By Spilios Argyropolous;Adrian Feeney;David Nutt
In medical perform, advanced sufferers with comorbidity of temper and anxiousness issues are arguably the norm. those volumes specialise in this zone, offering updated reports of the conceptual concerns that confront the clinician while comparing those sufferers Concise and easy-to-read, additionally they current a pragmatic method of the administration and remedy of sufferers with comorbid temper and anxiousness problems.
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Additional info for Anxiety Disorders Comorbid with Depression: Pocketbook: Panic Disorder and Agoraphobia
However, if the tract linking the hippocampus and amygdala is severed, the rat no longer displays fear when confronted by the cage, although it continues to do so with the tone. If the amygdala is lesioned, the rat responds to the cage but not to the tone (Kim and Fanselow 1992). Higher centres processing sensory information Cortex: prefrontal somatosensory Central nucleus or amygdala Sensory thalamus Hippocampus Involved in conditioned learning Hypothalamus Paraventricular Lateral Locus Periaqueductal Parabrachial Dorsal nucleus nucleus ceruleus grey area nucleus nerve of vagus Autonomic arousal Release of adrenocorticoids Postural freezing Noradrenaline Blood pressure Heart rate Hyperventilation Gastrointestinal distress Symptoms of arousal Figure 8 Neuroanatomical model of panic disorder.
This theory thus accommodates the evidence already detailed above that a variety of challenges is capable of precipitating panic attacks. The postulated abnormally sensitive fear circuit responds to unsettling afferent sensory information, which would normally be tolerated, by setting in train the autonomic responses and also accompanying cognitions characteristic of panic disorder. The SSRIs may serve to damp down this autonomic arousal and benzodiazepines may modulate the impaired appraisal of threat, which leads to these characteristic cognitions (Middleton 1991) (Figure 9).
It has been suggested, however, that this is an oversimplification of the course of panic, arising from methodological short comings of the follow-up studies (Katschnig and Amering 1998). Patient selection bias has been blamed for producing a worse overall outcome than in real life (Shinoda et al 1999). This is explained by the fact that patients with a quick recovery would stop attending follow-up sessions, so that subjects remaining in these studies represent more severely ill patients than the general population of patients with panic disorder.