RESUMEN
Recent studies have recognized similarities between the peptides involved in the neuropathology of Alzheimer's disease and prions. The Tau protein and the Amyloid ß peptide represent the theoretical pillars of Alzheimer's disease development. It is probable that there is a shared mechanism for the transmission of these substances and the prion diseases development; this presumption is based on the presentation of several cases of individuals without risk factors who developed dementia decades after a neurosurgical procedure. This article aims to present the role of Aß and Tau, which underlie the pathophysiologic mechanisms involved in the AD and their similarities with the prion diseases infective mechanisms by means of the presentation of the available evidence at molecular (in-vitro), animal, and human levels that support the controversy on whether these diseases might be transmitted in neurosurgical interventions, which may constitute a wide public health issue.
Asunto(s)
Enfermedad de Alzheimer/etiología , Enfermedad de Alzheimer/metabolismo , Péptidos beta-Amiloides/metabolismo , Procedimientos Neuroquirúrgicos/efectos adversos , Proteínas Priónicas/metabolismo , Proteínas tau/metabolismo , Enfermedad de Alzheimer/genética , Péptidos beta-Amiloides/genética , Humanos , Procedimientos Neuroquirúrgicos/tendencias , Proteínas Priónicas/genética , Factores de Riesgo , Proteínas tau/genéticaRESUMEN
Pain originating from sacroiliac joint may also cause pain in the lumbar and gluteal region in 15% of the population. The clinical manifestation represents a public health problem due to the great implications on the quality of life and health-related costs. However, this is a diagnosis that is usually ignored in the general clinical practice; probably because of the unknown etiology, making harder to rule out the potential etiologies of this pathology, or maybe because the clinical criteria that support this pathology are unknown. By describing several diagnostic techniques, many authors have studied the prevalence of this pathology, finding more positive data than expected; coming to the conclusion that even though there is no diagnostic gold standard yet, an important amount of cases might be detected by properly applying several tests at the physical examination. Thus, it is necessary to have knowledge of the physiopathology and clinical presentation so that diagnosis can be made to those patients that manifest this problem. We present a clinical approach for the neurosurgeon.
RESUMEN
RESUMEN El Síndrome de Locked-In también conocido como Síndrome de Enclaustramiento, de Deseferentización o de Encerramiento, se definió por primera vez en 1966 por Plum y Posner. Las causas pueden agruparse en vasculares y no vasculares, siendo las primeras las más frecuentes. Clínicamente este síndrome se caracteriza porque la conciencia y el estado de vigila están conservados, pero existe cuadriplejía, anartria, disfagia y dificultad para coordinar la mecánica ventilatoria, representando las complicaciones pulmonares la principal causa de muerte. En la mayoría de los casos, el paciente conserva la movilidad ocular vertical, por tanto, el único método de comunicación es por medio de parpadeo ocular y movimientos verticales oculares. A continuación, se hace la presentación de un caso y revisión de la literatura con los aspectos fisiopatológicos, clínicos, diagnósticos y terapéuticos más relevantes.
ABSTRACT Locked-In Syndrome, also known as Enclaustration, Deseferentization, or Enclosure Syndrome, was first defined in 1966 by Plum and Posner. Causes can be grouped into vascular and non-vascular, the former being the most frequent. Clinically this syndrome is characterized by consciousness and the state of watch conserved, but there is quadriplegia, anartria, dysphagia and difficulty to coordinate the ventilatory mechanics, representing pulmonary complications the main cause of death. In most cases, the patient retains vertical eye mobility, so the only method of communication is through eye blinking and vertical eye movements. Next, a case presentation and review of the literature with the most relevant pathophysiological, clinical, diagnostic and therapeutic aspects is done.
RESUMEN
Resumen La hidrocefalia de presión normal es una patología reversible que forma parte de las demencias. A pesar del tiempo que ha transcurrido desde su descubrimiento, su fisiopatología no ha sido claramente establecida y se han planteado dos teorías que buscan explicar el proceso. Una está basada en cambios en el flujo de líquido cefalorraquideo y la otra en el flujo sanguíneo cerebral. Además, el proceso de evaluación y diagnóstico no está determinado, puesto que no existe un método estándar y los síntomas son similares a otras patologías de sistema nervioso central, haciendo que el diagnóstico se realice gracias a la suma de los síntomas clínicos y ciertos hallazgos imagenológicos que no son siempre constantes.
Abstract Normal pressure hydrocephalus is a pathology causing dementia that is reversible. Despite the time elapsed since its discovery, its pathophysiology has not been clearly established and two theories have been proposed that try to explain the process, one based on changes in cerebrospinal fluid flow and the other on cerebral blood flow. In addition, the evaluation and diagnosis process is not determined, since there is no standard method and the symptoms are similar to other pathologies of the central nervous system, leading to the diagnosis as the summation of clinical symptoms and some findings in imaging which are not always constant.