1/5. Persistence of attacks of cluster headache after trigeminal nerve root section.cluster headache is a strictly unilateral headache that occurs in association with cranial autonomic features. We report a patient with a trigeminal nerve section who continued to have attacks. A 59-year-old man described a 14-year history of left-sided episodes of excruciating pain centred on the retro-orbital and orbital regions. These episodes lasted 1-4 h, recurring 2-3 times daily. The attacks were associated with ipsilateral ptosis, conjunctival injection, lacrimation, rhinorrhoea and facial flushing. From 1986 to 1988, he had trials of medications without any benefit. In February 1988, he had complete surgical section of the left trigeminal sensory root that shortened the attacks in length for 1 month without change in their frequency or character. In April 1988, he had further surgical exploration and the root was found to be completely excised; post-operatively, there was no change in the symptoms. From 1988 to 1999, he had a number of medications, including verapamil and indomethacin, all of which were ineffective. prednisolone 30 mg orally daily rendered the patient completely pain free. sumatriptan 100 mg orally and 6 mg subcutaneously aborted the attack after approximately 45 and 15 min, respectively. He was completely anaesthetic over the entire left trigeminal distribution. Left corneal reflex was absent. Motor function of the left trigeminal nerve was preserved. Neurological and physical examination was otherwise normal. MRI scan showed a marked reduction in the calibre of the left trigeminal nerve from the nerve root exit zone in the pons to Meckel's cave. An ECG-gated three-dimensional multislab MRI inflow angiogram was performed. No dilatation was observed in the left internal carotid artery during the cluster attack. Blink reflexes were elicited with a standard electrode and stimulus. Stimulation of the left supraorbital nerve produced neither ipsilateral nor contralateral blink reflex response. Stimulation of the right supraorbital nerve produced an ipsilateral response with a mean R2 onset latency of 36 ms and a contralateral response with a mean R2 onset latency of 32 ms. Lack of ipsilateral vessel dilatation makes the role of vascular factors in the initiation of cluster attacks questionable. With complete section of the left trigeminal sensory root the brain would perceive neither vasodilatation nor a peripheral neural inflammatory process; however, the patient continued to have an excellent response to sumatriptan. The case illustrates that cluster headache may be generated primarily from within the brain, and that triptans may have anti-headache effects through an entirely central mechanism.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
2/5. Childhood-onset 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.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
3/5. Periods of cluster headache induced by nitrate therapy and spontaneous remission of angina pectoris during active clusters.Glyceryl trinitrate (GTN) is known to induce single extra attacks of cluster headache (CH) during active cluster periods, most probably via actions of nitric oxide (NO). Induction of whole periods of CH by organic nitrates has, however, attracted little attention in the literature. We report on eight patients with episodic CH and coexistent effort-induced angina pectoris. Cases 1-6 had been free of their headaches for many years but got recurrence of CH within a few weeks after the administration of long-acting organic nitrates (isosorbide-dinitrate, isosorbide-5-mononitrate or slow-release GTN) aimed at treating their chest pains. These nitrate-induced headache periods were more severe and had a longer duration than the previous spontaneous ones. Furthermore, one of the subjects and two additional cases experienced a marked reduction of their anginal attacks during successive CH periods. exercise time to effort-induced angina was increased in all three patients and one of them revealed a markedly elevated threshold for eliciting ischaemic cardiac symptoms by standardized physical exercise on a cycle ergometer. We hypothesize whether extra CH periods elicited by sustained nitrate therapy and remission of angina pectoris during active clusters are caused by central mechanisms involving inhibition of sympathetic tone and effects on both cranial vessels and cardiac functions.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
4/5. Serious neurological disorders in children with chronic headache.AIMS: To determine the prevalence of serious neurological disorders among children with chronic headache. methods: All children presenting to a specialist headache clinic over seven years with headache as their main complaint were assessed by clinical history, physical and neurological examination, neuroimaging where indicated, and by follow up using prospective headache diaries. RESULTS: A total of 815 children and adolescents (1.25-18.75 years of age, mean 10.8 years (SD 2.9); 432 male) were assessed. Mean duration of headache was 21.2 months (SD 21.2). neuroimaging (brain CT or MRI) was carried out on 142 (17.5%) children. The vast majority of patients had idiopathic headache (migraine, tension, or unclassified headaches). Fifty one children (6.3%) had other chronic neurological disorders that were unrelated to the headache. The headache in three children (0.37%, 95% CI 0.08% to 1.1%) was related to active intracranial pathology which was predictable on clinical findings in two children but was unexpected until a later stage in one child (0.12%, 95% CI 0.006% to 0.68%). CONCLUSIONS: Chronic headache in childhood is rarely due to serious intracranial pathology. Careful history and thorough clinical examination will identify most patients with serious underlying brain abnormalities. Change in headache symptomatology or personality change should lower the threshold for imaging.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
5/5. testosterone replacement therapy for treatment refractory cluster headache.OBJECTIVES: To describe the clinical characteristics and laboratory findings of cluster headache patients whose headaches responded to testosterone replacement therapy. BACKGROUND: Current evidence points to hypothalamic dysfunction, with increased metabolic hyperactivity in the region of the suprachiasmatic nucleus, as being important in the genesis of cluster headaches. This is clinically borne out in the circadian and diurnal behavior of these headaches. For years it has been recognized that male cluster headache patients appear overmasculinized. Recent neuroendocrine and sleep studies now point to an association between gonadotropin and corticotropin levels and hypothalamically entrained pineal secretion of melatonin. RESULTS: Seven male and 2 female patients, seen between July 2004 and February 2005, and between the ages of 32 and 56, are reported with histories of treatment resistant cluster headaches accompanied by borderline low or low serum testosterone levels. The patients failed to respond to individually tailored medical regimens, including melatonin doses of 12 mg a day or higher, high flow oxygen, maximally tolerated verapamil, antiepileptic agents, and parenteral serotonin agonists. Seven of the 9 patients met 2004 International classification for the diagnosis of Headache criteria for chronic cluster headaches; the other 2 patients had episodic cluster headaches of several months duration. After neurological and physical examination all patients had laboratory investigations including fasting lipid panel, PSA (where indicated), LH, FSH, and testosterone levels (both free and total). All 9 patients demonstrated either abnormally low or low, normal testosterone levels. After supplementation with either pure testosterone in 5 of 7 male patients or combination testosterone/estrogen therapy in both female patients, the patients achieved cluster headache freedom for the first 24 hours. Four male chronic cluster patients, all with abnormally low testosterone levels, achieved remission. CONCLUSIONS: Abnormal testosterone levels in patients with episodic or chronic cluster headaches refractory to maximal medical management may predict a therapeutic response to testosterone replacement therapy. In the described cases, diurnal variation of attacks, a seasonal cluster pattern, and previous, transient responsiveness to melatonin therapy pointed to the hypothalamus as the site of neurological dysfunction. prospective studies pairing hormone levels and polysomnographic data are needed.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |