Principales características epidemiologicas y clínicas del síndrome de Guillain-Barre en hospital clínico Herminda Martin de Chillan desde el año 2010 al 2016 / Main epidemiological and clinical characteristics of Guillain-Barre syndrome in Herminda Martin de Chillan clinical hospital from 2010 to 2016

INTRODUCCIÓN: El SGB es una polirradiculopatía aguda, que a menudo se asocia a una infección anterior. Constituye una emergencia neurológica. La tríada clásica es paresia simétrica y ascendente, abolición o disminución de reflejos osteotendíneos y parestesias. Se sospecha clínicamente. El tratamiento es de soporte, intercambio de plasma e inmunoglobulina intravenosa. OBJETIVO: Describir las características epidemiológicas y clínicas de pacientes con diagnóstico de SGB del Hospital Clínico Herminda Martin de Chillán entre los años 2010 a 2015. MATERIAL Y MÉTODO: Estudio descriptivo retrospectivo de fichas clínicas de 22 pacientes. Criterios de inclusión fueron tener el diagnóstico de SGB informado en ficha clínica y haber sido atendido en el HCHM durante enero de 2010 y mayo del 2015. Criterio de exclusión es no contar físicamente con la ficha clínica del paciente. Las variables investigadas fueron edad, sexo, estacionalidad, antecedente de infección previa, días de hospitalización y manifestaciones clínicas. RESULTADOS: Predominio de SGB en hombres (63,6%), en individuos de 0-20 años (45,4%), en la época deotoño-invierno (59%) y un 54,5% presentó infección previa. Las manifestaciones clínicas más frecuentes fueron: parestesia (86,3%), paresia muscular (95.4%), arreflexia osteotendínea (86.3%) y dolor muscular (54.5%). 50% de los pacientes tuvo una estadía hospitalaria mayor a cuatro semanas. DISCUSIÓN: La mayoría de las características epidemiológicas y clínicas concuerdan con la literatura y estadísticas internacionales. No obstante, existen diferencias en edad de presentación y estacionalidad.

INTRODUCTION: GBS is an acute polyradiculopathy, which is often associated with a previous infection. It constitutes a neurological emergency. The classic triad is symmetric and ascending paresis, abolition or diminution of osteotendine reflexes and paresthesias. It is clinically suspected. The treatment is support, plasma exchange and intravenous immunoglobulin. The aim of this study is to describe the epidemiological and clinical characteristics of patients with a diagnosis of GBS at the Clinical Hospital Herminda Martin de Chillán between 2010 and 2015. MATERIAL AND METHODS: Retrospective descriptiv estudy of 22 patients` medical records. Inclusion criteria were to have the diagnosis of GBS reported in theclinical record and to have been seen at the HCHM duringJanuary 2010 and May 2016. Exclusion criterion is not to physically counton the patient'sclinical record. The investigated variables were age, sex, seasonality, history of previous infection, clinical manifestations and recovery time. RESULTS: Predominance of GBS in males (63,6%), in the 0-20 years range (45,4%), debuting in autumn-winter (59%) and previous infection in 54,5% of patients. The most frequent clinical manifestations were: paresthesia (86.3%), muscle paresis (95.4%), osteotendinous areflexia (86.3%) and muscle pain (54.5%). 50% of patients recovered in more than four weeks. DISCUSSION: Most of the epidemiology and clinical features are consistent with the literature and international statistics. However, there are differences in age of presentation and seasonality

Polineuropatia secundária ao uso crônico de estatinas / Polineuropathy due to chronic use of statins

Os inibidores da 3-hidroxi-3-metilglutaryl coenzima-A (HMG-CoA)redutase têm eficácia comprovada em reduzir os níveis de colesterole prevenir a inflamação do endotélio coronariano, cerebral e periférico.Os efeitos adversos devem ser conhecidos, pois sua suspensão pode levar à completa reversibilidade dos sintomas. São descritas complicações musculares, entre elas, mialgia, miosite e rabdomiólise, além de complicações hepáticas, neuropatias e outras. Foram revistos 1 estudo experimental, 6 estudos populacionais, 25 relatos de casos e 2 revisões sobre o tema, a maioria apontando para a real existência dessa complicação. A neuropatia induzida por estatinas tem incidência aproximada de 12 por 100.000 pessoas-ano. Apresenta-se mais comumente como polineuropatia sensitivo-motora axonal de predomínio sensitivo. Em alguns casos, agravam neuropatias periféricas preexistentes. A fisiopatologia parece convergir para o comprometimento da cadeia respiratória mitocondrial. O diagnóstico baseia-se na relação temporal entre o uso ou suspensão da droga e o surgimento ou melhora dos sinais e sintomas. Os exames laboratoriais são fundamentais para excluir causas de neuropatias periféricas bem estabelecidas. O prognóstico relaciona-se com o momento de suspensão da droga, com relatos desde melhora completa até irreversibilidade.

Inhibitors of coenzyme A 3-hydroxy-3-metilglutaryl (HMG-CoA) reductaseinhibitors have proven to reduce cholesterol levels and prevent inflammation of the coronary, cerebral and peripheral endothelium. Adverse effects should be known, for its suspension can lead to complete reversibility of symptoms. Muscle complications are described, among them, myalgia, myositis and rhabdomyolysis, besides hepatic, neuropathies, and others. One experimental study and 6 population studies, 25 cases reports, and other 2 reviews were reviewed, most pointing to the actual existence of this complication. Statin induced neuropathy has an approximate incidence of 12 per 100,000 persons-year. It most commonly is presented as a sensorimotor axonal polyneuropathy predominantly sensory. In some cases it aggravates pre-existing peripheral neuropathies. The pathophysiology seems to converge to impairment of the mitochondrial respiratory chain. The diagnosis is based on the temporal relationship between the use or discontinuation of the drug and the emergence or improvement of signs and symptoms. Laboratory tests are essential to exclude well established causes of peripheral neuropathies. The prognosis is related to the moment of drug suspension, with reports from complete recovery to irreversibility.

Neuropatía hereditaria con susceptibilidad a la parálisis por presión. Estudio clínico, neurofisiológico y genético de 3 casos esporádicos / Hereditary neuropathy with liability to pressure palsy. Clinical, neurophysiological and genetic study of 3 sporadic cases

Introducción. La neuropatía hereditaria con susceptibilidad a la parálisis por presión (NHPP) es una enfermedad genética que afecta fundamentalmente al componente mielínico de los nervios periféricos. Este estudio pretende describir detalladamente tres casos no emparentados familiarmente, así como realizar una revisión bibliográfica actualizada sobre el tema. Casos clínicos. Pacientes de 23, 42 y 41 años estudiados por sospecha de neuropatía cubital (casos 1 y 2) y de síndrome del túnel carpiano bilateral (caso 3). Resultados. Los estudios neurofisiológicos mostraron la existencia de una polineuropatía sensitivo-motora de predominio desmielinizante y mayor intensidad en localizaciones susceptibles al atrapamiento nervioso. El estudio genético confirmó en todos ellos la existencia de una deleción a nivel del gen PMP22 (cromosoma 17p11.2). Conclusiones. Esta neuropatía hereditaria puede simular una simple neuropatía compresiva, estando por ello infradiagnosticada. Una anamnesis completa, así como un riguroso estudio neurofisiológico son fundamentales para una orientación diagnóstica adecuada.

Introduction. Hereditary neuropathy with liability to pressure palsy (HNPP) is a genetic disease that primarily affects the myelin of peripheral nerves. This study aims to describe in detail three cases with no familiar blood-ties and do an updated literature review on the topic. Clinical cases. 23, 42 and 41 years old patients studied for suspected ulnar neuropathy (cases 1 and 2) and bilateral carpal tunnel (case 3) syndrome. Results. The electromyographic examination revealed the existence of a sensory-motor demyelinating polyneuropathy of greater intensity in locations susceptible to nerve entrapment. The genetic study confirmed in all patients the existence of a deletion at the level of PMP22 gene (chromosome 17p11.2). Conclusions. This hereditary neuropathy can simulate a simple compressive neuropathy. Therefore it is underdiagnosed. A thorough anamnesis and a rigorous neurophysiological study are essential in a proper diagnostic orientation.

Encefalopatía de Wernicke posterior a cirugía bariátrica: más que una pérdida de peso: [revisión] / Wernicke encephalopathy following a bariatric surgery: more than a weight loss: [review]

La encefalopatía de Wernicke y polineuropatía por deficiencia de tiamina (vitamina B1) es una de las posibles complicaciones neurológicas que comúnmente se presentan en pacientes sometidos a cirugías bariátricas. Al tener un aumento del número de procedimientos también se ha observado un aumento de estas complicaciones relacionadas a déficit vitamínico, y haciendo de esta condición relevante que debería conocerse por todos los profesionales de la salud; ya que su pronóstico está estrechamente relacionado con su prevención prequirúrgica y con la instauración rápida del tratamiento al tener una sospecha diagnóstica. La siguiente es una revisión de la literatura acerca de esta entidad; su presentación clínica, factores de riesgo, diagnóstico diferencial, tratamiento y pronóstico.

Wernicke encephalopathy and polyneuropathy related with Thiamine deficiency, is one of the possible neurologic complications that are commonly presented in patients who undergo bariatric surgery. With increasing number of bariatric procedures done there is also an increase in complications related to vitamin deficiency, making this a relevant condition that must be known by all healthcare professionals; mainly because its prognosis is closely related to its pre-surgical prevention and the prompt treatment when there is a clinical suspicious of the condition. The following in a literature review about this condition; its clinical presentation, risk factors, differential diagnosis, treatment and prognosis.

Neuropatia diabética: diagnóstico e tratamento: relato de caso / Diabetic neuropathy: diagnosis and treatment: case report

JUSTIFICATIVA E OBJETIVOS: As neuropatias periféricas são frequentes e muitos pacientes permanecem sem causa definida, sendo importante a avaliação apropriada. O objetivo foi usando um relato de caso, discutir as alternativas para o diagnóstico, a fisiopatologia e o tratamento da neuropatia diabética.RELATO DO CASO: Paciente do sexo masculino, 65 anos, com queixa de dor nos pés há três anos, em queimação, agulhadas, picadas, e às vezes em choque. Ao exame físico havia diminuição da sensibilidade em ambos os pés até 5 cm proximal ao tornozelo, alodínia e diminuição do reflexo Aquileu. O paciente usava anti-inflamatórios não esteroides e 600 mg de carbamazepina ao dia sem resultado. A introdução de 900 mg/dia de gabapentina e 25 mg/dia de nortriptilina, e 200 mg/dia de tramadol produziram alívio adequado da dor.CONCLUSÃO: O diagnóstico de neuropatias de fibras finas requer a utilização de exame físico, neurológico e complementar pelos inúmeros diagnósticos diferenciais. O tratamento da dor consiste na introdução de forma progressiva de fármacos como os antidepressivos e os anticonvulsivantes.

BACKGROUND AND OBJECTIVES: Peripheral neuropathies are frequent and many patients remain without defined cause, being important the adequate evaluation. Our objective was, using a case report, to discuss diagnostic alternatives, pathophysiology and treatment of diabetic neuropathy.CASE REPORT: Male patient, 65 years old, with feet burning, needle prick, sting and sometimes shock pain complaint for three years. At physical evaluation there was decreased sensitivity of both feet up to 5 cm proximal to the ankle, allodynia and decreased Achilles reflex. Patient was under nonsteroid anti-inflammatory drugs and 600 mg carbamazepine per day without result. The introduction of 900 mg/day gabapentin, 25 mg/day nortriptyline and 200 mg/day tramadol has produced adequate pain relief.CONCLUSION: Thin fiber neuropathies diagnosis requires physical, neurological and complementary evaluation due to numerous differential diagnoses. Pain treatment consists on the progressive introduction of drugs such as antidepressants and anticonvulsivants.

Evaluación del funcionamiento del sistema nervioso autonómico en pacientes con polineuropatía de Charcot Marie Tooth tipo 1 / Evaluation of the functioning of the autonomic nervous system in patients with Charcot Marie Tooth 1 polyneuropathy

Se realizó este estudio para evaluar las alteraciones clínicas y electrofisiológicas del sistema autonómico en pacientes con la enfermedad de Charcot Marie Tooth 1 y conocer la sensibilidad de índices electrofisiológicos y clínicos disponibles para identificar y cuantificar disautonomías asociadas a esta enfermedad. Se hizo un estudio analítico de casos y controles. Se obtuvo una muestra de 15 pacientes con polineuropatía sensorimotora desmielinizante hereditaria tipo 1 y 20 controles pareados. A todos los pacientes se les aplicó un formulario clínico para disautonomía. También se monitoreó la frecuencia cardíaca, se observó la variabilidad en reposo y durante la maniobra de Valsalva, las respiraciones profundas y el ortostatismo. Se calcularon los coeficientes de variación y los índices de Valsalva (VS), de espiración/inspiración y máximo/mínimo al ortostatismo. Se halló que el 60 % (9 casos) de los pacientes padecían de frialdad en los pies y las manos, urgencia para la micción y digestiones lentas con llenado fácil durante el acto de comer. El coeficiente de Inspiración/espiración fue estadísticamente menor en los pacientes que en los controles (p = 0,01). No se encontraron diferencias estadísticamente significativas en el resto de los indicadores de VFC (índice Max/Min, RR medio, desviaciones estándar, y MSSD media) registrados en pacientes y controles. Se concluyó que los pacientes con CMT tienen en su cuadro clínico manifestaciones de disautonomía y que el índice de respiraciones profundas evidenció una lesión ligera parasimpática cardiovascular.

A study was conducted to evaluate the clinical and electrophysiological alterations of the autonomic nervous system in patients with Charcot Marie Tooth 1 disease and to know the sensitivity of electrophysiological and clinical indexes available to identify and quantify dysautonomies associated with this disease. An analytical case-control study was undertaken. It was obtained a sample of 15 patients with type 1 hereditary motor and sensory demyelinating polyneuropathy and 20 matched controls. All the patients were applied a clinical questionnaire for dysautonomy. Heart rate was monitored, and it was observed the variability at rest and during Valsalva's maneuver, deep breaths and orthostatism. The variation coefficients, the Valsalva's indexes, and the expiration/inspiration and maximum/minimum coefficients on orthatism were calculated. It was found that 60 % (9 cases) of the patients suffered from coldness in hands and feet, urgency for miction, had slow digestions and they easily filled up when eating. The expiration/inspiration coefficient was statistically lower in patients than in controls (p = 0.01). No statistically significant differences were found in the rest of the VFC indicators (Max/Min index, mean RR, standard deviations and mean MSSD) registered in patients and controls. It was concluded that the patients with CMT have manifestations of dysautonomy in their clinical picture and that the index of deep breaths evidenced a mild parasympathetic cardiovascular lesion.