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)

The author investigated neurotic symptoms of borderline patients by reviewing the clinical charts of twenty-six patients of longer than one year treatment period (8 men, 18 women; 23 patients with DSM III-R borderline personality disorder (BPD), 14 with schizotypal personality disorder (SPD), (11 BPD-SPD overlaps); age at the first contact: mean = 24.3 y. o., SD = 6.7 y. o.; treatment period: mean = 51 months, SD = 35 months). The diagnoses of the comorbid neurotic disorders were obsessive compulsive disorder: 5 cases (19% (BPD: 22%, SPD: 7%)), somatoform disorder: 5 (19% (BPD: 22%, SPD: 21%)), panic disorder: 4 (15% (BPD: 17%, SPD: 14%)), social phobia: 2 (8% (BPD: 9%, SPD: 7%)), dissociative disorder: 2 (8% (BPD: 9%, SPD: 0%)), and generalized anxiety disorder: 1 (4% (BPD: 4%, SPD: 7%)). The neurotic symptoms identified in the charts of the subjects were as follows; symptoms of social phobia: 11 cases (42% (BPD: 43%, SPD: 43%)) including 6 with anthropophobic symptoms (23% (BPD: 26%, SPD: 36%)), obsessive compulsive symptoms and diffuse and floating anxiety: 9 (35% (BPD: 39%, SPD: 38%)), panic attacks: 8 (31% (BPD: 35%, SPD: 36%)), conversion symptoms: 7 (27% (BPD: 30%, SPD: 21%)), dissociative episodes: 6 (23% (BPD: 26%, SPD: 7%)), depersonalization: 5 (19% (BPD: 22%, SPD: 14%)), multiple apprehensive expectations: 4 (15% (BPD: 17%, SPD: 14%)), derealization: 3 (12% (BPD: 13%, SPD: 14%)), hyperventilation attacks: 3 (12% (BPD: 13%, SPD: 7%)), and somatization: 1 (4% (BPD: 4%, SPD: 7%)). In short, 54% (BPD: 61%, SPD: 43%) of the subjects had comorbid neurotic disorders, and 92% (BPD: 91%, SPD: 93%) reported at least one, and 54% (BPD: 61%, SPD: 50%), more than two kinds of neurotic symptoms, though no specific symptom correlating with BPD or SPD diagnosis was found. These findings suggest that neurotic symptoms and neurotic disorders cannot be ignored as peripheral in the borderline symptomatology. By analyzing in detail the neurotic experiences, the author pointed out as their characteristics, ego syntonicity, deterioration of reality sense and symptomatic polymorphism, ambiguity and multiplicity (panneurosis). In the symptoms the author observed signs of defective personality functioning such as disavowal of reality, low anxiety tolerance, various forms of identity disturbances. The findings counted above, suggest that the borderline neurotic symptoms are more severe in nature than those of neurotics, and could be situated in between neurotic and psychotic levels of symptomatic severity. The results indicate that the neurotic experiences of borderline patients are, as a whole, deeply ingrained in the borderline psychopathology.
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PMID:[Neurotic symptoms of borderline patients: a case review study]. 143 98

In order to examine the validity of the distinction between generalized anxiety disorder (GAD) and panic disorder (PD) we compared 41 subjects with GAD and 71 subjects with PD. The GAD subjects had never had panic attacks. In contrast to the symptom profile in PD subjects suggestive of autonomic hyperactivity, GAD subjects had a symptom pattern indicative of central nervous system hyperarousal. Also, subjects with GAD had an earlier, more gradual onset of illness. In terms of coexisting syndromes, GAD subjects more often had simple phobias, whereas PD subjects more commonly reported depersonalization and agoraphobia. GAD subjects more frequently had first-degree relatives with GAD, whereas PD subjects more frequently had relatives with PD. A variety of measures indicated that our GAD subjects had a milder illness than those with PD. Also, fewer GAD subjects gave histories of major depression than did PD subjects. Among GAD subjects, coexisting major depression was associated with simple phobia and thyroid disorders and among PD subjects, comorbid depression was associated with social phobia and hypertension. Our findings indicate that the separation of GAD from PD is a valid one. They also indicate that, within disorders, unique patterns of comorbidity may exist that are important both clinically and theoretically.
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PMID:Generalized anxiety disorder vs. panic disorder. Distinguishing characteristics and patterns of comorbidity. 143 31

One hundred fifty patients with Panic Disorder (PD) with or without Phobic Avoidance were subdivided into two groups on the basis of presence/absence of derealization and/or depersonalization (D-D) during panic attacks. D-D was found in 34.7% of the sample. By comparing the two groups, the patients with D-D were found to be younger and had an earlier onset of the disorder; they had a higher prevalence of avoidance behavior and a higher severity of the agoraphobic spectrum phobias. They were also more frequently subject to concomitant disorders such as Generalized Anxiety, Obsessive-Compulsive, and depressive symptomatology. The authors have hypothesized a correlation between the presence of D-D during panic attacks and a more frequent clinical evolution toward agoraphobia. This view is supported by finding that D-D in panic attacks corresponds to severer forms of PD, both in terms of the earlier onset of PD, and because PD shows higher levels of anxiety, depression, and disability.
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PMID:Derealization and panic attacks: a clinical evaluation on 150 patients with panic disorder/agoraphobia. 292 66

This paper reviews anxiety, panic, and phobic disorders as they were described in landmark works, along with more recent epidemiologic studies of the disorders. The author discusses clinical syndromes of anxiety as outlined in the DSM-III: agoraphobia, social phobia, generalized anxiety disorder, panic disorder, simple phobic states, and obsessive-compulsive disorder, relating them to Phobic Anxiety-Depersonalization Syndrome and to earlier descriptions by Westphal and Benedict. The paper addresses the problem of delineating anxiety and phobic states from depressive disorders, with regard to diagnosis and treatment outcome. Various etiological bases of agoraphobia, panic, and anxiety disorders are suggested: heredity, life events and circumstances, family background and developmental history, the premorbid personality, and some psychological aspects. Several questions are explored on the relationships of agoraphobia, anxiety and panic attacks. For example, is agoraphobia a new disease or one stage in the development of severe chronic anxiety? Are the phobias of agoraphobia acquired by conditioning or learning? Are "panics" spontaneous or physiological? Are panic attacks the first event in the primary cause of agoraphobia? For future work the authors propose a reassessment of the prevalence of agoraphobia and related disorders, a more careful definition of the agoraphobic disorders, and thorough clinical investigation of the various treatment modalities in well-defined populations. The past twenty years' achievements in behavioural and pharmacological treatments for agoraphobia are briefly recapitulated.
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PMID:Anxiety, panic and phobic disorders: an overview. 305 59

Panic disorder is a subtype of anxiety manifested by discrete periods of apprehension or fear and at least four of the following somatic symptoms: dyspnea, palpitations, chest pain, choking, dizziness, depersonalization or derealization experience, paresthesias, hot and cold flashes, sweating, faintness, trembling, and fear of dying, going crazy, or doing something uncontrolled during an attack. Because the patient with panic disorder often selectively focuses on one of these somatic symptoms and may minimize or deny psychosocial distress, panic disorder is frequently misdiagnosed. As a result of the frightening nature of the symptoms, a pattern of overutilization of medical care systems frequently ensues. Panic disorder is usually precipitated by stressful life events, most commonly separation or loss, in a patient with a genetic or acquired vulnerability. As with other psychophysiologic illness (depression, duodenal ulcer) resolution of the acute stressful life event may not lead to resolutions of the physiologic changes. Two specific tricyclic antidepressants, imipramine and desipramine, have been shown to be effective therapeutic agents in treating panic disorder.
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PMID:Panic disorder. 663 52

The present study evaluated the efficacy of three tasks in inducing depersonalization (DP) and derealization (DR) in three different groups: (a) panic disorder patients who report these symptoms while panicking (PD + DD; n = 10); (b) panic disorder patients never experiencing these symptoms during panic attacks (PD; n = 10); and (c) nonanxious controls (NC; n = 10). Clinical features of the PD+DD and PD Ss were compared as well. Relative to PD Ss, PD + DD Ss evidenced higher levels of depression, trait anxiety, more fear of panic, and had a briefer duration of their disorder. A substantial proportion of NC Ss reported past DP and DR experiences. DP and DR induction procedures were the following: staring at a dot on the wall, staring in a mirror, and silent repetition of one's name. Results indicated two tasks (mirror and dot) successfully elicited these sensations above baseline levels with DP reported more frequently and intensely than DR for all Ss. The PD + DD Ss evidenced greater baseline-to-task increases in DP and DR relative to the other two groups and exhibited a differential fear response, particularly on the dot task, with 30% of these Ss intentionally distracting themselves or terminating the induction.
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PMID:The experimental induction of depersonalization and derealization in panic disorder and nonanxious subjects. 804 62

Pathogenetic mechanisms of "neuroses" were reconsidered based on a behavioristic framework which includes not only the traditional stimulus-response learning theory but also the concept of conflict proposed by Lewin. Most of the subtypes of "neuroses"--with the exception of panic disorder--were divided into two categories: conditioned fear-related disorders and conflict-related disorders. Phobias have been suggested to be caused by an escape or avoidance behavior motivated by an unconditioned or conditioned fear and obsessive compulsive disorder by an avoidance behavior motivated by a conditioned fear, while such disorders as posttraumatic disorder or hypochondriasis (nosophobia) were considered to be direct manifestations of conditioned fear. Generalized anxiety and depersonalization disorders were suggested to be caused by conflicts, but these conflicts seemed to persist even after the appearance of the symptoms. In contrast, appearances of conversion, somatization, somatoform pain, psychogenic fugue, or psychogenic amnesia were suggested to result in a temporary attenuation of the causative conflicts.
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PMID:A tentative classification of "neuroses" based on behavioristic consideration of the pathogenetic mechanisms. 820 88

Computerized EEG activity derived from the temporal lobes was investigated in normal subjects and panic disorder patients with and without depersonalization and/or derealization, in a resting condition and during an odor stimulation task. Panic patients without depersonalization or derealization showed an increase of fast and a decrease of slow activities independent of odor stimulation. Panic patients with depersonalization and/or derealization showed an increase of slow activity and bilateral lack of responsiveness in the fast alpha frequency band during odor stimulation. Findings suggest there are different EEG patterns in the temporal regions of the two different groups of panic patients during rest and activating conditions.
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PMID:EEG power modifications in panic disorder during a temporolimbic activation task: relationships with temporal lobe clinical symptomatology. 828 39

Since Cullen coined the term "neurosis" in the 18th century, medical investigators have searched the neural substrates of conditions we now classify as anxiety disorders. Harper and Roth in 1962 hypothesized that the temporal lobes might represent one such substrate for phobic-anxious patients with depersonalization-derealization (DD); the association between the presumed temporal lobe feature and phobic anxiety was so compelling that Roth (in 1959) described the condition as "phobic-anxiety-depersonalization" syndrome. Introduced into our current nosology as panic disorder-agoraphobia (PDA), this seemingly neuropsychiatric condition is nonetheless distinct from complex partial epilepsy (CPE), from which it is conventionally differentiated through clinical and anamnestic evaluation. Yet increasingly there are clinical-and laboratory-hints of certain overlap between manifestations of the two disorders, hitherto based largely on evaluation of psychosensorial phenomena in PDA or affective phenomena in CPE. We located only one systematic study that monitored 24-hour electroencephalogram (EEG) abnormalities in PDA. Finally, recent epidemiologic data suggest a significantly greater than chance association between PDA and a history of seizures. To further explore these intriguing links, the present study directly compared a group of 91 PDA outpatients with a group of 41 CPE outpatients with respect to DD and other psychosensorial symptoms. The broad similarities discovered between psychosensorial and related phenomena provide further support for the hypothesis that there may be a common neurophysiological substrate linking CPE phenomena with PDA.
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PMID:Psychosensorial and related phenomena in panic disorder and in temporal lobe epilepsy. 865 62

Using cluster analysis of 207 patients with panic disorder (PD), we investigated the relationships between several panic symptoms at the time of panic attacks, which included anticipatory anxiety, agoraphobia, and 13 clinical symptoms based on the Diagnostic and Statistics Manual-III-Revised. Cluster analysis revealed three panic symptom clusters: cluster A (dyspnea, choking, sweating, nausea, flushes/chills); cluster B (dizziness, palpitations, trembling or shaking, depersonalization, agoraphobia, and anticipatory anxiety); and cluster C (fear of dying, fear of going crazy, paresthesias, and chest pain or discomfort). Generally, cluster A was comprised exclusively of physiological symptoms, among which respiratory symptoms were prominent, cluster B included both panic and non-panic symptoms such as agoraphobia and anticipatory anxiety, and cluster C was comprised chiefly of fear symptoms.
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PMID:The symptom structure of panic disorder: a trial using factor and cluster analysis. 868 87


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