La migraña como factor de riesgo vascular / Migraine as a vascular risk factor

Introducción. Migraña e ictus se asocian con una frecuencia superior a lo esperable. Aunque controvertida, múltiples estudios demuestran una asociación significativa entre migraña y patología vascular no sólo cerebral, sino también en otros lechos arteriales. El espectro de la relación entre migraña e ictus comprende relaciones de coexistencia, semejanza y causalidad. Los mecanismos por los que la migraña llega a ser un factor de riesgo vascular y conduce al desarrollo de un ictus no son del todo conocidos, posiblemente porque sean múltiples, complejos e interrelacionados entre sí. Objetivo. Poniendo énfasis en los artículos más recientes, se revisa críticamente el estado actual acerca de la relación de causalidad entre migraña y enfermedad vascular, y se discute su fisiopatología. Desarrollo. La migraña es un factor de riesgo independiente de ictus, especialmente en el subgrupo de población comprendido por mujeres jóvenes, con migraña con aura, crisis frecuentes, fumadoras y en tratamiento con anticonceptivos orales. Además, se asocia con lesiones de la sustancia blanca y patología vascular en otros territorios arteriales. Disfunción del endotelio y musculatura vascular, hipercoagulabilidad, depresión propagada cortical, factores genéticos, foramen oval permeable, perfil desfavorable de riesgo vascular, disección arterial y el tratamiento específico de migraña se postulan como mecanismos patogénicos. Conclusiones. Si la enfermedad cerebrovascular es una importante causa de invalidez y mortalidad, y la migraña es un factor de riesgo de enfermedad vascular, comprender la relación entre migraña y enfermedad vascular es necesario para reducir riesgos y optimizar su manejo y tratamiento (AU)

Introduction. Migraine and stroke are associated with a higher frequency than expected. Numerous studies have shown a significant, but controversial, association between migraine and vascular disease, not only in cerebral but also in other arterial beds. The full spectrum of this relationship includes coexisting stroke and migraine, stroke with clinical features of migraine and migraine-induced stroke. Why migraine is a risk factor and how it leads to stroke is not entirely understood, possibly because the mechanisms involved are multiple, complex and interrelated. Aim. Emphasizing the most recent papers, we review critically the current knowledge about the causal relationship between migraine and vascular disease and discuss its pathophysiology. Development. Migraine is an independent risk factor for stroke, especially for young women with frequent migraine with aura attacks, who smoke and use oral contraceptives. Migraine has also been associated with lesions in the white matter and in other vascular territories. Potential pathogenic mechanisms include endothelium and vascular smooth muscle dysfunction, hypercoagulability, cortical spreading depression, genetic factors, patent foramen ovale, unfavourable vascular risk profile, arterial dissection and migraine-specific treatment. Conclusion. Considering that cerebrovascular disease is a major cause of disability and mortality and that migraine is a risk factor for vascular disease, understanding the relationship between migraine and vascular disease is necessary to reduce risks and optimize management and treatment (AU)

Angina de Prinzmetal en el aura de la migraña que se resuelve con la cefalea / Prinzmetal angina in the migraine's aura resolving with headache

No disponible

Duloxetina en el tratamiento de los síntomas somáticos dolorosos asociados a la depresión / Duloxetine in the treatment of somatic pain symptoms associated with depression

No disponible

No disponible

Orofacial Pain--Part II: Assessment and management of vascular, neurovascular, idiopathic, secondary, and psychogenic causes.

Chronic orofacial pain is a common health complaint faced by health practitioners today and constitutes a challenging diagnostic problem that often requires a multidisciplinary approach to diagnosis and treatment. The previous article by the same authors in this issue discussed the major clinical characteristics and the treatment of various musculoskeletal and neuropathic orofacial pain conditions. This second article presents aspects of vascular, neurovascular, and idiopathic orofacial pain, as well as orofacial pain due to various local, distant, or systemic diseases and psychogenic orofacial pain. The emphasis in this article is on the general differential diagnosis and various therapeutic regimens of each of these conditions. An accurate diagnosis is the key to successful treatment of chronic orofacial pain. Given that for many of the entities discussed in this article no curative treatment is available, current standards of management are emphasized. A comprehensive reference section has been included for those who wish to gain further information on a particular entity.

Aura with non-migraine headache.

The typical aura associated with migraine is characterized by visual or sensory and speech symptoms, with a mix of positive and negative features and complete reversibility within 1 hour. However, auras are not an exclusive migraine-dependent phenomenon. There have been descriptions of aura occurring in association with cluster headache, hemicrania continua, and even with chronic paroxysmal hemicrania. In addition, the occurrence of aura without headache or followed by a headache resembling the criteria of tension-type headache is encountered in clinical practice. This paper reviews the literature about auras in non-migraine headaches and the features involving this uncommon presentation. The possibility of a specific genetic origin for the auras, not related to the primary headache type, also is raised.

Chronic paroxysmal hemicrania, hemicrania continua and SUNCT syndrome in association with other pathologies: a review.

We present a review of 22 cases of headache mimicking chronic paroxysmal hemicrania (CPH) (17 female and five male; F : M ratio 3.4), nine cases mimicking hemicrania continua (HC) (seven female and two male) and seven cases mimicking SUNCT syndrome (five male and two female) found in association with other pathologies published from 1980 up to the present. All case reports were discussed with respect to diagnostic criteria proposed by International Headache Society (IHS) for CPH, by Goadsby and Lipton for HC and SUNCT, and evaluated to identify a possible causal relationship between the pathology and the onset of headache. The aim of the present review was to evaluate if the presence of associated lesions and their location could help elucidate the pathogenesis of trigeminal autonomic cephalalgias (TACs).

Non-lateralized pain in a case of chronic paroxysmal hemicrania?

We describe a man with chronic paroxysmal hemicrania, who remained free of headaches on indomethacin, 25 mg once or twice daily. However, in this case, in contrast to typical cases of paroxysmal hemicrania, the pain of the headaches was nonlateralized and was located in the centre of the forehead. The headaches were not associated with local autonomic symptoms or signs involving the eyes or nose. Initially, the pain of the headaches lasted for seconds only and was brought on by coughing.

The paroxysmal hemicrania-tic syndrome.

Two cases of paroxysmal hemicrania (PH) associated with trigeminal neuralgia are reviewed. The paroxysmal hemicrania component in one patient was episodic, while it was chronic in the other. Each headache type responded completely to separate treatment, highlighting the importance of recognizing this association. We review the six other cases of chronic paroxysmal hemicrania-tic (CPH-tic) reported, and suggest that the term paroxysmal hemicrania-tic syndrome (PH-tic) be used to describe this association.

Case reports: chronic paroxysmal hemicrania-tic syndrome.

The coexistence of chronic paroxysmal hemicrania and trigeminal neuralgia is called chronic paroxysmal hemicrania-tic syndrome. We describe the case of a man who has suffered both types of pain occurring synchronously but with different localization on the ipsilateral side. The pain attacks could be abolished with indomethacin and carbamazepine. To the best of our knowledge, this is the third case to be reported, the first in the male sex. We review this new disorder and discuss the pathophysiology.

Chronic paroxysmal hemicrania presenting as otalgia with a sensation of external acoustic meatus obstruction: two cases and a pathophysiologic hypothesis.

OBJECTIVE: To describe two cases of chronic paroxysmal hemicrania manifested by otalgia with a sensation of external acoustic meatus obstruction and to suggest that the trigeminal-autonomic reflex is a mechanism for the sensation of ear blockage. BACKGROUND: Maximum pain in chronic paroxysmal hemicrania is most often in the ocular, temporal, maxillary, and frontal regions. It is less often located in the nuchal, occipital, and retro-orbital areas. Review of the literature on chronic paroxysmal hemicrania found no reports of pain primarily localized to the ear and associated with a sensation of external acoustic meatus obstruction. METHODS: The history, physical examination, imaging studies, and successful treatment plan in two patients with otalgia and ear fullness and a subsequent diagnosis of chronic paroxysmal hemicrania are summarized. RESULTS: The first patient was a 42-year-old woman with a 10-year history of unilateral, severe, paroxysmal otalgia occurring five times a day with a duration of 2 to 60 minutes. During an attack, the ear became erythematous and the external acoustic meatus felt obstructed. There were no other associated autonomic signs. The second patient was a 49-year-old woman with a 3-year history of unilateral, severe, paroxysmal otalgia occurring 4 to 15 times a day with a duration of 3 to 10 minutes. During an attack, her ear felt obstructed, and she noted ipsilateral eyelid edema and ptosis. Both patients quickly became pain-free after taking indomethacin and required its continued use to prevent headache recurrence. CONCLUSIONS: Chronic paroxysmal hemicrania may be manifested by otalgia with a sensation of external ear obstruction. When the otalgia is paroxysmal, unilateral, severe, frequent, and associated with autonomic signs, one should consider the diagnosis of chronic paroxysmal hemicrania, especially because of the prompt response to indomethacin. The most important feature to consider when making the diagnosis of chronic paroxysmal hemicrania is the frequent periodicity of discrete, brief attacks of unilateral cephalgia separated by pain-free intervals. It is hypothesized that the sensation of ear obstruction in these patients is due to swelling of the external acoustic meatus mediated through increased blood flow by the trigeminal-autonomic reflex.

Orofacial pain with vascular-type features.

OBJECTIVE: To examine whether a classifiable primary vascular-type craniofacial pain subgroup exists that predominantly affects intraoral structures. STUDY DESIGN: Fifty-five patients were chosen prospectively according to the following inclusion criteria; periodic craniofacial pain that was unilateral, pulsatile, severe, and that may wake the patient from sleep. Accompanying phenomena could include local autonomic and/or systemic signs. Twenty-six cases could be further classified into one of the categories of vascular craniofacial pain. The remaining 29, all with predominantly intraoral pain, were not readily classifiable. RESULTS: Of the 29 patients 70% were women, with an average onset-age of 42.6 years. All reported severe, episodic pain that was usually unilateral and lasted minutes to hours. In all, 55% of patients had autonomic or systemic signs, 48% had pulsatile pain, and 35.4% of patients were awakened by the pain. CONCLUSION: Although clinical similarities were observed within these patients, further studies are needed to confirm vascular orofacial pain as a clear diagnostic category.

Headaches in the athlete.

Headache is one of the most common entities to affect mankind. In addition to headaches seen in the general population, there are numerous types of headaches that are related to physical activity and sports. This article discusses the mechanism, presentation, evaluation, treatment, and prevention of the most common causes of headache in the athlete.

Cluster headache and vertigo.

The term "cluster vertigo" was originally used by Gilbert to describe episodes of vertigo in patients with Ménière's syndrome. Since these patients also had co-existing cluster headache, he suggested that both disorders could have had a common pathophysiology. There is no evidence in the literature for an increased incidence of Ménière's syndrome in cluster headache patients, so the argument that cluster headache and Ménière's syndrome may have a common pathogenesis cannot be supported. Subsequent authors have used the term "cluster vertigo" to denote a variant form of cluster headache and have confused the matter further. This was not the intention of the original author. The terminology is misleading and should not be used to describe a sub-type of cluster headache. A case of cluster headache with accompanying vertigo is described as a contrast to the patients described by Gilbert in whom headache and episodes of vertigo occurred independently.

Shortlasting unilateral neuralgiform headache attacks with conjunctival injection, tearing, sweating, and rhinorrhea.

Three grown-up males with a long-lasting history of rather uniform, unilateral headache in the ocular-periocular area, in cluster fashion, are examined. Pain paroxysms of short duration (15-60 sec) appear up to 5-30 times per h. The headache is unilateral without side shift. Conjunctival injection appears at the very beginning of the attack and is partly massive, lasting the entire duration of the attack, and fading away at the end of it. Tearing (massive), forehead sweating (subclinical) and rhinorrhea, all on the symptomatic side, accompany the attack. In the youngest patient, the headache became chronic after clustering for six months initially, and after approximately 3 1/2 years it became bilateral. However, even in this patient, a clear unilateral pain preponderance prevails, and the autonomic disturbances are all on the original pain side. Attacks can partly be precipitated by chewing, eating (e.g. citrus fruits), moving the head, etc. The headache is completely refractory to drug therapy, including indomethacin.