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PubMed2003

[Cluster headache].

Cluster headache is characterized by recurrent unilateral attacks of headache of great intensity and brief duration (15-180 minutes), accompanied by local signs and symptoms of autonomic dysfunction including conjunctival injection, lacrimation, nasal congestion, rhinnorrhea, forehead and facial sweating, miosis, ptosis or eyelid edema. Attacks occur in so-called cluster periods lasting for weeks or months. About 10% of patients have chronic symptoms with no period of remission. There are only two abortive treatments with proven efficacy: subcutaneous sumatriptan and nasal oxygen inhalation. Prophylactic treatment is often needed to reduce the daily frequency of attacks: verapamil in episodic cluster headache and lithium in chronic cluster headache.

Cluster Headache↗
PubMed2003

Impairment of trigeminal sensory pathways in cluster headache.

Cluster headache (CH) typically presents in clusters of attacks of intense (peri)orbital, unilateral pain. The distribution of the pain implies involvement of central and/or peripheral trigeminal pathways. These can be investigated by means of trigeminal somatosensory evoked potentials (TSEP) and blink reflexes (BR). We aimed to relate functional changes in trigeminal sensory pathways to the presence of cluster periods. TSEP and BR were performed in 28 episodic CH patients during a cluster period and repeated in 22 outside a cluster period. TSEP latencies (N1, P1 and N2) and amplitude (N1-P1 and P1-N2) and BR latencies (R1, R2 ipsilateral and R2 contralateral) were compared between sides, during and outside a cluster period and with healthy control data (n = 22). During a cluster period, N2 TSEP latencies were longer on the symptomatic side compared with the non-symptomatic side (27.2 +/- 3.0 ms vs. 26.3 +/- 3.4 ms, P = 0.02), and compared with the same side outside the cluster period (26.7 +/- 3.1 ms vs. 25.1 +/- 3.0 ms, P = 0.01). N1, P1 and N2 latencies on the symptomatic side in patients during the cluster period (14.8 +/- 2.3 ms, 20.4 +/- 2.5 ms and 27.2 +/- 3.0 ms, respectively) were significantly longer than those of healthy controls (13.4 +/- 1.9 ms, 18.8 +/- 2.4 ms and 25.0 +/- 2.6 ms, respectively, P < 0.03). Outside the cluster period, N1 latencies of both sides (15.3 +/- 2.8 ms symptomatic side and 15.4 +/- 2.6 ms asymptomatic side) were longer compared with controls (13.4 +/- 1.9 ms, P < 0.04). TSEP amplitudes and BR latencies revealed no significant differences. We conclude that abnormalities of the afferent trigeminal pathway are present in patients with cluster headache, most prominent during the cluster period, and on the symptomatic side. This seems primarily due of changes within the higher cerebral regions of the system.

Adult↗
PubMed1994

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.

Animals↗
PubMed1989

Pericarotid cluster headache.

Cluster headache is generally not associated with recognised disease, and the pathogenesis remains unclear. The onset of typical cluster headaches is reported in a patient with nasopharyngeal carcinoma. The tumor encircled the internal carotid artery but did not extend intracranially. It thus appears possible that cluster headaches may be triggered by processes involving the carotid artery.

Carcinoma, Squamous Cell↗
PubMed2000

Cluster headache.

Cluster headache is a stereotypic, primary headache disorder that is marked by repeated short-lasting attacks of severe, unilateral head pain and associated autonomic symptoms. Cluster headache is probably due to an abnormality in the circadian hypothalamic generator with subsequent trigeminovascular activation. We have reviewed the clinical manifestations, pathophysiology, gender differences, and treatment options in cluster headache.

Cluster Headache↗
PubMed2004

A review of nonvalidated and complementary therapies for cluster headache.

Cluster headache is arguably the most disabling form of primary headache. There is a great deal of information available about alternative therapy for migraine, but very little regarding alternative therapy for cluster headaches. This article reviews the popular and scientific print and electronic sources of information about alternative and complementary treatments for cluster headache dietary supplements, herbal modalities, folk remedies, physical and manual therapies, and unlabeled use of prescription drugs such as botulinum toxin, baclofen, and methylphenidate.

Cluster Headache↗
PubMed2005

Management of cluster headache.

Cluster headache, an excruciating, unilateral headache usually accompanied by conjunctival injection and lacrimation, can occur episodically or chronically, and can be difficult to treat. Existing effective treatments may be underused because of underdiagnosis of the syndrome. Oxygen and sumatriptan have been demonstrated to be effective in the acute treatment of cluster headaches. Verapamil has been shown to be effective for prophylaxis. For cluster headache completely refractory to all treatments, surgical modalities and newer interventions such as the implantation of stereotactic electrodes may be useful. Patients should be encouraged to avoid possible triggers such as smoking or alcohol consumption, especially during the duster period. The intensity of duster headache pain leads to ethical concerns among researchers over the use of placebo, making randomized controlled trials difficult. As new technology and genetic studies clarify the etiology of duster headache, it is possible that more specific therapies will emerge.

Cluster Headache↗
PubMed2001

Melatonin in the preventive treatment of chronic cluster headache.

Cluster headache is a stereotypic headache disorder marked by short-lasting bouts of severe unilateral head pain and associated autonomic symptoms. Almost pathognomonic of this condition are nocturnal attacks that usually occur during the first random eye movement sleep phase of the evening. Melatonin levels have been found to be decreased in cluster headache patients. A lack of melatonin secretion may predispose the cluster sufferer to nocturnal and, possibly, daytime attacks. Leone et al. demonstrated that melatonin could rapidly alleviate cluster attacks, but only in episodic cluster patients. We report two chronic cluster headache patients who had both daytime and nocturnal attacks that were alleviated with melatonin.

Adult↗
PubMed1994

Psuedoaneurysm within the cavernous sinus presenting as cluster headache.

Cluster headache and its associated signs and symptoms have been described in medical literature for years. The etiology of this condition remains unresolved. We describe a unique patient who presented with a cluster headache syndrome concurrent with new-onset pseudoaneurysm within the cavernous sinus. Our review and analysis of this patient confirms current theories which describe the role of the cavernous sinus as a locus of pathology in cluster headache.

Angiography, Digital Subtraction↗
PubMed2001

Premonitory symptoms in cluster headache.

Cluster headache is one of the most excruciating headaches affecting human beings--especially the male sex. Most of the cluster headache cases are of episodic nature, with active cluster periods lasting generally between a few weeks and 2 or 3 months. A still undetermined percentage of patients report nonpainful sensations preceding the onset of the pain attack for a variable period of time. If occurring only a few minutes or a few hours before the onset of pain, such symptoms are called prodromal. When occurring for several days, weeks, or months before the pain, they are termed premonitory symptoms. The author believes that premonitory symptoms have not been properly diagnosed and emphasizes the need to investigate their presence, because by knowing them advances can be made in the understanding of the physiopathology of this particular cephalalgia. Furthermore, it can also allow the physician to be ahead, by giving preventive treatment and stopping or diminishing the intensity and duration of the pain attacks.

Adult↗
PubMed1993

Cluster headache.

Cluster headache is a rare condition that predominantly affects older men. The diagnosis is based on the history and clinical characteristics, which are distinctive. The headache is always unilateral, excruciating and, most uniquely, occurs in timed attacks, called "clusters." The etiology is unknown, but disturbances in the hippocampal areas controlling circadian rhythm may contribute to cluster headache. Various treatments to relieve individual attacks and to shorten active cluster periods have been used, including systemic corticosteroids, lithium, ergotamine and calcium channel blockers. Patient education and individualized treatment are important elements of the management plan.

Adult↗
PubMed1990

Diagnosis and management of cluster headaches.

Cluster headaches are vascular headaches that predominantly affect males and occur frequently, with cyclic regularity. Treatment is predominantly pharmacological in nature and is divided into symptomatic and prophylactic relief. This article discusses the pathogenesis, clinical features, and current prophylactic and symptomatic treatments used with cluster headaches.

Adult↗
PubMed1982

[Cluster headache].

Cluster headache is a defined disorder which is often mistaken in spite of its characteristic picture. The different types of cluster headache and their clinical symptoms are reviewed in detail. Predisposing factors, frequency of other medical disorders as well as personal and psychological characteristics are described. The treatment of the attack and the prophylaxis includes ergot alkaloids, methysergide, cortisone, lithium and oxygen. Some aspects of etiology and pathogenesis are discussed.

Adult↗
PubMed1994

The clinical profile of sumatriptan: cluster headache.

Cluster headache is a rare form of severe idiopathic headache characterized by unilateral short-lasting episodes of excruciating pain in association with autonomic disturbances. Subcutaneous sumatriptan has been investigated as an acute treatment for cluster headache in two randomized, double-blind, placebo-controlled, crossover trials. About 75% of patients given subcutaneous sumatriptan 6 mg reported headache relief within 15 min, in comparison with 26-35% given placebo (p < 0.001 in both studies). The need for rescue medication (100% oxygen by inhalation) at 15 min was significantly lower after sumatriptan treatment as were the severity of functional disability and incidence of non-headache symptoms. Results of a long-term study indicate that the tolerability and efficacy of sumatriptan 6 mg is maintained in long-term use, and that there is no evidence of tachyphylaxis.

Cluster Headache↗
PubMedDate not supplied

[Dexamethasone test in cluster headache].

Cluster headache and manic depressive illness share in common similarities like: periodic symptomatology, accessibility to lithium therapy, abnormalities in circadian rhythm of cortisol. Though, in contrast to periodic depression, D.S.T. was found normal in 9 patients with cluster headache.

Cluster Headache↗
PubMed1988

Cluster headaches.

Cluster headaches are episodes of excruciating unilateral facial pain, typically occurring in young men. Ipsilateral autonomic symptoms of nasal congestion, rhinorrhea, conjunctival injection and lacrimation are commonly present. Characteristic facial features may be found. Migraine and trigeminal neuralgia are two important considerations in the differential diagnosis. Prednisone and lithium are effective prophylactic medications for episodic and chronic forms of cluster headaches. Treatment with oxygen or ergotamines may be useful in aborting attacks.

Adult↗
PubMed2005

[Cluster headache].

Cluster headaches are characterized by attacks of strictly unilateral severe pain which is orbital, supraorbital, temporal or in any combination of these sites associated with one or more of the following, ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis, and eyelid edema. Most patients are usually unable to lie down, restless or agitated during an attack. The attacks last 15-180 minutes and occur from once every other day to 8 times a day. Cluster periods usually last for weeks or months separated by remission periods, however about 10-15% of patients have chronic symptoms without remission. Age at onset is usually 20-40 years and prevalence is 3-4 times higher in men than in women. Acute attacks involve activation of the posterior hypothalamic gray matter. Pharmacological treatment for cluster headache can be abortive, prophylactic, or a combination of both methods.

Adult↗
PubMed2004

Noxious chemical stimulation of rat facial mucosa increases intracranial blood flow through a trigemino-parasympathetic reflex--an experimental model for vascular dysfunctions in cluster headache.

Cluster headache is characterized by typical autonomic dysfunctions including facial and intracranial vascular disturbances. Both the trigeminal and the cranial parasympathetic systems may be involved in mediating these dysfunctions. An experimental model was developed in the rat to measure changes in lacrimation and intracranial blood flow following noxious chemical stimulation of facial mucosa. Blood flow was monitored in arteries of the exposed cranial dura mater and the parietal cortex using laser Doppler flowmetry. Capsaicin (0.01-1 mm) applied to oral or nasal mucosa induced increases in dural and cortical blood flow and provoked lacrimation. These responses were blocked by systemic pre-administration of hexamethonium chloride (20 mg/kg). The evoked increases in dural blood flow were also abolished by topical pre-administration of atropine (1 mm) and [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (0.1 mm), a vasoactive intestinal polypeptide (VIP) antagonist, onto the exposed dura mater. We conclude that noxious stimulation of facial mucosa increases intracranial blood flow and lacrimation via a trigemino-parasympathetic reflex. The blood flow responses seem to be mediated by the release of acetylcholine and VIP within the meninges. Similar mechanisms may be involved in the pathogenesis of cluster headache.

Animals↗