzable data were provided by 1,440 (77%). Parents responded to a standardized questionnaire with a validated headache module and specific questions about prenatal exposures. Odds of chronic daily headache (CDH) were significantly higher when maternal tabagism was reported. When active and passive smoking were reported, odds ratio (OR) of CDH were 2.29 [95% confidence intervals (CI)=1.6 vs. 3.6)]; for active tabagism, OR=4.2 (95% CI=2.1-8.5). Alcohol use more than doubled the chance of CDH (24% vs. 11%, OR=2.3, 95% CI=1.2-4.7). In multivariate analyses, adjustments did not substantially change the smoking/CDH association. Prenatal exposure to tobacco and alcohol are associated with increased rates of CDH onset in preadolescent children.
Alcohol is a widely consumed beverage that has significant effects on most organs of the body. The nervous system is a particular target for the damaging consequences of alcohol, caused either directly by the toxic effect of alcohol or by problems related to alcoholism. This article discusses the central nervous system effects of alcohol.
Migraine is a common and sometimes debilitating disorder. This review describes the epidemiology, pathophysiology, and preventive and symptomatic treatment of migraine, with special attention to drug therapy with the triptans.
Cluster headache (CH) is a relatively rare disease and episodic CH is more frequent than chronic CH. Few studies have described the characteristics of patients with chronic CH.
This was a descriptive study carried out by eight tertiary care specialist headache centres in France participating in the Observatory of Migraine and Headaches (OMH). From 2002 to 2005, OMH collected data from 2074 patients with CH, of whom 316 had chronic CH. From January to June 2005, 113 patients with chronic CH were interviewed using standardised questionnaires during a consultation.
The male to female ratio was 4.65:1. Median age was 42 years. The majority of patients were smokers or former smokers (87%). 46% had primary chronic CH (chronic at onset) and 54% secondary chronic CH (evolving from episodic CH). Most patients had unilateral pain during attacks and 7% had sometimes bilateral pain during an attack. 48% reported a persisting painful state between attacks. Symptoms anteceding pain onset (mainly discomfort/diffuse pain, exhaustion, mood disorders) and auras were reported by 55% and 20% of patients, respectively. The functional impact of chronic CH was estimated as severe by 74% of patients, and 75.7% suffered from anxiety, as assessed by the Hospital Anxiety and Depression scale. There was no substantial difference in clinical presentation between primary and secondary CH.
This study confirms the existence of auras and interictal signs and symptoms in patients with chronic CH, and male sex and smoking as CH risk factors. Primary and secondary chronic CH appear equally prevalent. Male sex does not appear to favour the shift from episodic to chronic CH.
Headache is undoubtedly among the most frequent ills to which the human flesh is heir. It is a complaint which has been known to mankind since the dawn of antiquity. Few contributions, however, have marked medical progress in this field.It is not my purpose to review or consider the differential diagnostic features of the various types of headaches and head pains which have been recorded in the literature but rather to describe a new syndrome of vascular headache and to report the results of treatment with histamine. Other less well defined types of headaches have also been treated with histamine and the results will be reported.This new syndrome of vascular headache, which MacLean, Craig and I1 tentatively called "erythromelalgia of the head" and which I shall call "histaminic cephalgia" hereafter, was first encountered and recognized at the Mayo Clinic in September 1937. At that time the syndrome
The etiological and physiopathological mechanisms of cluster headache (CH) are still largely unknown. The majority of the studies published on the possible risk factors and conditions associated with CH rely on either anecdotal observations or generalizations and have not been supported by serious epidemiological investigations. The aim of this case-control study was to evaluate the real association of life habits and general risk factors with CH. CH was associated only with cigarette smoking, head trauma and a positive family history for headache. Further epidemiologic studies are probably necessary in order to find clues to CH etiology.
SYNOPSIS
Forty-nine out of 51 consecutive male patients with episodic cluster headache were studied with regard to their smoking and drinking habits in general and in relation to cluster headache periods. Questionnaires were constructed for data regarding tobacco intake. Situation-related smoking behavior was registered according toFrith (1971). Screening for alcohol over-consumption was made using the Malmö modification of the brief Michigan Alcoholism Screening Test (Mm-MAST).
Eighty-three percent of the patients used tobacco on a regular basis at the time of the study, with an average consumption of 20 cigarettes per day. Only 3% had never used tobacco regularly. The smoking-related desire to smoke in different situations was consistent with what is found in a general population of smokers.
Sixty-seven percent of the patients had scores on the Mm-MAST indicative of alcohol over-consumption (i.e.heavy social drinking or alcoholism). During active headache periods 79% decreased their alcohol intake, whereas no consistent change in tobacco consumption was reported for the group as a whole. These findings were furthercorroborated by the fact that alcohol, but not tobacco intake, was reported by the majority of patients to elicit headache attacks during periods.
Thus, our study showed high alcohol and tobacco consumption to be prominent feature in male patients with episodic cluster headache. Since neither alcohol nor tobacco appear to have properties of ameliorating headache periods or attacks, the addictive behavior in our patients more likely reflects certain personality characteristics.
Comparison of 2 variables, stature and eye color, between cluster headache patients and controls reveal significant differences. The higher incidence of hazel eye color among patients with cluster headache in this study suggests a common constitutional or genetic factor. In addition, the cluster patients of this study revealed a taller stature than the non cluster patients. The cluster patients were shown to have a specific personality make up in common probably responsible for an increased smoking and drinking habit. The resultant effect of this habit is postulated as the cause of 'cluster facies'.
SYNOPSIS
Thirty-two patients with chronic cluster headache, not responding to conventional therapy, were treated with lithium carbonate for 32 weeks.
Treatment was discontinued in 4 cases because of intolerable side effects. Marked and continued improvement occurred in 27 of 28 patients throughout the treatment period. Twenty-five percent of all patients had mild or transient side effects without increased serum lithium levels. Long-term prophylactic lithium maintenance treatment is efficacious in selected cases of chronic cluster headache.
The author previously tried lithium in 5 male patients aged 26-57 yr with cluster headache, 3 of whom had chronic symptoms. Lithium was administered in the form of slow release tablets (Lithionit Durules, 6 meq), and the dose adjusted until a serum concentration of 0.7 to 1.2 mmol per liter was achieved. In all 3 patients with chronic symptoms lithium therapy resulted in an immediate, partial remission of the headache. The results of lithium in chronic cluster patients has recently been confirmed by Kudrow. He treated 32 patients, unresponsive to conventional prophylactic and systemic drugs. Therapy was maintained over a period of 32 wk. 6 patients had intolerable side-effects. Of the remaining 26 patients, 25 obtained marked improvement. Kudrow also compared lithium with methysergide or prednisone and found that it was significantly superior to these drugs (p <0.001). Some Scandinavian neurologists also noted good results with lithium in chronic cluster patients.
Forty-nine out of 51 consecutive male patients with episodic cluster headache were studied with regard to their smoking and drinking habits in general and in relation to cluster headache periods. Questionnaires were constructed for data regarding tobacco intake. Situation-related smoking behavior was registered according to Frith (1971). Screening for alcohol over-consumption was made using the Malmö modification of the brief Michigan Alcoholism Screening Test (Mm-MAST). Eighty-three percent of the patients used tobacco on a regular basis at the time of the study, with an average consumption of 20 cigarettes per day. Only 3% had never used tobacco regularly. The smoking-related desire to smoke in different situations was consistent with what is found in a general population of smokers. Sixty-seven percent of the patients had scores on the Mm-MAST indicative of alcohol over-consumption (i.e. heavy social drinking or alcoholism). During active headache periods 79% decreased their alcohol intake, whereas no consistent change in tobacco consumption was reported for the group as a whole. These findings were further corroborated by the fact that alcohol, but not tobacco intake, was reported by the majority of patients to elicit headache attacks during periods. Thus, our study showed high alcohol and tobacco consumption to be prominent features in male patients with episodic cluster headache. Since neither alcohol nor tobacco appear to have properties of ameliorating headache periods or attacks, the addictive behavior in our patients more likely reflects certain personality characteristics.
Changes in the male-to-female (M/F) ratio of cluster headache (CH) over the years were investigated through a comparative analysis of the distribution of the disease by sex and decade of onset in 482 patients (374M and 108F). Variations over the last few decades were also investigated in the employment rate, level of school education, smoking habit, and coffee and alcohol intake of the population living in the same area as the CH patients. The M/F ratio has fallen from 6.2:1 for patients with CH onset before 1960, to 5.6:1, 4.3:1, 3.0:1, and 2.1:1 for patients with CH onset in the 1960s, 1970s, 1980s, and 1990s, respectively. Correspondingly, in those same decades, the M/F ratio has fallen from 2.6:1 to 2.4:1, 2.2:1, and 1.7:1, respectively, for the employment rate, and from 8.6:1 to 7.8:1, 3.3:1, 2.5:1, and 1.9:1 for the smoking habit. Such a close correlation suggests that the significant changes that have occurred over the last few decades in the lifestyle of both sexes--and particularly that of women--may have played a major role in altering the gender ratio of CH.
To investigate the relation between cluster headache (CH) and lifestyle, some lifestyle factors were considered in a population of 374 CH male patients consecutively referred to the same headache center, including 306 with episodic CH, 22 with chronic CH unremitting from onset, 20 with chronic CH evolved from episodic, and 26 with CH periodicity undetermined CH patients had jobs involving greater responsibilities and were more frequently self-employed than controls. In addition, their past medical histories often reported head injury, either with loss of consciousness (13.4%) or without loss of consciousness (23.5% of cases). As regards nonessential consumption habits, both cigarette-smoking and coffee and alcohol intake were more frequently reported in CH patients than in the general population, with a higher prevalence in chronic CH as opposed to episodic CH sufferers. In particular, smokers accounted for 78.9% of episodic CH patients and 87.8% of chronic CH patients--12.9% of episodic CH patients and 19.6% of chronic CH patients smoked over 30 cigarettes a day. Alcohol abuse was reported in 16.2% of episodic and 26.8% of chronic CH patients, while coffee abuse was reported in 6.9% of episodic and in 36.6% of chronic CH patients. Rather than pointing to a single lifestyle factor directly implicated in CH onset, my review suggests a common trend among CH patients to overindulge in certain living habits.
Background: Cluster headache, when compared with migraine or tension-type headache, is an uncommon form of primary neurovascular headache. However, with a prevalence of approximately 0.1% and a lengthy history of disabling and distressing episodic pain, cluster headache is an important neurologic problem. Methods: Patients (n = 230) were recruited from our specialist clinic (24%) or from support groups (76%). All patients had a detailed history taken by at least two physicians and were assigned diagnoses according to the International Headache Society Diagnostic Guidelines. Results: The pain characteristics were of a strictly unilateral, predominantly retro-orbital (92%) and temporal pain (70%). Of the cranial autonomic features, lacrimation (91%) was the most common. Nausea (50%), photophobia (56%), and phonophobia (43%) often were noted, as was a sense of agitation or restlessness in 93% of patients. Typical migrainous aura was noted in 14% of this cohort. Most patients (79%) had episodic cluster headache, which was largely the same clinically as chronic cluster headache except for the persistence of attacks over time. The overall male-to-female ratio in this sample was 2.5:1, and this has decreased with time. Neither oral contraceptive use, menses, menopause, nor hormone replacement therapy had any consistent effect on cluster headache in women. Less than half of the patients had tried injectable sumatriptan, and many had not tried high-flow oxygen. Several unproven preventative agents that usually are used in migraine and an array of alternative therapies had been used; none of the latter was consistently effective. Conclusion: Patients with cluster headache offer a population of primary headache patients with devastating acute attacks of pain. The syndrome is stereotyped with effective evidence-based treatments that are prescribed in only half of patients having cluster headache.
To document the relationship between the use of subcutaneous (SQ) sumatriptan (sum) and a change in frequency pattern of cluster headache (CH) in six patients. To discuss the clinical and pathophysiological implications of this observation in the context of available literature.
Treatment with SQ sum may cause an increase in attack frequency of CH but data from literature are scant and controversial.
Six CH sum-naïve patients (three episodic and three chronic according to the International Headache Society (IHS) criteria) are described.
All six patients had very fast relief from pain and accompanying symptoms from the drug but they developed an increase in attack frequency soon after using SQ sum. In all patients, the CH returned to its usual frequency within a few days after SQ sum was withdrawn or replaced with other drugs. Five patients were not taking any prophylactic treatment and SQ sum was the only drug prescribed to treat their headache.
Physicians should recognize the possibility that treatment of CH with SQ sum may be associated with an increased frequency of headache attacks.
Nitroglycerin administration provokes spontaneous-like migraine attacks in migraine and cluster headache (CH) patients. Nitroglycerin-induced migraine-like headache has been used as an experimental model of migraine. In this paper, we evaluate the possibility of using the nitroglycerin provocative test (NPT) as a supportive measure in the diagnosis of primary neurovascular headaches by assessing its reliability on a large population and adopting strict criteria for rating the response as positive or negative. Our population consisted of 197 migraineurs, 42 subjects suffering from cluster headache and 53 healthy controls. In migraine without aura, the test sensitivity was 82.1%, specificity 96.2% and accuracy 85.5%, while in subjects suffering from migraine with aura, the reliability of the NPT was less satisfactory (sensitivity 13.6%, specificity 96.2% and accuracy 72%). In CH patients tested during the active phase of the disease the sensitivity was 80.6%, specificity 100% and accuracy 92.9%. NPT is an easy, low-cost and reliable method for supporting the diagnosis of migraine without aura and cluster headache.
Cluster headaches both episodic and chronic are some of the most challenging headaches to treat. Although effective treatments are now available, some patients continue to be unresponsive to standard therapy. We present 17 patients from our practice whom we treated preventively with frovatriptan, a new triptan with a long half-life. The promising results suggest that this medication may be an useful addition to our ammaterium against this painful disorder.
The vascular hypothesis of migraine has now been superseded by a more integrated theory that involves both vascular and neuronal components. It has been demonstrated that the visual aura experienced by some migraineurs arises from cortical spreading depression, and that this neuronal event may also activate perivascular nerve afferents, leading to vasodilation and neurogenic inflammation of the meningeal blood vessels and, thus, throbbing pain. The involvement of the parasympathetic system supplying the meninges also causes increased vasodilation and pain. As an acute attack progresses, sensory neurones in the trigeminal nucleus caudalis become sensitized, resulting in the phenomenon of cutaneous allodynia. Triptans may act at several points during the progression of a migraine attack. However, the development of central sensitization impacts upon the effectiveness of triptan therapy.
The International Classification of Headache Disorders, second edition (ICHD-II) was the result of 4 years' work by a large number of headache experts from different parts of the world. This article summarizes the main new features of ICHD-II, compared with the original International Headache Society classification: better definition of migraine with aura, inclusion of chronic migraine, inclusion of a number of new primary headaches (SUNCT, hypnic headache, benign thunderclap headache, new daily-persistent headache, hemicrania continua), better definition of the secondary headaches, introduction of medication-overuse headache and of headache attributed to psychiatric disorder. An appendix defines a number of entities for research purposes. The new classification has already been translated into many of the world's major languages and many more are in the pipeline. It is enormously important that headache experts support and encourage the use of the new classification in order to develop a common knowledge base, and that they research ways of further improving it.
Cluster headache is a stereotyped primary pain syndrome characterised by strictly unilateral severe pain, localised in or around the eye and accompanied by ipsilateral autonomic features. The syndrome is characterised by the circadian rhythmicity of the short-lived attacks, and the regular recurrence of headache bouts, which are interspersed by periods of complete remission in most individuals. Headaches often start about 1-2 h after falling asleep or in the early morning, and show seasonal variation, suggesting that the hypothalamus has a role in the illness. Consequently, the vascular theory has been superseded by recognition that neurovascular factors are more important. The increased familial risk suggests that cluster headache has a genetic component in some families. Neuroimaging has broadened our pathophysiological view and has led to successful treatment by deep brain stimulation of the hypothalamus. Although most patients can be treated effectively, some do not respond to therapy. Fortunately, time to diagnosis of cluster headache has improved. This is probably the result of a better understanding of the pathophysiology in combination with efficient treatment strategies, leading to a broader acceptance of the syndrome by doctors.
Cluster headache (CH) is diagnosed according to criteria of the International Headache Society (IHS), but, in clinical practice, these criteria seem too restrictive. As part of a nation-wide study, we identified a group of patients who met all criteria minus one (IHS-CH-1), and assessed in which way they differed from CH patients meeting all criteria (IHS-CH). We performed a nation-wide questionnaire study for CH and CH-like syndromes, including questions based on the IHS criteria, and additional features such as restlessness during attacks, nocturnal onset of attacks, circadian rhythmicity of attacks and response to treatment. IHS-CH and IHS-CH-1 patients were compared. Of 1452 responders to two questionnaires, 1163 were IHS-CH and 289 were IHS-CH-1. The majority of the IHS-CH-1 patients were classified as such because their attacks exceeded 3 h (64%, median attack duration: 5 h), or came in a frequency of less than 1 per 2 days (16%). Age at onset was similar between the groups. The male to female ratio was 3.7 : 1 in the IHS-CH group and around 1.6 : 1 in the IHS-CH-1 groups (P < 0.005). Patients with attacks exceeding 3 h less often reported a circadian rhythmicity (IHS-CH-1: 49%, IHS-CH: 64%), episodic periodicity (IHS-CH-1: 65%, IHS-CH: 78%), nocturnal attacks (IHS-CH-1: 67%, IHS-CH: 78%), smoking (IHS-CH-1: 90%, IHS-CH: 80%) and restlessness during attacks (IHS-CH-1: 64%, IHS-CH: 76%) than IHS-CH patients (P < 0.005). Photo- or phono-phobia (IHS-CH-1: 67%, IHS-CH: 54%) and nausea (IHS-CH-1: 38%, IHS-CH: 27%) were more frequently reported by patients who reported to have attacks exceeding 3 h (P < 0.005). Similar proportions reported effect of verapamil on their attacks (IHS-CH-1: 54%, IHS-CH 61%). We conclude that average attack duration exceeding 3 h was frequently the reason for not fulfilling IHS CH criteria. Symptoms often accompanying CH such as restlessness, nocturnal attacks and an episodic attack pattern were relatively frequently present in IHS-CH-1 patients with longer attacks. These patients may therefore be diagnosed with CH. Attack frequency may not be a useful criterion for the diagnosis of CH. The upper limit of 3 h should be increased in future diagnostic criteria.
The purpose of this study was to identify predictors of hazardous alcohol consumption in patients with cluster headache (CH). We investigated 246 German CH patients with the Alcohol Use Disorders Identification Test (AUDIT). The average daily alcohol consumption was 6.5 g. Predictors for hazardous drinking (AUDIT>or=5 points; 21.5% of patients) were male gender [odds ratio (OR) 4.15, 95% confidence interval (CI) 1.35, 12.71], episodic as opposed to chronic CH (OR 4.8, 95% CI 1.38, 16.67) and a low demanding job as opposed to a high demanding job (OR 2.28, 95% CI 1.15, 4.51). Our data indicate that CH patients drink less alcohol compared with the German population and that CH seems to protect against hazardous alcohol consumption. Moreover, predictors for hazardous alcohol consumption in CH patients are not different from the general population.
Cluster headache (CH) is a rare but severe headache form with a distinct clinical presentation. Misdiagnoses and mismanagement among these patients are high.
To characterize clinical features and medical treatment in patients with CH.
We established a cohort of 246 clinic-based and non-clinic-based CH patients. The diagnosis of CH was verified according to International Headache Society (IHS) criteria. We used standardized questionnaires to assess associated factors as well as success or failure of treatments.
The majority (75.6%) was not treated before at our clinic-77.6% were males; 74.8% had episodic CH, 16.7% had chronic CH, in the remaining patients, the periodicity was undetermined because they were newly diagnosed. Cranial autonomic features were present in 98.8%, nausea and vomiting in 27.8%, and photophobia or phonophobia in 61.2% of CH patients. Most (67.9%) reported restlessness during attacks and 23% a typical migrainous aura preceding the attacks. The rate of current smoking was high (65.9%). Half of the patients reported that alcohol (red wine in 70%) triggered CH attacks. Eighty-seven percent reported the use of drugs of first choice (triptans 77.6%, oxygen 71.1%) with sumatriptan subcutaneous injection being the most effective drug for acute therapy (81.2%). The most frequently used preventive medications were verapamil (70.3%) and glucocorticoids (57.7%) with equally high effectiveness.
Apart from the IHS criteria additional features like nausea/vomiting and migrainous aura may guide the diagnosis of CH. A large number of CH patients do not receive adequate treatments.
Cluster headache and the other trigeminal-autonomic cephalalgias [paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) syndrome] are rare but very disabling conditions with a major impact on the patient's quality of life. The objective of this study was to give evidence-based recommendations for the treatment of these headache disorders based on a literature search and consensus amongst a panel of experts. All available medical reference systems were screened for any kind of studies on cluster headache, paroxysmal hemicrania and SUNCT syndrome. The findings in these studies were evaluated according to the recommendations of the European Federation of Neurological Societies resulting in level A, B or C recommendations and good practice points. For the acute treatment of cluster headache attacks, oxygen (100%) with a flow of at least 7 l/min over 15 min and 6 mg subcutaneous sumatriptan are drugs of first choice. Prophylaxis of cluster headache should be performed with verapamil at a daily dose of at least 240 mg (maximum dose depends on efficacy or tolerability). Although no class I or II trials are available, steroids are clearly effective in cluster headache. Therefore, the use of at least 100 mg methylprednisone (or equivalent corticosteroid) given orally or at up to 500 mg i.v. per day over 5 days (then tapering down) is recommended. Methysergide, lithium and topiramate are recommended as alternative treatments. Surgical procedures, although in part promising, require further scientific evaluation. For paroxysmal hemicranias, indomethacin at a daily dose of up to 225 mg is the drug of choice. For treatment of SUNCT syndrome, large series suggest that lamotrigine is the most effective preventive agent, with topiramate and gabapentin also being useful. Intravenous lidocaine may also be helpful as an acute therapy when patients are extremely distressed and disabled by frequent attacks.
It has long been suggested that some of the neuropharmacological, neurochemical and behavioural effects of ethanol are mediated by its first metabolite, acetaldehyde. In spite of the well documented psychoactivity of acetaldehyde, the precise role of this compound in alcohol abuse remains a matter of intense debate among scientists devoted to the study of alcoholism. Very frequently, the main drawback has been related to the presence of adequate levels of acetaldehyde or its derivatives inside the brain after ethanol ingestion. Since penetration into the central nervous system from blood of peripherically derived acetaldehyde is very low due to the high aldehyde dehydrogenase activity at the blood-brain barrier, several authors called into question the acetaldehyde implication in the toxicity and neurobehavioral effects of ethanol. The confirmation in several laboratories of the existence of enzymatic mechanisms of ethanol oxidation in the brain has revitalized the old theories supporting the acetaldehyde contribution to alcohol abuse and alcoholism. In this paper, we review current data on the brain metabolism of ethanol. We focused on the description of the enzymatic mechanisms involved in this metabolic process, reviewing the constitutive expression, catalytic activity and inhibition and inducibility of the enzymes involved in brain ethanol metabolism. We also analyze old and recent data on their regional distribution and cellular localization in the central nervous system, with special reference to the mesocorticolimbic system, a dopaminergic brain pathway that plays an important role in drug and ethanol reinforcement.