Estudio LAM: conducta y calidad de vida en pacientes diagnosticados de epilepsia tratados con lacosamida / LAM study: Effects of lacosamide on behaviour and quality of life in patients with epilepsy

Introducción: La comorbilidad psiquiátrica es común en epilepsia, de ahí la importancia de considerar en qué medida los fármacos antiepilépticos pueden influir en el estado de ánimo. El objetivo de este trabajo es analizar el efecto de lacosamida en la calidad de vida y en la conducta del paciente epiléptico en la práctica clínica. Métodos: Estudio multicéntrico, observacional y prospectivo en pacientes diagnosticados de epilepsia, mal controlados que recibieron tratamiento adyuvante con lacosamida. Mediante 4 visitas durante 12 meses se valoró el impacto del fármaco en la calidad de vida y el estado de ánimo utilizando el cuestionario de calidad de vida QOLIE-10, la escala hospitalaria de ansiedad y depresión (HADS) y la escala de impulsividad de Barratt (BIS-11), además se determinó su eficacia y seguridad. Resultados: Se incluyeron 55 pacientes, edad media 47,1 ± 18,4 años; porcentaje inicial de comorbilidad psiquiátrica 34,5% y número medio de crisis/mes previo 3,6 ± 4,3. Las escalas QOLIE-10 y HADS reflejaron mejoras estadísticamente significativas en pacientes que partían de una situación basal desfavorable (ansiedad, depresión y/o baja calidad de vida). La escala BIS-11 no detectó la aparición de conductas impulsivas durante el seguimiento. Tras 12 meses de tratamiento el 51,9% de los pacientes estuvo sin crisis, y un 77,8% presentó una educción ≥ 50%. La mayoría de efectos adversos fueron leves, obligando a retirar el fármaco en 10 casos (18,2%). Conclusiones: Lacosamida ofrece un perfil de eficacia y seguridad favorable, y podría constituir una opción terapéutica útil en pacientes con epilepsia y comorbilidad psiquiátrica

Introduction: Psychiatric comorbidities are common in epileptic patients, and evaluating the impact of antiepileptic drugs on patients’ moods is therefore essential. The aim of this study is to assess the effects of lacosamide on behaviour and quality of life in people with epilepsy. Methods: We conducted a multicentre prospective observational study of poorly-controlled epileptic patients who received lacosamide as an adjuvant treatment. Patients were evaluated on 4 occasions during a 12-month period. The impact of lacosamide on patients’ mood and quality of life was assessed with the Quality of Life in Epilepsy Inventory-10 (QOLIE-10), the Hospital Anxiety and Depression Scale (HADS), and the Barratt Impulsiveness Scale (BIS-11). As a secondary objective, we evaluated the effectiveness and safety of lacosamide. Results: We included 55 patients with a mean age of 47.1 ± 18.4 years. At baseline, 34.5% of the patients had psychiatric comorbidities; the mean number of crises in the previous month was 3.6 ± 4.3. The QOLIE-10 and HADS scales revealed statistically significant improvements in patients with a poor baseline condition (anxiety, depression, and/or poor quality of life). The BIS-11 scale detected no impulsive behaviour during follow-up. After 12 months of treatment, 51.9% of the patients were seizure-free and 77.8% experienced a reduction of at least 50% in seizure frequency. Adverse effects were mild in most cases; lacosamide was discontinued in 10 patients (18.2%)

LAM study: Effects of lacosamide on behaviour and quality of life in patients with epilepsy. / Estudio LAM: conducta y calidad de vida en pacientes diagnosticados de epilepsia tratados con lacosamida.

INTRODUCTION: Psychiatric comorbidities are common in epileptic patients, and evaluating the impact of antiepileptic drugs on patients' moods is therefore essential. The aim of this study is to assess the effects of lacosamide on behaviour and quality of life in people with epilepsy. METHODS: We conducted a multicentre prospective observational study of poorly-controlled epileptic patients who received lacosamide as an adjuvant treatment. Patients were evaluated on 4 occasions during a 12-month period. The impact of lacosamide on patients' mood and quality of life was assessed with the Quality of Life in Epilepsy Inventory-10 (QOLIE-10), the Hospital Anxiety and Depression Scale (HADS), and the Barratt Impulsiveness Scale (BIS-11). As a secondary objective, we evaluated the effectiveness and safety of lacosamide. RESULTS: We included 55 patients with a mean age of 47.1±18.4 years. At baseline, 34.5% of the patients had psychiatric comorbidities; the mean number of crises in the previous month was 3.6±4.3. The QOLIE-10 and HADS scales revealed statistically significant improvements in patients with a poor baseline condition (anxiety, depression, and/or poor quality of life). The BIS-11 scale detected no impulsive behaviour during follow-up. After 12 months of treatment, 51.9% of the patients were seizure-free and 77.8% experienced a reduction of at least 50% in seizure frequency. Adverse effects were mild in most cases; lacosamide was discontinued in 10 patients (18.2%). CONCLUSIONS: Lacosamide is a safe and effective treatment option for patients with epilepsy and psychiatric comorbidities.

Disautonomía progresiva como presentación del síndrome anti-Hu / Progressive dysautonomia as initial manifestation of anti-Hu antibody-related syndrome

Introducción. Los anticuerpos antineuronales anti-Husuelen estar asociados al desarrollo de síndromes paraneoplásicosdel sistema nervioso central como la neuropatíasensorial, la ataxia cerebelosa o la encefalitis límbica. Laafectación del sistema nervioso autónomo aislado comopresentación de un síndrome paraneoplásico asociado a anticuerposanti-Hu es muy poco frecuente. Caso clínico. Un hombre de 68 años comenzó a ser estudiadopor estreñimiento pertinaz al que 2 meses más tardese fue añadiendo progresivamente clínica de disautonomíacon hipotensión ortostática, impotencia, sequedad deboca, seudoobstrucción intestinal y retención urinaria. Al finalde la evolución, tras 4 meses desde inicio de la clínica,presentó parestesias en las cuatro extremidades, paresiaoculomotora y tetraparesia. Los anticuerpos anti-Hu en sangrey líquido cefalorraquídeo fueron positivos. En el estudiorealizado no se pudo demostrar un tumor primario. Conclusiones. Aunque la disautonomía no asociada aotros síntomas de la encefalomielitis/neuropatía sensitiva esuna presentación excepcional del síndrome anti-Hu, se debeconsiderar la posibilidad de origen paraneoplásico en pacientescon cuadros de disautonomía progresiva

Introduction. The anti-Hu antibody are associatedwith central nervous system paraneoplastic syndromessuch as sensory neuropathy, cerebellar ataxia or limbicencephalitis. The isolated autonomic dysfunction as thepresenting manifestation of anti-Hu antibody-relatedparaneoplastic syndrome is extremely infrequent. Case report. A 68 year-old male presented with atwo-month history of severe constipation following oforthostatic hypotension, impotence, urinary retentionand intestinal pseudo-obstruction as manifestations ofprogressive dysautonomia. Four months after the onsetof these symptoms, he developed paresthesias in thehands and feet, motor weakness in both upper and lowerlimbs and ophtalmoplegia. Anti-Hu antibodies were positivein serum and cerebrospinal fluid, although tumorwas not found

[Progressive dysautonomia as initial manifestation of anti-Hu antibody-related syndrome]. / Disautonomía progresiva como presentación del síndrome anti-Hu.

INTRODUCTION: The anti-Hu antibody are associated with central nervous system paraneoplastic syndromes such as sensory neuropathy, cerebellar ataxia or limbic encephalitis. The isolated autonomic dysfunction as the presenting manifestation of anti-Hu antibody-related paraneoplastic syndrome is extremely infrequent. CASE REPORT: A 68 year-old male presented with a two-month history of severe constipation following of orthostatic hypotension, impotence, urinary retention and intestinal pseudo-obstruction as manifestations of progressive dysautonomia. Four months after the onset of these symptoms, he developed paresthesias in the hands and feet, motor weakness in both upper and lower limbs and ophtalmoplegia. Anti-Hu antibodies were positive in serum and cerebrospinal fluid, although tumor was not found. CONCLUSIONS: Progressive dysautonomia may result from a number of diseases. We encourage to consider also the possibility of anti-Hu antibody-related syndrome, despite the case that it is a very unusual isolated initial manifestation.

[Solitary costal plasmacytoma: a rare cause of subacute demyelinating polyradiculoneuropathy]. / Plasmocitoma solitario costal: causa excepcional de polirradiculoneuropatía desmielinizante subaguda.

INTRODUCTION: The solitary plasmacytoma (SP) is a non-frequent, localized variant of multiple myeloma with a single bone lesion and earlier appearance. Polyradiculoneuropathy is the most frequent neurological manifestation. We report the case of a young male who developed a subacute demyelinating polyradiculoneuropathy as the initial symptomatology of a costal SP, which constitutes an extremely infrequent association, given age and site of the lesion. CASE REPORT: A 32-year old, previously healthy, man presented with a one month history of progressive symmetrical paraparesis and paresthesias in feet. The neurological examination revealed 4/5 paraparesis, global arreflexia and hypopalesthesia in legs. Cerebrospinal fluid examination revealed elevated proteins (83 mg/dl) with normal cell count and glucose content. Investigations showed high levels of beta(2)-microglobulin (3 mg/l), and a monoclonal IgG lambda gammapathy. The chest X-ray and thoracic CT revealed an osteolytic lesion in the left third rib. Nerve conduction studies showed sensitive and motor polyneuropathy with secondary axonal degeneration. Bone marrow biopsy was normal. Second and third left ribs were excised, revealing a pathologic diagnosis of plasmacytoma. The patient became asymptomatic after corticosteriod administration lesion excision and local radiotherapy. Conclusions. Subacute demyelinating polyradiculoneuropathy can be due to multiple causes. SP can be one of its etiologies and occur at infrequent ages and localizations.

Plasmocitoma solitario costal: causa excepcional de pollirradiculoneuropatía desmielinizante subaguda / Solitary costal plasmacytoma: a rare cause of subacute demyelinating polyradiculoneuropathy

Introducción. El plasmocitoma solitario (PS) es una variante infrecuente del mieloma múltiple caracterizado por una lesión ósea única y aparición más temprana. La manifestación neurológica más frecuente es la polirradiculoneuropatía. Presentamos el caso de un paciente joven con una polirradiculopatía desmielinizante subaguda como inicio de un PS costal, lo que constituye un hecho extremadamente infrecuente dada la edad y localización de la lesión. Caso clínico. Varón de 32 años sano que ingresó por cuadro subagudo de un mes de evolución de paraparesia y parestesias en los pies. En la exploración neurológica se objetivó una paraparesia 4/5 con arreflexia universal y disminución de la sensibilidad profunda en los pies. El estudio del líquido cefalorraquídeo mostró una proteinorraquia de 83 mg/dl sin pleocitosis. Tenía una beta (2)-microglobulina de 3 mg/l y un pico monoclonal IgG lambda. La radiografía costal y la TC toracoabdominal evidenciaron una lesión única de características líticas en el tercer arco costal izquierdo. El estudio neurofisiológico descubrió una polineuropatía sensitivomotora mixta con degeneración axonal secundaria de predominio en miembros inferiores. La biopsia de médula ósea fue normal. Se realizó la exéresis de la lesión costal con resultado patológico de plasmocitoma. Tras la administración de corticoides, la exéresis de la lesión y radioterapia local se consiguió la desaparición de la sintomatología. Conclusiones. Las polirradiculoneuropatías desmielinizantes subagudas tienen un amplio espectro etiológico. Aunque extremadamente raro, el PS puede ser una causa de las mismas y presentarse tanto en edades como en localizaciones infrecuentes (AU)

Introduction: The solitary plasmacytoma (SP) is a non-frequent, localized variant of multiple myeloma with a single bone lesion and earlier appearance. Polyradiculoneuropathy is the most frequent neurological manifestation. We report the case of a young male who developed a subacute demyelinating polyradiculoneuropathy as the initial symptomatology of a costal SP, which constitutes an extremely infrequent association, given age and site of the lesion. CASE Report: A 32-year old, previously healthy, man presented with a one month history of progressive symmetrical paraparesis and paresthesias in feet. The neurological examination revealed 4/5 paraparesis, global arreflexia and hypopalesthesia in legs. Cerebrospinal fluid examination revealed elevated proteins (83 mg/dl) with normal cell count and glucose content. Investigations showed high levels of beta (2)-microglobulin (3 mg/l), and a monoclonal IgG lambda gammapathy. The chest X-ray and thoracic CT revealed an osteolytic lesion in the left third rib. Nerve conduction studies showed sensitive and motor polyneuropathy with secondary axonal degeneration. Bone marrow biopsy was normal. Second and third left ribs were excised, revealing a pathologic diagnosis of plasmacytoma. The patient became asymptomatic after corticosteriod administration lesion excision and local radiotherapy. Conclusions. Subacute demyelinating polyradiculoneuropathy can be due to multiple causes. SP can be one of its etiologies and occur at infrequent ages and localizations (AU)

Presumed macular choroidal watershed vascular filling, choroidal neovascularization, and systemic vascular disease in patients with age-related macular degeneration.

PURPOSE: To investigate the possible association of presumed macular choroidal watershed vascular filling (PMWF), choroidal neovascularization, and systemic vascular disease in patients with age-related macular degeneration. METHODS: In a retrospective study, we evaluated 74 randomly selected indocyanine green videoangiograms of 74 patients with age-related macular degeneration. We also reviewed the charts of 20 randomly selected, age-matched control patients without age-related macular degeneration, initially referred for uniocular conditions, and subsequently performed indocyanine green videoangiography on their normal fellow eyes. We evaluated these videoangiograms for the presence of PMWF, manifesting as characteristic early choroidal hypofluorescence and its relation to choroidal neovascularization when present. Additionally, the incidence of hypertension, coronary artery disease, peripheral vascular disease, and diabetes mellitus was determined. RESULTS: Forty-one (55.4%) of 74 patients with age-related macular degeneration vs three (15.0%) of 20 normal control patients exhibited PMWF on indocyanine green videoangiography (P = .0014). Of the 61 patients with age-related macular degeneration and choroidal neovascularization, 36 (59.0%) exhibited PMWF on videoangiography. Associated choroidal neovascularization arose from the PMWF zone in 33 (91.7%) of these cases. Hypertension was observed in 24 (58.5%) of 41 patients with age-related macular degeneration and PMWF vs nine (27.3%) of 33 patients with age-related macular degeneration who did not exhibit PMWF (P = .007). CONCLUSIONS: An increased incidence of PMWF occurs in patients with age-related macular degeneration with a possible predisposition for the development of associated choroidal neovascularization. Additionally, PMWF may be accentuated by associated hypertensive choroidal microvascular insult.