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Amidarone (AMD) is an antiarrhythmic drug with side effects on the nervous system. Cerebellum is seldom involved: We describe the case of a 56 years old male patient with a history of 4 month of cerebellar involvement characterized by gait unsteadiness, ataxia, nistagmus and vertigo. He was on treatment with AMD because of ventricular arrythmia. The cerebellar syndrome progressively disappeared after drug withdrawal and he was symptoms-free 4 months later. Similar symptoms appeared after another one month of automedication with the same drug. Structural lesions, metabolic, nutritional deficiencies or toxics were excluded. Mechanisms of cerebellar toxicity of AMD are yet unknown. The knowledge of the toxic effects of this drug, widely used in our country, would allow its early recognition.

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Fueron examiandos 11 pacientes adultos con el diagnostico presuntivo de neurocisticercosis, 8 de ellos provenientes de Bolivia y los restantes del interior de la Argentina. Como manifestación clínica inicial el 82 por ciento de ellos mostro convulsiones t el 73 por ciento cefaleas. Ambas alteraciones podian estar combinadas en el mismo paciente o presentarse en forma independiente. La tomografia computada de cerebro evidencio calcificaciones y quistes en 5 enfermos, solo calcificaciones en 3, hidrocefalia en 2 y un unico quiste en 1. En 7 casos se efectuo ELISA en el LCR, de ellos 6 resultaron positivos. El tratamiento medico se hizo en base a la administración de praziquantel o albendazolcon buena evolución de los pacientes en todos los casos. El tratamiento quirurgico fue indicado en el caso en que una lesión actuase como masa ocupante con aumento de la presión endocraneana (1 caso) o produjera obstrucción de la circulación del LCR llevando a una hidrocefalia (2 casos). El estudio presente pretende alertar sobre la posibilidad que nuevas regiones, como la Ciudad de Buenos Aires, puedan ingresar dentor del area endemica latinoamericana a consecuencia de los movimientos migratorios internos y externos y el asentamiento de portadores de la parasitosis en el perimetro urbano

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Eleven patients with diagnosis of possible neurocistycercosis were studied in our Department since 1986. All of them were adults. Eight were Bolivian citizens. The commonest neurological clinical manifestation were seizures and/or headache. Brain CT scans showed cystic lesions and calcifications in 5 patients, only calcifications in 3, enlarged ventricles in 2 and an isolated frontal cystic lesion in 1. Six out of 7 patients who were submitted to spinal fluid ELISA test showed positive response for cysticercosis. Patients were put on praziquantel (50 mg/Kg/d) or albendazol (15 mg/Kg/d) with good outcome for all them. Surgery was carried on for treatment of enlarged ventricles (2 patients) and for a like-expansive lesion (1 patient). The aim of this work is to underscore the fact that in Buenos Aires city, which previously was not within the endemic latin american area for cysticercosis, is now possible to find patients with the neurological manifestations of this parasitosis, most probably due to migration of people coming from the north provinces or from countries situated at its border where the disease is endemic.

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We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8%) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0%), 2) rheumatic heart disease in 14 (20.3%), 3) nonischemic dilated cardiomyopathy in 13 (18.8%). Nine of these (69%) had cardiac involvement due to Chagas' disease, 4) ischemic heart disease in 11 (15.9%), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9%), six patients had previous strokes, and 14 patients (20.3%) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2%), and 28.6% of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas' disease.

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We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8

) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0

), 2) rheumatic heart disease in 14 (20.3

), 3) nonischemic dilated cardiomyopathy in 13 (18.8

). Nine of these (69

) had cardiac involvement due to Chagas disease, 4) ischemic heart disease in 11 (15.9

), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9

), six patients had previous strokes, and 14 patients (20.3

) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2

), and 28.6

of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas disease.

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We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8

) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0

), 2) rheumatic heart disease in 14 (20.3

), 3) nonischemic dilated cardiomyopathy in 13 (18.8

). Nine of these (69

) had cardiac involvement due to Chagas disease, 4) ischemic heart disease in 11 (15.9

), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9

), six patients had previous strokes, and 14 patients (20.3

) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2

), and 28.6

of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas disease.

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Nine-hundred-eighty-nine patients with diagnosis of lymphoma were studied. Forty-six cases (4.6%) had compressions of the spinal cord or roots. Forty-two patients (4.2%) had Herpes zoster virus infections, which in 6 cases were of disseminated type. The major predisposing factors for infection were: advanced stage of lymphoma, previous systemic chemotherapy and splenectomy. Toxic polyneuropathy secondary to chemotherapy was found in 39 patients (3.9%). In 14 cases, the polyneuropathic symptoms were the main complaint (Group 1), while in the remaining 25 cases the diagnosis was made during neurological consultations because of unrelated symptoms (Group 2). Both groups did not have significant differences in the total dose of chemotherapy received. The electrophysiological studies showed an axonal neuropathy in both groups. The discontinuation of chemotherapy was found to be a limiting factor in the appearance of neuropathic symptoms. Other less frequent forms of involvement were: compression of peripheral nerves or nerve plexi from lymphadenopathies (3 cases), radiation myelopathy (1 case), and Guillain-Barré Syndrome associated with Hodgkin's Lymphoma (1 case).

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Nine-hundred-eighty-nine patients with lymphoma were studied. Fifty-three cases (5.3%) had lymphomatous craniocerebral infiltration. The principal factors of risk for this complication were: advanced stage of the lymphoma (III or IV), diffuse histiocytic, diffuse poorly differentiated lymphocytic, or mixed cellularity lymphoma histological type, bone marrow involvement, and previous systemic chemotherapy. Thirty-two per cent of the cases of meningeal lymphomatous infiltration were asymptomatic and represented autopsy findings. CT-scan was an useful test to detect brain focal parenchymatous infiltration, as opposed to meningeal infiltration. Mean survival time in patients with lymphomatous meningeal infiltration was 4.3 months, following the combined use of systemic chemotherapy, radiation therapy and intrathecal methotrexate. Two cases had primary cerebral lymphoma, although without associated immunodeficiency. Twenty patients (2%) had intracranial hemorrhage, in clear relationship with platelet alterations. Fifteen patients (1.5%) had CNS infection, caused by common bacteria or opportunistic agents. In 7 cases, the diagnosis was made at autopsy. Thirty-six autopsies were performed. In 8 cases (22%), pathologic findings such as, demyelination, microcalcifications, coagulative necrosis, or gliosis, suggested complications from treatment.

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Fueron estudiados 41 pacientes portadores de linfomas, que desarrollaron, en algún momento de su enfermedad complicaciones del Sistema Nervioso Central (SNC). La incidencia de este grupo con respecto a la población linfomatosa en general fue del 6,6%. Consideramos en nuestra serie un 57% de linfomas No Hodgkin (LNH) y un 43% de linfomas Hodgkin (LH), predominando ambos grupos en el sexo masculino. Fueron realizadas un total de 27 necropsias. El mecanismo lesional más frecuentemente observado fue la infiltración (68%), ya sea meníngea, parenquimatosa u ósea. Los tipos histológicos que predominaron fueron el difuso (en el caso de los LNH) y el de celularidad mixta (tratándose de los LH). La incidencia de infecciones fue mayoritaria en el grupo de los LH. La mayor frecuencia de complicaciones en el SNC se observó en estadios avanzados de la enfermedad (IV A y B), mostrando una tendencia decreciente en las formas más benignas. Los tiempos de latencia entre el diagnóstico del linfoma y la aparición de la complicación neurológica, fueron de 60 meses para los LH, en tanto que disminuyó a 21 meses en el grupo de los LNH. Los signos y síntomas más frecuentemente ballados fueron el compromiso de los pares craneales (especialmente oculomotores y el facial) y las alteraciones del estado de conciencia, sumadas a variables déficits focales. El compromiso de la Médula Osea se relacionó en forma directa con los casos en que se confirmó compromiso del SNC por mecanismo infiltrativo. Los métodos complementarios de diagnóstico por imágenes fueron eficaces en un 68%, aportando escasa utilidad en la identificación de las leptomeningitis linfomatosas (LML). El pronóstico más severo se verificó en el grupo de las LML (3,8 meses de sobrevida)...

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Fueron estudiados 41 pacientes portadores de linfomas, que desarrollaron, en algún momento de su enfermedad complicaciones del Sistema Nervioso Central (SNC). La incidencia de este grupo con respecto a la población linfomatosa en general fue del 6,6%. Consideramos en nuestra serie un 57% de linfomas No Hodgkin (LNH) y un 43% de linfomas Hodgkin (LH), predominando ambos grupos en el sexo masculino. Fueron realizadas un total de 27 necropsias. El mecanismo lesional más frecuentemente observado fue la infiltración (68%), ya sea meníngea, parenquimatosa u ósea. Los tipos histológicos que predominaron fueron el difuso (en el caso de los LNH) y el de celularidad mixta (tratándose de los LH). La incidencia de infecciones fue mayoritaria en el grupo de los LH. La mayor frecuencia de complicaciones en el SNC se observó en estadios avanzados de la enfermedad (IV A y B), mostrando una tendencia decreciente en las formas más benignas. Los tiempos de latencia entre el diagnóstico del linfoma y la aparición de la complicación neurológica, fueron de 60 meses para los LH, en tanto que disminuyó a 21 meses en el grupo de los LNH. Los signos y síntomas más frecuentemente ballados fueron el compromiso de los pares craneales (especialmente oculomotores y el facial) y las alteraciones del estado de conciencia, sumadas a variables déficits focales. El compromiso de la Médula Osea se relacionó en forma directa con los casos en que se confirmó compromiso del SNC por mecanismo infiltrativo. Los métodos complementarios de diagnóstico por imágenes fueron eficaces en un 68%, aportando escasa utilidad en la identificación de las leptomeningitis linfomatosas (LML). El pronóstico más severo se verificó en el grupo de las LML (3,8 meses de sobrevida)...(AU)

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Se presenta un caso de paracoccidioidomicosis de localización cerebral pura cuyo cuadro de presentación corresponde a un síndrome de bipertensión endocraneana de instalación progresiva asociado a signos deficitarios motores. El estudio tomográfico cerebral fue compatible con un proceso tumoral maligno con afectación secundaria de los plexos coroideos. La biopsia cerebral efectuada descartó la etiología neoplásica del cuadro, informándose como proceso granulomatoso de origem micótico. La serología de LCR confirmó el diagnóstico de paracoccidioidomicosis. Descartadas otras localizaciones extraneurológicas, se comenzó tratamiento con ketokonazol, observándo-se en el seguimiento clínico-tomográfico buena respuesta al tratamiento instituido. El presente caso es el tercero de la bibliografía con afectación restringida al sistema nervioso. Se citan otras formas clínicas de la enfermedad con compromiso neurológico

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Se presenta un caso de paracoccidioidomicosis de localización cerebral pura cuyo cuadro de presentación corresponde a un síndrome de bipertensión endocraneana de instalación progresiva asociado a signos deficitarios motores. El estudio tomográfico cerebral fue compatible con un proceso tumoral maligno con afectación secundaria de los plexos coroideos. La biopsia cerebral efectuada descartó la etiología neoplásica del cuadro, informándose como proceso granulomatoso de origem micótico. La serología de LCR confirmó el diagnóstico de paracoccidioidomicosis. Descartadas otras localizaciones extraneurológicas, se comenzó tratamiento con ketokonazol, observándo-se en el seguimiento clínico-tomográfico buena respuesta al tratamiento instituido. El presente caso es el tercero de la bibliografía con afectación restringida al sistema nervioso. Se citan otras formas clínicas de la enfermedad con compromiso neurológico (AU)

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The Argentine hemorrhagic fever (AHF) is an infectious disease, endemo-epidemical, of viral etiology, produced by the Junin virus and limited to the Buenos Aires Province, South of Córdoba, East of La Pampa, and South of Santa Fe. It generally assails rural workers at harvest-time, especially during corn-harvest. The incubation period of the disease does not exceed 12 days. A feverish syndrome with asthenia, adynamia, myalgias, migraine, photophobia, epigastralgia etc., appear. The patient has a facial erythema, petechias on the skin, enantema on the palate, conjunctive micropolyadenopaty injection. The laboratory shows a low erytro, leukopenia with aneosinophilia, thrombopenia and a urine with albuminuria and virous cells. After the fourth day, hemorrhage and a neurological case appears. The laboratory tends to normalize and cast appears in the urine. The most striking neurological signs are the following: muscular hypotonia, proprioceptive hyporreflexia or arreflexia, marinesco reflex, shakings, difficulty to stand and walk, oscillations in consciousness level, and ocular disturbances. The cytochemical test of the C.L. Rachis in the usual ways of the AHF is within its normal characteristics; on the other hand there are modifications in the nervous cases: the total proteins are nearly always increased and the cells augmented with a great predominance of mononuclear cells. The electroencephalogrammes were always abnormal, varying from a brief disorganization up to a diffusive and permanent slowness. The half of which additionally presented paroxisms generalized by slow waves. The pathological anatomy over the central nervous system makes us think that the lesion would not primitively neuronal but that the action of the virus would be indirectly done through the capillar wall. This capillar lesion is produced by multiple focuses. The neuronal destruction with necrosis by microinfarcts is minimum. The symptoms and neurological signs are present in 10% of the clinical cases; the death-rate in the nervous clinical cases having reached 50% of them. The premature treatment allows the death-rate to diminish and the cases that survive have not many after effects.

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