Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depersonalization disorder is classified in DSM-III-R (APA 1987) as a dissociative disorder characterized by altered perception or experience of the self. To date, there are no known reports of the neurobiological features of this disorder. We report clinical and biological correlates in a patient with depersonalization disorder previously unresponsive to a variety of anticonvulsant, monoamine oxidase inhibitor, and tricyclic antidepressant trials, but for whom fluoxetine partially reduced depersonalization symptoms, but not associated anxiety and depression. Neurophysiological, neuroanatomical and neuropsychological findings revealed left hemispheric frontal-temporal activation and decreased left caudate perfusion. These findings suggest a similarity to the neuropsychiatric data reported in obsessive-compulsive disorder patients.
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PMID:Left hemispheric activation in depersonalization disorder: a case report. 152 79

Depersonalisation disorder may occur during severe anxiety or following a traumatic event, suggesting a possible role of stress hormones. This study investigated basal activity of the hypothalamic-pituitary-adrenal (HPA) axis in patients with depersonalisation disorder. Salivary cortisol levels were measured at four time points over 12 h in patients with depersonalisation disorder (N=13), major depressive disorder (MDD, N=14) and healthy controls (N=13). Beck Depression Inventory scores were significantly higher in depersonalised subjects than controls, while MDD subjects demonstrated higher scores than both groups. Basal cortisol levels of depersonalised subjects were significantly lower than those of MDD subjects but not healthy controls. These results point to reduced basal activity of the HPA axis in depersonalisation disorder. This pilot study supports the distinction between depersonalisation disorder and major depressive disorder which should be examined in a larger sample.
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PMID:Basal activity of the hypothalamic-pituitary-adrenal axis in patients with depersonalization disorder. 1160 Jan 92

Depersonalisation disorder is characterised by prominent depersonalisation and often derealisation, without clinically notable memory or identity disturbances. The disorder has an approximately 1 : 1 gender ratio with onset at around 16 years of age. The course of the disorder is typically long term and often continuous. Mood, anxiety and personality disorders are often comorbid with depersonalisation disorder but none predict symptom severity. 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. A variety of psychotherapeutic techniques has been used to treat depersonalisation disorder (including trauma-focused therapy and cognitive-behavioural techniques), although again none of these have established efficacy to date. Overall, novel therapeutic approaches are clearly needed to help individuals experiencing this refractory disorder.
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PMID:Depersonalisation disorder: a contemporary overview. 1508 2

Depersonalization disorder is considered to be a common clinical phenomenon and disorder with an enormous gap between prevalence and detection partly due to the common interpretation of depersonalization (DP) being a negligible variant of anxiety and depression. Therefore, we sought to analyze (1) the prevalence rate of DP in a large community sample (n=5000) according to a recently developed ultra brief two-item depersonalization screener; (2) the associations with depression, anxiety, physical and mental health status; and 93) whether DP contributes independently to the health status beyond anxiety and depression. The prevalence of clinically significant DP was 0.8% (n=41), and 8.5% (n=427) endorsed at least one symptom of DP. DP was independently associated with impairment of mental and physical health status as well as with a medical history of any depressive or anxiety disorder. Despite the consistent association of DP with anxiety and depression, the shared variances were small, and DP was clearly separated from symptoms of anxiety and depression in the principal component analysis. Therefore, we conclude that the implementation of depersonalization screening might be recommended.
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PMID:Distinctiveness and overlap of depersonalization with anxiety and depression in a community sample: results from the Gutenberg Heart Study. 2112 25

Low-dose ketamine administration mimics, both clinically and on gross neuroimaging, depersonalization disorder. The perceptual effects of ketamine may be due to secondary stimulation of glutamate release and lamotrigine, possibly by inhibited glutamate release, may reduce some of ketamine's so-called dissociative effects. However, lamotrigine does not seem to be useful in the treatment of depersonalization disorder. Glutamate release in prefrontal cortex is increased by subanaesthetic doses of ketamine, resulting in increased inhibition, possibly via intercalated GABAerg cells, of projections from amygdala, affecting structures critically involved in depersonalization. I speculate that, in depersonalization disorder, the increased glutamate activity in prefrontal cortex is due to intrinsic imbalance, resulting in long-term potentiation, at the postsynaptic glutamate receptors on the GABAerg interneurons while the same receptor abnormality at the synapses on the intercalated GABAerg cells of the amygdala result in long-term depression in the case of either normal or high glutamate release.
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PMID:Depersonalization disorder may be related to glutamate receptor activation imbalance. 2174 42

Depersonalization is a frequent symptom in depression and obsessive-compulsive disorder (OCD), but sometimes, it may be severe and concurrently diagnosed as a disorder. The treatment of depersonalization disorder both alone and comorbid with other psychiatric disorders is as yet unclear. This report presents the successful treatment with aripiprazole of concurrent depersonalization disorder in 3 patients with depression or OCD. The psychiatric disorders were diagnosed through structured clinical interviews. Assessments were by means of Yale-Brown Obsessive-Compulsive Scale, the Clinical Global Impression-Improvement Scale, and the 17-item Hamilton Rating Scale for Depression. Aripiprazole may be a beneficial psychotropic drug in the treatment of depersonalization disorder comorbid with OCD or depression, which is an important problem in clinical practice.
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PMID:Aripiprazole in depersonalization disorder comorbid with major depression and obsessive-compulsive disorder: 3 cases. 2499 87

Case reports and an open trial have reported promising responses to repetitive transcranial magnetic stimulation (rTMS) to prefrontal and temporo-parietal sites in patients with depersonalization disorder (DPD). We recently showed that a single session of rTMS to the ventrolateral prefrontal cortex (VLPFC) was associated with a reduction in symptoms and increase in physiological arousal. Seven patients with medication-resistant DSM-IV DPD received up to 20 sessions of right-sided rTMS to the VLPFC for 10 weeks. Stimulation was guided using neuronavigation software based on participants' individual structural MRIs, and delivered at 110% of resting motor threshold. A session consisted of 1Hz repetitive TMS for 15min. The primary outcome measure was reduction in depersonalization symptoms on the Cambridge Depersonalization Scale (CDS). Secondary outcomes included scores on the Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI). 20 sessions of rTMS treatment to right VLPFC significantly reduced scores on the CDS by on average 44% (range 2-83.5%). Two patients could be classified as "full responders", four as "partial" and one a non-responder. Response usually occurred within the first 6 sessions. There were no significant adverse events. A randomized controlled clinical trial of VLPFC rTMS for DPD is warranted.
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PMID:Ventrolateral prefrontal cortex repetitive transcranial magnetic stimulation in the treatment of depersonalization disorder: A consecutive case series. 2710 26

High frequency repetitive transcranial magnetic stimulation (rTMS) was approved by the US Food and Drug Administration in 2008 to treat major depressive disorder in those who did not respond to at least 1 antidepressant trial. Previous studies have shown that both high frequency rTMS to the left dorsolateral prefrontal cortex (DLPFC) and low frequency rTMS to the right DLPFC have antidepressant efficacy in treatment-resistant depression. Although rTMS has been widely used in the treatment of depression, very few studies of rTMS in patients with depersonalization disorder (DPD) have been published so far. DPD involves persistent or recurrent experiences of unreality and feelings of detachment causing distress or functional impairment while insight remains intact. The prevalence of DPD is approximately 1% to 2%. Studies of the pharmacological treatment of DPD are limited, and medications have proven to be of limited benefit. We present the case of a 30-year-old man with major depressive disorder and DPD who did not respond to pharmacotherapy. After the patient was treated with low frequency rTMS to the right DLPFC followed by high frequency rTMS to the left DLPFC, there was a significant reduction in his depersonalization symptoms. Given its effectiveness in our patient, the use of both low frequency rTMS to the right DLPFC and high frequency rTMS to the left DLPFC for treatment of DPD should be further explored.
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PMID:Treatment of Depersonalization Disorder With Repetitive Transcranial Magnetic Stimulation. 2829 Oct 42