Headache CurrentsPub Date : 2006-03-28DOI: 10.1111/j.1743-5013.2006.00025.x
Robert W. Baloh M.D.
{"title":"Migraine and Vertigo: Epidemiology, Genetics, and Mechanism(s)","authors":"Robert W. Baloh M.D.","doi":"10.1111/j.1743-5013.2006.00025.x","DOIUrl":"10.1111/j.1743-5013.2006.00025.x","url":null,"abstract":"<p> <i>Both migraine and vertigo are highly prevalent in the general population, but the co-occurrence of migraine and vertigo is much higher than would be expected by chance alone with a lifetime prevalence of migrainous vertigo in the range of 1%. Genetic factors are important for determining the threshold for migraine symptoms but so far, mutations have been identified in only two genes for the relatively rare syndrome of familial hemiplegic migraine. Numerous genetic loci and candidate genes have been identified for the more common syndromes of migraine with aura and migraine without aura, but the results are conflicting and largely unreplicated. Recently, a susceptibility locus for familial benign recurrent vertigo was identified on chromosome 22q, but as with the susceptibility loci for migraine syndromes, this will need to be replicated in other patient populations. How migraine leads to recurrent vertigo is poorly understood; there may be multiple mechanisms affecting both peripheral and central vestibular pathways. Vasospasm involving the labyrinthine arteries is an intriguing possibility since vasospasm has been identified with retinal migraine. An ion channel mutation shared by ear and brain could explain the combination of central and peripheral vestibular signs and the common triggers for migraine symptoms. Finally, in some patients with migrainous vertigo, the inner ear may be damaged resulting in a form of Meniere's disease.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"3 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2006-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2006.00025.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90077583","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 : 2006-03-28DOI: 10.1111/j.1743-5013.2006.00027.x
Thomas Brandt M.D., F.R.C.P., Michael Strupp M.D.
{"title":"Migraine and Vertigo: Classification, Clinical Features, and Special Treatment Considerations","authors":"Thomas Brandt M.D., F.R.C.P., Michael Strupp M.D.","doi":"10.1111/j.1743-5013.2006.00027.x","DOIUrl":"10.1111/j.1743-5013.2006.00027.x","url":null,"abstract":"<p> <i>Vestibular migraine is a recognized medical entity in most dizziness units. It accounts for approximately 10% of these ‘dizzy’ patients and is the most common cause of spontaneous episodic vestibular vertigo. In about one third of the patients it is not associated with headache. Vestibular migraine is characterized by an extremely varied manifestation; its attacks last from seconds to days; it can occur at any time in life; and its diagnosis is difficult, especially since it must be differentiated from Meniere's disease, vestibular paroxysmia, and transient ischemic attacks. During the attack pathological spontaneous or positional nystagmus and postural imbalance are found in 70–90%; during the attack-free interval less severe ocular motor signs are found in about 60%. This review delineates the clinical features of vestibular migraine and distinguishes it from motion sickness-like symptoms and nonvestibular dizziness in migraine. Finally, the case is made for including the term ‘vestibular migraine’ in the International Headache Classification as a subcategory of migraine which is distinct from ‘basilar-type migraine’ and ‘benign paroxysmal vertigo of childhood.’</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"3 1","pages":"12-19"},"PeriodicalIF":0.0,"publicationDate":"2006-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2006.00027.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84412761","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 : 2006-03-28DOI: 10.1111/j.1743-5013.2006.00026.x
Joanna C. Jen M.D., Ph.D.
{"title":"Migraine and Vertigo: Genetics and Mechanisms—Scientific Abstracts and Commentary","authors":"Joanna C. Jen \u0000 M.D., Ph.D.","doi":"10.1111/j.1743-5013.2006.00026.x","DOIUrl":"10.1111/j.1743-5013.2006.00026.x","url":null,"abstract":"","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"3 1","pages":"8-11"},"PeriodicalIF":0.0,"publicationDate":"2006-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2006.00026.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81412622","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 : 2005-12-06DOI: 10.1111/j.1743-5013.2005.00022.x
Irene Tracey Ph.D.
{"title":"The Neural Matrix of Pain Processing and Placebo Analgesia: Evidence from Functional Imaging","authors":"Irene Tracey Ph.D.","doi":"10.1111/j.1743-5013.2005.00022.x","DOIUrl":"10.1111/j.1743-5013.2005.00022.x","url":null,"abstract":"<p> <i>Recent functional imaging studies in humans have given us unprecedented opportunities to define the neuroanatomical basis for the placebo effect. Though these studies have largely been conducted in the field of pain and analgesia, the findings could well provide models for more general placebo effects in other clinical situations. Key regions that mediate the placebo effect include prefrontal cortices, anterior cingulate cortex (ACC) and brainstem structures, whereas the specific analgesic effects produced subsequent to a placebo response are mediated by a decreased activation in key pain processing brain regions, similar to that seen via pharmacological means. These new methods provide powerful tools with which to study the placebo response in pain and other diseases as they allow correlations to be made between cognitive manipulations and behavioral outcomes with changes in functionally defined neuroanatomical brain regions. Researchers are harnessing these methods to construct generalized models for the placebo effect that can be tested beyond the field of pain and analgesia.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 6","pages":"123-126"},"PeriodicalIF":0.0,"publicationDate":"2005-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.00022.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77717389","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 : 2005-12-06DOI: 10.1111/j.1743-5013.2005.00023.x
Damien G Finniss M.Sc.Med., Fabrizio Benedetti M.D.
{"title":"The Neural Matrix of Pain Processing and Placebo Analgesia: Implications for Clinical Practice","authors":"Damien G Finniss M.Sc.Med., Fabrizio Benedetti M.D.","doi":"10.1111/j.1743-5013.2005.00023.x","DOIUrl":"10.1111/j.1743-5013.2005.00023.x","url":null,"abstract":"<p> <i>The placebo response has been the focus of increased research attention in recent years, particularly in the field of pain. Advances in research have improved our understanding about the psychological and neurobiological mechanisms underpinning this response, ultimately demonstrating the complexity of the mind–brain–body interaction. This has also allowed for the discussion of possible clinical implications of this research, both in clinical trial design and clinical practice. The ability to harness and maximize the mechanisms of the placebo response presents an exciting challenge for further research and clinical practice. This review presents an overview of the mechanisms of the placebo response and discusses the implications on clinical trial design and clinical practice.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 6","pages":"132-138"},"PeriodicalIF":0.0,"publicationDate":"2005-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.00023.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82815124","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 : 2005-10-24DOI: 10.1111/j.1743-5013.2005.00019.x
Yolande Knight B.Med.Sc., Ph.D.
{"title":"Brainstem Modulation of Caudal Trigeminal Nucleus: A Model for Understanding Migraine Biology and Future Drug Targets","authors":"Yolande Knight B.Med.Sc., Ph.D.","doi":"10.1111/j.1743-5013.2005.00019.x","DOIUrl":"10.1111/j.1743-5013.2005.00019.x","url":null,"abstract":"<p> <i>There is now considerable clinical and experimental evidence implicating a role for the brainstem in migraine pathophysiology. Studies point toward a possible dysfunction in sites such as the periaqueductal gray, nucleus raphe magnus, nucleus tractus solitarius, and locus coeruleus, since these structures affect the control of anti- and pronociception as well as cerebral blood flow. Numerous neurotransmitters in these structures provide potential pharmacological targets, notably adenosine (A1), opiates, GABA, cannabinoids, cholecystokinin and compounds targeting voltage-sensitive calcium channels. The possible mechanisms by which brainstem structures could drive a dysfunction in trigeminal nociception homeostasis are reviewed.</i> </p>","PeriodicalId":100600,"journal":{"name":"Headache Currents","volume":"2 5","pages":"108-118"},"PeriodicalIF":0.0,"publicationDate":"2005-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1743-5013.2005.00019.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77048549","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}