Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future.

@article{citeulike:1305310, abstract = {The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.}, address = {Psychiatric Neuroscience Division, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA.}, author = {Rauch, S. L. and Shin, L. M. and Phelps, E. A. }, citeulike-article-id = {1305310}, doi = {http://dx.doi.org/10.1016/j.biopsych.2006.06.004}, issn = {0006-3223}, journal = {Biol Psychiatry}, keywords = {fmri, neuroimaging, psychotherapy, ptsd, review}, month = {August}, number = {4}, pages = {376--382}, posted-at = {2007-05-18 14:37:48}, priority = {2}, title = {Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future.}, url = {http://dx.doi.org/10.1016/j.biopsych.2006.06.004}, volume = {60}, year = {2006} }

TY - JOUR ID - citeulike:1305310 L3 - citeulike-article-id:1305310 TI - Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future. JF - Biol Psychiatry VL - 60 IS - 4 SP - 376 EP - 382 AD - Psychiatric Neuroscience Division, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA. SN - 0006-3223 N2 - The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD. KW - fmri KW - neuroimaging KW - psychotherapy KW - ptsd KW - review AU - Rauch, SL AU - Shin, LM AU - Phelps, EA PY - 2006/08/15/ UR - http://dx.doi.org/10.1016/j.biopsych.2006.06.004 ER -