result of a medical disorder. Cognitive behavioral therapy (CBT) is effective for anxiety disorders and is a first line treatment. CBT appears to be equally effective when carried out via the internet. While evidence for mental health apps is promising, it is preliminary. Psychopharmacological treatment can be used in parallel to CBT or can be used alone. As a general rule, most anxiety disorders respond well to first-line agents. Such drugs, also used as anti-depressants, are the selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors, that work by blocking the reuptake of specific neurotransmitters and resulting in the increase in availability of these neurotransmitters. Additionally, benzodiazepines are often prescribed to individuals with anxiety disorder. Benzodiazepines produce an anxiolytic response by modulating GABA and increasing its receptor binding. A third common treatment involves a category of drug known as serotonin agonists. This category of drug works by initiating a physiological response at 5-HT1A receptor by increasing the action of serotonin at this receptor. Other treatment options include pregabalin, tricyclic antidepressants, and moclobemide, among others. Anxiety is considered to be a serious psychiatric illness that has an unknown true pervasiveness due to affected individuals not asking for proper treatment or aid, and due to professionals missing the diagnosis. Prevention The above risk factors give natural avenues for prevention. A 2017 review found that psychological or educational interventions have a small yet statistically significant benefit for the prevention of anxiety in varied population types. Pathophysiology Anxiety 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. In the central nervous system (CNS), the major mediators of the symptoms of anxiety disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). Other neurotransmitters and peptides, such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic nervous system, mediates many of the symptoms. Increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients are the diagnostic factors for prevalence of anxiety disorder. The amygdala is central to the processing of fear and anxiety, and its function may be disrupted in anxiety disorders. Anxiety processing in the basolateral amygdala has been implicated with expansion of dendritic arborization of the amygdaloid neurons. SK2 potassium channels mediate inhibitory