Neurobiologia do transtorno de personalidade anti-social

Abstract

ResumoNos últimos anos, tem havido um interesse crescente a respeito de uma melhor compreensão sobre o comportamento anti-social. O aumento da criminalidade e violência urbanas pode ter contribuído para esse maior interesse. Além de fatores psicossociais, outros biológicos têm sido implicados na fisiopatogenia do transtorno de personalidade anti-social (TPAS). Estudos de neuroimagem apontam o envolvimento de estruturas cerebrais frontais, especialmente o córtex orbitofrontal, e a amígdala. Também tem sido sugerido que prejuízos na função serotonérgica estariam associados à ocorrência de comportamento antisocial, já que pacientes com diagnóstico de TPAS apresentam respostas hormonais atenuadas a desafios farmacológicos com drogas que aumentam a função serotonérgica cerebral e redução da concentração de receptores serotonérgicos. Uma abordagem ampla dos diferentes fatores possivelmente envolvidos na fisiopatogenia do TPAS poderia contribuir para o desenvolvimento de novas técnicas de prevenção e intervenção.Palavras-chave: Transtorno de personalidade anti-social, psicopatia, serotonina, neuroimagem. AbstractViolence and crime have been increasing considerably in urban societies. As a consequence, some efforts have been made aiming at a better understanding of antisocial bevaviour. Apart from psychosocial factors, some evidences suggest the occurrence of biological factors in the pathogenesis of antisocial personality disorders (ASPD). Neuroimaging studies have shown the involvement of prefrontal areas, especially orbitofrontal cortex, and amygdala. Also, impaired serotonin (5-HT) neurotransmission has been implicated, since patients with ASPD present alterations in measures of 5-Ht system, such as blunted hormonal response to 5-HT pharmacological challenges and reduced 5-HT receptors numbers. A comprehensive approach of antisocial behavior, including biological and psychosocial aspects could lead to the development of new techniques for prevention and intervention in ASPD.

Qualitative and quantitative EEG abnormalities in violent offenders with antisocial personality disorder

“…Abnormalities within the anterior-inferior regions of the temporal lobes are associated with violence. 4,7 Results of this research may serve as support to the growing evidence of brain dysfunction underlying the diagnosis of ASPD in subject authors of crimes. The use of non-invasive technology like the EEG appears to allow accurate identification of substantial CNS abnormalities.…”

“…1 Several studies indicate an interaction between biological factors and social factors in the development of antisocial behaviour. [2][3][4][5][6][7] In the last years there has been an increased interest in studying the neurobiology of personality disorders [8][9][10] , and in particular ASPD. 11,12 The brain regions more compromised in antisocial populations include frontal and temporal lobes.…”

Novas problemáticas sociais: o uso do crack em mulheres e a perspectiva de gênero

“…Tal transtorno constitui um padrão invasivo de desrespeito e violação dos direitos, iniciando na infância ou adolescência e continua na idade adulta (APA, 2002). Além disso, caracteriza-se pela impulsividade, expressa na dificuldade de planejar o futuro, através de escolhas que tragam a satisfação imediata e desconsideram as consequências e leis (Del-Bem, 2005). Desta forma, os tratamentos necessitam contemplar tanto o Transtorno por Uso de Substâncias, como o de Personalidade Anti-Social (Bordin & Offord, 2000).…”

Quantification of tryptophan in plasma by high performance liquid chromatography

“…1 It has a role in physiological (nerve transmission, immune response) and pathological processes (depression, stress, and sleep and appetite disorders) 2 and therefore its plasma levels are linked to changes in mood, behavior, anxiety, sleep, fatigue and appetite suppression. 3 These characteristics have led research centers to focus their studies on the creation of methods allowing the determination and quantification of this amino acid, as well as the identification of possible relationships between plasma levels of tryptophan with diseases and metabolic disorders.…”