The role of vagus nerve stimulation in the treatment of refractory epilepsy: clinical outcomes and impact on quality of life.

BACKGROUND: Vagus nerve stimulation (VNS) is used as a complementary therapy to pharmacological treatment in patients with refractory epilepsy. This study aims to evaluate the efficacy of VNS in reducing seizure frequency, severity, and duration; reducing the number of antiepileptic drugs administered; and improving patients' quality of life. MATERIAL AND METHODS: We analysed the clinical progression of 70 patients with refractory epilepsy treated with VNS at Hospital Universitario de Alicante and Hospital Clínico de Valencia. Data were collected before and after the procedure. The difference in seizure frequency pre- and post-VNS was classified using the McHugh scale. Data were also collected on seizure duration and severity, the number of drugs administered, and quality of life. RESULTS: According to the McHugh classification, 12.86% of the patients were Class I, 44.29% were Class II, 40% were Class III, and the remaining 2.86% of patients were Class IV-V. A ≥ 50% reduction in seizure frequency was observed in 57.15% of patients. Improvements were observed in seizure duration in 88% of patients and in seizure severity in 68%; the number of drugs administered was reduced in 66% of patients, and 93% reported better quality of life. CONCLUSIONS: VNS is effective for reducing seizure frequency, duration, and severity and the number of antiepileptic drugs administered. It also enables an improvement in patients' quality of life.

The role of vagus nerve stimulation in the treatment of refractory epilepsy: Clinical outcomes and impact on quality of life. / Papel de la estimulación del nervio vago en el tratamiento de la epilepsia refractaria. Resultados clínicos e impacto en la calidad de vida.

BACKGROUND: Vagus nerve stimulation (VNS) is used as a complementary therapy to pharmacological treatment in patients with refractory epilepsy. This study aims to evaluate the efficacy of VNS in reducing seizure frequency, severity, and duration; reducing the number of antiepileptic drugs administered; and improving patients' quality of life. MATERIAL AND METHODS: We analysed the clinical progression of 70 patients with refractory epilepsy treated with VNS at Hospital Universitario de Alicante and Hospital Clínico de Valencia. Data were collected before and after the procedure. The difference in seizure frequency pre- and post-VNS was classified using the McHugh scale. Data were also collected on seizure duration and severity, the number of drugs administered, and quality of life. RESULTS: According to the McHugh classification, 12.86% of the patients were Class I, 44.29% were Class II, 40% were Class III, and the remaining 2.86% of patients were Class IV-V. A≥50% reduction in seizure frequency was observed in 57.15% of patients. Improvements were observed in seizure duration in 88% of patients and in seizure severity in 68%; the number of drugs administered was reduced in 66% of patients, and 93% reported better quality of life. CONCLUSIONS: VNS is effective for reducing seizure frequency, duration, and severity and the number of antiepileptic drugs administered. It also enables an improvement in patients' quality of life.

[Peripheral and optical myeloneuropathy in a folic acid deficient alcoholic patient]. / Mieloneuropatía periférica y óptica en un paciente alcohólico deficiente en ácido fólico.

INTRODUCTION: In Western countries, neurological disorders secondary to toxic nutritional problems usually present as isolated cases that are generally associated to identifiable causes (alcoholism, eating disorders, absorption disorders, use of medicines) that reduce the availability of basic nutrients, especially B group vitamins, but also folic acid (FA). The optic nerves and the peripheral axons are frequent target organs in this type of pathology, but leukoencephalopathy and spinal cord involvement may also appear, often in combination. CASE REPORT: We describe the case of a 38-year-old female smoker with a heavy alcohol habit, who developed a subacute clinical pattern of, predominantly axonal, sensitive peripheral polyneuropathy, with vegetative fibre involvement. She also presented involvement of the posterior spinal cord, which gave rise to an ataxic disorder in the gait, as well as a severe bilateral retrobulbar optic neuropathy. Likewise, she presented macrocytosis (MCV: 118) due to megaloblastosis. She was also found to have a FA deficit but a normal vitamin B12 metabolism. With the help of supplementary vitamins, stopping drinking and the regularisation of her diet, the patient presented progressive clinical improvement, and was able to walk without support at 3 months and almost completely recovered her sight, which was corroborated by an improvement in the studies of both visual and somatosensorial evoked potentials. CONCLUSIONS: In our community, alcoholism is a frequent cause of nutritional deficiencies, which lead to neurological problems. FA is one of the nutrients that become deficient in alcoholics. More and more descriptions are being reported of peripheral polyneuropathy, retrobulbular optic neuropathy, myelopathy or leukoencephalopathy associated to FA deficiency, above all in patients with a history of alcoholism.

Mieloneuropatía periférica y óptica en un paciente alcohólico deficiente en ácido fólico / Peripheral and optical myeloneuropathy in a folic acid deficient alcoholic patient

Introducción. En los países occidentales, los trastornos neurológicos secundarios a problemas toxiconutricionales suelen presentarse como casos aislados, generalmente asociados a causas identificables (alcoholismo, aberraciones dietéticas, trastornos de la absorción, uso de fármacos), que disminuyen la disponibilidad de algunos nutrientes básicos, fundamentalmente vitaminas del grupo B, pero también de ácido fólico (AF). Los nervios ópticos y los axones periféricos son dianas frecuentes en este tipo de patologías, pero también pueden aparecer, frecuentemente en combinación, leucoencefalopatía y afectación medular. Caso clínico. Mujer de 38 años, fumadora y con hábito alcohólico importante, que desarrolló un cuadro subagudo de polineuropatía periférica, sensitiva, con afectación de las fibras vegetativas, y de predominio axonal, junto a afectación cordonal posterior, que provocó trastorno atáxico de la marcha, así como neuropatía óptica retrobulbar bilateral grave. Igualmente presentaba macrocitosis (VCM: 118) debida a megaloblastosis. Se halló deficiencia de AF con un metabolismo de la vitamina B12 normal. Con suplementos vitamínicos, el abandono del hábito alcohólico y la normalización de la dieta, la paciente presentó una mejoría clínica progresiva, y fue capaz de deambular sin apoyo a los tres meses, con una recuperación casi completa de la función visual, todo ello corroborado por una mejoría en los resultados de los estudios de potenciales evocados, tanto visuales como somatosensoriales. Conclusiones. En nuestro medio, el alcoholismo es una causa frecuente de deficiencias nutricionales, que ocasionan problemas neurológicos. El AF es uno de los nutrientes que se hace deficitario en el alcoholismo. Cada vez aparecen más descripciones de polineuropatía periférica, neuropatía óptica retrobulbar, mielopatía o leucoencefalopatía asociadas a una deficiencia de AF, sobre todo en pacientes con abuso de alcohol (AU)

Introduction. In Western countries, neurological disorders secondary to toxic-nutritional problems usually present as isolated cases that are generally associated to identifiable causes (alcoholism, eating disorders, absorption disorders, use of medicines) that reduce the availability of basic nutrients, especially B group vitamins, but also folic acid (FA). The optic nerves and the peripheral axons are frequent target organs in this type of pathology, but leukoencephalopathy and spinal cord involvement may also appear, often in combination. Case report. We describe the case of a 38-year-old female smoker with a heavy alcohol habit, who developed a subacute clinical pattern of, predominantly axonal, sensitive peripheral polyneuropathy, with vegetative fibre involvement. She also presented involvement of the posterior spinal cord, which gave rise to an ataxic disorder in the gait, as well as a severe bilateral retrobulbar optic neuropathy. Likewise, she presented macrocytosis (MCV: 118) due to megaloblastosis. She was also found to have a FA deficit but a normal vitamin B12 metabolism. With the help of supplementary vitamins, stopping drinking and the regularisation of her diet, the patient presented progressive clinical improvement, and was able to walk without support at 3 months and almost completely recovered her sight, which was corroborated by an improvement in the studies of both visual and somatosensorial evoked potentials. Conclusions. In our community, alcoholism is a frequent cause of nutritional deficiencies, which lead to neurological problems. FA is one of the nutrients that become deficient in alcoholics. More and more descriptions are being reported of peripheral polyneuropathy, retrobulbular optic neuropathy, myelopathy or leukoencephalopathy associated to FA deficiency, above all in patients with a history of alcoholism (AU)