Headache CurrentsPub Date : 2005-10-24DOI: 10.1111/j.1743-5013.2005.00017.x
Katharina Haerter M.D., Cenk Ayata M.D., Michael A. Moskowitz M.D.
{"title":"Cortical Spreading Depression: A Model for Understanding Migraine Biology and Future Drug Targets","authors":"Katharina Haerter M.D., Cenk Ayata M.D., Michael A. Moskowitz M.D.","doi":"10.1111/j.1743-5013.2005.00017.x","DOIUrl":"10.1111/j.1743-5013.2005.00017.x","url":null,"abstract":"<p> <i>Cortical spreading depression (CSD) is an intense and steady depolarization of neuroglial membranes, and cessation of spontaneous or evoked synaptic activity. CSD can be evoked by simultaneous depolarization of a minimum volume of brain tissue, such as during cerebral ischemia, trauma, or cortical drug application. Once triggered, it slowly spreads to contiguous areas regardless of functional cortical divisions or arterial territories. A pathophysiological overlap between CSD and migraine aura has long been suspected. Both migraine aura and headache result from CSD. Neurological symptoms during migraine aura spread, and the speed of spread on retinotopic maps is consistent with the speed of CSD in experimental animals. Migraine headache results from CSD-induced activation of nociceptors in meninges and large blood vessels in concert with modulation of central pain mechanisms. Insights into causes and consequences of CSD have come from studies in animals with genetically modified neuronal Ca<sup>2+</sup> channel subtypes that influence CSD threshold; therefore, genetic variations may influence CSD susceptibility in humans. Identification of CSD as an important cause of migraine headache provides new insights into mechanisms leading to an attack, and the potential for development of new prophylactic agents.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 5","pages":"97-103"},"PeriodicalIF":0.0,"publicationDate":"2005-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.00017.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76397369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Headache CurrentsPub Date : 2005-08-08DOI: 10.1111/j.1743-5013.2005.20415.x
Anna S. Cohen M.R.C.P., Holger Kaube M.D.
{"title":"Primary Headache Disorders and Circadian Biology: A Clinical, Imaging, and Therapy Perspective","authors":"Anna S. Cohen M.R.C.P., Holger Kaube M.D.","doi":"10.1111/j.1743-5013.2005.20415.x","DOIUrl":"10.1111/j.1743-5013.2005.20415.x","url":null,"abstract":"<p> <i>Primary headache syndromes such as hypnic headache, and trigeminal autonomic cephalgias (TACs) such as cluster headache, paroxysmal hemicrania, and SUNCT (Short-lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and Tearing), are associated with varying degrees with attacks that occur with circadian rhythmicity. In hypnic headache, the attacks occur exclusively during sleep, and in cluster headache the attacks predominate in sleep in 75% of patients. The TACs, especially cluster headache and SUNCT, have been associated on functional imaging with activation of the hypothalamus during attacks. There is also evidence in patients with cluster headache of altered secretory rhythms of a variety of hypophyseal hormone systems including melatonin, cortisol, and others. Given the role of the suprachiasmatic nucleus in the diurnal cycle, the hypothalamus is implicated as a generator of headaches with a prominent circadian rhythm. This article discusses the physiological and biochemical mechanisms that implicate the hypothalamus in the generation of a variety of primary headache disorders.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 4","pages":"86-92"},"PeriodicalIF":0.0,"publicationDate":"2005-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.20415.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83520649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Headache CurrentsPub Date : 2005-08-08DOI: 10.1111/j.1743-5013.2005.20416.x
Ramadevi Gourineni M.D., Phyllis C. Zee M.D., Ph.D.
{"title":"The Hypothalamus and Primary Headache Disorders","authors":"Ramadevi Gourineni M.D., Phyllis C. Zee M.D., Ph.D.","doi":"10.1111/j.1743-5013.2005.20416.x","DOIUrl":"10.1111/j.1743-5013.2005.20416.x","url":null,"abstract":"<p> <i>A prominent feature of primary headache disorders is the diurnal variation in their timing, and their relationship to sleep. In particular, the temporal and seasonal distribution of cluster headaches and accompanying hormonal changes in migraine, indicate that the circadian system and other sleep and wake generating areas in the hypothalamus may play an important role in their pathophysiology. This article provides a review of the basic neurobiology of circadian rhythms and sleep and its potential implications for understanding the central triggers of some primary headache disorders. The strongest and most direct evidence for a role of the hypothalamus in cluster headache derives from functional brain imaging studies. Furthermore, alteration in the timing and amplitude of hormonal circadian rhythms point to a possible role of the suprachiasmatic nucleus (SCN) in cluster headaches. Improved understanding of the relationship between circadian rhythms, sleep and primary headache disorders is an exciting area of investigation which could lead to innovative circadian and sleep based treatment strategies.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 4","pages":"77-80"},"PeriodicalIF":0.0,"publicationDate":"2005-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.20416.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82914993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Headache CurrentsPub Date : 2005-06-01DOI: 10.1111/j.1743-5013.2005.20312.x
H. C. Diener M.D., Ph.D., T. Kurth M.D., Sc.D.
{"title":"Migraine as a Risk Factor for White Matter Lesions, Silent Infarctions, and Ischemic Stroke: The Potential Mechanisms and Therapeutic Implications","authors":"H. C. Diener M.D., Ph.D., T. Kurth M.D., Sc.D.","doi":"10.1111/j.1743-5013.2005.20312.x","DOIUrl":"10.1111/j.1743-5013.2005.20312.x","url":null,"abstract":"<p> <i>The high prevalence of migraine among young individuals with stroke as well as dysfunction of cerebral arteries during the migraine attack has led to the hypothesis that migraine may be a risk factor for ischemic stroke. Advances in brain imaging have provided further evidence that migraine may not only be associated with stroke, but also with silent infarctions and with white matter lesions in the brain. In this review, we discuss the current scientific evidence, plausable biological mechanisms, and potential treatment options.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 3","pages":"53-57"},"PeriodicalIF":0.0,"publicationDate":"2005-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.20312.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74003707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Headache CurrentsPub Date : 2005-06-01DOI: 10.1111/j.1743-5013.2005.20309.x
Mark C. Kruit M.D., Lenore J. Launer Ph.D., Mark A. Van Buchem M.D., Ph.D., Gisela M. Terwindt, Michel D. Ferrari M.D., Ph.D.
{"title":"Migraine as a Risk Factor for White Matter Lesions, Silent Infarctions, and Ischemic Stroke: The Evidence for a Link","authors":"Mark C. Kruit M.D., Lenore J. Launer Ph.D., Mark A. Van Buchem M.D., Ph.D., Gisela M. Terwindt, Michel D. Ferrari M.D., Ph.D.","doi":"10.1111/j.1743-5013.2005.20309.x","DOIUrl":"10.1111/j.1743-5013.2005.20309.x","url":null,"abstract":"<p> <i>For decades, migraine has been considered to be an episodic, neurovascular disorder, without long-term consequences to the brain. Associations between migraine and clinical stroke and migraine and white matter hyperintense lesions have been suggested in numerous studies, but due to various methodological problems no definite conclusion could be drawn from these studies. Recently, data from a population-based cross-sectional MRI study in were published. Data from this study established migraine to be a true and independent risk factor for white matter lesions (in female migraine patients) and subclinical posterior circulation territory infarcts. In this review, the methodology and results of previous investigations of a relationship between migraine and clinical ischemic stroke, silent infarction and white matter lesions are reviewed, and integrated in the results from the new MRI study. The conclusion comprises that brain infarction occurs far more frequently than expected in migraine patients, most pronounced in migraine with aura: 8% have subclinical cerebellar infarcts, although most infarcts remain clinically silent. Female migraine patients are at increased risk of deep white matter lesions, independent of the effects of cardiovascular risk factors. The influence of migraine severity (attack frequency) on the risk of both types of lesions suggests a causal relationship between migraine severity and lesion load. Future studies are needed to assess whether these (probably) ischemic lesions have relevant (long-term) functional correlates.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 3","pages":"62-70"},"PeriodicalIF":0.0,"publicationDate":"2005-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.20309.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89123944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Headache CurrentsPub Date : 2005-06-01DOI: 10.1111/j.1743-5013.2005.20310.x
Gretchen E. Tietjen M.D.
{"title":"Migraine as a Risk Factor for White Matter Lesions, Silent Infarctions, and Ischemic Stroke","authors":"Gretchen E. Tietjen \u0000 M.D.","doi":"10.1111/j.1743-5013.2005.20310.x","DOIUrl":"10.1111/j.1743-5013.2005.20310.x","url":null,"abstract":"","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 3","pages":"71-75"},"PeriodicalIF":0.0,"publicationDate":"2005-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.20310.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76552913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Headache CurrentsPub Date : 2005-06-01DOI: 10.1111/j.1743-5013.2005.20311.x
David W. Dodick M.D.
{"title":"Migraine as a Risk Factor for White Matter Lesions, Silent Infarctions, and Ischemic Stroke","authors":"David W. Dodick \u0000 M.D.","doi":"10.1111/j.1743-5013.2005.20311.x","DOIUrl":"10.1111/j.1743-5013.2005.20311.x","url":null,"abstract":"","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 3","pages":"58-61"},"PeriodicalIF":0.0,"publicationDate":"2005-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.20311.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86862350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}