[Cognitive and emotional alterations in chronic insomnia]. / Alteraciones cognitivas y emocionales en el insomnio crónico.

INTRODUCTION: Little is known about the cognitive and emotional alterations associated with chronic insomnia. DEVELOPMENT: After reviewing the aetiology and pathophysiology of chronic insomnia, taking into account the patient's vulnerability and its inheritability, this study reports on the knowledge currently held about the cognitive deficits and emotional alterations observed in patients with chronic insomnia. CONCLUSIONS: Most aetiological models include factors that predispose an individual to insomnia, as well as precipitating and maintaining it. Predisposing factors can be of a biological or psychosocial nature. One predisposing factor that plays an important role is the vulnerability to insomnia, which is related to a non-adaptive way of coping with stress (focused on the emotion rather than on the problem) and the internalisation of negative emotions, which favours a state of physiological, cognitive and emotional hyperactivation that disrupts sleep and may lead to insomnia. This vulnerability is largely hereditary. Two phenotypes, based on the objective duration of sleep, have been described, the difference between them being the severity of the disorder. Insomniacs with an objective sleep time below six hours present significant cognitive deficits. These become manifest in tasks that require a large number of cognitive resources, complex attention tasks, changes in the focus of attention, the process of consolidation of memory during sleep, and working memory. These data suggest the existence of a prefrontal dysfunction. Comorbidity between insomnia and anxiety-depression is high. The anxiety-depression triggered by the internalisation of emotions predisposes the individual to insomnia and this, in turn, intensifies the depression.

TITLE: Alteraciones cognitivas y emocionales en el insomnio cronico.Introduccion. Las alteraciones cognitivas y emocionales asociadas al insomnio cronico son poco conocidas. Desarrollo. Tras revisar la etiologia y fisiopatologia del insomnio cronico, considerando la vulnerabilidad a este y su heredabilidad, se describe el estado actual de conocimientos acerca de los deficits cognitivos y las alteraciones emocionales observados en el insomnio cronico. Conclusiones. La mayoria de los modelos etiologicos incluye factores que predisponen al insomnio, que lo precipitan y que lo mantienen. Los factores predisponentes pueden ser de tipo biologico o psicosocial. Un factor predisponente que desempeña un importante papel es la vulnerabilidad al insomnio, que se relaciona con un modo no adaptativo de afrontar el estres (centrado en la emocion en vez de en el problema) y la internalizacion de las emociones negativas, lo cual favorece un estado de hiperactivacion fisiologica, cognitiva y emocional que altera el sueño y puede desembocar en insomnio. Esta vulnerabilidad es en gran parte hereditaria. Se han descrito dos fenotipos, basados en la duracion objetiva del sueño, que difieren en la gravedad del trastorno. Los insomnes con duracion objetiva del sueño menor de seis horas presentan deficits cognitivos significativos. Estos se manifiestan en tareas que requieren gran cantidad de recursos cognitivos, tareas de atencion complejas, cambio de foco de atencion, proceso de consolidacion de la memoria durante el sueño y memoria operativa. Estos datos sugieren la existencia de una disfuncion prefrontal. Se da una alta comorbilidad entre insomnio y ansiedad-depresion. La ansiedad-depresion provocada por la internalizacion de las emociones predispone al insomnio, y este, a su vez, intensifica la depresion.

Alteraciones cognitivas y emocionales en el insomnio crónico / Cognitive and emotional alterations in chronic insomnia

Introducción. Las alteraciones cognitivas y emocionales asociadas al insomnio crónico son poco conocidas. Desarrollo. Tras revisar la etiología y fisiopatología del insomnio crónico, considerando la vulnerabilidad a éste y su heredabilidad, se describe el estado actual de conocimientos acerca de los déficits cognitivos y las alteraciones emocionales observados en el insomnio crónico. Conclusiones. La mayoría de los modelos etiológicos incluye factores que predisponen al insomnio, que lo precipitan y que lo mantienen. Los factores predisponentes pueden ser de tipo biológico o psicosocial. Un factor predisponente que desempeña un importante papel es la vulnerabilidad al insomnio, que se relaciona con un modo no adaptativo de afrontar el estrés (centrado en la emoción en vez de en el problema) y la internalización de las emociones negativas, lo cual favorece un estado de hiperactivación fisiológica, cognitiva y emocional que altera el sueño y puede desembocar en insomnio. Esta vulnerabilidad es en gran parte hereditaria. Se han descrito dos fenotipos, basados en la duración objetiva del sueño, que difieren en la gravedad del trastorno. Los insomnes con duración objetiva del sueño menor de seis horas presentan déficits cognitivos significativos. Éstos se manifiestan en tareas que requieren gran cantidad de recursos cognitivos, tareas de atención complejas, cambio de foco de atención, proceso de consolidación de la memoria durante el sueño y memoria operativa. Estos datos sugieren la existencia de una disfunción prefrontal. Se da una alta comorbilidad entre insomnio y ansiedad-depresión. La ansiedad-depresión provocada por la internalización de las emociones predispone al insomnio, y éste, a su vez, intensifica la depresión (AU)

Introduction. Little is known about the cognitive and emotional alterations associated with chronic insomnia. Development. After reviewing the aetiology and pathophysiology of chronic insomnia, taking into account the patient’s vulnerability and its inheritability, this study reports on the knowledge currently held about the cognitive deficits and emotional alterations observed in patients with chronic insomnia. Conclusions. Most aetiological models include factors that predispose an individual to insomnia, as well as precipitating and maintaining it. Predisposing factors can be of a biological or psychosocial nature. One predisposing factor that plays an important role is the vulnerability to insomnia, which is related to a non-adaptive way of coping with stress (focused on the emotion rather than on the problem) and the internalisation of negative emotions, which favours a state of physiological, cognitive and emotional hyperactivation that disrupts sleep and may lead to insomnia. This vulnerability is largely hereditary. Two phenotypes, based on the objective duration of sleep, have been described, the difference between them being the severity of the disorder. Insomniacs with an objective sleep time below six hours present significant cognitive deficits. These become manifest in tasks that require a large number of cognitive resources, complex attention tasks, changes in the focus of attention, the process of consolidation of memory during sleep, and working memory. These data suggest the existence of a prefrontal dysfunction. Comorbidity between insomnia and anxiety-depression is high. The anxiety-depression triggered by the internalisation of emotions predisposes the individual to insomnia and this, in turn, intensifies the depression (AU)

Insomnia with objective short sleep duration is associated with deficits in neuropsychological performance: a general population study.

STUDY OBJECTIVES: To examine the joint effect of insomnia and objective short sleep duration on neuropsychological performance. DESIGN: Representative cross-sectional study. SETTING: Sleep laboratory. PARTICIPANTS: 1,741 men and women randomly selected from central Pennsylvania. INTERVENTIONS: None. MEASUREMENTS: Insomnia (n = 116) was defined by a complaint of insomnia with a duration > or = 1 year and the absence of sleep disordered breathing (SDB), while normal sleep (n = 562) was defined as the absence of insomnia, excessive daytime sleepiness, and SDB. Both groups were split according to polysomnographic sleep duration into 2 categories: > or = 6 h of sleep ("normal sleep duration") and < 6 h of sleep ("short sleep duration"). We compared the groups' performance on a comprehensive neuropsychological battery that measured processing speed, attention, visual memory, and verbal fluency, while controlling for age, race, gender, education, body mass index, and physical and mental health. RESULTS: No significant differences were detected between insomniacs and controls. However, the insomnia with short sleep duration group compared to the control with normal or short sleep duration groups showed poorer neuropsychological performance in variables such as processing speed, set-switching attention, and number of visual memory errors and omissions. In contrast, the insomnia with normal sleep duration group showed no significant deficits. CONCLUSIONS: Insomnia with objective short sleep duration is associated with deficits in set-switching attentional abilities, a key component of the "executive control of attention." These findings suggest that objective sleep duration may predict the severity of chronic insomnia, including its effect on neurocognitive function.