[Brain vasculitis associated with drugs]. / Vasculitis cerebral asociada a drogas.

INTRODUCTION: Vasculitis or angiitis is the term used to define the inflammation of the vessels, either blood or lymphatic, which causes may be primary related to immunological disorders, or secondary, with great variety of causal factors. CASE REPORT: We present a very uncommon case of a 36 year old man with brain vasculitis associated with drugs with very peculiar characteristics in the imaging studies and with definite diagnosis through histopathology obtained by biopsy, which differs from the few reports in the literature until our days. CONCLUSIONS: Our report is an uncommon case of cerebral vasculitis whose clinical features were confusing with impressing neuroimaging studies that showed possible lesions due to vasculitis that was confirmed through a cerebral biopsy and considering that the immunological tests were negative for a primary vasculitic process, we concluded that it was a vasculitis secondary to drug abuse which represents a special interest in view of the few existing reports in literature with definite diagnostic methods, such as cerebral biopsy or autopsy.

Vasculitis cerebral asociada a drogas / Brain Vasculitis associated with drugs

Introduction. Vasculitis or angiitis is the term used to define the inflammation of the vessels, either blood or lymphatic, which causes may be primary related to immunological disorders, or secondary, with great variety of causal factors. Case report. We present a very uncommon case of a 36 year old man with brain vasculitis associated with drugs with very peculiar characteristics in the imaging studies and with definite diagnosis through histopathology obtained by biopsy, which differs from the few reports in the literature until our days. Conclusions. Our report is an uncommon case of cerebral vasculitis whose clinical features were confusing with impressing neuroimaging studies that showed possible lesions due to vasculitis that was confirmed through a cerebral biopsy and considering that the immunological tests were negative for a primary vasculitic process, we concluded that it was a vasculitis secondary to drug abuse which represents a special interest in view of the few existing reports in literature with definite diagnostic methods, such as cerebral biopsy or autopsy (AU)

Introducción. Vasculitis, o angeítis, es el término que se emplea para definir la inflamación de los vasos, ya sean sanguíneos o linfáticos, cuyas causas pueden ser primarias, relacionada más con alteraciones inmunológicas, o secundarias, con una gran heterogeneidad de factores causales. Caso clínico. Presentamos el caso poco común de un hombre de 36 años de edad con vasculitis cerebral asociada a la utilización de drogas, el cual cuenta con estudios de imagen peculiares, pero con confirmación histopatológica de una muestra obtenida mediante biopsia cerebral, la cual difiere de los pocos informes similares que existen en la literatura hasta la actualidad. Conclusiones. Este comunicado corresponde a un caso poco común de vasculitis cerebral cuyas manifestaciones iniciales eran confusas, con estudios de neuroimagen que mostraron posibles lesiones por vasculitis, lo que se corroboró mediante biopsia cerebral; considerando que las pruebas inmunológicas resultaron negativas para un proceso vasculítico primario, concluimos, por los antecedentes del paciente, que se trataba de una vasculitis secundaria a abuso de drogas; esto tiene un interés especial, dados los escasos comunicados existentes en la literatura con métodos diagnósticos definitivos, como la biopsia cerebral o la necropsia (AU)

[Ergotism. A case report and review of the literature]. / Ergotismo. Presentación de un caso y revisión de la bibliografía.

INTRODUCTION: Ergotism is characterised by an intensive generalised vasoconstriction of small and large blood vessels. The symptoms derive from the regional ischemia caused by the vasospasm produced by ergotamine. Nowadays, ergotism is almost exclusively due to the excessive ingestion of ergotamine tartrate used in the treatment of migraine. The main treatment consists in withdrawing the medication. CASE REPORT: Our study involves a 53-year-old male with a history of migraine since his youth, who was treated with ergotaminic preparations up until the day before admission to hospital. He was admitted because of a 7-day history of symptoms including bilateral and symmetrical anaesthesia of the fingers and a general feeling of weakness, associated with intense pain and cyanosis of the right thenar eminence. On admission, it was not possible to measure his AT in the upper limbs and his peripheral pulses dropped in a generalised manner. Aetiologies involving vasculitis were ruled out. An angiography study showed segmented stenosis of arteries in the upper and lower limbs. Ergotaminic agents were withdrawn and nifedipine was indicated. The symptoms disappeared, the physical examination was normal and results of a control angiography study were also normal. CONCLUSIONS: Ergotamine intoxication can be detected by a thorough interview and physical examination; it should be suspected when faced with symptoms that are compatible with vasospasms and a history of ingestion of the drug, in the absence of any prothrombotic, liver, kidney or vasculitic pathology. This condition is treated by withdrawing the drug and administration of vasodilators if the symptoms are intense. In this paper, we review the history, pathophysiology, initial symptoms and signs, diagnosis and treatment of ergotamine poisoning.

Ergotismo. Presentación de un caso y revisión de la bibliografía / Ergotism. A case report and review of the literature

Introducción. El ergotismo se caracteriza por una intensa y generalizada vasoconstricción de los vasos sanguíneos pequeños y grandes. Los síntomas resultan de la isquemia regional causada por el vasoespasmo que produce la ergotamina. En la actualidad, el ergotismo resulta casi exclusivamente de la ingesta excesiva de tartrato de ergotamina para el tratamiento de la migraña. El principal tratamiento es la suspensión del fármaco. Caso clínico. Se trata de un hombre de 53 años con historia de migraña desde su juventud, tratada con ergotamínicos hasta un día antes de su ingreso. Ingresó por manifestaciones de siete días de evolución, con anestesia bilateral y simétrica de los dedos de las manos y sensación de debilidad generalizada, asociados a dolor intenso y cianosis de la eminencia tenar derecha. Cuando ingresó no fue posible medir la tensión arterial en las extremidades superiores, y sus pulsos periféricos estaban disminuidos de manera generalizada. Se descartaron etiologías de vasculitis. Una angiografía mostró estenosis segmentaria de las arterias en las extremidades superiores e inferiores. Se suspendieron los ergotamínicos y se indicó nifedipina. La sintomatología desapareció, la exploración física fue normal y una angiografía de control fue normal. Conclusiones. La intoxicación por ergotamina puede detectarse mediante un interrogatorio y exploración física completos; se debe sospechar ante manifestaciones compatibles con vasoespasmo y el antecedente de ingesta del fármaco, en ausencia de patología protrombótica o vasculítica, hepatopatía o nefropatía. El tratamiento del cuadro es con suspensión del fármaco, y vasodilatadores si las manifestaciones son intensas. En este artículo se revisa la historia, fisiopatología, síntomas y signos de presentación, diagnóstico y tratamiento de la intoxicación por ergotamina

Introduction. Ergotism is characterised by an intensive generalised vasoconstriction of small and large blood vessels. The symptoms derive from the regional ischemia caused by the vasospasm produced by ergotamine. Nowadays, ergotism is almost exclusively due to the excessive ingestion of ergotamine tartrate used in the treatment of migraine. The main treatment consists in withdrawing the medication. Case report. Our study involves a 53-year-old male with a history of migraine since his youth, who was treated with ergotaminic preparations up until the day before admission to hospital. He was admitted because of a 7-day history of symptoms including bilateral and symmetrical anaesthesia of the fingers and a general feeling of weakness, associated with intense pain and cyanosis of the right thenar eminence. On admission, it was not possible to measure his AT in the upper limbs and his peripheral pulses dropped in a generalised manner. Aetiologies involving vasculitis were ruled out. An angiography study showed segmented stenosis of arteries in the upper and lower limbs. Ergotaminic agents were withdrawn and nifedipine was indicated. The symptoms disappeared, the physical examination was normal and results of a control angiography study were also normal. Conclusions. Ergotamine intoxication can be detected by a thorough interview and physical examination; it should be suspected when faced with symptoms that are compatible with vasospasms and a history of ingestion of the drug, in the absence of any prothrombotic, liver, kidney or vasculitic pathology. This condition is treated by withdrawing the drug and administration of vasodilators if the symptoms are intense. In this paper, we review the history, pathophysiology, initial symptoms and signs, diagnosis and treatment of ergotamine poisoning

[Non-convulsive epileptic status associated with Lafora disease: two case reports]. / Estado epiléptico no convulsivo asociado a enfermedad de Lafora: presentación de dos casos.

INTRODUCTION: Lafora s disease is a type of progressive myoclonic epilepsy with poor prognosis, is characterized by myoclonic crisis, tonic clonic seizures, absence or partial complex seizures and other neurological manifestations with a progressive course and a poor response to the treatment. It has not been considered as a cause of epileptic status. CASE REPORTS: Two women without important past medical history with normal psychomotor development before their suffering, with manifestations of 2 years of evolution the first one and 8 years on the second case characterized by myoclonic generalized, partial complex seizures and progressive deterioration of the mental functions that joined to our institution in a non convulsive epileptic status and they featured with a different evolution. The first patient with favorable control of the event with a single medication and functionality recover later, the second one with torpid evolution complicated with an epileptic status convulsive widespread condition and a prolonged permanency in the unit of intensive therapy. In both patients the diagnosis of Lafora s disease was established based in the findings of the skin axilar biopsy. DISCUSSION AND CONCLUSION: We believe that Lafora s disease must be suspected as a probable cause of non convulsive epileptic status in patients with myoclonic epilepsy associated with other neurological manifestations and a refractary response to the medical treatment. The evolution and clinical response will depend on the evolutionary stage of the disease.

[Diabetic neuropathy: vascular disease?]. / Neuropatía diabética: una enferemedad vascular?

INTRODUCTION: The major neurologic complications of diabetes are: 1) Neuropathy, both peripheral and autonomic, with principal manifestations in the lower limbs; 2) Microvascular disease, mainly affecting the retina, resulting in blindness; and 3) Macrovascular disease, presenting with atherosclerosis in the cerebral arteries causing ischemic cerebrovascular disease and stroke. METHOD: The definition of diabetic neuropathy has changed over the last 50 years. Over the last 20 years there have been three main pathogenetic theories to explain diabetic neuropathy: the polyol pathway theory, the microvascular theory, and the glycosylation end product theory. It is apparent that several pathophysiologic factors probably operate simultaneously, and it may be too simplistic to attempt to explain the many clinical and pathologic findings of diabetic neuropathy through a single theory. Diabetic peripheral neuropathy is not caused by large vessel peripheral vascular disease, however, it does appear that small vessel disease plays a role. CONCLUSION: It seems likely, that microangiopathy on the one hand and changes of various metabolic pathways due to hyperglycemia on the other hand are much more related to each other than it was suggested previously.

Neuropatía diabética: ¿una enfermedad vascular? / Diabetic neuropathy: vascular disease?

Introducción. Las principales complicaciones neurológicas de la diabetes son: 1) Neuropatía periférica y autonómica, cuyas manifestaciones principales ocurren en las extremidades inferiores; 2) Enfermedad microvascular, que afecta principalmente a la retina y desencadena ceguera, y 3) Enfermedad macrovascular, presente con aterosclerosis en las arterias cerebrales y que causa enfermedad isquémica cerebrovascular. Desarrollo. La definición de la neuropatía diabética (ND) ha cambiado en los últimos 50 años; en los últimos veinte se han propuesto tres teorías patogénicas principales para explicar la ND: la teoría de la vía poliol, la teoría microvascular y la teoría del producto final de la glucosilación. Probablemente, varios factores patofisiológicos actúan simultáneamente, y puede parecer muy simplista explicar que muchas manifestaciones clínicas y hallazgos patológicos en la ND pueden ser resultado de un solo mecanismo. La ND periférica no la ocasiona la enfermedad vascular periférica de grandes vasos; sin embargo, parece que la enfermedad de pequeños vasos desempeña un papel importante. Conclusión. Es probable que la microangiopatía, por un lado, y las alteraciones de varias vías metabólicas por la hiperglucemia, por otro, se relacionen más entre sí que como se había descrito anteriormente (AU)

Introduction. The major neurologic complications of diabetes are: 1) Neuropathy, both peripheral and autonomic, with principal manifestations in the lower limbs; 2) Microvascular disease, mainly affecting the retina, resulting in blindness; and 3) Macrovascular disease, presenting with atherosclerosis in the cerebral arteries causing ischemic cerebrovascular disease and stroke. Method. The definition of diabetic neuropathy has changed over the last 50 years. Over the last 20 years there have been three main pathogenetic theories to explain diabetic neuropathy: the polyol pathway theory, the microvascular theory, and the glycosylation end product theory. It is apparent that several pathophysiologic factors probably operate simultaneously, and it may be too simplistic to attempt to explain the many clinical and pathologic findings of diabetic neuropathy through a single theory. Diabetic peripheral neuropathy is not caused by large-vessel peripheral vascular disease, however, it does appear that small-vessel disease plays a role. Conclusion. It seems likely, that microangiopathy on the one hand and changes of various metabolic pathways due to hyperglycemia on the other hand are much more related to each other than it was suggested previously (AU)