Cognitive-Affective Neuroscience of Depression and Anxiety by Dan J Stein

By Dan J Stein

Data on melancholy and anxiousness problems now spans quite a number fields from molecular neuroscience, via cognitive and affective technological know-how, and directly to evolutionary psychology. the writer right here integrates this paintings into one quantity, delivering the clinician with a theoretical synthesis in addition to an invaluable functional framework. This guidebook is helping pros in those numerous fields to control sufferers with significant melancholy, generalized nervousness disease, obsessive-compulsive ailment, panic ailment, post-traumatic rigidity illness and social anxiousness ailment. Neuroscientists, neurologists, pharmacologists, psychiatrists and psychological well-being practitioners will reap the benefits of this text.

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Another significant issue is whether OCD really is an anxiety disorder (Montgomery, 1993). Certainly, the primary emotion in OCD does not appear to be fear. Indeed, some authors have begun to suggest rather that the emotion that is particularly relevant to OCD is that of disgust (Stein et al, 2001). Interestingly, the neurobiology 33 of fear and disgust can be dissociated on neurobiological studies; whereas fear involves the amygdala (see Chapter 5), disgust is mediated by the CSTC circuits which are so central to OCD.

Sensory information, while efferents from the central amygdala nucleus and lateral bed nucleus of the stria terminalis (BNST) (or extended amygdala) include a range of structures which mediate the ‘fight-or-flight’ response. Such structures include the lateral nucleus (autonomic arousal and sympathetic discharge) and paraventricular 37 nucleus (increased adrenocorticoid release) of the hypothalamus, as well as the locus ceruleus (increased noradrenaline release), parabrachial nucleus (increased respiratory rate), periaqueductal grey (defensive behaviours and postural freezing), and nucleus pontine reticularis (startle response) in the brainstem.

Thus, patients with SP have a greater reduction in putamen volume with ageing (Potts et al, 1994), reduced choline and creatinine signal:noise ratios in subcortical, thalamic, and caudate areas (Davidson et al, 1993a), and decreased N-acetylaspartate (NAA) levels and a lower ratio of NAA to other metabolites in cortical and subcortical regions (Davidson et al, 1993a; Tupler et al, 1997). Furthermore, striatal dopamine systems may be abnormal in SP. Finally, frontal areas may play a role in social anxiety.

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