Clinical meaning
Anxiety disorders involve dysregulation of the fear circuitry centered on the amygdala, prefrontal cortex, and hippocampus. In generalized anxiety disorder (GAD), the amygdala is hyperresponsive to ambiguous stimuli while prefrontal cortex top-down inhibition is impaired, resulting in chronic, excessive, uncontrollable worry. GABAergic inhibitory neurotransmission is deficient (explaining benzodiazepine efficacy), and serotonergic modulation from the dorsal raphe to the amygdala is disrupted (explaining SSRI/SNRI efficacy). GAD diagnostic criteria require excessive anxiety and worry about multiple events/activities for ≥ 6 months with ≥ 3 somatic symptoms (restlessness, fatigue, concentration difficulty, irritability, muscle tension, sleep disturbance). In panic disorder, the locus coeruleus noradrenergic system generates 'false alarm' responses with sudden autonomic activation: recurrent unexpected panic attacks (palpitations, sweating, trembling, dyspnea, chest pain, derealization, fear of dying/losing control) reaching peak intensity within minutes. The NP differentiates panic attacks from cardiac, endocrine (pheochromocytoma, hyperthyroidism), respiratory, and substance-induced causes. Treatment integrates pharmacotherapy (SSRIs/SNRIs first-line for both; benzodiazepines short-term for panic) with cognitive-behavioral therapy (CBT), which has the strongest evidence base for anxiety disorders and addresses catastrophic cognitions and avoidance behaviors.