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Behavioral therapy

In cognitive behavioral therapy (CBT) along with the use of drugs (imipramine), the application of both imipramine and CBT varies significantly with the use of placebos. Imipramine alone was seen to produce a higher quality of response but the combination of imipramine and CBT appears offer a more substantial advantage in the long run (Barlow, Gorman, Shear & Woods, 2000). In a classical conditioning approach to panic disorder, a noxious stimulus like a panic attack that occurs within a neutral stimulus like a bus ride or an elevator ride can result in the avoidance of the neutral stimulus (Sadock, Kaplan & Sadock, 2007).

An additional behavioral model offers that panic attacks arise when people recognize some somatic sensations to be significantly more perilous than they actually are; they then proceed to interpret this as a sign of imminent disaster. For instance some may misinterpret nervous, trembling sensibilities as indications of impending insanity. A criticism to this approach is the fact that those who suffer from panic disorders still misinterpret somatic symptoms even if the predicted imminent catastrophes do not occur.

But because these people take precautions to thwart the event of an attack, they do not actually realize that panic attacks will

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not conclude to catastrophic incidents. Biological models suggest that the range of biological abnormalities in brain structure and function coincide with the symptoms of panic disorders. Studies show that individuals having temporal lobe aberrations were notably younger during the start of panic disorder and have had more panic attacks as compared to individuals with healthy MRI scans; this indicates that panic disorder can possibly result to temporal lobe damage.

Respiration is predominantly unstable in panic disorder, which underlines the magnitude of respiratory structure and physiology in comprehending this disorder. It has also been observed that panic disorder and coronary artery disease (CAD) are linked in non-cardiology situations, and persistent panic attacks can actually be the cause of CAD, detection of any of the two conditions generally leads the physician to consider the other (Katerndahl, 2004).

Evidence indicates that the abnormal regulation of brain noradrenergic systems is involved in the pathophysiology of panic disorder (Sadock, et al. , 2007). The major neurotransmitter systems that have been implicated are those for norepinephrine, serotonin and y-aminobutyric acid (GABA). Serotonin dysfunction is quite evident in panic disorder and various studies with mixed serotonin agonist-antagonist drugs have demonstrated increased rates of anxiety, such responses may be caused by postsynaptic serotonin hypersensitivity in panic disorders (Sadock, et al. , 2007).

It has been seen that the delivery of evidence-based cognitive behavioral therapy (CBT) and medication using the collaborative care model and the presence of a CBT-naive, midlevel behavioral health specialist is practical and comparatively more effective than usual care for primary care panic disorder (Roy-Byrne, Craske, Stein, Sullivan, Bystritsky, Katon, Golinelli & Sherbourne, 2005).

Existing proofs imply that CBT and pharmacotherapy which specifically include, selective serotonin reuptake inhibitors or serotonin-nor epinephrine reuptake inhibitors are effective front-line agents and that CBT presents a significant cost effectiveness relative to both pharmacotherapy on its own and joint pharmacotherapy and CBT (McHugh, Smits, & Otto, 2009).

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