An interaction between biophysical factors and traumatic situations may cause anxiety disorders. Neurotransmitters of the central nervous system like norepinephrine and serotonin, peptides like corticotropin-releasing factor are the major mediators for the cause of anxiety disorder.
Low levels of GABA, a neurotransmitter that reduces activity in the central nervous system, contribute to anxiety. A number of anxiolytics achieve their effect by modulating the GABA receptors. Selective serotonin reuptake inhibitors, the drugs most commonly used to treat depression, are frequently considered as a first line treatment for anxiety disorders. A 2004 study using functional brain imaging techniques suggests that the effects of SSRIs in alleviating anxiety may result from a direct action on GABA neurons rather than as a secondary consequence of mood improvement. Severe anxiety and depression can be induced by sustained alcohol abuse which in most cases abates with prolonged abstinence. Even moderate, sustained alcohol use may increase anxiety and depression levels in some individuals. Caffeine, alcohol and benzodiazepine dependence can worsen or cause anxiety and panic attacks. Anxiety commonly occurs during the acute withdrawal phase of alcohol and can persist for up to 2 years as part of a post-acute withdrawal syndrome, in about a quarter of people recovering from alcoholism. In one study in 1988–1990, illness in approximately half of patients attending mental health services at one British hospital psychiatric clinic, for conditions including anxiety disorders such as panic disorder or social phobia, was determined to be the result of alcohol or benzodiazepine dependence. In these patients, an initial increase in anxiety occurred during the withdrawal period followed by a cessation of their anxiety symptoms.
There is evidence that chronic exposure to organic solvents in the work environment can be associated with anxiety disorders. Painting, varnishing and carpet-laying are some of the jobs in which significant exposure to organic solvents may occur. People with obsessive-compulsive disorder (sometimes considered an anxiety disorder), evince increased grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, while decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. These findings contrast with those in people with other anxiety disorders, who evince decreased (rather than increased) grey matter volumes in bilateral lenticular/caudate nuclei, while also decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. Ingestion of caffeine may cause or exacerbate anxiety disorders. A number of clinical studies have shown a positive association between caffeine and anxiogenic effects and/or panic disorder. Anxiety sufferers can have high caffeine sensitivity.
The amygdala is central to the processing of fear and anxiety, and its function may be disrupted in anxiety disorders. Sensory information enters the amygdala through the nuclei of the basolateral complex (consisting of lateral, basal, and accessory basal nuclei). The basolateral complex processes sensory-related fear memories and communicates their threat importance to memory and sensory processing elsewhere in the brain, such as the medial prefrontal cortex and sensory cortices. Another important area is the adjacent central nucleus of the amygdala, which controls species-specific fear responses, via connections to the brainstem, hypothalamus, and cerebellum areas. In those with general anxiety disorder, these connections functionally seem to be less distinct, with greater gray matter in the central nucleus. Another difference is that the amygdala areas have decreased connectivity with the insula and cingulate areas that control general stimulus...
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