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Articles On Generalized Anxiety Disorder

Neurobiological Factors and generalized anxiety disorder
There is little research into the biological factors associated with generalized anxiety disorder specifically, although a large body of work has examined the role of biological factors in anxiety generally. The majority of the biochemical work has centered on the role of the benzodiazepine receptor complex. Discovery of a specific brain receptor for the benzodiazepines led to speculation that there must be a naturally occurring neurotransmitter that uses this receptor and therefore may be involved in producing anxiety. A number of chemicals were examined with this role in mind, and the research is still continuing. A specific anxiety neurotransmitter has proven difficult to identify, but some researchers have attempted to examine the interaction between various neurotransmitter systems and neuroanatomical sites. The main research of this type has been conducted by Jeffrey Gray, who has been involved in a systematic course of research examining the neuropsychology of anxiety.
Although Gray’s model is very involved, it centers largely around the septohippocampal system, which (according to Gray) acts as a type of comparator, comparing actual with expected stimuli. The system ‘‘turns on’’ (i.e., anxiety) when there is a mismatch between actual and expected stimuli or when the expected stimuli are aversive. Gray does not really apply his model to specific anxiety disorders, but it could be suggested that generalized anxiety disorder involves some type of dysfunction in the septohippocampal system. Whether one is specifying neurotransmitter systems or neuroanatomical pathways, it is clear that biological correlates of anxiety cannot be isolated to one neurotransmitter or one pathway. Any useful neurobiological model of anxiety will have to be very comprehensive. Currently, Gray’s model most closely approaches this characteristic. Another interesting neurobiological process recently discovered in individuals with generalized anxiety disorder is a distinct lack of autonomic reactivity, or what has come to be called ‘‘autonomic inflexibility’’. Interestingly, this process seems directly associated with the cognitive process of worry described before. Further investigations revealed that this psychophysiological characteristic is mediated by low vagal tone resulting in a high unstable heart rate and decreased heart rate reactivity, among other responses. In fact, a similar relationship was noted by several researchers such as Kagan who observed autonomic inflexibility in behaviorally inhibited children. Borkovec relates autonomic inflexibility in generalized anxiety disorder patients to the fact that the stimuli feared by these patients are not produced by external environmental stressors but are internally generated thoughts about potential future events.
Thus, these individuals are caught up in a perpetual state of scanning for danger studying free ranging baboons in Africa observed a similar process in his baboons who were subject to chronic stress. He suggests that this process, if chronic, leads to hippocampal lesions. Brain imaging is beginning to confirm the generality of these observations in patients with anxiety disorders. These f indings supported the substantial change in the symptoms that comprise the somatic criteria for DSM-IV definitions of generalized anxiety disorder. Several studies demonstrated the construct validity of these changes suggesting that symptoms of motor tension and vigilance and scanning are more strongly correlated with measures of generalized anxiety disorder (e.g., the Penn State Worry Questionnaire) than symptoms that reflect autonomic hyperactivity. More recent structural equation modeling has demonstrated the unique and important contribution of autonomic inflexibility to generalized anxiety disorder in the context of all anxiety and mood disorders.

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