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Cluster Headache (cluster + headache)
Kinds of Cluster Headache Selected AbstractsHaplotype Analysis Confirms the Association Between the HCRTR2 Gene and Cluster HeadacheHEADACHE, Issue 7 2008Innocenzo Rainero MD Background., Several studies suggested that genetic factors play a role in cluster headache (CH) susceptibility. We found a significant association between the 1246 G>A polymorphism of the hypocretin receptor-2 (HCRTR2) gene and the disease. This association was confirmed in a large study from Germany but was not replicated in a dataset of CH patients from Northern Europe. Objective., The purpose of this study was to further evaluate the association between CH and the HCRTR2 gene using new polymorphisms, estimating the frequency of different gene haplotypes, searching for gene mutations, and evaluating the effects of the examined polymorphisms on hypocretin binding sites. Methods., We genotyped 109 CH patients and 211 healthy controls for 5 new polymorphisms of the HCRTR2 gene and we inferred different gene haplotypes. Complete HCRTR2 sequencing was undertaken for 11 independent CH patients, 5 of whom had a positive family history. The effects of the 1246 G>A polymorphism on the hypocretin binding sites were evaluated using different computer-assisted analyses. Results., Three new polymorphisms of the HCRTR2 gene resulted significantly associated with CH. The GTAAGG haplotype resulted more frequent in cases than in controls (OR: 3.68; 95% CI: 1.85-7.67). No point mutation of the HCRTR2 gene was found. Binding analyses showed that the 1246 G>A polymorphism (substitution of valine at position 308 by isoleucine) has no effect on the hypocretin binding sites but could influence the dimerization process of the receptor. Conclusion., Our data confirm previous studies suggesting that the HCRTR2 gene or a linked locus significantly modulates the risk for CH. In addition, we suggest that the V308I substitution of the HCRTR2 may interfere with the dimerization process of the receptor, thereby influencing its functional activity. [source] Cluster Headache and Internal Carotid Artery Dissection: Two Cases and Review of the LiteratureHEADACHE, Issue 3 2008Andrea Rigamonti MD We describe 2 patients with cluster headache attacks associated with a dissection of the ipsilateral internal carotid artery at the extra,intracranial passage. These cases highlight the need for extensive neuroradiological investigation in cluster headache patients when atypical features are present. We also performed a PubMed search to review the current literature data about this association. [source] Clomiphene Citrate for Treatment Refractory Chronic Cluster HeadacheHEADACHE, Issue 2 2008Todd Rozen MD A treatment refractory chronic cluster headache patient is presented who became cluster-free on clomiphene citrate. The author has previously reported a SUNCT patient responding to clomiphene citrate. Hypothalamic hormonal modulation therapy with clomiphene citrate may become a new preventive choice for trigeminal autonomic cephalalgias. The possible mechanism of action of clomiphene citrate for cluster headache prevention will be discussed. [source] Effect on Sleep of Posterior Hypothalamus Stimulation in Cluster HeadacheHEADACHE, Issue 7 2007Roberto Vetrugno MD Objective.,To evaluate the structure and quality of sleep and the circadian rhythm of body core temperature (BcT°) in patients with drug-resistant chronic cluster headache (CH) before and during deep brain stimulation (DBS) of the posterior hypothalamus. Background.,Chronic CH is a severe primary headache and frequently associated with disturbances in sleep. Posterior hypothalamus DBS is performed as an effective treatment of drug-resistant chronic CH. The effects of posterior hypothalamus DBS on sleep and the circadian rhythm of BcT° are unknown. Methods.,Three male patients with chronic drug-resistant CH underwent 48-hour consecutive polysomnography (PSG) by means of the VITAPORT® system with determination of BcT° by means of a rectal probe. Recordings were done before electrode implantation in the posterior hypothalamus and after optimized DBS of posterior hypothalamus. Results.,Before electrode implantation PSG showed nocturnal CH attacks, reduced sleep efficiency, fragmented sleep and increased periodic limb movements in sleep (PLMS). During DBS nocturnal CH attacks were abolished and sleep efficiency and PLMS improved. BcT° circadian rhythm was normal both before and during DBS. Conclusions.,Our data show that DBS of posterior hypothalamus in drug-resistant chronic CH is effective in curtailing nocturnal CH attacks, and is associated with improved sleep structure and quality. Chronic CH displays a normal circadian rhythm of BcT°, unchanged during hypothalamic DBS. [source] Repeat Trigeminal Nerve Radiosurgery for Refractory Cluster Headache Fails to Provide Long-Term Pain ReliefHEADACHE, Issue 2 2007Shearwood McClelland III MD Objective/Background.,Medically refractory cluster headache (MRCH) is a debilitating condition that has proven resistant to many modalities. Previous reports have indicated that radiosurgery for MRCH provides little long-term pain relief, with moderate/significant morbidity. However, there have been no reports of repeated radiosurgery in this patient population. We present our findings from the first reports of repeat radiosurgery for MRCH. Methods.,Two patients with MRCH underwent repeat gamma knife radiosurgery at our institution. Each fulfilled clinical criteria for treatment, including complete resistance to pharmacotherapy, pain primarily localized to the ophthalmic division of the trigeminal nerve, and psychological stability. Both patients previously received gamma knife radiosurgery (75 Gy) for MRCH with no morbidity, but no long-term improvement of pain relief (Patient 1 = 5 months, Patient 2 = 10 months) after treatment. For repeat radiosurgery, each patient received 75 Gy to the 100% isodose line delivered to the root entry zone of the trigeminal nerve, and was evaluated postretreatment. Pain relief was defined as: excellent (free of MRCH with minimal/no medications), good (50% reduction of MRCH severity/frequency with medications), fair (25% reduction), or poor (less than 25% reduction). Results.,Following repeat radiosurgery, long-term pain relief was poor in both patients. Neither patient sustained any immediate morbidity following radiosurgery. Patient 2 experienced right facial numbness 4 months postretreatment, while Patient 1 experienced no morbidity. Conclusion.,Repeat radiosurgery of the trigeminal nerve fails to provide long-term pain relief for MRCH. Given the reported failures of initial and repeat radiosurgery for MRCH, trigeminal nerve radiosurgery should not be offered for MRCH. [source] Gene Expression Profiling in Cluster Headache: A Pilot Microarray StudyHEADACHE, Issue 10 2006Christina Sjöstrand MD Background.,Cluster headache (CH) is a primary neurovascular headache disorder characterized by attacks of excruciating pain accompanied by ipsilateral autonomic symptoms. CH pathophysiology is presumed to involve an activation of hypothalamic and trigeminovascular systems, but inflammation and immunological mechanisms have also been hypothesized to be of importance. Objective.,To identify differentially expressed genes during different clinical phases of CH, assuming that changes of pathophysiological importance would also be seen in peripheral venous blood. Methods.,Blood samples were drawn at 3 consecutive occasions from 3 episodic CH patients: during attacks, between attacks and in remission, and at 1 occasion from 3 matched controls. Global gene expression was analyzed with microarray tehnology using the Affymetrix Human Genome U133 2.0 Plus GeneChip® Set, covering more than 54,000 gene transcripts, corresponding to almost 22,000 genes. Quantitative RT-PCR on S100P gene expression was analyzed in 6 patients and 14 controls. Results.,Overall, quite small differences were seen intraindividually and large differences interindividually. However, pairwise comparisons of signal values showed upregulation of several S100 calcium binding proteins; S100A8 (calgranulin A), S100A12 (calgranulin C), and S100P during active phase of the disease compared to remission. Also, annexin A3 (calcium-binding) and ICAM3 showed upregulation. BIRC1 (neuronal apoptosis inhibitory protein), CREB5, HLA-DQA1, and HLA-DQB1 were upregulated in patients compared to controls. The upregulation of S100P during attack versus remission was confirmed by quantitative RT-PCR analysis. Conclusions.,The S100A8 and S100A12 proteins are considered markers of non-infectious inflammatory disease, while the function of S100P is still largely unknown. Furthermore, upregulation of HLA-DQ genes in CH patients may also indicate an inflammatory response. Upregulation of these pro-inflammatory genes during the active phase of CH has not formerly been reported. Data from this pilot microarray study provide a basis for further studies in CH. [source] Outpatient Intravenous Dihydroergotamine for Refractory Cluster HeadacheHEADACHE, Issue 3 2004E. Magnoux MD Objective.,To evaluate the efficacy and safety of outpatient intravenous dihydroergotamine (DHE) for treatment of refractory cluster headache. Method.,Medical records were retrospectively reviewed of all patients with cluster headache who received outpatient intravenous DHE for treatment of refractory cluster headache between January 1992 and May 2000. Results.,One hundred four treatments were identified in 70 patients. There were 7 dropouts. Of the 97 completed treatments, 60 were for episodic cluster headache and 37 were for chronic cluster headache. Results for all treatments showed complete resolution of pain during the intravenous phase at 1 month in 61 (63%) of 97 cases, partial resolution in 13 cases (15%), and failure in 23 cases (24%). For the treatment of episodic cluster headache, there was complete resolution in 44 (73%) of 60 cases, partial resolution in 9 cases (13%), and failure in 7 cases (12%). For treatment of chronic cluster headache, there was complete resolution in 17 (46%) of the 37 cases, partial resolution in 4 cases (11%), and 16 failures (43%). As regards side effects and safety, the treatment triggered chest pain suspected of being vasospastic angina in 1 patient on day 7 of the treatment, when she was in the subcutaneous phase. Two patients dropped out due to fear of the injection, 1 because of palpitations, 1 because of chest tightness, and 2 others because of leg cramps, nausea, and diarrhea. Conclusions.,Outpatient intravenous DHE is a safe treatment. It is useful for refractory cluster headache, is more effective for the episodic form than the chronic form, and has a rapid onset of action. It did not change the evolution of the episodic form, but it did appear to induce remission in the chronic form or transform it to the episodic form. We advance a hypothesis to explain this. [source] Soluble Interleukin-2 Receptors Increase During the Active Periods in Cluster HeadacheHEADACHE, Issue 1 2003M. Empl MD Objective.,To investigate whether cytokines are altered during the active period of cluster headache. Background.,Patients with cluster headache show activation of the hypothalamus in PET studies and via endocrinologic parameters. Data also suggest an inflammatory process occurs in cluster headache. A connection between the presumed inflammatory cause, an immunological activation, and the hypothalamus could be generated by certain cytokines. Design and Methods.,ELISA was used to determine the serum levels of soluble interleukin-2 receptors, interleukin-1, interleukin-6, and 2 soluble interleukin-6 receptors (sIL-6R and soluble gp130) in 18 patients with cluster headache (6 women and 12 men) during the cluster period and in 17 healthy controls who were headache-free (3 women and 14 men). Results.,Patients with cluster headache had significantly increased soluble interleukin-2 receptors (413.6±223 U/mL vs. 290.0±112 U/mL; P < .05) compared with controls. Serum levels of interleukin-1 (0.29±0.30 pg/mL vs. 0.13±0.13 pg/mL, n.s.), interleukin-6 (0.87±0.6 pg/mL vs. 0.91±0.7 pg/ml; n.s.), soluble interleukin-6 receptors (33,131±8,349 pg/mL vs. 35,063±7,606 pg/mL; n.s.), or soluble gp130 (289±59 pg/mL vs. 283±20 pg/mL; n.s.) did not differ between the 2 groups, although patients with cluster tended to have higher interleukin-1 values. Conclusions.,Because elevated soluble interleukin-2 receptors indicate T cell activation, our findings suggest immune activation during cluster headache. Because interleukin-2 can activate the hypothalamus and stimulate the release of Corticotropin-releasing Factor (CRF), interleukin-2 could link a putative immunological cause of cluster headache with the observed hypothalamic activation. Systemic changes of interleukin-1 or the interleukin-6 system do not seem to play a role in cluster headache, as no alterations of serum levels were observed. Even so, unchanged serum levels do not exclude limited local production. [source] Upper and Lower Cluster Headache: Clinical and Pathogenetic Observations in 608 PatientsHEADACHE, Issue 7 2002Carola Cademartiri MD Objective, Background, and Methods.,Ever since it was proposed by Ekbom and Kugelberg back in 1968 on the basis of the different location of head pain during attacks, the differentiation of cluster headache into an upper syndrome (US) and a lower syndrome (LS) has been regarded as a purely academic distinction. To evaluate whether this differentiation is indeed well founded and to understand its possible significance in the light of current pathogenetic knowledge, we rigorously applied Ekbom and Kugelberg's classification criteria to a sample of 608 patients with cluster headache (CH; 440 men and 168 women), including 483 with episodic CH, 69 with chronic CH, and 56 with CH periodicity undetermined. Results.,Of these patients, 278 could be classified as US sufferers and 330 as LS sufferers. Our data analysis showed statistically significant clinical differences between the two syndromes: pain location was more common in the ocular, temporal, and nuchal regions among LS sufferers; in addition, patients with LS reported not only a higher rate of autonomic symptoms, but also a higher predominance of nasal congestion, ptosis, and forehead and facial sweating among these symptoms. Conclusions.,Based on current anatomofunctional knowledge and on the most recent pathogenetic findings, we believe that changes in hypothalamic activity posteroinferiorly may lead to activation of the caudal part of the spinal trigeminal nucleus by way of the hypothalamus, midbrain, and trigeminal nerve fibers and consequently to activation of the trigeminovascular system with a different location in the two syndromes. More specifically, there seems to be a larger and more extensive involvement of the subnucleus caudalis in LS compared with US, where only its ventrocaudal portions are likely to be affected. [source] Naratriptan in the Prophylaxis of Cluster HeadacheHEADACHE, Issue 1 2002Elizabeth Loder MD A 36-year-old man with cluster headache refractory to trials of standard prophylactic treatment and only partially responsive to parenteral sumatriptan and inhaled oxygen was admitted to an inpatient pain unit. The diagnosis of cluster headache was confirmed by direct observation of a typical attack. Despite efforts at prophylaxis, the patient continued to experience three to four severe headaches per day. Attempts to control his headaches with scheduled parenteral dihydroergotamine were successful, but headaches recurred when the medication was tapered, and continuous or intermittent use of parenteral dihydroergotamine was not felt to be a practical option for the patient. Naratriptan 2.5 mg twice daily completely abolished his headaches, which recurred when the medication was discontinued. No electrocardiographic or laboratory abnormalities were observed during treatment, and the patient reported no side effects. [source] Antiepileptic Drugs in Migraine, Cluster Headache, and Mood DisordersHEADACHE, Issue 2001F. Michael Cutrer MD No abstract is available for this article. [source] Antiepileptic Drugs in the Management of Cluster Headache and Trigeminal NeuralgiaHEADACHE, Issue 2001Todd D. Rozen MD Cluster headache and trigeminal neuralgia are relatively rare but debilitating neurologic conditions. Although they are clinically and diagnostically distinct from migraine, many of the same pharmacologic agents are used in their management. For many patients, the attacks are so frequent and severe that abortive therapy is often ineffective; therefore, chronic preventive therapy is necessary for adequate pain control. Cluster headache and trigeminal neuralgia have several distinguishing clinical features. Cluster headache is predominantly a male disorder; trigeminal neuralgia is more prevalent in women. Individuals with cluster headaches often develop their first attack before age 25; most patients with trigeminal neuralgia are between age 50 and 70. Cluster headaches are strongly associated with tobacco smoking and triggered by alcohol consumption; trigeminal neuralgia can be triggered by such stimuli as shaving and toothbrushing. Although the pain in both disorders is excruciating, cluster headache pain is episodic and unilateral, typically surrounds the eye, and lasts 15 to 180 minutes; the pain of trigeminal neuralgia lasts just seconds and is usually limited to the tissues overlying the maxillary and mandibular divisions of the trigeminal nerve. Cluster headache is unique because of its associated autonomic symptoms. Although the pathophysiology of cluster headache and trigeminal neuralgia are not completely understood, both appear to have central primary processes, and these findings have prompted investigations of the effectiveness of the newer antiepileptic drugs for cluster headache prevention and for the treatment of trigeminal neuralgia. The traditional antiepileptic drugs phenytoin and carbamazepine have been used for the treatment of trigeminal neuralgia for a number of years, and while they are effective, they can sometimes cause central nervous system effects such as drowsiness, ataxia, somnolence, and diplopia. Reports of studies in small numbers of patients or individual case studies indicate that the newer antiepileptic drugs are effective in providing pain relief for trigeminal neuralgia and cluster headache sufferers, with fewer central nervous system side effects. Divalproex has been shown to provide effective pain control and to reduce cluster headache frequency by more than half in episodic and chronic cluster headache sufferers. Topiramate demonstrated efficacy in a study of 15 patients, with a mean time to induction of cluster headache remission of 1.4 weeks (range, 1 day to 3 weeks). In the treatment of trigeminal neuralgia, gabapentin has been shown to be effective in an open-label study. When added to an existing but ineffective regimen of carbamazepine or phenytoin, lamotrigine provided improved pain relief; it also may work as monotherapy. Topiramate provided a sustained analgesic effect when administered to patients with trigeminal neuralgia. The newer antiepileptic drugs show considerable promise in the management of cluster headache and trigeminal neuralgia. [source] Antiepileptic Drugs in Migraine, Cluster Headache, and Mood DisordersHEADACHE, Issue 2001Article first published online: 31 MAR 200 No abstract is available for this article. [source] Olanzapine as an Abortive Agent for Cluster HeadacheHEADACHE, Issue 8 2001Todd D. Rozen MD Objective.,To evaluate olanzapine as a cluster headache abortive agent in an open-label trial. Background.,Cluster headache is the most painful headache syndrome known. There are very few recognized abortive therapies for cluster headache and fewer for patients who have contraindications to vasoconstrictive drugs. Methods.,Olanzapine was given as an abortive agent to five patients with cluster headache in an open-label trial. The initial olanzapine dose was 5 mg, and the dose was increased to 10 mg if there was no pain relief. The dosage was decreased to 2.5 mg if the 5-mg dose was effective but caused adverse effects. To be included in the study, each patient had to treat at least two attacks with either an effective dose or the highest tolerated dose. Results.,Five patients completed the investigation (four men, one woman; four with chronic cluster, one with episodic cluster). Olanzapine reduced cluster pain by at least 80% in four of five patients, and two patients became headache-free after taking the drug. Olanzapine typically alleviated pain within 20 minutes after oral dosing and treatment response was consistent across multiple treated attacks. The only adverse event was sleepiness. Conclusions.,Olanzapine appears to be a good abortive agent for cluster headache. It alleviates pain quickly and has a consistent response across multiple treated attacks. It appears to work in both episodic and chronic cluster headache. [source] Sudden Worsening of Cluster Headache: A Signal of Aneurysmal Thrombosis and EnlargementHEADACHE, Issue 8 2000Juanita G. McBeath MD We report a 55-year-old man presenting with symptoms of cluster headache, including throbbing pain behind the left eye, tearing, and rhinorrhea. Magnetic resonance imaging and magnetic resonance angiography revealed no abnormalities. Two days of intravenous dihydroergotamine resolved his pain. His headaches were somewhat relieved with a treatment regimen of 100 mg of imipramine each night, 40 mg of propranolol twice a day, 250 mg of divalproex three times a day, and dihydroergotamine nasal spray for breakthrough headaches. Two months later, the severity of his pain increased dramatically. Repeat imaging revealed a large thrombosed left posterior communicating artery aneurysm. Following obliterative surgery, his headaches are infrequent and mild and resemble tension headaches. Dramatic changes in headache characteristics can be an indicator of aneurysmal enlargement and thrombosis. This case illustrates the importance of repeat imaging when a patient's headache significantly worsens. [source] Alteration in Nature of Cluster Headache During Subcutaneous Administration of SumatriptanHEADACHE, Issue 1 2000Rachel Hering-Hanit MD Objectives., To document the relationship between the 5-HT receptor agonist sumatriptan and a change in the nature of cluster headache in four cases. To relate the findings to the literature on the use of sumatriptan in both cluster headache and migraine. Background., Studies of the efficacy and adverse effects of long-term treatment with sumatriptan in cluster headache are limited and report conflicting findings. Methods., Four cases are described. Results., All four patients developed a marked increase in the frequency of attacks 3 to 4 weeks after initiating treatment with the drug for the first time. Three patients also developed a change in headache character, and 2 experienced prolongation of the cluster headache period. Withdrawal of the drug reduced the frequency of headaches and eliminated the newly developed type of headache. Conclusions., Determination of the effects of long-term use of sumatriptan will result in more precise guidelines for the frequency and duration of treatment with this otherwise extremely beneficial drug. [source] Sphenopalatine Endoscopic Ganglion Block: A Revision of a Traditional Technique for Cluster HeadacheTHE LARYNGOSCOPE, Issue 8 2006Giovanni Felisati MD The diagnosis of chronic cluster headache (CH), the most painful form of headache, is based on typical clinical features characterized by strictly unilateral pain with no side shift and ipsilateral oculofacial autonomic phenomena. The attacks occur several times a day for periods of 1 to 2 months in the episodic form of the disease or less frequently on a daily basis in the chronic form. The pathogenesis of CH involves the activation of parasympathetic nerve structures located within the sphenopalatine ganglion (SPG), which explains many of the associated symptoms, whereas the activation of the ipsilateral hypothalamic gray matter may explain its typical circadian and circannual periodicity. A number of surgical approaches have been tried in cases of chronic CH resistant to pharmacologic therapy, of which SPG blockade has been shown to have certain efficacy. We have adopted a new technique based on endoscopic ganglion blockade that approaches the pterigo-palatine fossa by way of the lateral nasal wall and consists of the injection of a mixture of local anesthetics and corticosteroids, which was performed in 20 selected patients with chronic CH, according to the International Headache Society criteria (18 male, 2 female; mean age 40 yr), who were selected for SPG blockade because they were totally drug resistant. The symptoms improved significantly, but always only temporarily, in 11 cases. These results should be considered rather good because, unlike other frequently used techniques, SPG blockade is not invasive and should therefore always be attempted before submitting patients to more invasive surgical approaches. [source] Gene Expression Profiling in Cluster Headache: A Pilot Microarray StudyHEADACHE, Issue 10 2006Christina Sjöstrand MD Background.,Cluster headache (CH) is a primary neurovascular headache disorder characterized by attacks of excruciating pain accompanied by ipsilateral autonomic symptoms. CH pathophysiology is presumed to involve an activation of hypothalamic and trigeminovascular systems, but inflammation and immunological mechanisms have also been hypothesized to be of importance. Objective.,To identify differentially expressed genes during different clinical phases of CH, assuming that changes of pathophysiological importance would also be seen in peripheral venous blood. Methods.,Blood samples were drawn at 3 consecutive occasions from 3 episodic CH patients: during attacks, between attacks and in remission, and at 1 occasion from 3 matched controls. Global gene expression was analyzed with microarray tehnology using the Affymetrix Human Genome U133 2.0 Plus GeneChip® Set, covering more than 54,000 gene transcripts, corresponding to almost 22,000 genes. Quantitative RT-PCR on S100P gene expression was analyzed in 6 patients and 14 controls. Results.,Overall, quite small differences were seen intraindividually and large differences interindividually. However, pairwise comparisons of signal values showed upregulation of several S100 calcium binding proteins; S100A8 (calgranulin A), S100A12 (calgranulin C), and S100P during active phase of the disease compared to remission. Also, annexin A3 (calcium-binding) and ICAM3 showed upregulation. BIRC1 (neuronal apoptosis inhibitory protein), CREB5, HLA-DQA1, and HLA-DQB1 were upregulated in patients compared to controls. The upregulation of S100P during attack versus remission was confirmed by quantitative RT-PCR analysis. Conclusions.,The S100A8 and S100A12 proteins are considered markers of non-infectious inflammatory disease, while the function of S100P is still largely unknown. Furthermore, upregulation of HLA-DQ genes in CH patients may also indicate an inflammatory response. Upregulation of these pro-inflammatory genes during the active phase of CH has not formerly been reported. Data from this pilot microarray study provide a basis for further studies in CH. [source] Cluster headache: aetiology, diagnosis and management.HEADACHE, Issue 3 2003K Ekbom Drugs. 2002;62(1):61-69 Cluster headache is characterised by repeated attacks of strictly unilateral pain in the orbital region associated with local autonomic symptoms or signs. The attacks are brief but of a very severe, almost excruciating intensity. For unknown reasons males are affected more often than females. Recent studies suggest that an autosomal dominant gene has a role in some families with cluster headache. Hormonal studies indicate a dysfunction in the central nervous system. Neuroimaging has revealed primary defects in the hypothalamic grey matter. Local homolateral dilatation in the intracranial segment of the internal carotid and ophthalmic arteries during attacks is the result of a generic neurovascular activation, probably mediated by trigeminal parasympathetic reflexes. Sumatriptan 6mg subcutaneously is the drug of choice in the treatment of acute attacks. Inhalation of 100% oxygen can also be recommended. In the prophylactic treatment, verapamil is the first option. Other drugs that can be considered are corticosteroids, which may induce a remission of frequent, severe attacks, and lithium. Oral ergotamine tartrate may be sufficient for patients with night attacks and/or short, rather mild to moderately severe cluster headache periods. Third line drugs are serotonin inhibitors (methysergide and pizotifen) and valproic acid. Patients should be encouraged to keep headache diaries and be carefully instructed about the nature and treatment of the headaches. Alcohol can bring on extra attacks and should not be consumed during active periods of cluster headache. Comment: A useful review of clinical options. Given the effectiveness of injectable sumatriptan and the prophylactic use of ergotamine mentioned, one might speculate that the new intranasal formulations of triptans (eg, zolmitriptan) and triptans with a longer half-life (eg, frovatriptan) may prove to be effective in the treatment of cluster headache. DSM [source] Cluster headache: the challenge of clinical trials.HEADACHE, Issue 3 2003K Moore Curr Pain Headache. Rep 2002 Feb;6(1):52-56 The design and execution of clinical trials poses special problems for cluster headache. Although there is less inter-individual and intra-individual variability of attacks than seen with migraine, the brevity of attacks, spontaneous remissions unrelated to treatment, and the relative rarity of cluster headaches challenge investigators. The International Headache Society has developed guidelines that represent a compromise between scientific rigor and practicality. Only injectable sumatriptan for acute attacks and verapamil for prophylaxis have demonstrated a robust therapeutic effect in controlled clinical trials. Comment: Kenneth Moore raises important methodological considerations. It is possible to undertake crossover trials comparing different active treatments? He is correct in his assertion that few agents show robust efficacy. A major issue relates to the proportion of patients with episodic versus chronic cluster headache where efficacy of active treatments can vary. For example, oral zolmitriptan was effective against placebo only in those patients with episodic disease (Bahra A, Gawel MJ, Hardebo JE, Millson DS, Breen SA, Goadsby PJ. Oral zolmitriptan is effective in the acute treatment of cluster headache. Neurology. 2000;54:1832-1839). And a set of small studies on melatonin and cluster demonstrate the problems Dr. Moore describes. In one study (Leone M, D'Amico D, Moschiano F, Fraschini F, Busonne G. Metalonin versus placebo in the prophylaxis of cluster headache: a double-blind pilot study with parallel groups. Cephalalgia. 1996;16:494-496), the melatonin worked only in episodic, not chronic cluster patients. In the second study (Prinsheim T, Magnoux E, Dobson CF, Hamel E, Aube M. Melatonin as adjuctive therapy in the prophylaxis of cluster headache: a pilot study. Headache. 2002;42:787-792), melatonin did not work better than placebo in either episodic or chronic cluster patients. Furthermore, the paper abstracted above by Torelli and Manzoni suggests that episodic cluster may progress to chronic cluster as a result of extrinsic factors such as smoking. Finally, there are ethical issues in placebo-controlled cluster studies, given the severity of the pain and the availability of effective acute and chronic treatments. As noted above, Dr. Peter Goadsby points out the need to persevere with these studies to find nonvasoactive treatments for patients with cluster headache. DSM and SJT [source] Antiepileptic Drugs in the Management of Cluster Headache and Trigeminal NeuralgiaHEADACHE, Issue 2001Todd D. Rozen MD Cluster headache and trigeminal neuralgia are relatively rare but debilitating neurologic conditions. Although they are clinically and diagnostically distinct from migraine, many of the same pharmacologic agents are used in their management. For many patients, the attacks are so frequent and severe that abortive therapy is often ineffective; therefore, chronic preventive therapy is necessary for adequate pain control. Cluster headache and trigeminal neuralgia have several distinguishing clinical features. Cluster headache is predominantly a male disorder; trigeminal neuralgia is more prevalent in women. Individuals with cluster headaches often develop their first attack before age 25; most patients with trigeminal neuralgia are between age 50 and 70. Cluster headaches are strongly associated with tobacco smoking and triggered by alcohol consumption; trigeminal neuralgia can be triggered by such stimuli as shaving and toothbrushing. Although the pain in both disorders is excruciating, cluster headache pain is episodic and unilateral, typically surrounds the eye, and lasts 15 to 180 minutes; the pain of trigeminal neuralgia lasts just seconds and is usually limited to the tissues overlying the maxillary and mandibular divisions of the trigeminal nerve. Cluster headache is unique because of its associated autonomic symptoms. Although the pathophysiology of cluster headache and trigeminal neuralgia are not completely understood, both appear to have central primary processes, and these findings have prompted investigations of the effectiveness of the newer antiepileptic drugs for cluster headache prevention and for the treatment of trigeminal neuralgia. The traditional antiepileptic drugs phenytoin and carbamazepine have been used for the treatment of trigeminal neuralgia for a number of years, and while they are effective, they can sometimes cause central nervous system effects such as drowsiness, ataxia, somnolence, and diplopia. Reports of studies in small numbers of patients or individual case studies indicate that the newer antiepileptic drugs are effective in providing pain relief for trigeminal neuralgia and cluster headache sufferers, with fewer central nervous system side effects. Divalproex has been shown to provide effective pain control and to reduce cluster headache frequency by more than half in episodic and chronic cluster headache sufferers. Topiramate demonstrated efficacy in a study of 15 patients, with a mean time to induction of cluster headache remission of 1.4 weeks (range, 1 day to 3 weeks). In the treatment of trigeminal neuralgia, gabapentin has been shown to be effective in an open-label study. When added to an existing but ineffective regimen of carbamazepine or phenytoin, lamotrigine provided improved pain relief; it also may work as monotherapy. Topiramate provided a sustained analgesic effect when administered to patients with trigeminal neuralgia. The newer antiepileptic drugs show considerable promise in the management of cluster headache and trigeminal neuralgia. [source] Olanzapine as an Abortive Agent for Cluster HeadacheHEADACHE, Issue 8 2001Todd D. Rozen MD Objective.,To evaluate olanzapine as a cluster headache abortive agent in an open-label trial. Background.,Cluster headache is the most painful headache syndrome known. There are very few recognized abortive therapies for cluster headache and fewer for patients who have contraindications to vasoconstrictive drugs. Methods.,Olanzapine was given as an abortive agent to five patients with cluster headache in an open-label trial. The initial olanzapine dose was 5 mg, and the dose was increased to 10 mg if there was no pain relief. The dosage was decreased to 2.5 mg if the 5-mg dose was effective but caused adverse effects. To be included in the study, each patient had to treat at least two attacks with either an effective dose or the highest tolerated dose. Results.,Five patients completed the investigation (four men, one woman; four with chronic cluster, one with episodic cluster). Olanzapine reduced cluster pain by at least 80% in four of five patients, and two patients became headache-free after taking the drug. Olanzapine typically alleviated pain within 20 minutes after oral dosing and treatment response was consistent across multiple treated attacks. The only adverse event was sleepiness. Conclusions.,Olanzapine appears to be a good abortive agent for cluster headache. It alleviates pain quickly and has a consistent response across multiple treated attacks. It appears to work in both episodic and chronic cluster headache. [source] Prevention and treatment of cluster headachePROGRESS IN NEUROLOGY AND PSYCHIATRY, Issue 3 2009Anna S Cohen PhD Cluster headache is an excruciatingly painful primary headache syndrome with rapid onset attacks that are relatively short, typically up to three hours. Management strategies involve avoidance of possible triggers to attacks, such as alcohol and naps, and pharmacological treatments aimed at either quickly aborting acute attacks, or preventive therapies to suppress the attacks entirely, or reduce their frequency, severity or duration. Copyright © 2009 Wiley Interface Ltd [source] Diagnostic delays and mis-management in cluster headacheACTA NEUROLOGICA SCANDINAVICA, Issue 3 2004A. Bahra Objectives , Cluster headache is a stereotyped form of primary headache that while common in terms of neurologic illnesses is much less common as a cause of disabling headache than migraine. Materials and methods , We directly interviewed 230 patients with cluster headache. National support groups contributed 76% and 24% came from the National Hospital for Neurology and Neurosurgery Headache Clinic. Results , Seventy-two percent were men and 28% women, giving a male to female (M:F) ratio of 2.5:1. Episodic cluster headache (ECH) was recorded in 79% while 21% had chronic cluster headache (CCH). The mean time to diagnosis has dropped from 22 years in the 1960s to 2.6 years in the 1990s, although the mean number of GPs seen before a diagnosis was made remains at three. Conclusions , While there has been improvement in the time to diagnosis for cluster headache, a number of physicians will be consulted, and better education is likely to reduce the overall patient suffering. [source] Effect of deep brain stimulation of the posterior hypothalamic area on the cardiovascular system in chronic cluster headache patientsEUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2007P. Cortelli The objective of this study was to determine the cardiovascular effects of chronic stimulation of the posterior hypothalamic area (PHA) in cluster headache (CH) patients. Systolic and diastolic blood pressure (SBP, DBP), cardiac output, total peripheral resistance (TPR), heart rate (HR) and breathing were monitored at supine rest and during head-up tilt test (HUTT), Valsalva manoeuvre, deep breathing, cold face test and isometric handgrip in eight drug-resistant chronic CH patients who underwent monolateral electrode implantation in the PHA for therapeutic purposes. Autoregressive power spectral analysis (PSA) of HR variability (HRV) was calculated at rest and during HUTT. Each subject was studied before surgery (condition A) and after chronic deep brain stimulation (DBS) of PHA (condition B). Baseline SBP, DBP, HR and cardiovascular reflexes were normal and similar in both conditions. With respect to condition A, DBP, TPR and the LF/HF obtained from the PSA of HRV were significantly (P < 0.05) increased during HUTT in condition B. In conclusion, chronic DBS of the PHA in chronic CH patients is associated with an enhanced sympathoexcitatory drive on the cardiovascular system during HUTT. [source] The use of gabapentin in chronic cluster headache patients refractory to first-line therapyEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2007S. Schuh-Hofer Chronic cluster headache (CCH) is a rare but challenging condition. About 20% of CCH patients get refractory to treatment. Gabapentin has recently been reported to be efficacious in the treatment of CCH. To test the potential of gabapentin as second-line drug, we prospectively studied the efficacy of gabapentin as add-on drug in eight patients suffering from CCH refractory to first-line treatment. Six of eight CCH patients responded to treatment. After the end of the study phase, the patients' clinical course was further followed up until January 2006. The longest period of being continuously pain-free under gabapentin treatment was 18 months. In some individuals, increasing doses were needed with time. We conclude that gabapentin may be offered as treatment trial in patients refractory to first-line treatment. However, patients may fail to respond to treatment and drug tolerance may occur with time. [source] Cluster Attacks Responsive to Recreational Cannabis and DronabinolHEADACHE, Issue 6 2009Matthew S. Robbins MD Pharmacological preparations of cannabinoid compounds have a variety of therapeutic uses in medicine, including different pain syndromes, but have not been previously reported as beneficial for cluster headache. We present a patient with cluster headache who was refractory to multiple acute and preventive medications but successfully aborted his attacks with recreational marijuana use; subsequent use of dronabinol provided equally effective pain relief. The beneficial effect may be related to the high concentration of cannabinoid receptors in the hypothalamus, which has been implicated as a site of dysfunction in neuroimaging studies of patients with cluster headache. [source] Haplotype Analysis Confirms the Association Between the HCRTR2 Gene and Cluster HeadacheHEADACHE, Issue 7 2008Innocenzo Rainero MD Background., Several studies suggested that genetic factors play a role in cluster headache (CH) susceptibility. We found a significant association between the 1246 G>A polymorphism of the hypocretin receptor-2 (HCRTR2) gene and the disease. This association was confirmed in a large study from Germany but was not replicated in a dataset of CH patients from Northern Europe. Objective., The purpose of this study was to further evaluate the association between CH and the HCRTR2 gene using new polymorphisms, estimating the frequency of different gene haplotypes, searching for gene mutations, and evaluating the effects of the examined polymorphisms on hypocretin binding sites. Methods., We genotyped 109 CH patients and 211 healthy controls for 5 new polymorphisms of the HCRTR2 gene and we inferred different gene haplotypes. Complete HCRTR2 sequencing was undertaken for 11 independent CH patients, 5 of whom had a positive family history. The effects of the 1246 G>A polymorphism on the hypocretin binding sites were evaluated using different computer-assisted analyses. Results., Three new polymorphisms of the HCRTR2 gene resulted significantly associated with CH. The GTAAGG haplotype resulted more frequent in cases than in controls (OR: 3.68; 95% CI: 1.85-7.67). No point mutation of the HCRTR2 gene was found. Binding analyses showed that the 1246 G>A polymorphism (substitution of valine at position 308 by isoleucine) has no effect on the hypocretin binding sites but could influence the dimerization process of the receptor. Conclusion., Our data confirm previous studies suggesting that the HCRTR2 gene or a linked locus significantly modulates the risk for CH. In addition, we suggest that the V308I substitution of the HCRTR2 may interfere with the dimerization process of the receptor, thereby influencing its functional activity. [source] Functional Imaging in Primary Headache DisordersHEADACHE, Issue 5 2008F. Michael Cutrer MD Over the past two decades, the development of new functional neuroimaging techniques has improved our understanding of the brain events underlying several primary headache disorders. In migraine and cluster headache, the advent of these techniques has shifted the emphasis in pathophysiological research away from the vessel and back to the brain. [source] Effect on Sleep of Posterior Hypothalamus Stimulation in Cluster HeadacheHEADACHE, Issue 7 2007Roberto Vetrugno MD Objective.,To evaluate the structure and quality of sleep and the circadian rhythm of body core temperature (BcT°) in patients with drug-resistant chronic cluster headache (CH) before and during deep brain stimulation (DBS) of the posterior hypothalamus. Background.,Chronic CH is a severe primary headache and frequently associated with disturbances in sleep. Posterior hypothalamus DBS is performed as an effective treatment of drug-resistant chronic CH. The effects of posterior hypothalamus DBS on sleep and the circadian rhythm of BcT° are unknown. Methods.,Three male patients with chronic drug-resistant CH underwent 48-hour consecutive polysomnography (PSG) by means of the VITAPORT® system with determination of BcT° by means of a rectal probe. Recordings were done before electrode implantation in the posterior hypothalamus and after optimized DBS of posterior hypothalamus. Results.,Before electrode implantation PSG showed nocturnal CH attacks, reduced sleep efficiency, fragmented sleep and increased periodic limb movements in sleep (PLMS). During DBS nocturnal CH attacks were abolished and sleep efficiency and PLMS improved. BcT° circadian rhythm was normal both before and during DBS. Conclusions.,Our data show that DBS of posterior hypothalamus in drug-resistant chronic CH is effective in curtailing nocturnal CH attacks, and is associated with improved sleep structure and quality. Chronic CH displays a normal circadian rhythm of BcT°, unchanged during hypothalamic DBS. [source] |