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Statistics: The statistics related to Somatic symptom disorder, The SSD-12 has good item characteristics and excellent reliability (Cronbach α = .95). Confirmatory factor analyses suggested that a three-factorial structure that reflects the three psychological criteria interpreted as cognitive, affective, and behavioral aspects (n = 663, Comparative Fit Index > 0.99, Tucker-Lewis Index > 0.99, Root Mean Square Error of Approximation = 0.06, 90% confidence interval = 0.01-0.08). SSD-12 total sum score was significantly associated with somatic symptom burden (r = 0.47, p < .001) and health anxiety (r = 0.71, p < .001), and moderately associated with general anxiety (r = 0.35, p < .001) and depressive symptoms (r = 0.22, p < .001). Patients with a higher SSD-12 psychological symptom burden reported higher general physical and mental health impairment and significantly higher health care use.
Pathophysiology: Depersonalization disorder is one of a group of conditions called dissociative disorders. Dissociative disorders are mental illnesses that involve disruptions or breakdowns of memory, consciousness, awareness, identity, and/or perception. When one or more of these functions is disrupted, symptoms can result. These symptoms can interfere with a person's general functioning, including social and work activities and relationships. Depersonalization disorder is marked by periods of feeling disconnected or detached from one's body and thoughts (depersonalization). The disorder is sometimes described as feeling like you are observing yourself from outside your body or like being in a dream. However, people with this disorder do not lose contact with reality; they realize that things are not as they appear.
Treatment: Most people with depersonalization disorder who seek treatment are concerned about symptoms such as depression or anxiety, rather than the disorder itself. In many cases, the symptoms will go away over time. Treatment usually is needed only when the disorder is lasting or recurrent, or if the symptoms are particularly distressing to the person. The best treatment approach depends on the individual and the severity of his or her symptoms, but most likely will include some combination of the treatment methods including psychotherapy, cognitive therapy, medication, family therapy, Creative therapies (art therapy, music therapy), clinical hipnosis, etc
Major research on disease: The most common immediate precipitants of the disorder are severe stress, depression and panic, and marijuana and hallucinogen ingestion. Depersonalisation disorder has also been associated with childhood interpersonal trauma, in particular emotional maltreatment. Neurochemical findings have suggested possible involvement of serotonergic, endogenous opioid and glutamatergic NMDA pathways. Brain imaging studies in depersonalisation disorder have revealed widespread alterations in metabolic activity in the sensory association cortex, as well as prefrontal hyperactivation and limbic inhibition in response to aversive stimuli. Depersonalisation disorder has also been associated with autonomic blunting and hypothalamic-pituitary-adrenal axis dysregulation. To date, treatment recommendations and guidelines for depersonalisation disorder have not been established. There are few studies assessing the use of pharmacotherapy in this disorder. Medication options that have been reported include clomipramine, fluoxetine, lamotrigine and opioid antagonists. However, it does not appear that any of these agents have a potent anti-dissociative effect.