Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011551 (depersonalization)
 1,117 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Do patients with borderline personality disorder (BPD) display psychotic symptoms as part of their syndrome? This question has important theoretical significance, since it bears on the question of whether BPD lies 'on the border' of psychotic functioning, or whether it is unrelated to psychotic disorders. A review of available evidence suggests that 'narrowly defined' psychotic symptoms, such as those included under the DSM-III definition of psychosis, are rare in BPD. Furthermore, when such symptoms have been reported in BPD, they may have been attributable to a concomitant, possibly independent, disorder suffered by the patient, such as substance abuse or major affective disorder. Broadly defined psychotic symptoms, such as depersonalization, are much more often reported in BPD, but many of these symptoms have also been reported frequently in patients with non-psychotic disorders and in normals. Finally, the prevalence of factitious psychotic symptoms in BPD has not been systematically investigated. Thus, the evidence for psychotic symptoms in BPD remains equivocal.
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PMID:Psychosis in borderline personality disorder. 639 40

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
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PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14

According to the ICD 10 only acute psychotic disorders and transitory acute disorders are specified, whereas DSM IV index, in the same class, schizophreniform disorder, schizoaffectif disorder and atypical psychosis. State biological markers of these disorders are present during the acute episode and disappear with it. A few studies concerns trait predispositional markers of these acute psychotic disorders. In addition, several studies of acute psychotic states are indexed as a partition of usual schizophrenic disorder, as a simple occurrence of that chronic disease. From the biological point of view, dysfunctions of norepinephrine and dopaminergic metabolisms are reported within these acute schizophrenic disorganisation, especially hyperdopaminergia, causality, consequence or evidence of the state syndrome. Those kinds of data are also reported in mood disorder with delusional symptoms. A hypothetic dysregulation of the balance between oxydation and antioxydation system has been searched in these acute states of schizophrenia. From the electrophysiologic perspective, no abnormalities are found for ocular movement functions during these acute psychotic disorders. Besides the clouding of consciousness of confusional states, neuropsychological abnormalities are reported: attention disorders, lack of inhibition of non relevant informations, abnormalities of working memory. Brain imaging can substantiate a diminution of the caudate nucleus size and a possible increase of D2 receptors number. Also, in these acute psychotic states abnormalities of humoral and cellular immunologic system have been found. Lastly, street drugs can originate confusional states and depersonalization, through their serotoninergic, dopaminergic and anticholinergic properties. Ethical drugs can also create an acute psychosis disorder: individual vulnerability and somatic disease cooccurrence act as risk-factors.
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PMID:[Biological approaches to acute psychoses]. 1059 92

The phenomenology of dissociative disorders may be complex and sometimes confusing. We describe here two cases who were initially misdiagnosed. The first case concerned a 61 year-old woman, who was initially diagnosed as an isolated dissociative fugue and was actually suffering from severe major depressive episode. The second case concerned a 55 year-old man, who was suffering from type I bipolar disorder and polyvascular disease, and was initially diagnosed as dissociative fugue in a mooddestabilization context, while it was finally a stroke. Yet dissociative disorders as affective disorder comorbidity are relatively unknown. We made a review on this topic. Dissociative disorders are often studied through psycho-trauma issues. Litterature is rare on affective illness comorbid with dissociative disorders, but highlight the link between bipolar and dissociative disorders. The later comorbidity often refers to an early onset subtype with also comorbid panic and depersonalization-derealization disorder. Besides, unipolar patients suffering from dissociative symptoms have more often cyclothymic affective temperament. Despite the limits of such studies dissociative symptoms-BD association seems to correspond to a clinical reality and further works on this topic may be warranted.
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PMID:[Dissociative disorders and affective disorders]. 2555 Feb 42

This study inquires into neurobiological response to stress and its clinical correlates among adolescents with post-traumatic stress disorder (PTSD). Structural magnetic resonance imaging (MRI) measures of cerebral anatomy were carried out on 23 female adolescents with PTSD related to severe childhood sexual abuse and 21 matched healthy controls. Clinician Administered PTSD Scale for Children and Adolescents, Adolescent Dissociative Experiences Scale, Childhood Trauma Questionnaire, Schedule for Affective Disorders and Schizophrenia for School Age Children, Beck Depression Scale, and a set of neuro-cognitive tests were administered to all participants. Compared to controls, PTSD group bilaterally had smaller amygdala, hippocampus, anterior cingulate, and thinner prefrontal cortex but normal thalamus. Further analyses within the PTSD group suggested an association between symptoms of PTSD and sizes of right brain structures including smaller amygdala but larger hippocampus and anterior cingulate. Thinner right prefrontal cortex and larger right thalamus seemed to be related to denial and response prevention, respectively. Being related to both hemispheres, dissociative amnesia was negatively associated with proportion of the right amygdala to right thalamus and to both left and right prefrontal cortex. Suggesting a neuro-protective effect against traumatic stress at least through adolescence, depersonalization-derealization and identity alteration were correlated with thicker left prefrontal cortex. Unlike the lateralization within PTSD group, correlations between regions of interest were rather symmetrical in controls. The graded response to stress seemed to be aimed at mental protection by lateralization of brain functions and possibly diminished connection between two hemispheres. A Tri-Modal Reaction (T-MR) Model of protection is proposed.
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PMID:Lateralization of Neurobiological Response in Adolescents with Post-Traumatic Stress Disorder Related to Severe Childhood Sexual Abuse: the Tri-Modal Reaction (T-MR) Model of Protection. 2828 21

How deep are the historical roots of our concept of major depression (MD)? I showed previously that psychiatric textbooks published in 1900-1960 commonly described 18 characteristic depressive symptoms/signs that substantially but incompletely overlapped with the current DSM (Diagnostic and Statistical Manual of Mental Disorders) MD criteria. I here expand that inquiry to the key years of 1880-1900 during which our major diagnostic categories of manic-depressive illness (MDI) and dementia praecox were developed. I review the symptoms of depression/melancholia in 28 psychiatric textbooks and 8 other relevant documents from this period including monographs, reviews and the first portrayal of melancholia Kraepelin in 1883. Descriptions of melancholia in the late nineteenth and twentieth century textbooks closely resembled each other, both reporting a mean of 12.4 characteristic symptoms, and emphasizing core features of mood change and alterations in cognitive content and psychomotor behavior. The detailed monographs, reviews and the early description of Kraepelin were more thorough, reporting a mean of 16.6 of these characteristic symptoms. These nineteenth century texts often contained phenomenologically rich descriptions of changes in mood and cognition, loss of interest and anhedonia and emphasized several features not in DSM including changes in volition/motivation, posture/facial expression and derealization/depersonalization. In the early nineteenth century, melancholia was often defined primarily by delusions or as the initial phase of a unitary psychosis transitioning to mania and then dementia. By 1880, the concept of depression as an independent mood disorder with characteristic symptoms/signs and a good prognosis had stabilized. Kraepelin incorporated this syndrome into his diagnostic concept of MDI, changing its name to 'Depressive States', but did not alter its underlying nature or clinical description.
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PMID:The genealogy of major depression: symptoms and signs of melancholia from 1880 to 1900. 2878 9