31 31.36

B R I T I S H J O U R N A L O F P S YC H I AT RY ( 2 0 0 4 ) , 1 8 5 , 3 1 ^ 3 6 fog?’). After a telephone screening, poten- tially suitable individuals were seen for aninitial clinical evaluation. For inclusion in the study, individuals had to have takenno psychotropic medication for a period oxidase inhibitors or investigational drugs).
Applicants were not eligible if they hadpreviously undergone an adequate fluox-etine trial, defined as a minimum of 10 mgdaily for 4 weeks, or if they reported fluox-etine intolerance or hypersensitivity.
Depersonalisation disorder is characterised ten informed consent was obtained after a full explanation of the study by the princi- order is diagnosed when depersonalisation is persistent or recurrent, causes marked distress or impairment, and is not part of another psychiatric or medical condition.
The illness is often chronic and debilitating, bipolar disorder or organic mental disorder were excluded from the study, as were indi- viduals with current substance use disorder or eating disorder. Lifetime Axis I disorders were assessed using the Structured Clinical (First et al, 1995), and Axis II personality disorders were assessed with the Structured et al, 1990; Fichtner et al, 1992; Ratliff & orders (Pfohl et al, 1995). Participants were allowed to enter the trial if they had been masked, placebo-controlled trial. We pre- psychotherapy or were receiving specialised treatment such as cognitive–behavioural therapy and hypnosis were excluded. Indi- viduals with acute or unstable medical ill- nesses, as well as those with a history of seizure disorder or major head trauma,were also excluded. All participants had a normal baseline routine laboratory evalua- tion with negative urine toxicology screen- People eligible for the study were adults required to use an effective birth control aged 18–65 years, who met DSM–IV diag- nostic criteria for current depersonalisation disorder by semi-structured clinical inter- view and by the Structured Clinical Inter- ised, parallel, flexible-dosage comparison of fluoxetine v. placebo for the treatment and postulate persistent depersonalisation, of depersonalisation disorder. After a 2- with intact reality testing, not occurring exclusively in the context of another diag- identical-appearing fluoxetine or placebo Association, 1994). Participants were self- capsules. Participants were assigned to the referred by responding to newspaper adver- fluoxetine or placebo group by the institu- tisements for research (‘do you frequently tion’s pharmacy on the basis of a standard investigators. Fluoxetine dosage was 10 mg in the past week only; in this context it other controlling for depression and anxiety per day for the first week, flexibly increased has been shown to be sensitive to treatment to 20 mg, 40 mg or 60 mg per day over the change (Ellason & Ross, 1997; Lubin et al, baseline scores were used as the only co- following 3 weeks, according to tolerabil- factor analysis of the DES in people with additional covariates in order to control the previously anecdotally reported efficacy for baseline and treatment effects in anxi- of higher dosages (Hollander et al, 1990), three factors – absorption, amnesia and de- ety, depression and social anxiety, using not required if not tolerated. No concomi- as well as change scores in these variables tant medication was allowed for the entire between baseline and week 10. Obsessive– on the particular factor analysis (mean of Table 3). Specifically for the CGI–I ana- lyses, the baseline CGI–S score was used adjusted the medication dose. Subsequently, The Depersonalization Severity Scale (DSS; as the covariate, and for the four people the independent evaluator (O.G.), to whom Simeon et al, 2001) is a six-item, clinician- participants had been requested to report visit, a CGI–I score of 4 was assumed. For all symptoms accurately but without refer- experiences rated 0–3, applied to the past week, which takes into account both symp- 0.80 in detecting group differences with a two-tailed test at the 0.5 level of signifi- cance, the effect size (difference between convergent and divergent validity, and to A categorical analysis of responders v.
come measures were used, in order to give test, defined as a CGI–I score of 2 or 1, were clinician-administered at each visit.
Depression was measured using the 17-item measures. Chi-squared tests were also used The Clinical Global Impression scale (CGI; acteristics of the two groups where appro- Guy, 1976) is a standard clinician-rated, Rating Scale for Anxiety (HRSA; Hamilton, response in relation to the presence of Axis was applied at the initial visit, and the I or Axis II disorders. For all 262 w2 tests during all subsequent visits, specifically to social anxiety and consequent avoidance.
measured using the Yale–Brown Obsessive al, 1989), a ten-item scale that measures Bernstein-Carlson & Putnam, 1993) is by far the most widely applied measure of dis- record of total number of panic attacks. In research studies to date. It is a 28-item addition to these scales, CGI–I scores were self-report questionnaire of dissociative applied to all existent comorbid disorders to measure treatment change in each.
Fifty-four people entered the placebo run-in period, of whom four were not randomised: has been shown to have good test–retest reliability (intraclass correlation coefficient sequent visit, one experienced a complete formed, with last observation carried for- resolution of depersonalisation symptoms, (Cronbach’s a¼0.95) and strong conver- and one experienced severe adverse effects gent, discriminant and criterion validity.
complete the trial. For each of the three on placebo. Of the 50 participants random- ised, 25 to fluoxetine and 25 to placebo, three-quarters (37) completed the trial, 16 patients are asked to rate their experience F LUOX E T I N E T R E AT M E N T O F D E P E R S ON A L I S AT I ON was a trend toward more people withdepressive disorders in the fluoxetine groupand more people with anxiety disorders in fluoxetine was not superior to placebo in treating depersonalisation, with the excep- tion of a statistically significant improve- although statistically greater than the pla-cebo mean improvement of 3.6. Bi-weekly categorical analysis of responder status re- (n¼6) and a 20% response rate on placebo (n¼5) (w2¼0.12, d.f.¼1, P¼0.73).
two groups as a whole. However, if the par-ticipants who had a diagnosis of depressive (Table 2), those taking fluoxetine consis- tently tended to have better responses than CGI–I scores of 2 or 1 for the particular dis- order: 50% v. 0% for major depression,75% v. 25% for dysthymia, 50% v. 40% for generalised anxiety disorder, 100% v.
25% for obsessive–compulsive disorder,50% v. 40% for panic disorder and 33% (w2¼2.60, d.f.¼1, P¼0.11). The mean daily tion (CGI–I 1). Withdrawals from the pla- depersonalisation disorder CGI–I score in fluoxetine and 46 mg for placebo (t¼0.45, for as follows: two persons before week 2, only primary outcome variable to show dif- to covarying for anxiety and depression.
For the fluoxetine group, end-point CGI–I to seek private treatment and one with wor- not significantly differ according to the pre- sening anxiety; three persons before week 4, one to attempt impregnation (CGI–I 5), istics of the 50 participants with DSM–IV (CGI–I) in comorbid depressive disorders one to seek private treatment (CGI–I 4) (w2¼5.07, d.f.¼4, P¼0.28). However, end- and one discontinued by the investigators point CGI–I for depersonalisation disorder for worsening depression (CGI–I 3); two did marginally differ according to the pre- marised in Table 2. It can be seen that the tion) before week 8 (CGI–I 2 and 4); and (w2¼5.76, d.f.¼2, P¼0.06). In effect, of (48% fluoxetine, 20% placebo) and de-creased sexual arousal (24% fluoxetine,4% placebo). Only one person from the fluoxetine group discontinued the trial pre- maturely because of adverse effects, in this case heightened anxiety. Therefore, to ourknowledge, the greater withdrawal the medication arm was not due to adverse possible efficacy suggested by earlier anec- dotal data. Previous reports had found that improvement in depersonalisation was clo- sely related to the presence of other symp-toms responsive to serotonin reuptake spective treatment reviews in depersonalisa- efficacy for serotonin reuptake inhibitor in both treatment groups, which was clini- cally not noteworthy and statistically no CGI–I score in the fluoxetine group, before effects, was also not clinically significant, approximately 3, i.e. minimal change.
Indeed, a number of the participants whoexperienced some improvement tine expressed this effect in words, stating fluoxetine, 4% placebo), muscle stiffness to take less notice or be less bothered by responders were all depersonalisation dis- them. The study finding of slight improve- 40% placebo), excitation or hyperactivity whose anxiety disorder did not respond to fluoxetine, only one was a depersonalisa- responder status did not significantly differ in the presence or absence of personality placebo), stomach ache (12% both groups), disorder (w2¼0.00, d.f.¼1, P¼1.00).
It is possible that some alleviation of co- morbid anxiety and depression contributed to an overall more tolerable affective state, Side-effects occurring at a frequency of at which led participants to experience their least 10% in at least one of the two study depersonalisation as less troubling although fluoxetine, 24% placebo), decreased libido essentially unchanged. Indeed, a mediating F LUOX E T I N E T R E AT M E N T O F D E P E R S ON A L I S AT I ON effect of comorbid anxiety and depression is suggested by the loss of statistically ised depersonalisation as a universal pre- formed functional response of the brain to covaried for baseline and change in anxiety and depression, as well as by the greaterimprovement improvement in anxiety disorders in those fluoxetine, compared with non-responders.
Strengths of the study include the fluoxetine well-validated dissociation measures, both for decades, and it would be fair to say that clinician-rated and self-reported; the use relationship of depersonalisation to phobic anxiety (Roth, 1959), depression (Sedman, stringent selection criteria for the partici- pants with primary DSM–IV depersonalisa- arm, and the medium size of the sample.
and anxiety disorders (Baker et al, 2003).
An alternative view, however, is thatextreme emotional states such as severe depression or anxiety are one type of ‘trau- Our study suggests that first-line use of matic stress’, among many others, that may serotonin reuptake inhibitors for the treat- ment of depersonalisation disorder is not with an underlying vulnerability; in some indicated, except possibly in selected indi- viduals with troublesome anxiety or depres- chronic and autonomous of the precipitat- sion; in such individuals, improved affective ing stressor (Simeon et al, 2003). The lack of responsiveness of depersonalisation to tolerance of their dissociative symptoms.
fluoxetine supports the latter concept, that depersonalisation disorder is a distinct dis- study are important in light of the absence sociative disorder. Indeed, as long ago as depersonalisation, and the common clinicalpractice of the past decade of using seroto- nin reuptake inhibitors on the basis ofpromising early anecdotal reports and the frequent presence of comorbid anxietyand depression. In the future, investigating other classes of medications that may have

Source: http://www.elizabethselwyn.50webs.com/PDF%20Papers%20about%20Depersonalization%20Disorder/D.%20SIMEON%202004.pdf


Is adaptability a normative and spontaneous concept? A review of the literature on social-ecological systems literature and resilience Björn Nykvist1,2* and Thomas Hahn1 1 Stockholm Resilience Centre 2 Stockholm Environment Institute, and Department of Systems Ecology, Stockholm University * Corresponding author: Tel: +46 (0)8-674 7513 Fax: +46 (0)8-674 7020 Emial: bjorn.nykvist@sei.

Mise en page

Dell™ Latitude™ 131L Innovative Design: Designed with usability in mind • UltraSharp™, wide-aspect LCD for increased Smart, affordable technology for business • Freedom to work longer, with 9-cell extended life• Dual Core processor option to help boost• Easy to customise with Dell QuickSet™ software• Windows® VistaTM Capable1: support for Microsoft’snext-gene

Copyright © 2010-2014 Internet pdf articles