RESUMO
There is no sense organ specifically dedicated to time perception, as there is for other senses such as hearing and vision. However, this subjective sense of time is fundamental to our conception of reality and it creates the temporal course of events in our lives. Here, we explored neurobiological relations from the clinical perspective, examining timing ability in patients with different neurological and psychiatric conditions (e.g. Parkinson's disease, depression, bipolar disorder, anxiety disorders and schizophrenia). The neural bases of present distortions in time perception and temporal information processing still remain poorly understood. We reviewed: a) how the brain is capable of encoding time in different environments and multiple tasks, b) different models of interval timing, c) brain structures and neurotransmitters associated with time perception, d) the relationship between memory and time perception, e) neural mechanisms underlying different theories in neural and mental processes, and f) the relationship between different mental diseases and time perception. Bibliographic research was conducted based on publications over the past thirteen years written in English in the databases Scielo, Pubmed/MEDLINE, ISI Web of Knowledge. The time perceptions research are executed to evaluate time perception in mental diseases and can provide evidence for future clinical applications.
Assuntos
Transtornos Mentais/complicações , Doenças do Sistema Nervoso/complicações , Transtornos da Percepção/etiologia , Percepção do Tempo/fisiologia , Feminino , Humanos , Masculino , Transtornos Mentais/patologia , Doenças do Sistema Nervoso/patologia , Transtornos da Percepção/diagnóstico , Transtornos da Percepção/patologiaRESUMO
En este trabajo se revisa y discute el síndrome de neglect considerando diferentes modelos teóricos explicativos; de dirección atencional, de asimetrías hemisféricas cerebrales, del sesgo atencional o el modelo de atención selectiva. Se consideran los aspectos cognitivos, emocionales y neuroconductuales. El Síndrome de Neglect generalmente es consecuencia de un accidente cerebrovascular, afecta al hemisferio cerebral derecho y señala directamente al lóbulo parietal. Este es el resultado de una definición anatómica vasta más que una unidad fisiológica o funcional. El síndrome se manifiesta por déficits en la atención perceptiva y en la respuesta a estímulos presentados en el hemicampo contralesional. Es un síndrome heterogéneo. Pese a la preponderancia de las teorías de déficits atencionales, las explicaciones de déficits perceptivos y de representación del espacio están presentes. Son variaciones del síndrome la heminatención, la extinción, la hemicinesia y el neglect hemiespacial. Se resalta la importancia de incluir los aspectos emocionales y neuroconductuales junto con los cognitivos y la rehabilitación motora en el proceso de rehabilitación neuropsicológica del síndrome. Son característicos los síntomas de anosognosia, extinción, desinhibición de conducta, conducta de utilización o la falta de afecto. En cuanto a la recuperación y a cómo ocurre esta, se discuten varias explicaciones alternativas y se apunta el papel de la motivación como factor importante en el éxito de los tratamientos.
This paper reviews the syndrome Neglect considering different theoretical models: attentional direction; of cerebral hemispheric asymmetry, attentional bias, selective attention model. The cognitive, emotional and neurobehavioral characteristics are high lighted. Neglect syndrome usually results from a stroke that affects the right cerebral hemisphere and points directly to the parietal lobe. This is the result of an extensive anatomical definition more than that one functional unit or physiological. The syndrome is manifested by deficits in attention and perceptual responses to stimuli presented in the contralesional hemispace. Neglect is a heterogeneous syndrome. Despite the preponderance of theories of the attentional deficit, explanations of perceptual deficits and representation of space are present. The syndrome manifestations are the heminatención, the extinction, the hemispatial hemicinesia and the neglect. They are very important the emotional aspects as the cognitive, neurobehavioral and motor rehabilitation, in the neuropsychological rehabilitation process of syndrome. Symptoms of anosognosia, extinction, behavioral disinhibition, and the utilization behavior or lack of affection are the most prominent in the syndrome. In terms of recovery, how to happen this? We discuss several alternative explanations and the role of motivation as an important factor in the success of treatments.
Assuntos
Humanos , Acidente Vascular Cerebral/complicações , Modelos Neurológicos , Transtornos da Percepção/patologia , Transtornos da Percepção/reabilitação , Sintomas Afetivos , Agnosia , Modelos Teóricos , Testes Neuropsicológicos , Síndrome , Transtornos da Percepção/etiologia , Transtornos da Percepção/fisiopatologiaRESUMO
Prenatal lipopolysaccharide (LPS) exposure causes reproductive, behavioral and neurochemical defects in both dams and pups. The present study evaluated male rats prenatally treated with LPS for behavioral and neurological effects related to the olfactory system, which is the main sensorial path in rodents. Pregnant Wistar rats received 100 µg/kg of LPS intraperitoneally (i.p.) on gestational day (GD) 9.5, and maternal behavior was evaluated. Pups were evaluated for (1) maternal odor preference, (2) aversion to cat odor, (3) monoamine levels and turnover in the olfactory bulb (OB) and (4) protein expression (via immunoblotting) within the OB dopaminergic system and glial cells. Results showed that prenatal LPS exposure impaired maternal preference and cat odor aversion and decreased dopamine (DA) levels in the OB. This dopaminergic impairment may have been due to defects in another brain area given that protein expression of the first enzyme in the DA biosynthetic pathway was unchanged in the OB. Moreover, there was no change in the protein expression of the DA receptors. The fact that the number of astrocytes and microglia was not increased suggests that prenatal LPS did not induce neuroinflammation in the OB. Furthermore, given that maternal care was not impaired, abnormalities in the offspring were not the result of reduced maternal care.