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panic disorder biological perspective

There is a long history of research into biological aspects of panic disorder. Most of the evidence in humans has come from biological challenge procedures and pharmacological treatment and manipulation studies. More recently, evidence has accumulated from neuroimaging studies of people with panic attacks. A large number of chemical substances, it has been found, produce panic attacks in individuals with panic disorder. These substances include sodium lactate, carbon dioxide, flumazenil, and caffeine. Yohimbine is a relatively specific alpha-2-adrenergic receptor antagonist that, by blocking the alpha-adrenergic autoreceptors in the locus coeruleus, results in increased levels of norepinephrine in the central nervous system (CNS). The fact that this substance can produce panic attacks provides evidence for the role of increased f iring of the locus coeruleus in panic.
However, it must be remembered that the response to biological challenge procedures is also markedly influenced by psychological factors. Other research provided evidence for the importance of serotonin in panic attacks. Pharmacologically, it has been found that drugs that block panic attacks affect both the noradrenergic and serotonergic systems. Obviously, locating the biological basis of any disorder in one or two broad neurochemical systems is too simplistic. Recently, some researchers have begun to develop more extensive and detailed models of panic disorder. One example described a model in terms of both neurochemistry and brain structures, centering on the amygdala and all of its afferent and efferent pathways, including the noradrenergic system.
Many of the biological challenge substances have also been linked to panic attacks through their putative action on the central medullary carbon dioxide (CO2) chemoreceptor. Specifically, it has been suggested that the CO2 receptors of individuals with panic disorder have greater sensitivity. Anatomically, it has been found that the CO2 chemoreceptors in the medulla and the norepinephrine receptors of the locus coeruleus are closely linked. A recent model of the neurobiology of panic disorder has argued that the main pathology in people with panic disorder is hypersensitivity of their central CO2 chemoreceptors. These receptors act as a suffocation alarm mechanism, and this alarm fires in people with panic disorder earlier than it should. Therefore, people with panic disorder will frequently experience breathlessness as their respiratory mechanisms try to keep their CO2 levels lower and even a relatively minor increase in CO2 can trigger a suffocation alarm (panic attack).

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