Hartside Unit, St Nicholas Hospital, Gosforth, Newcastle NE3 3XT
Depersonalisation Research Unit, Institute of Psychiatry, London
Correspondence: Anthony David, Section of Cognitive Neuropsychiatry, Box 68, Institute of Psychiatry, DeCrespigny Park, London SE5 8AF, UK. Tel: +44 (0)20 7848 0138; fax: +44 (0)20 7848 0572; e-mail: a.david{at}iop.kcl.ac.uk
![]() |
ABSTRACT |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Aims To carry out a large and comprehensive clinical and psychopathological survey of a series of patients who made contact with a research clinic.
Method A total of 204 consecutive eligible referrals were included: 124 had a full psychiatric examination using items of the Present State Examination to define depersonalisation/derealisation and 80 had either a telephone interview (n=22) or filled out a number of self-report questionnaires. Cases assessed were diagnosed according to DSMIV criteria.
Results The mean age of onset was 22.8 years; early onset was associated with greater severity. There was a slight male preponderance. The disorder tended to be chronic and persistent. Seventy-one per cent met DSMIV criteria for primary depersonalisation disorder. Depersonalisation symptom scores correlated with both anxiety and depression and a past history of these disorders was commonly reported. Dissociative amnesia was not prominent.
Conclusions Depersonalisation disorder is a recognisable clinical entity but appears to have significant comorbidity with anxiety and depression. Research into its aetiology and treatment is warranted.
![]() |
INTRODUCTION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
As well as describing the cohort, we sought to address two main questions:
![]() |
METHOD |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Participants
A total of 204 people with a putative diagnosis of depersonalisation
disorder seeking help or information were recruited via clinical referrals to
the Depersonaliation Research Unit at the Institute of Psychiatry, London
(n=130), and through the Unit's website (n=55), media
announcements (n=14) and patient support organisations
(n=5).
Assessments
Demographic details, along with medical and psychiatric history, were
obtained from all participants. A detailed history of the nature and course of
their depersonalisation was also obtained. A total of 124 referrals had a full
psychiatric interview and assessment at the request of the individual and
their referring clinician. The clinical assessment incorporated the Present
State Examination (PSE; Wing et
al, 1974). An additional 22 participants had a telephone
interview using the key PSE items and the remaining 58 supplied detailed
written information on a clinic form and by completing several questionnaires.
The PSE includes items for depersonalisation and derealisation. To summarise
definitions given in the glossary, for each item: 0=not present; 1=moderately
intense or transient; and 2=intense and persistent. Our case definition
required a total score of 2 without an obvious additional clinical
diagnosis or prominent non-dissociative symptomatology. This has been shown
previously to have good sensitivity and specificity when measured against a
new and established self-report measure (see below)
(Lambert et al,
2000). A final clinical diagnosis was made according to
DSMIV criteria, with the PSE items being used to help define the core
symptoms of depersonalisation and derealisation.
Self-report questionnaires
The Beck Anxiety Inventory (BAI; Beck
et al, 1988a) and the Beck Depression Inventory
(BDI; Beck et al,
1988b) were used. A score of 10 on either scale is
considered within the normal range and a score of
30 above
is severe.
The Dissociative Experiences Scale, version II (DES; Bernstein & Putnam, 1986; Carlson & Putnam, 1993), was also used. This is a 28-item self-report questionnaire with a cut-off score of 30 for severe dissociative disorders (Carlson & Putnam, 1993). Factor analysis shows this scale to have three main sub-scales: depersonalisation/derealisation (DESDP/DR); amnesia for dissociative experiences (DESAmnesia); and absorption and imaginative involvement (DESAbsorption) (Carlson et al, 1991). Eight items make up the taxon sub-scale (DESTaxon) (Simeon et al, 1998); this is sensitive to the detection of depersonalisation disorder, with a cut-off score of 13.
![]() |
RESULTS |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
|
Course
The most common description of the lifetime pattern of depersonalisation
was chronic (64%) and with little or no fluctuation (78%)
(Table 2). The longest single
episode for the majority (69%) was 1 year or more. Seventy-nine per cent of
participants reported impaired social and/or work functioning (see Appendix
for clinical descriptions).
|
Onset and duration
The mean age at onset of depersonalisation was 22.8 years, range 4-69
(Table 1), although 30%
reported the onset before the age of 16 years. We divided the sample into one
of three groups, depending upon age at onset: early (0-16 years); mid (17-39
years) and late (40+ years). One-way analysis of variance (ANOVA) revealed
that the early-onset group scored significantly more highly than the mid-onset
group, who in turn scored more highly than the late-onset group (see
Table 3) on all the DES
sub-scales and nearly significantly on DESTaxon (F=2.748,
d.f.=195, P=0.07). No effect of age at onset was observed for the
BDI, BAI or PSE ratings (see Appendix).
|
Dissociative Experiences Scale (DES)
Mean scores from the DES (Tables
1 and
3) showed that female
participants tended towards higher scores across all sub-scales than the
males, but none reached statistical significance. Eighty per cent of
participants scored on or above the DESTaxon cut-off score of 13 for
depersonalisation disorder and 90% scored on or above 8 on the DESDP/DR
sub-scale (76% >15 and 69% >20), with only 30% scoring in the
dissociative disorders range. Scores on the DESAmnesia sub-scale were
noticeably lower than in other groups of patients with mixed dissociative
disorders (Dubester & Braun,
1995; Putnam et al,
1996).
The early- and late-onset groups were more likely to report hearing voices
(2=14.47, d.f.=4, P=0.006) than the mid-onset group
but were no more likely to use alcohol or drugs, have other psychiatric
diagnoses, to have been hospitalised or to have suffered head trauma (90%
thought that the voices were not real). The mean reported
duration of depersonalisation was 13.9 years, range 0.5-69 (see
Table 1). There were no
significant correlations between length of illness (all r<0.1) and
other clinical variables.
Subjects found it difficult to categorise the onset of their disorder,
although just over one-third (38%) described a sudden onset
(Table 2). These participants
were more likely to experience seeing flashes of light
(2=4.671, d.f.=1, P=0.04) and had a significantly
lower mean score of 6.7 (s.d.=8.6) on the DESAmnesia sub-scale compared
with the gradual and unclear onset groups: mean DESAmnesia=12.3
(s.d.=14.7), t=2.68 and P=0.008. No other sub-scale scores
from the DES were significantly different.
Clinical assessment and PSE ratings
Comparisons were made between participants who were assessed clinically
with an interview (n=124) and the remainder (n=80). There
were no significant differences between the two groups on age
(t=-0.56, P=0.58), gender (2=0.47,
P=0.49), duration of illness (t=0.93, P=0.35), age
at onset (t=-0.45, P=0.65), DESMean (t=0.34,
P=0.74), DESTaxon (t=0.62, P=0.54) and any
sub-scale. There was no difference on the BDI score (t=-0.48,
P=0.63) but there was a trend for slightly higher BAI anxiety scores
(t=1.7, P=0.09) in the non-interviewed group. There were no
differences between those participants with PSE ratings (including telephone
interviewees) and those without. The main reasons why some subjects did not
have a clinical assessment were: problems traveling to the clinic; lack of a
responsible clinician to sanction the referral; and the need not to complicate
existing clinical care.
Of those clinically assessed or with PSE ratings, formal diagnosis by a qualified psychiatrist in the clinic (according to DSMIV) revealed 71% with primary depersonalisation disorder, 18% with depersonalisation secondary to major depression or dysthymic disorder, generalised anxiety disorder, agoraphobia (with and without panic) and obsessivecompulsive disorder, 3% with transient depersonalisation and 8% who were not assigned or where the diagnosis was unsure. MannWhitney tests revealed that PSE scores were significantly higher for participants designated with primary depersonalisation disorder, including transient cases (n=108; 74%), compared with those designated with secondary depersonalisation or other disorder (n=38) for both depersonalisation (P<0.001; depersonalisation mean= 1.65, median=2; secondary: mean=1.44, median=1) and derealisation ratings (P<0.001; derealisation mean=1.46, median=2; secondary: mean=0.79, median=1). There were no differences in terms of age or gender.
According to PSE ratings, depersonalisation was present in 96% and intense in 66% of cases. Symptoms of derealisation were present in 80% and intense in 49% of cases. Seventy-three per cent reported symptoms of depersonalisation and derealisation, 21% reported depersonalisation symptoms only and 6% reported derealisation symptoms only.
Attributions
Many participants (n=111) gave causal attributions for
depersonalisation. Factors identified were psychological (15%), traumatic
event (14%), substance misuse (14%), multiple (20%) and none obvious (27%).
Participants were asked about factors that improved depersonalisation
symptoms: 27% reported none, 19% physical (diet/exercise), 13% psychological,
8% social, 8% situational, 5% alcohol/drugs and the remaining 20% identified
multiple factors. Psychological stress (16%), environmental lighting (10%) and
physical stressors such as fatigue (12%) were identified as factors known to
worsen depersonalisation.
Past medical and psychiatric history
Of all the participants, 62% reported no significant previous or current
(60%) medical condition. Conditions mentioned included head injury
(n=5), asthma (n=5), irritable bowel syndrome (n=4)
and thyroid problems (n=3). Forty-two per cent reported undergoing a
brain scan. Sixteen participants (8%) attributed a physical
illness, specifically a viral infection, as the cause of the depersonalisation
disorder. Tinnitus was mentioned in 29% of respondents and migraine in 31%,
one-third of whom believed that their headaches and depersonalisation were
connected.
For all participants (n=204), 50% reported a previous psychiatric diagnosis. The biggest single diagnostic category was depression in 62% (Table 2); 42% had experienced psychiatric hospitalisation and, of these, 57% had had more than one admission. The primary reason cited was major depression in (35%). Seventy-three per cent reported current panic attacks and 59% said they were afraid to go out alone. The majority (72%) described persistent thoughts (mainly about depersonalisation) but only 26% said that they carried out any associated behaviours, for example checking or rituals. Seventy per cent of participants were currently taking psychotropic medication and these included the gamut of antidepressants and anxiolytics.
Alcohol and drugs
Of the participants who answered questions relating to alcohol and illicit
drug use (n=154), six reported being previously treated for alcohol
misuse (one current) and eight for drug misuse (two current). Forty-six people
said that they had used illegal drugs in the past, with the majority reporting
cannabis use only (n=20) and the remainder LSD, ecstasy, cocaine and
various combinations of drugs. Forty participants reported using illicit drugs
and 28 using alcohol just before the initial onset of depersonalisation; the
role of drugs and alcohol in depersonalisation will be reported
separately.
Family history
There was a suggestive family history (first- or second-degree relative) of
depersonalisation disorder in 10% of cases. For all participants
(n=204), 30% reported a history of some psychiatric disorder in a
first-degree relative. The largest single diagnostic category was depression
(28%), followed by alcohol misuse (15%) and panic (14%).
Anxiety and depression
The mean BAI score was 21.1 (s.d.=12.2) and the mean BDI score 22.0
(s.d.=11.5) for the entire sample. The BAI scores correlated significantly
(r=0.25-0.41; all P<0.05), as did the BDI scores
(r=0.35-0.52; all P<0.01), with all sub-scale scores from
the DES. We used BDI and BAI scores to define operationally both primary and
secondary depersonalisation. One-way ANOVA showed that participants scoring in
the normal range (0-11) on both the BAI and BDI had
significantly lower mean scores on all sub-scales of the DES (except
DESAmnesia, which was generally low) than all other groups. Out of the
19 with no depression or anxiety, seven (37%) scored more than the
DESTaxon cut-off of 13 and may be said to have pure
depersonalisation. Their mean (s.d.) DESTaxon score compared
with the remaining 185 subjects was 12.0 (12.1) v. 39.7 (21.5);
F 5.54; P<0.001. Out of 57 with no or minimal depression
or anxiety (scores of 18 on the BAI and BDI, respectively), 22 (38.6%) had
pure depersonalisation.
![]() |
DISCUSSION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Limitations
The main limitation of this study was the criterion used to detect
depersonalisation: 61% of the sample underwent a full psychiatric examination
whereas the remainder were assessed on the basis of completed questionnaires
(supplemented by a telephone interview in some). However, there were no
significant differences between the two groups on a number of demographic and
clinical variables. In addition, this sample was not epidemiologically based.
Various biases will have affected self- and practitioner referrals. The option
of contact through the internet may have biased the sample towards relatively
high educational attainment and perhaps male gender
(Senior et al, 1997)
and less depression (Lambert et
al, 2000), although a similar gender ratio was reported by
Simeon et al (1997)
in the USA, whose clinic attracts patients via media
advertisements. Furthermore, family and past psychiatric history were
based on self-report and an unstructured clinical interview without
independent corroboration.
Clinical course
There was no uniform pattern to the mode of onset. Sudden onset did not
appear to mark out a distinct subgroup. Depersonalisation disorder tended to
occur around 23 years of age (range 4-69), which is somewhat later than Simeon
et al's 1997 series but similar to older series (e.g.
Sedman, 1966). With our larger
sample we were able to separate an early-onset group (5-16 years) who appeared
to have a more severe disorder in that they were more likely to report higher
depersonalisation disorder symptomatology and greater levels of anxiety and
depression (see also Brauer et al,
1970). They also endorsed a question regarding hallucinations of
voices. However, it is reassuring that in most cases several years had passed
without any suggestion of a psychotic illness developing. These
phenomenological differences between early and late onset were not accounted
for by a greater use of illicit drugs or alcohol underlying the psychiatric
diagnosis. Depersonalisation symptoms in general appear to improve with age
(Sedman, 1966), but in line
with classical descriptions and Simeon et al's findings
(1997) we found that
depersonalisation disorder tends to run a chronic and unremitting course (see
Appendix).
Depersonaliation and derealisation
Seventy-three per cent of participants reported symptoms of both
depersonalisation and derealisation, the latter as a single phenomenon being
rare (see also Sedman, 1966).
The majority of participants were designated as having a clinical diagnosis of
primary depersonalisation disorder (DSMIV
depersonalisation disorder). The main symptoms focused on emotional and
sensory/perceptual disturbances such as self-reported flattening or
blunting of affect, feeling as if the world and/or the self was
unreal or like seeing the world through a goldfish bowl.
This supports the placing together of depersonalisation and derealisation as
in the ICD10 classification and not their separation as in the
DSMIV. Pure derealisation does exist and may well have a distinct
neurophysiological basis because it resembles the syndrome of visual
hypoemotionality (Sierra et al,
2002a). However, current and previous work have failed to
show any clinical factors unique to idiopathic derealisation
(Lambert et al,
2000).
Associations: other psychiatric disorders
Clues to aetiology come from some of the clinical associations. Just under
half of all participants reported seeing flashes of light,
suffered from tinnitus and/or migraine. Patients with migraine have been noted
to experience symptoms of depersonalisation, suggesting that this association
may not be due to chance (Lambert et
al, 2002). Indeed, such an association (38%) was noted by
Shorvon et al in 1946. No cases of temporal lobe disorder were
uncovered, although further specific tests such as electroencephalography and
magnetic resonance imaging were not carried out (see
Lambert et al, 2002).
Trauma (including physical/sexual abuse) was recorded as a contributing factor
in 14% of cases compared with the 43% reported by Simeon et al
(1997) who had been subjected
to childhood abuse including domestic violence. Again, specific study of such
antecedents may be worthwhile. Factors that were identified by some to improve
depersonalisation, such as diet, exercise, alcohol and fatigue, were listed by
others as worsening the condition.
The main risk factor was a past (and family) psychiatric history, although this was non-specific. Half of the sample reported being diagnosed formally with one or more psychiatric disorders (besides depersonalisation disorder), the most common being depression and/or anxiety (Dixon, 1963). The majority of participants reported having panic attacks (Cassano et al, 1989; Segui et al, 2000), prompting a reevaluation of Roth's phobic anxietydepersonalisation syndrome concept (Roth, 1959), generalised anxiety, low or flat mood (Ackner, 1954; Brauer et al, 1970; Sedman, 1970) as well as symptoms specific to depersonalisation disorder.
Other comorbid diagnoses were not made using a structured clinical interview but scores on the BAI and BDI will enable comparison with other case series. Correlations between depersonalisation-specific symptoms from the DES were highest with depression ratings, suggesting a degree of overlap. On the other hand, it has been shown that prognosis of anxiety disorder, particularly panic, is worsened if accompanied by depersonalisation (Segui et al, 2000). The reasons why some people develop depersonalisation as a complication of another neurotic disorder deserves further investigation.
Clearly, the clinical distinction between primary and secondary depersonalisation seems easy to make but is not absolute. We were able to extract a small group who had no symptoms of either depression or anxiety, more than one-third of whom scored above a validated cut-off for depersonalisation disorder. Links with anxiety and depression appear to be stronger than dissociation, given the low scores on amnesia items in the DES (Dubester & Braun, 1995). Many authorities regard amnesia recurrent discontinuities in conscious awareness as the hallmark of dissociation (Putnam et al, 1996). The relatively low level of childhood abuse in this cohort again supports a separation from other dissociative disorders, as does the lack of significant female preponderance in this and other series (Shorvon et al, 1946; Simeon et al, 2001). All in all, these clinical features favour placing depersonalisation disorder with anxiety and mood disorders (as in the ICD10) rather than with dissociative disorders (as in the DSMIV).
Comorbidity may arise from attempts to cope with depersonalisation, such as anxious or obsessive checking of symptoms change leading to compulsive behaviours (Simeon & Hollander, 1993), cognitive and behavioural avoidance of potential exacerbating factors or, instead, feelings of hopelessness. Differing appraisals currently are being explored through the development of theoretical cognitivebehavioural models, and in practice using a variety of therapeutic techniques including attention training (Senior et al, 2001). In view of the chronicity and persistence of the condition, research into its aetiology and possible treatments, both pharmacological and psychological, is urgently required.
![]() |
Clinical Implications and Limitations |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
LIMITATIONS
![]() |
APPENDIX |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Case 1
A 26-year-old male student with depersonalistion disorder for 9 years who
failed to complete his studies owing to illness.
Onset and attribution Acute onset following illicit drug use at a party. Believes that cannabis was spiked with unknown chemical.
Subjective description Reported feeling emotionally numb and cut-off from other people. Visual disturbance of hands and feet appearing to increase and decrease in size when I stare at them. Said that he felt as if I am living in a film it's all black and white and 2D. I know that it is not real but that is how it feels.
Diagnosis The disorder is constant and chronic. Previous psychiatric differential diagnoses were of anxiety, panic, depression and schizophrenia.
Case 2
A 30-year-old male journalist with depersonalistion disorder for 15
years.
Onset and attribution Acute onset following alcohol binge at a party when aged 15 years. Patient believes that parental abuse was a contributing factor.
Subjective description I'm Unreal and truly alone like an outsider looking in... When I walk down the street I feel as if I am swaying and the pavement is moving. I feel as if I can't connect normally to people on a mental level. I just don't feel anything I think I have gone mad.
Diagnosis The disorder is constant and chronic, with a previous psychiatric diagnosis of depression.
Case 3
A 29-year-old female sales manager with depersonalistion disorder for 6
months who is married with a family business.
Onset and attribution Current episode: gradual onset following recent marriage. Previous episode: acute onset at age 20 years following a prolonged period of stress (duration of disorder=5 years).
Subjective description I don't know who I am of course I am **** but I feel like a robot, like I am listening to someone else talking, like I am looking at myself from the outside, but it is not another voice or body it is mine, it is me, it just doesn't feel like it... I spend all day trying to figure it out. Maybe I am too analytical. Nothing makes it better but being with other people makes it worse.
Diagnosis The disorder is episodic and becoming chronic. There was no previous psychiatric diagnosis.
Case 4
A 54-year-old married female barrister with depersonalistion disorder for
30 years.
Onset and attribution Unsure of onset. Patient recalls feeling the disorder all of her life.
Subjective description I feel nothing never have. When my children were born nothing. I am not sure what love is, I have been married 30 years, it drives my husband mad when I talk about it. I just feel nothing not pain, not anxiety, not happiness. I am not depressed I am nothing.
Diagnosis The disorder is constant and chronic, with a previous psychiatric diagnosis of depression.
Case 5
A 40-year-old divorced male with depersonalistion disorder for 2 years who
is unemployed.
Onset and attribution Gradual onset over 6 months for two separate episodes. Both episodes attributed to unhappy relationships.
Subjective description These feelings are unbearable. It is like walking around with a goldfish bowl on your head... I can't drive, can't work. You try taking photos when everything you look at feels... like it is the wrong colour and depth is all wrong... When you try and tell people they think you're mad.
Diagnosis The disorder is constant and chronic within each episode. There was a previous diagnosis of anxiety and depression.
Case 6
A 28-year-old male, unemployed shop assistant with depersonalistion
disorder for 4 years.
Onset and attribution Gradual onset over several months with each separate episode becoming more intense. No attribution made or significant life events reported.
Subjective description This sounds mad but I am not me. I look in the mirror and I don't see me. I don't know who it is that I see and I don't know where the real me has gone. Logically that cannot be the case, but that is how it feels. I spend all day checking myself and it's never me. I panic and try to solve where I am. I feel so depressed, like I can't go on living this way but I live in hope that one day I will wake up and it will be me.
Diagnosis The disorder is constant and chronic with anxiety and depression. There was a previous psychiatric diagnosis of panic and obsessivecompulsive disorder.
![]() |
ACKNOWLEDGMENTS |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
![]() |
REFERENCES |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Aderibigbe, Y. A., Bloch, R. M. & Walker, W. R. (2001) Prevalence of depersonalization and derealization experiences in a rural population. Social Psychiatry and Psychiatric Epidemiology, 36, 63-69.[CrossRef][Medline]
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSMIV). Washington, DC: APA.
Beck, A. T., Epstein, N., Brown, G., et al (1988a) An inventory for measuring clinical anxiety: psychometric properties. Journal of Consulting and Clinical Psychology, 56, 893-897.[CrossRef][Medline]
Beck, A. T., Steer, R. A. & Garbin, M. G. (1988b) Psychometric properties of the Beck Depression Inventory: twenty-five years of evaluation. Clinical Psychology Review, 8, 77-100.[CrossRef]
Bernstein, E. & Putnam, F. (1986) Development, reliability and validity of a dissociation scale. Journal of Nervous and Mental Disease, 174, 727-735.[Medline]
Brauer, R., Harrow, M. & Tucker, G. J. (1970) Depersonalisation phenomena in psychiatric patients. British Journal of Psychiatry, 117, 509-515.[Medline]
Carlson, E. B. & Putnam, F. W. (1993) An update on the Dissociative Experiences Scale. Dissociation, 6, 16-27.
Carlson, E. B., Putnam, F. W., Ross, C. A., et al (1991) Factor analysis on the dissociative experiences scale: a multicentre study. In Proceedings of the Eighth International Conference on Multiple Personality and Dissociative States (eds B. G. Braun & E. B. Carlson). Chicago, IL: Rush.
Cassano, G. B., Petracca, A., Perugi, G., et al (1989) Derealization and panic attacks: evaluation on 150 patients with panic disorder/agoraphobia. Comprehensive Psychiatry, 30, 5-12.[Medline]
Dixon, J. C. (1963) Depersonalisation phenomena in a sample population of college students. British Journal of Psychiatry, 109, 371-375.
Dubester, K. A. & Braun, B. G. (1995) Psychometric properties of the Dissociative Experiences Scale. Journal of Nervous and Mental Disease, 183, 231-235.[Medline]
Grigsby, J. & Kaye, K. (1993) Incidence and correlates of depersonalization following head trauma. Brain Injury, 7, 507-513.[Medline]
Kihlstrom, J. F., Gilsky, M. L. & Angiulo, M. J. (1994) Dissociative tendencies and dissociation disorders. Journal of Abnormal Psychology, 103, 117-124.[CrossRef][Medline]
Lambert, M. V., Senior, C., Phillips, M. L., et al (2000) Depersonalization in cyberspace. Journal of Nervous and Mental Disease, 188, 764-771.[CrossRef][Medline]
Lambert, M. V., Senior, C., Fewtrell, D. W., et al (2001a) Primary and secondary depersonalisation disorder: a psychometric study. Journal of Affective Disorders, 63, 249-256.[CrossRef][Medline]
Lambert, M. V., Senior, C., Phillips, M. L., et al (2001b) Visual imagery and depersonalisation. Psychopathology, 34, 259-264.[CrossRef][Medline]
Lambert, M. V., Sierra, M., Phillips, M. L., et al (2002) The spectrum of organic depersonalisation: a review plus four new cases. Journal of Neuropsychiatry and Clinical Neuroscience, 14, 141-154.[CrossRef][Medline]
Mayou, R., Bryant, R. & Ehlers, A. (2001)
Prediction of psychological outcomes one year after a motor vehicle accident.
American Journal of Psychiatry,
158,
1231-1238.
McGuire, P. K., Cope, H. & Fahy, T. A. (1994) Diversity of psychopathology associated with use of 3,4-methylenedioxymethamphetamine (Ecstasy). British Journal of Psychiatry, 165, 391-395.[Abstract]
Noyes, R. & Kletti, R. (1977) Depersonalisation in response to life-threatening danger. Comprehensive Psychiatry, 18, 375-384.[Medline]
Phillips, M. L., Medford, N., Senior, C., et al (2001a) Depersonalisation disorder: thinking without feeling. Psychiatry Research: Neuroimaging, 108, 145-160.[CrossRef]
Phillips, M. L., Sierra, M., Hunter, E., et al
(2001b) Service innovations: a depersonalisation
research unit progress report. Psychiatric Bulletin,
25,
105-108.
Putnam, F. W., Carlson, E. B., Ross, C. A., et al (1996) Patterns of dissociation in clinical and nonclinical samples. Journal of Nervous and Mental Disease, 184, 673-679.[CrossRef][Medline]
Ross, C. A., Joshi, S. & Currie, R. (1990) Dissociative experiences in the general population. American Journal of Psychiatry, 147, 1547-1552.[Abstract]
Roth, M. (1959) The phobic anxietydepersonalisation syndrome. Journal of Neuropsychiatry, 1, 293-306.
Sedman, G. (1966) Depersonalisation in a group of normal subjects. British Journal of Psychiatry, 112, 907-912.[Medline]
Sedman, G. (1970) Theories of depersonalisation: a re-appraisal. British Journal of Psychiatry, 117, 1-14.[Medline]
Segui, J., Maruez, M., Garcia, L., et al (2000) Depersonalization in panic disorder: a clinical study. Comprehensive Psychiatry, 41, 172-178.[Medline]
Senior, C., Phillips, M. & David, A. S. (1997) Psychiatry and the WWW: some implications. Psychiatric Bulletin, 21, 775-778.
Senior, C., Hunter, E., Lambert, M. V., et al (2001) Depersonalisation. Psychologist, 14, 128-132.
Shorvon, H. J., Hill, J. D. N., Burkitt, E., et al (1946) The depersonalization syndrome. Proceedings of the Royal Society of Medicine, 39, 779-792.
Sierra, M. & Berrios, G. E. (1998) Depersonalization: neurobiological perspectives. Biological Psychiatry, 44, 898-908.[CrossRef][Medline]
Sierra, M., Lopera, F., Lambert, M. V., et al
(2002a) Separating depersonalisation and
derealisation: the relevance of the lesion method.
Journal of Neurology, Neurosurgery and Psychiatry,
72,
530-532.
Sierra, M., Senior, C., Dalton, J., et al
(2002b) Autonomic response in depersonalization
disorder. Archives of General Psychiatry,
59,
833-838.
Simeon, D. & Hollander, E. (1993) Depersonalization disorder. Psychiatric Annals, 23, 382-388.
Simeon, D., Gross, S., Guralnik, O., et al (1997) Feeling unreal: 30 cases of DSMIIIR depersonalization disorder. American Journal of Psychiatry, 154, 1107-1113.[Abstract]
Simeon, D., Guralnik, O., Gross, S., et al (1998) The detection and measurement of depersonalisation disorder. Journal of Nervous and Mental Disease, 186, 536-542.[CrossRef][Medline]
Simeon, D., Guralnik, O., Schmeidler, J., et al
(2001) The role of childhood interpersonal trauma in
depersonalization disorder. American Journal of
Psychiatry, 158,
1027-1033.
Wing, J. K., Cooper, J. E. & Sartorius, N. (1974) Measurement and Classification of Psychiatric Symptoms. Cambridge: Cambridge University Press.
World Health Organization (1992) Tenth Revision of the International Classification of Diseases and Related Health Problems (ICD10). Geneva: WHO.
Received for publication July 17, 2002. Revision received December 4, 2002. Accepted for publication December 9, 2002.