The neuroanatomy of<unk>  largely overlaps with that of most anxiety disorders. Neuropsychological, neurosurgical, and neuroimaging studies implicate the insula, amygdala, hippocampus, anterior cingulate cortex (ACC), lateral prefrontal cortex, and periaqueductal grey. During acute<unk>  attacks, viewing emotionally charged words, and rest, most studies find elevated blood flow or metabolism. However, the observation of amygdala hyperactivity is not entirely consistent, especially in studies that evoke<unk>  attacks chemically. Hippocampus hyperactivity has been observed during rest and viewing emotionally charged pictures, which has been hypothesized to be related to memory retrieval bias towards anxious memories. Insula hyperactivity during the onset of and over the course of acute<unk>  episodes is thought to be related to abnormal introceptive processes; the perception that bodily sensations are "wrong" is a transdiagnostic finding(i.e. found across multiple anxiety disorders), and may be related to insula dysfunction. Rodent and human studies heavily implicate the periaqueductal grey in generating fear responses, and abnormalities related to the structure and metabolism in the PAG have been reported in<unk> . The frontal cortex is implicated in<unk>  by multiple lines of evidence. Damage to the dorsal ACC has been reported to lead to<unk> . Elevated ventral ACC and dorsolateral prefrontal cortex during symptom provocation and viewing emotional stimuli have also been reported, although findings are not consistent. Researchers studying some individuals with<unk>  propose they may have a chemical imbalance within the limbic system and one of its regulatory chemicals GABA-A. The reduced production of GABA-A sends false information to the amygdala which regulates the body's "fight or flight" response mechanism and, in return, produces the physiological symptoms that lead to the disorder. Clonazepam, an anticonvulsant benzodiazepine with a long half-life, has been successful in keeping the condition under control. Recently, researchers have begun to identify mediators and moderators of aspects of<unk> . One such mediator is the partial pressure of carbon dioxide, which mediates the relationship between<unk>  patients receiving breathing training and anxiety sensitivity; thus, breathing training affects the partial pressure of carbon dioxide in a patient's arterial blood, which in turn lowers anxiety sensitivity. Another mediator is hypochondriacal concerns, which mediate the relationship between anxiety sensitivity and<unk>  symptomatology; thus, anxiety sensitivity affects hypochondriacal concerns which, in turn, affect<unk>  symptomatology. Perceived threat control has been identified as a moderator within<unk> , moderating the relationship between anxiety sensitivity and agoraphobia; thus, the level of perceived threat control dictates the degree to which anxiety sensitivity results in agoraphobia. Another recently identified moderator of<unk>  is genetic variations in the gene coding for galanin; these genetic variations moderate the relationship between females suffering from<unk>  and the level of severity of<unk>  symptomatology.
Panic disorder
Hyperthyroidism
Depression 
Cardiovascular disease
Late life depression
Hypochondriasis
Blood phobia
Anxiety disorder