RESUMEN
The Restless legs syndrome (RLS) and Parkinson's disease (PD) are two disorders that can co-exist, whether or not they share a common pathophysiology. If, and to what extent RLS and PD share the same pathophysiology, is still under debate. Sleep disturbances are prevalent in PD, and as PD progresses, nocturnal disturbances become even more evident, in association not only with motor symptoms but also with non-motor symptoms. Alertness to, and recognition of, RLS in PD patients with sleep disorders could improve customized treatment and quality of life of these patients. In this article the prevalence of RLS in PD, the clinical profile of RLS in PD, the PD profile of patients with RLS, RLS mimics specifically related to PD and impact of RLS in PD will be reviewed.
Asunto(s)
Enfermedad de Parkinson/complicaciones , Enfermedad de Parkinson/epidemiología , Síndrome de las Piernas Inquietas , Progresión de la Enfermedad , Humanos , Calidad de Vida , Síndrome de las Piernas Inquietas/complicaciones , Síndrome de las Piernas Inquietas/diagnóstico , Síndrome de las Piernas Inquietas/epidemiologíaAsunto(s)
Movimientos de la Cabeza , Trastornos del Movimiento/diagnóstico , Enfermedades Neuromusculares/diagnóstico , Anciano , Diagnóstico Diferencial , Femenino , Movimientos de la Cabeza/fisiología , Humanos , Masculino , Trastornos del Movimiento/etiología , Debilidad Muscular/diagnóstico , Debilidad Muscular/etiología , Miastenia Gravis/complicaciones , Miastenia Gravis/diagnóstico , Músculos del Cuello , Enfermedades Neuromusculares/etiología , SíndromeRESUMEN
To gain a greater insight into the relationship between hyperactivity of the corticotropin-releasing hormone (CRH) system and autonomic and physiological changes associated with chronic stress, we developed a transgenic mouse model of central CRH overproduction. The extent of central and peripheral CRH overexpression, and the amount of bioactive CRH in the hypothalamus were determined in two lines of CRH-overexpressing (CRH-OE) mice. Furthermore, 24 h patterns of body temperature, heart rate, and activity were assessed using radiotelemetry, as well as cumulative water and food consumption and body weight gain over a 7-day period. CRH-OE mice showed increased amounts of CRH peptide and mRNA only in the central nervous system. Despite the presence of the same CRH transgene in their genome, only in one of the two established lines of CRH-OE mice (line 2122, but not 2123) was overexpression of CRH associated with increased levels of bioactive CRH in the hypothalamus, increased body temperature and heart rate (predominantly during the light (inactive) phase of the diurnal cycle), decreased heart rate variability during the dark (active) phase, and increased food and water consumption, when compared with littermate wildtype mice. Because line 2122 of the CRH transgenic mice showed chronic stress-like neuroendocrine and autonomic changes, these mice appear to represent a valid animal model for chronic stress and might be valuable in the research on the consequences of CRH excess in situations of chronic stress.