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By
Andrew R. Gilbert, Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh, PA, USA,
Alison M. Gilbert, Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh, PA, USA,
Jorge R. C. de Almeida, Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh, PA, USA,
Philip R. Szeszko, Department of Psychiatry The Zucker Hillside Hospital Glen Oaks, NY, USA and Albert Einstein College of Medicine Bronx, NY, USA
This chapter presents findings from structural neuroimaging studies of obsessive-compulsive disorder (OCD) in both pediatric and adult populations. It reviews the structural neuroimaging literature with a focus on regions strongly implicated in the pathophysiology of OCD, including the orbitofrontal cortex, anterior cingulate cortex, basal ganglia, and thalamus. Structural neuroimaging studies have identified abnormalities in CST neural systems, especially in the orbitofrontal cortex and have informed many of the dominant neurobiological models of OCD. The emergence of magnetic resonance (MR) imaging techniques advanced the field by providing higher-resolution images without the potential risk of ionizing radiation. Several structural neuroimaging studies reported less gray matter in the amygdala and hippocampus in adult patients with OCD compared to healthy controls, although Kwon et al. reported larger amygdala volume in patients. Recently, investigators have used diffusion tensor imaging (DTI) to investigate the potential role of white matter abnormalities in the pathogenesis of OCD.
By
Rebecca P. Smith, Assistant Clinical Professor World Trade Center Worker and Volunteer Mental Health Screening, Monitoring and Interventions Programs,
Craig L. Katz, Assistant Clinical Professor Psychiatry Mount Sinai School of Medicine,
Dennis S. Charney, Professor Psychiatry Mount Sinai School of Medicine,
Steven M. Southwick, Professor Section of Child Study Center Yale University
Edited by
Robert J. Ursano, Uniformed Services University of the Health Sciences, Maryland,Carol S. Fullerton, Uniformed Services University of the Health Sciences, Maryland,Lars Weisaeth, Universitetet i Oslo,Beverley Raphael, University of Western Sydney
This chapter reviews the findings of human and animal studies which have characterized normal function in the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis, and then briefly describes post-traumatic stress disorder (PTSD)-associated abnormalities seen in each system. Neurobiological models of the structure, function and neurochemistry of the brain have evolved significantly as a result of recent input from findings of neuroimaging studies. In recent years several neurochemicals have been associated with resilience. In humans, neuroimaging studies of PTSD have primarily focused on the amygdala, the hippocampus, medial prefrontal cortex, and anterior cingulate cortex. Multidisciplinary studies that use neurochemical, neuroimaging, genetic, and psychosocial approaches may in the future clarify the complex relationships between genotype, phenotype, and psychobiological responses to stress. Pharmacological intervention aimed at treating early severe symptoms which are known to be predictive of later PTSD, such as excessive arousal, is one possible avenue of study.
This chapter shows how olfactory testing could be applied to investigations of orbitofrontal cortex (OFC) function and related behavioural outcomes. It discusses how tasks such as olfactory identification may offer insights into the development and maintenance of substance use disorders (SUD). Although imaging and neuropsychological studies demonstrate abnormalities in OFC function within addicted populations, it is unclear whether these deficits are related to premorbid vulnerability, a direct consequence of chronic exposure to addictive substances, or a combination of both. In humans, there is growing evidence that an earlier onset age of substance abuse may be related to more marked neurobiological and cognitive deficits. Adolescence is a developmental period associated with increased risk-taking and experimentation with drugs, and is also a time of increased vulnerability to the development of SUD. Experimentation with drugs also occurs during a period of substantial brain development and remodelling.
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