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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

13, mostly male, cases of cluster headache and 15, mostly female, cases of atypical facial neuralgia were submitted to the psychosomatic anamnestic interview of Seguin. A very high proportion of patients in both groups had suffered from early deprivation of physical gratification. Pain itself started initially after a sequence of masked depression followed by dental or facial intervention in most atypical facial neuralgias, and by emotional stress in half of the patients with cluster headaches. Pain afterwards still hid and expressed a current underlying depression in both groups.
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PMID:The onset of facial pain. A psychological study. 744 41

In 11 patients with Horton's headache morphological investigations (differential white blood cell count), cytoenzymatic determinations (alkaline and acid phosphatase, non-specific esterase) and cytoimmunological tests (IgM and IgG binding) were carried out on capillary blood neutrophils obtained from the area of pain, non-painful area of the skin on the head on the contralateral side, and from the finger. The observed changes suggest an active participation of neutrophils in the pathological mechanism of Horton's headache and anaphylactoidal background of the disease.
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PMID:[Cytoenzymatic and cytoimmunological changes in capillary blood neutrophils of patients with Horton's headache]. 745 19

Cluster headache is almost always idiopathic, but, in rare cases, associated intracranial lesions have been found. We describe a patient who had chronic cluster headache for more than 20 years. The headache immediately resolved upon resection of a tentorial meningioma. Prior reports of cluster headache as a manifestation of structural disease are briefly reviewed. In the patient described, the pain was referred from the right tentorium cerebelli to the right side of the face, in accordance with reported studies on the subjective localization of pain referred from posterior fossa structures. The accompanying abnormalities of autonomic function may have been mediated by central autonomic reflexes that are also involved in the pathogenesis of idiopathic cluster headache.
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PMID:Resolution of chronic cluster headache after resection of a tentorial meningioma: case report. 869 12

We report the case of a 74-year-old women admitted to the hospital because of rapidly developing diplopia. The admission anamnesis revealed fronto-temporal headaches and pain in the maxilla for three days. A cerebral cT scan was normal, and a corticosteroid therapy was initiated. Diagnosis of Horton's syndrome was confirmed by the good response to treatment and by biopsy of the temporal artery. Different ocular and neurologic complications of Horton's disease, their clinical appearances and therapeutic measures are discussed by the authors.
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PMID:[Horton's disease: ophthalmological and neurological complication]. 749 58

Cluster headache is a rare very severe disorder that is clinically well characterized with a relatively poorly understood pathophysiology. In this study patients with episodic cluster headache fulfilling the criteria of the International Headache Society were examined during an acute spontaneous attack of headache to determine the local cranial release of neuropeptides. Blood was sampled from the external jugular vein ipsilateral to the pain before and after treatment of the attack. Samples were assayed for calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), substance P and neuropeptide Y. Attacks were treated with either oxygen inhalation, sumatriptan or an opiate. Thirteen patients were studied of whom 10 were male and three female. All had well-established typical attacks of cluster headache when blood was sampled. During the attacks external jugular vein blood levels of CGRP and VIP were raised while there was no change in neuropeptide Y or substance P. Calcitonin gene-related peptide levels rose to 110 +/- 7 pmol/l (normal: < 40) while VIP levels rose to 20 +/- 3 pmol/l (normal: < 7). Treatment with both oxygen and subcutaneous sumatriptan reduced the CGRP level to normal, while opiate administration did not alter the peptide levels. These data demonstrate for the first time in vivo human evidence for activation of the trigeminovascular system and the cranial parasympathetic nervous system in an acute attack of cluster headache. Furthermore, it is shown that both oxygen and sumatriptan abort the attacks and terminate activity in the trigeminovascular system.
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PMID:Human in vivo evidence for trigeminovascular activation in cluster headache. Neuropeptide changes and effects of acute attacks therapies. 751 21

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.
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PMID:The clinical profile of sumatriptan: cluster headache. 783 81

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.
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PMID:The pathogenesis of cluster headache. 808 23

A large body of evidence points to an inflammatory process in the cavernous sinus and tributary veins as being primarily responsible for cluster headaches. The inflammation obliterates the venous outflow from the cavernous sinus on one side and injures the through-running sympathetic fibers to the eye, upper eye lid, forehead skin, and the intracranial internal carotid artery and its branches. The active period ends when the inflammation is suppressed and the sympathetic fibers partially or fully recover. Evidence is presented that the symptoms suggestive of an enhanced parasympathetic activity during attacks may alternatively be explained as local pain fiber activation or a stasis in the outflow from the cavernous sinus. Vasodilator agents like nitroglycerin induce an attack by enhancing the venous load on the cavernous sinus. Constriction of the proximal intracranial internal carotid artery, spontaneously induced by stressful pain activation of the perivascular sympathetic nerves, or by exogenous administration of serotonin 1D-like receptor agonists or oxygen, terminates the venous load and thus the pain and associated symptoms.
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PMID:How cluster headache is explained as an intracavernous inflammatory process lesioning sympathetic fibers. 820 Jul 85

Cluster headache (CH) is a rare form of headache occurring in both episodic and chronic forms. The painful attacks are short-lived, occur unilaterally, and are associated with signs and symptoms of autonomic involvement. Attacks frequently occur at night and can be precipitated by ingestion of alcohol. In the episodic form, attacks occur daily for some weeks followed by a period of remission. In the chronic form, attacks can continue for years. Inheritance is not a factor in CH. Treatment can be symptomatic or prophylactic. Agents used to treat individual attacks include inhalation of oxygen, rapidly acting forms of ergotamine and dihydroergotamine, and sumatriptan. Prophylactic treatment employs calcium-channel-blocking agents, methysergide, lithium, and corticosteroids. Surgical modalities, notably thermocoagulation of the gasserian ganglion, can provide relief in those who are resistant to medical management.
J Pain Symptom Manage 1993 Apr
PMID:Diagnosis and treatment of cluster headache. 816 60

Episodic paroxysmal hemicrania (EPH) is a rare, benign disorder characterized by discrete bouts of hemicranial headaches separated by periods of pain-free remissions. EPH is frequently mistaken for episodic cluster headache because they have similar temporal profiles and clinical features. EPH is differentiated from cluster headaches by an increased frequency and a shorter duration of individual attacks. Establishing the diagnosis of EPH is important because of its unique response to treatment with indomethacin and not standard anti-cluster headache medications.
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PMID:Episodic paroxysmal hemicrania: 3 new cases and a review of the literature. 849 58


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