By Sherry H. Stewart, Patricia Conrod
Issues of hysteria and substance use are, for a few cause, hardly taken care of in an built-in style via pros. This well timed quantity addresses this obtrusive omission with dispatches from the frontlines of analysis and remedy. Thirty-four foreign specialists supply findings, theories, and intervention options for this universal kind of twin illness, throughout various ingredients and of hysteria problems, to offer the reader accomplished wisdom in a realistic structure.
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Extra resources for Anxiety and Substance Use Disorders: The Vicious Cycle of Comorbidity (Series in Anxiety and Related Disorders)
Sample text
Anxiety can lead to SUD in the form of self-medication. Conversely, any use of sedative anti-anxiety drugs, which act via receptors of the inhibitory neurotransmitter GABA (specifically GABAA receptors), can produce dependence and withdrawal that can generate significant anxiety disorder. Positive feedback between self-medication and withdrawal can thus sustain co-morbidity of SUD and anxiety disorder. Consistent with the epidemiological conclusions of Kushner et al. (this volume), neurobiology suggests multiple causal routes (particularly via stress systems) to co-morbidity of SUD and anxiety.
As a result, tricyclic drugs, clomipramine, monoamine oxidase inhibitors and selective serotonin reuptake inhibitors all increase monoamine function and so have both anti-anxiety and anti-panic effects. ) Likewise, many of the structures of the anxiety system (right hand side of Fig. 1) show coordinated rhythmic electrical activity (‘‘theta rhythm’’) controlled from subcortical areas such as the hypothalamus. Theta rhythm is altered by all anti-anxiety drugs including those that are not also anti-panic, such as buspirone (McNaughton & Coop, 1991).
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