Depersonalization/derealization and its relationship to mood and anxiety disorders in the National Comorbidity Survey-Replication (NCS-R)

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Depersonalization/derealization and its relationship to mood and anxiety disorders in the National Comorbidity Survey-Replication (NCS-R)

https://doi.org/10.21203/rs.3.rs-4874891/v1

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Depersonalization/derealization (dpdr) is known to occur across mood and anxiety disorders (MAD) and has been proposed as a marker of worse illness. However, despite the well-known clinical association, there are no epidemiological data on the relationship between dpdr and MAD. In this NCS-R analysis clinically significant dpdr (DPDR-C) was defined as “sometimes” or “often” past-month endorsement of depersonalization and/or derealization in the absence of other pathological dissociation. Six past-month MAD diagnoses were examined: DSM-IV generalized anxiety disorder, panic disorder, social phobia, major depression, bipolar I, and bipolar II. National DPDR-C one-month prevalence was 0.9%. After excluding all cases with past-month posttraumatic stress disorder or non-dpdr pathological dissociation, 21.2% of DPDR-C cases were accounted for by MAD while 3.0% of MAD cases endorsed DPDR-C, ranging from 0% (generalized anxiety disorder) to 11.8% (comorbid mood and anxiety disorder). DPDR-C was not uniquely related to any MAD disorder, and was not associated with MAD age of onset, chronicity, or impairment. Rather, DPDR-C was significantly associated with number of comorbid MAD disorders and with mood/anxiety comorbidity. In conclusion, at the epidemiologic level DPDR-C was uncommon in MAD but was more likely to occur in the presence of combined mood and anxiety disturbance, which may cause greater disruption to the usual sense of self and thus trigger unreality experiences.

dissociation

depersonalization/derealization

epidemiology

prevalence

mood disorders

anxiety disorders

severity

comorbidity

impairment

Depersonalization/derealization (dpdr) can be a transient experience, or a more enduring dissociative condition that portends clinical significance. Unlike many psychiatric disorders, the dissociative disorders, including depersonalization/derealization disorder (DDD), have received little epidemiologic attention. Both the fourth and the fifth edition of the Diagnostic and Statistical Manual for Mental Disorders (American Psychiatric Association, 1994; American Psychiatric Association, 2013) specify that in order for a DDD diagnosis to be made, dpdr episodes must not only be persistent or recurrent, and associated with distress or impairment, but must also have a separate standing of their own, predating, extending past, and not limited to episodes of other psychiatric disorders, the most common ones being anxiety disorders, mood disorders, posttraumatic stress disorder, and other dissociative disorders. The overarching purpose of this report was to examine the relationship of dpdr to mood and anxiety disorders in a nationally representative U.S. sample; the relationship of dpdr to posttraumatic stress disorder and to pathological dissociation/dissociative disorders has been examined elsewhere (Stein et al., 2013; Simeon & Putnam, 2022).

The relationship between dpdr and mood/anxiety disorders (MAD) has been of longstanding interest for decades, though the pertinent literature remains scant to this day. Dpdr is known to occur trans-diagnostically across all the major mood and anxiety disorders. From an epidemiologic standpoint, two German national surveys examined the relationship of clinically significant dpdr (DPDR-C) to mood and anxiety. The first survey reported a 0.9% 6-month prevalence for DPDR-C, with 72% of cases accounted for by generalized anxiety, panic disorder, social phobia, or depression (Michal et al., 2009). The second survey found a 3.4% two-week prevalence, and only 3.5% of DPDR-C cases did not have comorbid anxiety or depression (Michal et al., 2011). Additionally, dpdr-related impairment was greater in the presence of depression or panic disorder (Michal et al., 2009), and dpdr at baseline was prospectively associated with elevated depressive and anxiety symptoms over a 2.5-year follow-up period (Schlax et al., 2020).

Clinical studies of DDD have established extensive comorbidity with mood and anxiety disorders. In a U.S. sample of 117 DDD patients, lifetime comorbidity was 67% for major depression, 33% for social phobia, 31% for panic disorder, and 19% for generalized anxiety disorder, though current comorbidity was much lower (10%, 28%, 12%, and 16% respectively) (Simeon et al., 2003). In a German cohort of 223 DDD patients, current comorbidity was 85% for depressive disorders and 43% for anxiety disorders; functional impairment was worse in the DDD group than in the comparison group with depression (Michal et al., 2016). In a U.K. cohort of 204 DDD patients, self-reported psychiatric history was 62% for depression, 41% for anxiety disorder, and 8% for bipolar disorder; dpdr severity was associated with current depression and anxiety scores suggesting that dpdr may be a severity marker in MAD (Baker et al., 2003).

Several clinical studies in the anxiety disorders have examined dpdr and its associations. Back in 1959, Sir Martin Roth astutely delineated an essentially transdiagnostic “phobic anxiety-depersonalization syndrome.” Segui et al. (2000) reported a 24% prevalence of dpdr during attacks in 274 patients diagnosed with panic disorder (PD); dpdr was associated with greater PD severity, more frequent attacks, and worse functioning. In another study of 104 outpatients with PD, 48% reported dpdr during attacks while 20% had DDD; PD patients with comorbid DDD had significantly more severe PD (Mendoza et al., 2011). Cassano et al. (1989) reported a 35% prevalence of dpdr during panic attacks, predicted by earlier age of onset, higher avoidance and agoraphobia, and greater comorbidity with generalized anxiety and depressive symptoms. Dpdr is also elevated in social phobia (SP), and dpdr severity has been associated with social anxiety severity (Gül et al., 2014). While Hoyer et al. (2013) found that dpdr in social anxiety disorder was associated with more safety behaviors and post-event processing thus contributing to the maintenance of social anxiety, Schweden et al. (2016) reported that baseline dpdr neither predicted nor mediated cognitive behavioral treatment response in SP. Less is known about the prevalence and clinical significance of dpdr in GAD; Noyes et al. (1992) reported than dpdr was more common in panic than in generalized anxiety, while in a GAD patient sample dpdr ranked fourth out of ten significant discriminators from healthy controls (Beck et al., 1999).

The prevalence and correlates of dpdr in mood disorders have received less attention than in anxiety disorders, though reliable comparisons of prevalence and clinical significance in the two classification categories are, in fact, lacking. Further, the relationship between dpdr and comorbid MAD has not been well explored. A large patient sample compared major depressive disorder (MDD) without comorbid anxiety disorders to PD without comorbid mood disorders, and found similar dpdr loadings for cognitive depression (.25) and anxiety (.30), with inverse loading for vegetative depression (-.21) (Porter et al., 2017). Dpdr was not associated with poorer response to electroconvulsive therapy in “endogenous” depression, but only in “neurotic” depression (Ackner & Grant, 1960). Of note, the distinction between affective depersonalization and depressive anhedonia can be challenging one (Mula et al., 2010), and dpdr in MDD has been associated with reduced connectivity between the extrastriate body area and the default mode network (Paul et al., 2019). Dpdr can also occur in bipolar disorder (BP); one study of 91 adults reported comparable dpdr in BP-I and BP-II, associated with earlier BP onset and PD comorbidity (Mula et al., 2009).

Mula et al. (2007) hypothesized that dpdr in mood and anxiety disorders “may represent a clinical index of disease severity, poorer response to treatment, and high level of comorbidity.” Though adult inpatients with MAD scored significantly higher on the Structured Clinical Interview for the Depersonalization-Derealization Spectrum than healthy controls, the issue of whether dpdr was associated with greater severity, more impairment, or worse treatment prognosis was not reported on (Mula et al., 2008).

All in all, though there is clear evidence documenting that dpdr is encountered in both anxiety and mood anxiety disorders, and that it might be associated with greater illness severity, more impairment, greater comorbidity, and worse prognosis, findings to date by no means draw a definitive picture. Thus, the goal of the present study was to investigate dpdr in the National Comorbidity Survey-Replication sample, with the following aims. 1. To determine the prevalence of clinically significant depersonalization/derealization (DPDR-C) occurring in the absence of other pathological dissociation or posttraumatic stress presumably indicative of dissociative disorders other than DDD (Simeon & Putnam, 2022) or the dissociative subtype of PTSD (Stein et al., 2013). 2. To investigate the prevalence and associations of 1-month? DPDR-C with x-month? mood disorders, anxiety disorders, and comorbid mood-anxiety disorders. 3. To determine whether DPDR-C is a marker of greater MAD severity, impairment, or comorbidity.

2.1. Participants

The NCS-R was a U.S. face-to-face household survey of adult English-speakers conducted from 2001 to 2003 in a multi-stage clustered area probability sample of the U.S. population (Kessler & Merikangas, 2004). The primary sampling areas, metropolitan and non-metropolitan counties, were selected with stratification to guarantee representativeness of the U.S. population on a wide range of geographic and sociodemographic characteristics. Recruitment within clustered probability samples of households within sampling areas began with an advance letter and study brochure followed by in-person interviewer visits to explain study goals and procedures and randomly select a household respondent. Response rate was 71%, and a probability subsample of non-responders completed a follow-up survey so as to adjust for differential probabilities of selection and non-response biases. The study was approved by the human subject committees of Harvard Medical School and the University of Michigan.

2.2. Assessment

The seven NCS-R items inquiring about pathological dissociation were derived verbatim from the pathological dissociation “taxon” (Waller et al., 1996) of the Dissociative Experiences Scale (DES; Bernstein-Carlson & Putnam, 1993). Items were rated on a scale of 1 to 4 (4 - never, 3 - rarely, 2 - sometimes, 1 - often) applied to the past month, and were inversely converted to a 0–3 scale (0 - never, 1 - rarely, 2 - sometimes, 3 - often). Of the seven items three inquired about dpdr, two about depersonalization (DES7: “Some people sometimes have the experience of feeling as though they are standing next to themselves or watching themselves do something and they actually see themselves as if they were looking at another person; DES13: “Some people have the experience of feeling that their body does not seem to belong to them”), and one about derealization (DES12: “Some people have the experience of feeling that other people, objects, and the world around them are not real”).

At least one of the three items had to be scored as “sometimes” or “often” for an individual to be deemed as experiencing clinically significant dpdr (DPDR-C), the same cutoff employed to delineate the dissociative subtype of PTSD (presence of clinically significant depersonalization and/or derealization) in the World Mental Health Survey (Stein et al., 2013). Dpdr score was calculated as the sum of the three dpdr items. Confirming the validity of using these three taxon items to reliably detect clinically significant dpdr, Simeon et al. (2003) previously found that in a sample of 117 individuals diagnosed with depersonalization disorder by semi-structured interview, mean scores for the three items were 28 (DES7), 67 (DES12), and 51 (DES13), well within the “sometimes” to “often” range. Furthermore, these three items were highly sensitive in detecting DPDR-C as only 3% of the sample did not score at least 20 (“sometimes,” see Simeon & Putnam (2022) for NCS-R to DES conversion scoring) on any of the three items. To conservatively exclude all other pathological dissociation, DPDR-C was defined as a rating of “never” on the remaining four items (DES 5, 8, 22, and 27) indicative of amnesia or identity alteration (Simeon & Putnam, 2022).

Demographic, MAD, and impairment variables were extracted from the database. NCS-R psychiatric diagnoses employed a structured, lay-administered interview based on DSM-IV diagnostic criteria. The following past-month MAD were included: anxiety disorders (GAD, PD, SP); and mood disorders (MDD, BP-I, BP-II). Three relevant groups were identified after excluding all cases with other pathological dissociation or past-month PTSD. Group 1 included all DPDR-C cases without past-month MAD; Group 2 included past-month MAD cases with DPDR-C; and Group 3 included past-month MAD cases without DPDR-C.

To explore onset and course characteristics of MAD in relation to dpdr, MAD age of onset as well as past-year status were examined. Remission was defined as MAD endorsed for the past year but not the past month. Chronicity was defined as MAD endorsed for the past year and unremitted or recurring in the past month. Recency was defined as MAD not endorsed for the past year but endorsed for the past month.

Past-month impairment was assessed by the World Health Organization Disability Assessment Scale (WHODAS), which inquired about functional impairment in six domains: time out of role, self-care, mobility, cognition, role functioning, and social functioning (Rehm et al., 1999).

2.3. Statistical analysis

Statistical analyses were conducted with SPSS version 29 and employed two-tailed comparisons with a probability significance value of .05. Between-group comparisons were conducted with ANOVAs or chi-square tests as applicable, with Bonferroni-corrected post-hoc comparisons. A stepwise linear regression analysis was used to examine the prediction of dpdr score by the six MAD disorders. Pearson’s correlations were used to examine the relationship between dpdr score and MAD age of onset, number of MAD comorbid disorders, and impairment scores.

3.1. Prevalence of DPDR-C

Of a total of 6,644 participants who responded to all items of the pathological dissociation questionnaire (completion rate 99.8%), DPDR-C was endorsed by 60 individuals (0.9%); 8 of these cases were accounted for by past-month PTSD. Past-month MAD was endorsed by 597 of the 6,644 participants. After excluding past-month PTSD (n = 157) and non-dpdr pathological dissociation (n = 1,667) a subsample of 4,908 individuals was generated, of whom 52 endorsed DPDR-C and 365 endorsed past-month MAD. Group 1 comprised the 41 DPDR-C participants without past-month MAD; Group 2 the 11 DPDR-C participants with past-month MAD; and Group 3 the 354 past-month MAD participants without DPDR-C.

The three groups differed in age (Group 1: 37.37 (SD 14.29), Group 2: 49.18 (SD 18.13), Group 3: 42.52 (SD 14.67); F (2, 405) = 3.53, p = .03; Bonferroni-corrected post-hocs: Groups 1–2: p = .06; Groups 1–3: p = .10; Groups 2–3: p = .42), but not gender (Group 1: 22F / 19M, Group 2: 5F / 6M, Group 3: 230F / 124M; ꭓ² (2) = 3.57, p = .17). The three groups differed significantly in dpdr score (Group 1: 2.49 (SD 0.84), Group 2: 3.18 (SD 1.33), Group 3: 0.10 (SD 0.38); F (2, 405) = 624.46, p < .001; all three Bonferroni-corrected post-hocs p < .001).

Table 1 presents the prevalence of DPDR-C in MAD by mood and anxiety classifications and by MAD disorders.

Table 1

Prevalence of clinically significant depersonalization/derealization (DPDR-C) in past-month mood and anxiety disorders (MAD).
	total n	n with DPDR-C	Prevalence (%)
Anxiety Disorder	262	9	3.4
Generalized Anxiety Disorder	51	0	0
Panic Disorder	48	3	6.3
Social Phobia	174	8	4.6
Mood Disorder	137	6	4.4
Major Depressive Disorder	116	4	3.4
Bipolar I Disorder	12	1	8.3
Bipolar II Disorder	9	1	11.1
Anxiety Disorder only	228	5	2.2
Mood Disorder only	103	2	1.9
Comorbid Anxiety & Mood Disorder	34	4	11.8
Any MAD Disorder	365	11	3.0

3.2. Predictors of dpdr in MAD

In the combined Group 2 and 3 MAD sample (n = 365), dpdr score was not predicted by any of the six MAD disorders. There was comorbidity amongst MAD diagnoses, with a mean of 1.12 (SD 0.36) diagnoses per individual (range 1–3). Number of comorbid MAD disorders was significantly correlated with dpdr score (r = .17, n = 365, p < .001). Comparison of DPDR-C prevalence between the anxiety disorder only group, the mood disorder only group, and the comorbid anxiety and mood disorder group (see Table 1) revealed significantly more DPDR-C in the comorbid group (ꭓ² (2) = 8.84, p = .007; Bonferroni corrected post-hocs at p = .017 significance value: Anxiety vs Comordid p = .004; Mood vs Comorbid p = .015; Anxiety vs Mood: p = .88).

Descriptive examination of the eleven MAD cases with DPDR-C revealed that 6 had more than one MAD disorder and 5 had mood-anxiety comorbidity. [case-by-case: PD/SP/MDD x 2; MDD x 2; PD/SP; SP x 4; PD/BP-II; SP/BP-I].

3.3. Relationship of dpdr to MAD illness characteristics

MAD age of onset was available for a minority of cases. In combined groups 2 and 3, all Pearson’s correlations between age of MAD onset and dpdr score were not significant. Comparison of MAD age of onset between groups 2 and 3 revealed no difference for SP (t (109) = 0.61, p = .55) and MDD (t (153) = 0.66, p = .51); the other four MAD disorders lacked data for Group 2.

Of 851 individuals with past-year MAD remitted by the past month, only 5 endorsed DPDR-C (0.6%) [GAD: 1 of 76 (1.3%); PD: 0 / 121 (0%); SP: 2 / 342 (0.6%); MDD: 1 / 348 (0.3%); BP-I: 0 / 35 (0%); BP-II: 1 / 41 (2.4%)]. Of 75 individuals with chronic MAD (past year and past month), none endorsed DPDR-C (0%). Of 343 individuals with recent MAD (past month but not past year), 11 endorsed DPDR-C (3.2%).

3.4. Relationship of dpdr to functional impairment

WHODAS scores were available for 238 of the 406 cases in the three groups. There was no between-group difference in functional impairment (Group 1: 2.78 (SD 6.08), Group 2: 0.00 (SD 0.00), Group 3: 3.31 (SD 6.50); F (2, 237) = 0.79, p = .45). There was also no association between dpdr score and impairment in the combined sample (r = − .05, n = 238, p = .44).

The main study findings can be summarized as follows. The national 1-month prevalence of clinically significant depersonalization/derealization (DPDR-C) without other pathological dissociation was 0.9%, 13.3% of which was associated with past-month PTSD. Of the remaining DPDR-C cases, a minority (21.2%) was associated with past-month MAD. The overall rate of DPDR-C in past-month MAD was 3.0%, comparable for mood and anxiety disorders, and ranged from 0% (GAD) to 11.8% (comorbid mood and anxiety). Dpdr was not uniquely related to any single MAD disorder, but rather was associated with both number of comorbid MAD disorders and mood/anxiety comorbidity. Dpdr was not significantly associated with MAD age of onset, chronicity, or impairment.

The 0.9% one-month prevalence of DPDR-C in this U.S. national sample is comparable to the 0.8% − 2.4% prevalence reported by prior epidemiologic studies (Johnson et al. 2006; Michal et al., 2009; Ross, 1991; Sar et al., 2007), at the low end of the range as expected for a one-month assessment period. Though diagnoses cannot be inferred without interviewing, the rigorously extracted 41 DPDR-C cases free of the four major exclusionary diagnostic categories (mood disorders, anxiety disorders, posttraumatic stress disorder, and other pathological dissociation) have a reasonable likelihood of DDD diagnosis. According to DSM-IV and, similarly, DSM-5 criteria (American Psychiatric Association, 1994; American Psychiatric Association, 2013), the one-month occurrence of dpdr would need to qualify as a “persistent” or “recurrent” episode, as the diagnostic criteria do not specify a minimum duration. Additionally, the dpdr symptoms would have to be associated with distress or impairment. It is even conceivable that a portion of the 11 DPDR-C cases with comorbid MAD might have met DDD criteria, if dpdr symptoms were not occurring exclusively in the context of a mood or anxiety episode; the data do not permit further exploration of this question. Notably, past-year MAD remitted by the past month had a very low DPDR-C prevalence of 0.6% which could maximally account for 5 of the 41 putative DDD cases, a relevant fact since it is clinically known that dpdr symptoms can lag in remission vis-à-vis mood and anxiety symptoms (Simeon et al., 2003).

The co-occurrence of DPDR-C and MAD was notably lower in the NCS-R than that reported by the two German national surveys (Michal et al., 2009; Michal et al., 2011). Though the NCS-R used items from the Dissociative Experiences Scale while the German surveys used items from the Cambridge Depersonalization Scale, the questions are comparable. The German studies, however, did not employ structured interviewing to establish MAD diagnoses but rather relied on anxiety and mood questionnaire cutoffs, so the prevalence of MAD may have been overestimated. Another likely explanation is that the German surveys did not inquire about, and therefore did not exclude, other pathological dissociation; the dissociative identity disorder spectrum is known to be highly comorbid with MAD (Ellason et al., 1996). Interestingly, dpdr severity was significantly lower in Group 1 (no MAD) than in Group 2 (MAD), consistent with clinical and epidemiological reports that the presence of mood or anxiety disturbances intensifies dpdr experiences (Baker et al., 2003; Michal et al., 2009).

Clinical studies of mood and anxiety disorders that have examined dpdr (see Introduction) generally report higher prevalence than that found in the NCS-R. The most likely explanation for this discrepancy is the nonclinical nature of the NCS-R sample, since clinical samples typically reflect the greater disorder severity of those who seek treatment. Along the same lines, the NCS-R sample did not support the contention that dpdr may be a marker of worse MAD illness, as reported by many (Baker et al., 2003; Cassano et al., 1989; Gul et al., 2014; Hoyer et al., 2013; Mendoza et al., 2011; Michal et al., 2009; Mula et al., 2009; Schlax et al., 2020; Segui et al., 2000), but not all (Ackner & Grant, 1960; Schweden et al., 2016) clinical studies. However, the NCS-R sample clearly demonstrated that the risk of dpdr was higher in the presence of MAD comorbidity, as proposed by Mula et al. (2007). Though comorbid mood and anxiety disorders accounted for less than a tenth of the MAD sample, they accounted for nearly half of the DPDR-C cases. It is plausible that concomitant disturbance of both mood and anxiety is of a magnitude more likely to disrupt self-experience and self-constancy to the point of precipitating the unreality sense of dpdr. Neurobiological factors could also be at play (Mula et al., 2006), as both mood (Anand et al., 2009) and anxiety (Gold et al., 2016) have been associated with corticolimbic dysconnectivity, as has dpdr (Sierra & Berrios, 1998).

The findings of this epidemiologic study carry implications for clinicians. Since only a minority of DPDR-C was accounted for by MAD diagnoses, and conversely only a small minority of those with MAD diagnoses had DPDR-C, in the clinical evaluation of any patient it is important to determine the longitudinal course of both conditions, and the extent to which dpdr can be consistently accounted for by MAD episodes throughout a patient’s lifetime history, or instead has a distinct course of its own and qualifies for a DDD diagnosis.

The strengths of this study lie in the large and nationally representative sample, the diagnostic assessment of MAD by structured interviewing, and the use of three well-validated questions for the detection of dpdr. Limitations include the absence of both dissociative disorder diagnostic interviewing and any information about dissociation prior to the past month. Also, in order to examine “pure” dpdr, nearly 40% of past-month MAD cases had to be excluded due to the presence of non-dpdr pathological dissociation or PTSD, and that MAD group may differ from the MAD sample included in this report. Finally, there were missing data for functional impairment.

On an epidemiologic scale, DPDR-C was dissectible from MAD and was largely not accounted for by MAD. DPDR-C in MAD had low prevalence, was not differentially associated with any MAD disorder or with anxiety versus mood, but instead was predicted by comorbidity.

Competing Interests

Dr. Stein has received consultancy honoraria from Discovery Vitality, Johnson & Johnson, Kanna, L’Oreal, Lundbeck, Orion, Sanofi, Servier, Takeda and Vistagen.

Author Contribution

DS did the analysis and wrote a first draft of the manuscript. DJS provided further inputs on the manuscript. Both authors reviewed the final draft.

Ackner B, Grant AFR, American Psychiatric Association (1960) The prognostic significance of depersonalization in depressive illnesses treated with electroconvulsive therapy. J Neurol Neurosurg Psychiat 23, 242–246. https://doi.org/10.1136/jnnp.23.3.242 American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders, 5th edition. APA, Washington, D.C. (2013). Diagnostic and statistical manual of mental disorders, 5th edition. APA, Washington, D.C
Anand A, Li Y, Wang Y, Lowe MJ, Dzemidzic M (2009) Resting state corticolimbic connectivity abnormalities in unmedicated bipolar disorder and unipolar depression. Psychiatry Res 171:189–198. https://doi.org/10.1016/j.pscychresns.2008.03.012
Baker D, Hunter E, Lawrence E, Medford N, Patel M, Senior C, Sierra M, Lambert MV, Phillips ML, David AS (2003) Depersonalisation disorder: Clinical features of 204 cases. BJ Psych 182:428–433. https://doi.org/10.1192/bjp.182.5.428
Beck JG, Stanley MA, Zebb BJ (1999) Effectiveness of the Hamilton Rating Scale with older generalized anxiety disorder patients. Clin Geropsych 5:281–290. https://doi.org/10.1023/A:1022962907930
Bernstein-Carlson E, Putnam FW (1993) An update on the Dissociative Experiences Scale. Dissociation 6:16–27
Cassano GB, Petracca A, Perugi G, Toni C, Tundo A, Roth M (1989) Derealization and panic attacks: A clinical evaluation on 150 patients with Panic Disorder/agoraphobia. Compr Psychiatry 30:5–12. https://doi.org/10.1016/0010-440X(89)90112-0
Ellason JW, Ross CA, Fuchs DL (1996) Lifetime axis I and II comorbidity and childhood trauma history in dissociative identity disorder. Psychiatry 59:255–266. https://doi.org/10.1080/00332747.1996.11024766
Gold AL, Shechner T, Farber MJ, Spiro CN, Leibenluft E, Pine DS et al (2016) Amygdala-Cortical Connectivity: Associations with Anxiety, Development, and Threat. Depress Anxiety 33:917–926. https://doi.org/10.1002/da.22470
Gul AI, Simsek GG, Inanir S, Karaaslan O (2014) Is there a dissociative subtype of generalized social phobia? J Psychiatry 17:14–68
Hoyer J, Braeuer D, Crawcour S, Klumbies E, Kirschbaum C (2013) Depersonalization/derealization during acute social stress in social phobia. J Anxiety Disord 27:178–187. https://doi.org/10.1016/j.janxdis.2013.01.002
Johnson JG, Cohen P, Kasen S, Brook JS (2006) Dissociative disorders among adults in the community, impaired functioning, and axis I and II comorbidity. J Psychiatric Res 40:131–140. https://doi.org/10.1016/j.jpsychires.2005.03.003
Kessler RC, Merikangas KR (2004) The National Comorbidity Survey Replication (NCS-R): background and aims. Int J Method Psychiatric Res 13:60–68. https://doi.org/10.1002/mpr.166
Mendoza L, Navines R, Crippa JA, Fagundo AB, Gutierrez F, Nardi AE, Bulbena A, Valdes M, Martin-Santos R (2011) Depersonalization and personality in panic disorder. Compr Psychiatry 52:413–419. https://doi.org/10.1016/j.comppsych.2010.09.002
Michal M, Adler J, Wiltink J, Reiner I, Tschan R, Wolfling K, Weimert S, Tuiin I, Subic-Wrana C, Beutel ME, Zwerenz R (2016) A case series of 223 patients with depersonalization-derealization syndrome. BMC Psychiatry 16:203–213. https://doi.org/10.1186/s12888-016-0908-4
Michal M, Glaesmer H, Zwerentz R, Knebel A, Wiltink J, Brahler E, Beutel ME (2011) Base rates for depersonalization according to the 2-item version of the Cambridge Depersonalization Scale (CDS-2) and its associations with depression/anxiety in the general population. J Affect Disord 128:106–111. https://doi.org/10.1016/j.jad.2010.06.033
Michal M, Wiltnik J, Subic-Wrana C, Zwerenz R, Tuin I, Lichy M, Brähler E, Beutel ME (2009) Prevalence, correlates, and predictors of depersonalization experiences in the German general population. J Nerv Ment Dis 197:499–506. https://doi.org/10.1097/NMD.0b013e3181aacd94
Mula M, Pini S, Calugi S, Preve M, Masini M, Giovannini I, Conversano C, Rucci P, Cassano GB (2008) Validity and reliability of the Structured Clinical Interview for Depersonalization-Derealization Spectrum (SCI-DER). Neuropsychiatric Dis Treat 4:977–986. https://doi.org/10.2147/NDT.S3622
Mula M, Pini S, Calugi S, Preve M, Masini M, Giovannini I, Rucci P, Cassano GB (2010) Distinguishing affective depersonalization from anhedonia in major depression and bipolar disorder. Compr Psychiatry 51:187–192. https://doi.org/10.1016/j.comppsych.2009.03.009
Mula M, Pini S, Cassano GB (2007) The neurobiology and clinical significance of depersonalization in mood and anxiety disorders: A critical reappraisal. J Affect Disord 99:91–99. https://doi.org/10.1016/j.jad.2006.08.025
Mula M, Pini S, Preve M, Masini A, Giovannini I, Cassano GB (2009) Clinical correlates of depersonalization symptoms in patients with bipolar disorder. J Affect Disord 115:252–256. https://doi.org/10.1016/j.jad.2008.08.001
Noyes R, Woodman C, Garvey MJ, Cook BL, Suelzer M, Clancy J, Anderson DJ (1992) Generalized Anxiety Disorder vs. Panic Disorder: Distinguishing Characteristics and Patterns of Comorbidity. J Nerv Ment Dis 180:369–379. https://doi.org/10.1097/00005053-199206000-00006
Paul ER, Farmer M, Kampe R, Cremers HR, Hamilton JP (2019) Functional connectivity between extrastriatal body area and default mode network predicts depersonalization symptoms in major depression: Findings from an a priori specified multinetwork comparison. Biol Psychiatry: Cogn Neurosci Neuroimaging 4:627–635. https://doi.org/10.1016/j.bpsc.2019.03.007
Porter E, Chambless DL, McCarthy KS, DeRubeis RJ, Sharpless BA, Barrett MS, Milrod B, Hollon SD, Barber JP (2017) Psychometric Properties of the Reconstructed Hamilton Depression and Anxiety Scales. J Nerv Ment Dis 205:656–664. https://doi.org/10.1097/NMD.0000000000000666
Rehm J, Ustun TB, Saxena S, Nelson CB, Chatterji S (1999) On the development and psychometric testing of the WHO screening instrument to assess disablement in the general population. Int J Methods Psychiatric Res 8:110–122. https://doi.org/10.1002/mpr.61
Ross C (1991) The epidemiology of multiple personality disorder and dissociation. Psychiatric Clin N Am 14:503–517
Roth M (1959) The phobic anxiety-depresonalization syndrome. proc. of the R. Society of Medicine 52:587–595
Sar V, Akyüz G, Doğan O (2007) Prevalence of dissociative disorders among women in the general population. Psychiatry Res 149:169–176. https://doi.org/10.1016/j.psychres.2006.01.005
Schlax J, Wiltink J, Beutel ME, Munze T, Pfeiffer N, Wild P, Blettner M, Kerahrod JG, Michal M (2020) Symptoms of depersonalization/derealization are independent risk factors for the development or persistence of psychological distress in the general population: Results from the Gutenberg health study. J Affect Disord 273:41–47. https://doi.org/10.1016/j.jad.2020.04.018
Schweden TLK, Pittig A, Bräuer D, Klumbies E, Kirschbaum C, Hoyer J (2016) Reduction of depersonalization during social stress through cognitive therapy for social anxiety disorder: A randomized controlled trial. J Anxiety Disord 43:99–105. https://doi.org/10.1016/j.janxdis.2016.09.005
Segui J, Marquez M, Garcia L, Canet J, Salvador-Carulla L, Ortiz M (2000) Depersonalization in panic disorder: a clinical study. Compr Psychiatry 4:172–178. https://doi.org/10.1016/S0010-440X(00)90044-0
Sierra M, Berrios GE (1998) Depersonalization: neurobiological perspectives. Biol Psychiatry 44:898–908. https://doi.org/10.1016/S0006-3223(98)00015-8
Simeon D, Knutelska M, Nelson D, Guralnik O (2003) Feeling unreal: A depersonalization disorder update of 117 cases. J Clin Psychiatry 64:990–997. https://doi.org/10.4088/jcp.v64n0903
Simeon D, Putnam F (2022) Pathological dissociation in the National Comorbidity Survey Replication (NCS-R): Prevalence, morbidity, comorbidity, and childhood maltreatment. J Trauma Dissociation 23:490–503. https://doi.org/10.1080/15299732.2022.2064580
Stein DJ, Koenen KC, Friedman MJ, Hill E, McLaughlin KA, Petukhova M et al (2013) Dissociation in posttraumatic stress disorder: evidence from the world mental health surveys. Biol Psychiatry 73:302–312. https://doi.org/10.1016/j.biopsych.2012.08.022
Waller NG, Ross CA (1997) The prevalence and biometric structure of pathological dissociation in the general population: Taxometric and behavior genetic findings. J Abnorm Psychol 106:499–510. https://doi.org/10.1037/0021-843X.106.4.499
Zikić O, Cirić S, Mitković M (2009) Depressive phenomenology in regard to depersonalization level. Psychiatria Danubina 21:320–326

Competing interest reported. Dr. Stein has received consultancy honoraria from Discovery Vitality, Johnson & Johnson, Kanna, L’Oreal, Lundbeck, Orion, Sanofi, Servier, Takeda and Vistagen.

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Depersonalization/derealization and its relationship to mood and anxiety disorders in the National Comorbidity Survey-Replication (NCS-R)

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Abstract

1. INTRODUCTION

2. METHODS

2.1. Participants

2.2. Assessment

2.3. Statistical analysis

3. RESULTS

3.1. Prevalence of DPDR-C

3.2. Predictors of dpdr in MAD

3.3. Relationship of dpdr to MAD illness characteristics

3.4. Relationship of dpdr to functional impairment

4. DISCUSSION

5. CONCLUSION

Declarations

Author Contribution

References

Additional Declarations

Status:

Version 1