Social anxiety disorder
Panic disorder appears to be a genetically inherited neurochemical dysfunction that may involve autonomic imbalance; decreased GABA-ergic tone; allelic polymorphism of the catechol-O-methyltransferase (COMT) gene; increased adenosine receptor function; increased cortisol; diminished benzodiazepine receptor function; and disturbances in serotonin, serotonin transporter (5-HTTLPR) and promoter (SLC6A4) genes, norepinephrine, dopamine, cholecystokinin, and interleukin-1-beta. Some theorize that panic disorder may represent a state of chronic hyperventilation and carbon dioxide receptor hypersensitivity. Some epileptic patients have panic as a manifestation of their seizures. Genetic studies suggest that the chromosomal regions 13q, 14q, 22q, 4q31-q34, and probably 9q31 may be associated with the heritability of panic disorder phenotype.
The cognitive theory regarding panic is that patients with panic disorder have a heightened sensitivity to internal autonomic cues (eg, tachycardia). Triggers of panic can include the following:
- Interpersonal conflict or loss
- Use of cannabis (can be associated with panic attacks, perhaps because of breath-holding)
- Use of stimulants, such as caffeine, decongestants, cocaine, and sympathomimetics (eg, amphetamine, MDMA ["ecstasy"])
- Certain settings, such as stores and public transportation (especially in patients with agoraphobia)
- Sertraline can induce panic in previously asymptomatic patients.
- The SSRI discontinuation syndrome can induce symptoms similar to those experienced by panic patients.
In experimental settings, symptoms can be elicited in people with panic disorder by hyperventilation, inhalation of carbon dioxide, caffeine consumption, or intravenous infusions of hypertonic sodium lactate or hypertonic saline, cholecystokinin, isoproterenol, flumazenil, or naltrexone. The carbon dioxide inhalation challenge is especially provocative of panic symptoms in smokers.
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