La cognición socialy su contribución a la rehabilitación de los trastornos de la conducta por traumatismo craneal / Social Cognition and its Contribution to the Rehabilitation of Behavioural Disorders in Traumatic Brain Injury

Resumen Las alteraciones de la conducta social por traumatismo craneoencefálico son el resultado de la disfunción de procesos psíquicos involucrados en las relaciones sociales e interpersonales. El concepto de cognición social se ha desarrollado en el estudio de la esquizofrenia, el autismo y la discapacidad intelectual. Los límites del concepto y su estructura interna distan de estar asentados, pero conceptos como teoría de la mente, empatía y procesamiento emocional están presentes en todos los modelos publicados. Las intervenciones propuestas para mejorar la conducta social se centran en la mejora de procesos cognitivos como la memoria de trabajo, el reconocimiento y el procesamiento de las emociones, la capacidad empática o el entrenamiento en habilidades sociales. La evidencia sobre la eficacia de las estrategias que se centran en la cognición social es todavía escasa.

Abstract Social behaviour disorders in traumatic brain injury are caused by the dysfunction of cognitive processes involved in social and interpersonal interaction. The concept of social cognition was introduced by authors studying schizophrenia, autism or mental retardation. The boundaries and the content of the concept have not yet been definitively defined, but theory of mind, empathy and emotional processing are included in all the models proposed.The strategies proposed to improve social behaviour focus on the restoration of cognitive processes such as working memory, emotional recognition and processing, and empathy, as well as social skills. To date, there is very little evidence on the efficacy of the aforementioned social cognition strategies.

[Social Cognition and its Contribution to the Rehabilitation of Behavioural Disorders in Traumatic Brain Injury]. / La cognición social y su contribución a la rehabilitación de los trastornos de la conducta por traumatismo craneal.

Social behaviour disorders in traumatic brain injury are caused by the dysfunction of cognitive processes involved in social and interpersonal interaction. The concept of social cognition was introduced by authors studying schizophrenia, autism or mental retardation. The boundaries and the content of the concept have not yet been definitively defined, but theory of mind, empathy and emotional processing are included in all the models proposed. The strategies proposed to improve social behaviour focus on the restoration of cognitive processes such as working memory, emotional recognition and processing, and empathy, as well as social skills. To date, there is very little evidence on the efficacy of the aforementioned social cognition strategies.

The source of the memory impairment in Parkinson's disease: acquisition versus retrieval.

Memory deficits are common in persons with Parkinson's disease (PD) even without the presence of a frank dementia. These memory deficits have traditionally been attributed to inability of patients to retrieve information from long-term memory, referred to as the "retrieval failure hypothesis." However, some studies additionally document problems in recognition memory, noted to be inconsistent with the retrieval failure hypothesis. Given the neuroanatomical abnormalities observed in the hippocampus of PD patients and the role of the hippocampus in learning new information, the current study was designed to specifically examine learning abilities in a nondemented PD sample through the application of a learning paradigm, the Open Trial Selective Reminding Test. We examined 27 patients with PD without dementia and 27 age-, gender-, and education-matched healthy controls (HCs) with a neuropsychological test battery designed to assess new learning and memory. Results indicated a significant difference between the groups in terms of their ability to learn a list of 10 semantically related words. However, once the groups were equated on learning abilities, no significant difference was noted between the PD and HC participants in recall or recognition of the newly learned material. The memory deficit observed in nondemented PD patients is thus largely the result of a deficit in learning new information. This finding should be used to guide treatment for memory deficits in persons with PD, and future research should seek to identify novel means of improving new learning in this population.