REM sleep behaviour disorder (RBD) is a parasomnia characterized by the loss of normal skeletal muscle atonia during REM sleep with prominent motor activity accompanying dreaming. The terminology relating to RBD, and mechanisms underlying REM sleep without atonia and RBD based on data in cat and rat are presented. Neuroimaging data from the few published human cases with RBD associated with structural lesions in the brainstem are presented, in which the dorsal midbrain and pons are implicated. Pharmacological manipulations which alter RBD frequency and severity are reviewed, and the data from human neuropathological studies are presented. An anatomic framework and new schema for the pathophysiology of RBD are proposed based on recent data in rat regarding the putative flip-flop switch for REM sleep control. The structure in man analogous to the subcoeruleus region in cat and sublaterodorsal nucleus in rat is proposed as the nucleus (and its associated efferent and afferent pathways) crucial to RBD pathophysiology. The association of RBD with neurological disease ('secondary RBD') is presented, with emphasis on RBD associated with neurodegenerative disease, particularly the synucleinopathies. The hypothesized pathophysiology of RBD is presented in relation to the Braak staging system for Parkinson's disease, in which the topography and temporal sequence of synuclein pathology in the brain could explain the evolution of parkinsonism and/or dementia well after the onset of RBD. These data suggest that many patients with 'idiopathic' RBD are actually exhibiting an early clinical manifestation of an evolving neurodegenerative disorder. Such patients may be appropriate for future drug therapies that affect synuclein pathophysiology, in which the development of parkinsonism and/or dementia could be delayed or prevented. We suggest that additional clinicopathological studies be performed in patients with dementia or parkinsonism, with and without RBD, as well as in patients with idiopathic RBD, to further elucidate the pathophysiology and also characterize the clinical and pathophysiological relevance of RBD in neurodegenerative disease. Furthermore, longitudinal studies in patients with idiopathic RBD are warranted to characterize the natural history of such patients and prepare for future therapeutic trials.

Background: Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), often termed Hashimoto encephalopathy, is a poorly understood and often misdiagnosed entity. Objective: To characterize the clinical, laboratory, and radiologic findings in patients with SREAT to potentially improve recognition of this treatable entity. Design: Retrospective analysis of clinical features and diagnostic test data. Setting: Two affiliated tertiary care referral institutions. Patients: Twenty consecutive (6 male) patients diagnosed as having SREAT from 1995 to 2003. Main Outcome Measures: Clinical features and ancillary test findings associated with SREAT. Results: The median age at disease onset was 56 years (range, 27-84 years). The most frequent clinical features were tremor in 16 (80%), transient aphasia in 16 (80%), myoclonus in 13 (65%), gait ataxia in 13 (65%), seizures in 12 (60%), and sleep abnormalities in 11 (55%). All patients were assigned an alternative misdiagnosis at

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Introducción: El MoCA-Test, es un instrumento breve de tamizaje, utilizado para la detección de cambios cognoscitivos en adultos mayores. Diferentes validaciones han demostrado que es un instrumento sensible y específico, para detectar el deterioro cognoscitivo leve, con puntos de corte que varían según las diferentes poblaciones estudiadas. Objetivo: Evaluar la confiabilidad y validez discriminante del MoCA-test, en un grupo de adultos de Bogotá, con diferentes escolaridades. Material y Métodos: Se evaluaron 1174 adultos mayores de 50 años, autónomos de las diferentes localidades de Bogotá, por medio de la aplicación del MoCA-Test y el MMSE. Los sujetos con puntajes

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Results from this study suggest that neurocysticercosis is a risk factor for cerebral glioma. The intense astrocytic gliosis that surrounds calcified cysticerci, together with the suppression of the cellular immune response induced by cysticerci, may contribute to the development of malignant glial cells in patients with neurocysticercosis.