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The authors discuss the problem of bilateral occurrence of symptoms in cluster headache. Literature survey shows that bilateral headache were observed in 10-13% of cases by various authors. In own material of 63 cases the authors found bilateral symptoms in 9.5% of cases and describe in more detail two cases. An own classification of bilateral cluster headaches in suggested.
In view of the still unexplained pathomechanism of Horton's cluster headaches 9 patients were given a challenge test with nitroglycerin while at the same time the attacks were blocked with indomethacin. The attacks were provoked with one dose (1 mg) of nitroglycerin. Then during 3 days the patients took 75-100 mg indomethacin which dose was quite sufficient for inhibition of the activity of arachidonic acid cyclooxygenase. On the fourth day another nitroglycerine provocation was done. No inhibitory effect of indomethacin on the attack was observed. It seems doubtful that products of arachidonic acid cyclooxygenation play any role in the pathomechanism of this headache.
Cluster headaches are rare in childhood. We identified 35 patients with cluster headaches starting at or before 18 years of age, including 7 patients with onset prior to age 10. All patients met the criteria of the International Headache Society for episodic or chronic cluster headaches. Patients experienced cluster headaches for as long as 20 years before seeking medical attention and required many medical contacts to establish the correct diagnosis. The clinical features of cluster headaches during childhood were similar to those which typically occur in adult life. Cluster headache patterns changed over 18 years of follow up. The frequency and duration of cluster periods increased in 14 subjects. The frequency of single headache attacks during cluster periods also increased in a similar number of subjects. We conclude that cluster headaches starting in childhood or adolescence closely resemble the adult form of the disease. In many patients, the frequency and duration of cluster periods and the frequency of the individual headache episodes increased over time. Cluster headache represent a treatable under-recognized cause of severe headaches in childhood and adolescence.
Cluster headache is an episodic form of primary neurovascular headache that is both severe and relatively rare. It is characterized by episodes of headache with cranial parasympathetic activation and sympathetic impairment that come in bouts, or clusters. Its pathophysiology can be divided into understanding the attack phenotype and the biotype of the periodicity. Acute attacks of cluster headache are marked by trigeminal nerve-mediated pain and with cranial autonomic activation, trigeminal-autonomic cephalalgia; an activation that characterizes the phenotype of a group of headaches. The signature feature of cluster headache is its periodicity, the daily cycle of attacks when the patient is in an active bout, or the circumannual, or other period, cycling that distinguishes the on period from the off period. Functional brain imaging with positron emission tomography and structural imaging with voxel-based morphometry have identified an area in the posterior hypothalamic gray as key in understanding cluster headache. This area is subtly enlarged in its gray matter volume, active during an acute cluster headache but inactive when patients are challenged between bouts. Cluster headache is likely to be a form of primary neurovascular pain whose phenotypic expression relies on the trigeminal-autonomic reflex, with a biotype determined by the brain area, the posterior hypothalamus, in which the lesion seems to be located. Understanding both the phenotypic expression and the biotype will, respectively, enable better acute attack treatments and better preventative management of this horrible form of headache.
Cluster headache is a rare, severe, clinically well-characterized disorder that occurs in both episodic and chronic forms. The painful short-lived attacks occur unilaterally and are associated with signs and symptoms of autonomic involvement. They are difficult to treat, and reported prophylactic therapies include ergotamine, steroids, methysergide, lithium carbonate, verapamil, valproate, capsaicin, leuprolide, clonidine, methylergonovine maleate, and melatonin. Baclofen, an antispastic agent, has been shown to have an antinociceptive action. Its efficacy in the treatment of neuralgias, central pain following spinal lesions or painful strokes, migraine, and medication misuse chronic daily headache suggested that it may prevent cluster headache attacks. Nine cluster headache patients received baclofen, 15 to 30 mg, in three divided doses. Within a week, six of nine patients reported the cessation of attacks. One was substantially better and became attack free by the end of the following week. In the remaining two patients, the attacks worsened and corticosteroids were prescribed. In this pilot study, baclofen seemed to be effective and well tolerated for the prevention of cluster headache.
Cluster headache is a rare very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. Although peripheral structures are postulated to be involved in triggering the pain attacks, chronobiological changes like the cluster period and the complex dysbalance of the sympathetic and parasympathetic nervous system point to a "central" genesis of cluster headache. To check neuroendocrine changes in cluster headache, in 12 patients (43.4 +/- 6.3 years) during the cluster period cortisol and ACTH were determined four-times a day (7.00, 12.00, 17.00, 23.00) in the plasma. To prove the central genesis of cluster headache, in the cerebrospinal fluid (CSF) the neurotransmitters norepinephrine, epinephrine, dopamine and the metabolites 5-hydroxyindolacetic acid (5-HIAA), homovanillic acid (HVA) and vanillymandelic acid (VMA) were determined. The values of cortisol and ACTH were significantly elevated in the morning (p < 0.01, p < 0.05) and at night (p < 0.01, p < 0.01) in comparison to the control patients. The daily mean value of cortisol was significantly increased compared to controls (p < 0.01). In the CSF norepinephrine (p < 0.05), HVA (p < 0.01) and 5-HIAA (p < 0.01) decreased to significant low levels compared to control patients. We found significant correlations between cortisol/ACTH and norepinephrine and 5-HIAA. Moreover, our results indicate that the higher cortisol the longer the duration of the cluster period. The results of this study confirm changes of the hypothalamic-pituitary-adrenal axis due to the chronobiological changes in cluster headache. The reduced values of neurotransmitters in the CSF are compatible with the hypothesis of a central genesis of cluster headache.
Cluster headache has been defined by the International Headache Society (IHS) as one of the primary headaches. A primary headache is a headache that has no other known cause, such as infection or trauma. Cluster headache is also listed as one of the trigeminal autonomic cephalalgias. These headaches are mediated by the trigeminal nerve with accompanying autonomic symptoms that may range from conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, and ptosis to eyelid edema. The IHS has described cluster headache as "attacks of severe, strictly unilateral pain that is orbital, supraorbital, temporal or in any combination of these sites, lasting 15 to 180 minutes." In the author's practice, as a dentist treating orofacial pain, patients with cluster headache have dental or midfacial complaints as a primary presentation. This paper introduces such presentations based on interviews with cluster headache patients, with the main purpose of having midfacial complaints considered as an important presentation to be added to the IHS diagnostic criteria for cluster headache.
Cluster headache, the most painful of the primary headaches, is a disorder with well-known diagnostic criteria. The condition usually begins in the second decade of life; the prevalence of childhood onset is approximately 0.1%. A 7-year-old female who suffered daily from severe strictly unilateral right orbital attacks lasting approximately 30 minutes associated with autonomic symptoms is reported herein. They were primarily misdiagnosed as psychogenic headaches. There was no family history for migraine or cluster headaches; physical and neurologic examinations and magnetic resonance imaging did not suggest any association with head trauma or vascular disorders. After a negative indomethacin test, daily intravenous administration of prednisolone terminated the attacks on the third day of the treatment. According to the classification and diagnostic criteria for headache disorders of the International Headache Society the child fulfilled the criteria for episodic cluster headaches. The pathogenesis, clinical manifestation, autonomic features, genetics, and family history of cluster headaches during childhood are reviewed in this report. Prophylactic medication and symptomatic treatment options are discussed, especially concerning the rationale of use of steroids in children with cluster headaches.
Cluster headache, the most severe primary headache, is characterised by unilateral pain, ipsilateral autonomic features, and, in many cases, restlessness. Recent epidemiological studies indicate that the prevalence of cluster headache is about one person per 500. Genetic epidemiological surveys indicate that first-degree relatives are five to 18 times-and second-degree relatives, one to three times-more likely to have cluster headache than the general population. Inheritance is likely to be autosomal dominant with low penetrance in some families, although there may also be autosomal recessive or multifactorial inheritance in others. To date, no molecular genetic clues have been identified for cluster headache. Identification of genes for cluster headache is likely to be difficult because most families reported have few affected members and genetic heterogeneity is likely. Future focus should be on ion channel genes and clock genes. This review summarises the epidemiology and genetics of cluster headache.
Cluster headache is characterized by regular periodicity, high frequency during a cluster period, relative brevity, and extreme intensity. Lancinations, as in trigeminal neuralgia, are rare. An important behavioral difference between migraine and cluster headache is that the patient is usually hyperactive during a cluster headache, whereas the migraineur retreats to a dark, quiet room. Cluster headache is more common in middle-aged men; migraine is more common in young women. Intermediate or overlap syndromes occur. Many of the same prophylactic and abortive treatments are effective in both, although in cluster headache there is a premium on rapid action.
Cluster headache is an uncommon yet distinctive neurovascular syndrome occurring in either episodic or chronic patterns. The most unique feature of cluster headache is the unmistakable circadian and circannual periodicity. The attacks are stereotypical, that is, of extreme intensity, of short duration, occurring unilaterally, and associated with robust signs and symptoms of autonomic dysfunction. Unlike migraine, during an attack the patient with cluster headache often paces about. Attacks frequently occur at night, awakening the patient from sleep. Although the pathophysiology of cluster headache remains to be fully elucidated, several seminal observations have recently been made. The medical treatment of cluster headache includes acute, transitional, and maintenance prophylaxis. Agents used for acute therapy include inhalation of oxygen and triptans, such as sumatriptan, and dihydroergotamine. Transitional prophylaxis refers to the short-term use of fast-acting agents. This typically involves either corticosteroids or ergotamine derivatives. The mainstay of prophylactic therapy is verapamil. Lithium, divalproex sodium, or topiramate may also be useful. As the sophistication of functional neuroimaging increases, so too will our ability to better understand the anatomic and metabolic perturbations that underlie cluster headache.
Cluster headache is a rare, very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. Alterations of the hypothalamic-pituitary axis due to chronobiological changes, such as typical temporal pattern of both cluster periods and attacks, point to a central etiopathogenesis. Multiple local and systemic autonomic symptoms are compatible with an altered balance of the sympathetic and parasympathetic nervous system. In this connection, too, a central etiology is postulated. To evaluate the activation of the sympathetic nervous system, in 12 cluster headache patients we investigated the plasma catecholamines norepinephrine and epinephrine four times a day (7.00, 12.00, 17.00, 23.00) in the cluster period. In the cerebrospinal fluid we determined the transmitters norepinephrine, epinephrine, dopamine and the metabolites homovanillic acid (HVA), vanillymandelic acid (VMA) and 5-hydroxyindoleacetic acid (5-HIAA). Values of plasma norepinephrine in the morning (p < 0.01), in the evening (p < 0.01) and the daily mean value (223.8 = 58.3 nmol/ml) were significantly decreased in the cluster headache group in comparison to the control group (328.8 = 53.0 nmol/ml, p < 0.01). The plasma epinephrine showed no significant changes. In the CSF of cluster headache patients norepinephrine (p < 0.05), HVA (p < 0.01), and 5-HIAA (p < 0.01) were significantly decreased. Plasma norepinephrine was correlated with CSF values of HVA and 5-HIAA. The longer the duration of the disease, the lower the values of HVA and 5-HIAA in the CSF of cluster headache patients. Moreover, plasma norepinephrine showed a significant correlation with the duration, the intensity and the frequency of the attacks. The results of this study implicate decreased activity of the sympathetic nervous system with alteration of circadian rhythmicity during the cluster period. The decreased CSF transmitter values may support the hypothesis of a central etiopathogenesis of cluster headache. Moreover, plasma norepinephrine seems to be involved in triggering and continuing the attacks. The anatomical region in which this interface of sympathetic and neurogenic inflammatory processes might be located is the trigemino-vascular system.
Cluster headache is a rare, clinically well-characterized disabling disorder that occurs in both episodic and chronic forms. The very painful short-lived unilateral headache attacks are associated with autonomic dysfunction. A large number of drugs such as ergotamines, steroids, methysergide, lithium carbonate, verapamil, valproate, capsaicin, leuprolide, clonidine, methylergovine maleate, methylphenidate, and melatonin are considered beneficial for prophylaxis. Nevertheless, this extremely painful condition is occasionally refractory to conventional treatment. The antispastic agent baclofen has been shown to possess an antinociceptive activity. Its efficacy in neuralgias, central pain following spinal lesions, painful strokes, migraine, and medication misuse chronic daily headache suggests that it may be useful for prevention of cluster headache attacks. Therefore, we treated 16 symptomatic patients with cluster headache with daily baclofen, 15 to 30 mg, in three divided doses for the cluster period and 2 weeks after. Within a week, 12 patients reported the cessation of attacks. One was substantially better and became attack free by the end of the following week. In the remaining three patients, the attacks worsened and corticosteroids were prescribed. One of these was also given verapamil. Three of the 16 patients had an additional cluster period, which cleared with a second course of baclofen. In this pilot study, baclofen seemed to be effective, safe, and well tolerated for cluster headache, and seemed to retain its efficacy on repeated clusters.
Cluster headache is rare, occurring in less than 1% of the population. Studies suggest that, in addition to the pain and associated autonomic disturbances recognized to be characteristic of the syndrome, patients also may experience nausea, photophobia, behavioral agitation, or restlessness. A decreasing male:female ratio also has been noted, perhaps attributable to lifestyle trends adopted by more women that were previously associated with men, such as tobacco use, alcohol consumption, and working outside of the home. The relationship between cluster headache and hormonal events does not appear to be strong. Hormonal influences on the chronic form of cluster headache in women are a subject of investigation. The emerging understanding of the genetics of cluster headache increasingly suggests a genetic component, with familial transmission now recognized to be more common than previously appreciated. Head trauma, coronary artery disease, and migraine appear to be present in more patients with cluster headache than can be explained by chance alone. Ethnic and racial differences in prevalence are less well understood.
Cluster headache is perhaps the most painful of the primary headache disorders. Its treatment includes acute, transitional, and preventive therapy. Despite the availability of many treatments, cluster headache patients can still be difficult to treat. We treated 14 cluster headache patients with greater occipital nerve block as transitional therapy (treatment initiated at the same time as preventive therapy). The mean number of headache-free days was 13.1 + 23.6. Four patients (28.5%) had a good response, five (35.7%) a moderate, and five (35.7%) no response. The greater occipital nerve block was well tolerated with no adverse events. Headache intensity, frequency and duration were significantly decreased comparing the week before with the week after the nerve block (P < 0.003, P = 0.003, P < 0.005, respectively). Greater occipital nerve blockade is a therapeutic option for the transitional treatment of cluster headache.
Cluster headache is an uncommon yet well-defined neurovascular syndrome occurring in both episodic and chronic varieties. The most striking feature of cluster headache is the unmistakable circadian and circannual periodicity. Inheritance may play a role in some families. The attacks are of extreme intensity, of short duration, occur unilaterally, and are accompanied by signs and symptoms of autonomic dysfunction. In contrast to migraine, during an attack the cluster patient prefers to pace about. Attacks frequently occur at night. Although the pathophysiology of cluster headache remains to be fully elucidated, several seminal observations have recently been made. The medical treatment of cluster headache includes both acute therapy aimed at aborting individual attacks and prophylactic therapy aimed at preventing recurrent attacks during the cluster period. Agents used for acute therapy include inhalation of oxygen, sumatriptan, and dihydroergotamine. Transitional prophylaxis involves the short-term use of either corticosteroids or ergotamine derivatives. The cornerstone of maintenance prophylaxis is verapamil, yet methysergide, lithium, and divalproex sodium may also be employed. In some patients, melatonin or topiramate may be useful adjunctive therapies.
Cluster headache is ordinarily managed medically, but may become refractory to such medical management. In this setting, surgical treatment has occasionally been performed, based on evidence that pertinent pain pathways and parasympathetic pathways may be interrupted at the main sensory root of the trigeminal nerve and at the nervus intermedius. Between 1976 and 1987, 13 patients underwent surgery for treatment of cluster headache that was refractory to medical therapy (15 procedures). Partial sectioning of the main sensory root and sectioning of the nervus intermedius were performed in nine patients; only partial sectioning of the main sensory root in one; only sectioning of the nervus intermedius in one; and nervus intermedius sectioning plus microvascular decompression of the trigeminal nerve in two. The average postoperative period for the 13 patients was 37 months (range 2 to 135 months). All patients had return of their headaches postoperatively except for one patient who obtained relief after a repeat procedure. Headache began to return between 2 days and 2 years postoperatively. Three patients are currently free of headache, including both patients who had nervus intermedius sectioning plus microvascular decompression of the trigeminal nerve. Together with recurrence of headache, cluster-associated autonomic disturbances recurred after 14 of the 15 operations but are currently absent in the three headache-free patients. Partial sectioning of the main sensory root and sectioning of the nervus intermedius, as performed in these patients, seem to have limited value in the treatment of cluster headache.
Cluster headache is characterized by attacks of severe periorbital pain. Repetitive burst activity in afferent fibers may induce plastic alterations in somatosensory synaptic processing as a prerequisite for recurring and chronic pain. This psychophysical study addressed hypothesized dysfunctions in craniofacial somatosensory processing in cluster headache disease. Thermal and mechanical sensory functions in the periorbital region were assessed by quantitative sensory testing (QST) in 25 cluster headache patients and 60 healthy volunteers. Perception of warmth (p<0.01), cold (p<0.000001), and pressure pain (p<0.05) was reduced on the cluster side as compared with the contralateral asymptomatic side. In contrast to healthy volunteers, warm detection threshold (WDT) and thermal sensory limen (TSL) on one side did not positively correlate with the other side. WDT and TSL negatively correlated with the elapsed time since last attack. All patients showed QST abnormalities on the headache side in comparison to healthy controls. Loss of sensory functions strongly preponderated gain. Several lines of evidence indicate a pivotal role of the hypothalamus in cluster headache pathophysiology. The impairment of warm and cold perception in patients may be based upon a dysfunction of the hypothalamus which is strongly involved in thermosensory control.