Baker 2003
Baker 2003
DAWN BAKER, ELAINE HUNTER, EMMA LAWRENCE, NICHOLAS MEDFORD, MAXINE PATEL, CARL
SENIOR, MAURICIO SIERRA, MICHELLE V. LAMBERT, MARY L. PHILLIPS and ANTHONY S. DAVID
BJP 2003, 182:428-433.
Access the most recent version at DOI: 10.1192/bjp.182.5.428
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428
D E P E R S ON A L I S AT I ON D I S O R D E R
written information on a clinic form and by Table 1 Mean (s.d.) age, age at onset and duration of depersonalisation disorder in all participants
completing several questionnaires. The PSE
includes items for depersonalisation and All participants Male Female
derealisation. To summarise definitions
(n¼204)
204) (n¼112)
112) (n¼92)
92)
given in the glossary, for each item: 0¼not
0 not
present; 1¼moderately
1 moderately intense or transient; Age (years) 36.3 (12.77) 35.2 (11.59) 37.5 (14.03)
and 2¼intense
2 intense and persistent. Our case
Age at onset (years) 22.8 (11.94) 21.5 (9.67) 24.3 (14.14)
definition required a total score of 52
Duration (years) 13.9 (13.43) 13.2 (12.4) 14.7 (14.62)
without an obvious additional clinical
DES^Mean score 23.84 (14.94) 22.89 (13.83)1 24.98 (16.17)1
diagnosis or prominent non-dissociative
symptomatology. This has been shown DES^Taxon score 24.78 (16.25) 23.75 (15.10)2 26.01 (17.53)2
previously to have good sensitivity and DES, Dissociative Experiences Scale.
specificity when measured against a new 1. Percentage above cut-off for dissociation: 30% for both males and females.
2. Percentage above cut-off for depersonalisation: 82% for males; 76% for females.
and established self-report measure (see
below) (Lambert et al, al, 2000). A final
clinical diagnosis was made according to some form of higher education; 38% were Table 2 Associated diagnoses, onset and course in
DSM–IV criteria, with the PSE items being not working or were unemployed. (n¼204)
depersonalisation disorder (n 204)
used to help define the core symptoms of
depersonalisation and derealisation.
Course n (%)
The most common description of the life-
time pattern of depersonalisation was Onset
Self-report questionnaires
‘chronic’ (64%) and with little or no fluc- Sudden 77 (38)
The Beck Anxiety Inventory (BAI; Beck et
tuation (78%) (Table 2). The longest single Gradual 33 (16)
al,
al, 1988a
1988a) and the Beck Depression Inven-
episode for the majority (69%) was 1 year Unclear 94 (46)
tory (BDI; Beck et al,al, 1988b
1988b) were used.
or more. Seventy-nine per cent of partici- Course
A score of 410 on either scale is considered
pants reported impaired social and/or work Chronic 131 (64)
within the ‘normal’ range and a score of
functioning (see Appendix for clinical Episodic, becoming chronic 37 (18)
530 above is ‘severe’.
descriptions). Long episodes 16 (8)
The Dissociative Experiences Scale,
version II (DES; Bernstein & Putnam, 1986; Brief episodes 10 (5)
Carlson & Putnam, 1993), was also used. Onset and duration Unsure 10 (5)
This is a 28-item self-report questionnaire The mean age at onset of depersonalisation Persistence
with a cut-off score of 30 for severe dissoci- was 22.8 years, range 4–69 (Table 1), No fluctuation 122 (55)
ative disorders (Carlson & Putnam, 1993). although 30% reported the onset before Little fluctuation 46 (23)
Factor analysis shows this scale to have the age of 16 years. We divided the sample Fluctuating symptoms
three main sub-scales: ‘depersonalisation/ into one of three groups, depending upon Specific triggers 16 (8)
derealisation’ (DES–DP/DR); ‘amnesia’ for age at onset: early (0–16 years); mid (17–
No specific triggers 28 (14)
dissociative experiences (DES–Amnesia); 39 years) and late (40+ years). One-way
and ‘absorption’ and imaginative involve- Other diagnoses1
analysis of variance (ANOVA) revealed
ment (DES–Absorption) (Carlson et al, al, Depression 127 (62)
that the early-onset group scored signifi-
1991). Eight items make up the ‘taxon’ Anxiety disorder 82 (41)
cantly more highly than the mid-onset
sub-scale (DES–Taxon) (Simeon et al, al, group, who in turn scored more highly than Obsessive^compulsive disorder 33 (16)
1998); this is sensitive to the detection of the late-onset group (see Table 3) on all the Agoraphobia 28 (14)
depersonalisation disorder, with a cut-off DES sub-scales and nearly significantly on Bipolar disorder 16 (8)
score of 13. DES–Taxon (F (F¼2.748,
2.748, d.f.¼195,
d.f. 195, P¼0.07).
0.07). Schizophrenia 14 (7)
No effect of age at onset was observed for Drug dependency 14 (7)
the BDI, BAI or PSE ratings (see Appendix). Alcohol dependency 10 (5)
RESULTS
1. According to patient self-report.
Demographic characteristics Dissociative Experiences Scale
The mean age of the 204 participants (112 (DES)
males and 92 females) was 36.3 years, Mean scores from the DES (Tables 1 and 3) 69% 420), with only 30% scoring in the
range 16–74 (Table 1). Around two-thirds showed that female participants tended to- dissociative disorders range. Scores on the
were from the greater London area. Others wards higher scores across all sub-scales DES–Amnesia sub-scale were noticeably
came from the rest of the UK or mainland than the males, but none reached statistical lower than in other groups of patients with
Europe (n (n¼16),
16), North America and significance. Eighty per cent of participants mixed dissociative disorders (Dubester &
Canada (n(n¼15)
15) and Australasia (n(n¼3).
3). scored on or above the DES–Taxon cut-off Braun, 1995; Putnam et al,
al, 1996).
Fifty-one per cent were single, 38% were score of 13 for depersonalisation disorder The early- and late-onset groups were
cohabiting and 11% were separated/ and 90% scored on or above 8 on the more likely to report hearing voices
divorced/widowed. Fifty-four per cent had DES–DP/DR sub-scale (76% 415 and (w2¼14.47,
14.47, d.f.¼4,
d.f. 4, P¼0.006)
0.006) than the
429
B AK ER E T AL
T
Table
able 3 Mean (s.d.) scores from Dissociative Experiences Scale (DES), Beck Anxiety Attributions
Inventory (BAI) and Beck Depression Inventory (BDI) for early-, mid- and late-onset participants and
Many participants (n (n¼111)
111) gave causal
(n¼199;
correlation of duration of illness with all measures (n 199; some missing data) attributions for depersonalisation. Factors
identified were psychological (15%), trau-
Onset 0^16 years Onset 17^39 years Onset 440 years matic event (14%), substance misuse
(n¼56)
56) (n¼128)
128) (n¼15)
15) (14%), multiple (20%) and none obvious
(27%). Participants were asked about
DES^Mean** 28.45 (18.13) 22.77 (13.69) 15.74 (8.27) factors that improved depersonalisation
DES^Taxon 28.14 (19.21) 24.34 (15.13) 17.50 (12.46) symptoms: 27% reported none, 19%
DES^DP/DR* 39.91 (20.31) 37.98 (21.97) 22.44 (17.18) physical (diet/exercise), 13% psychological,
DES^Amnesia* 13.48 (19.34) 7.95 (10.04) 6.83 (7.63) 8% social, 8% situational, 5% alcohol/
drugs and the remaining 20% identified
DES^Absorption** 32.10 (21.44) 25.09 (16.31) 18.15 (12.15)
multiple factors. Psychological stress
BAI 22.42 (12.26) 20.00 (12.27) 24.20 (9.94)
(16%), environmental lighting (10%) and
BDI 23.14 (14.39) 21.06 (9.89) 24.67 (11.11)
physical stressors such as fatigue (12%)
DP/DR, depersonalisation/derealisation. were identified as factors known to worsen
*P50.05 (ANOVA, two-tailed); **P
**P50.01 (ANOVA, two-tailed). depersonalisation.
mid-onset group but were no more likely to differences between those participants with
use alcohol or drugs, have other psychiatric PSE ratings (including telephone inter- Past medical and psychiatric
diagnoses, to have been hospitalised or to viewees) and those without. The main history
have suffered head trauma (90% thought reasons why some subjects did not have a Of all the participants, 62% reported no
that the voices were not ‘real’). The mean clinical assessment were: problems travel- significant previous or current (60%)
reported duration of depersonalisation ling to the clinic; lack of a responsible clin- medical condition. Conditions mentioned
was 13.9 years, range 0.5–69 (see Table ician to sanction the referral; and the need included head injury (n (n¼5),
5), asthma (n(n¼5),
5),
1). There were no significant correlations not to complicate existing clinical care. irritable bowel syndrome (n (n¼4)
4) and
between length of illness (all r50.1) and Of those clinically assessed or with PSE thyroid problems (n (n¼3).
3). Forty-two per cent
other clinical variables. ratings, formal diagnosis by a qualified reported undergoing a ‘brain scan’. Sixteen
Subjects found it difficult to categorise psychiatrist in the clinic (according to participants (8%) attributed a physical
the onset of their disorder, although just DSM–IV) revealed 71% with primary illness, specifically a viral infection, as the
over one-third (38%) described a sudden depersonalisation disorder, 18% with deper- cause of the depersonalisation disorder.
onset (Table 2). These participants were sonalisation secondary to major depression Tinnitus was mentioned in 29% of respon-
more likely to experience seeing flashes of or dysthymic disorder, generalised anxiety dents and migraine in 31%, one-third of
(w2¼4.671,
light (w 4.671, d.f.¼1,
d.f. 1, P¼0.04)
0.04) and had disorder, agoraphobia (with and without whom believed that their headaches and
a significantly lower mean score of 6.7 panic) and obsessive–compulsive disorder, depersonalisation were connected.
(s.d.¼8.6)
(s.d. 8.6) on the DES–Amnesia sub-scale 3% with transient depersonalisation and For all participants (n (n¼204),
204), 50%
compared with the gradual and unclear 8% who were not assigned or where the reported a previous psychiatric diagnosis.
onset groups: mean DES–Amnesia¼12.3
DES–Amnesia 12.3 diagnosis was unsure. Mann–Whitney tests The biggest single diagnostic category was
(s.d.¼14.7),
(s.d. 14.7), t¼2.68
2.68 and P¼0.008.
0.008. No revealed that PSE scores were significantly depression in 62% (Table 2); 42% had ex-
other sub-scale scores from the DES were higher for participants designated with pri- perienced psychiatric hospitalisation and,
significantly different. mary depersonalisation disorder, including of these, 57% had had more than one
transient cases (n(n¼108;
108; 74%), compared admission. The primary reason cited was
with those designated with secondary deper- major depression in (35%). Seventy-three
Clinical assessment and PSE sonalisation or other disorder (n (n¼38)
38) for per cent reported current ‘panic attacks’
ratings both ‘depersonalisation’ (P (P50.001; de- and 59% said they were ‘afraid to go out
Comparisons were made between par- personalisation mean¼
mean 1.65, median¼2;
median 2; alone’. The majority (72%) described per-
ticipants who were assessed clinically with secondary: mean¼1.44,
mean 1.44, median¼1)
median 1) and ‘de- sistent thoughts (mainly about depersonali-
an interview (n(n¼124)
124) and the remainder realisation’ ratings (P
(P50.001; derealisation sation) but only 26% said that they carried
(n¼80).
80). There were no significant dif- mean¼1.46,
mean 1.46, median¼2;
median 2; secondary: mean¼
mean out any associated behaviours, for example
ferences between the two groups on age 0.79, median¼1).
median 1). There were no differences checking or rituals. Seventy per cent of
(t¼770.56, P¼0.58),
0.58), gender (w (w2¼0.47,
0.47, in terms of age or gender. participants were currently taking psycho-
P¼0.49),
0.49), duration of illness (t (t¼0.93,
0.93, According to PSE ratings, depersonali- tropic medication and these included the
P¼0.35),
0.35), age at onset (t (t¼7
70.45, sation was ‘present’ in 96% and ‘intense’ gamut of antidepressants and anxiolytics.
P¼0.65),
0.65), DES–Mean (t (t¼0.34,
0.34, P¼0.74),
0.74), in 66% of cases. Symptoms of derealisation
DES–Taxon (t (t¼0.62,
0.62, P¼0.54)
0.54) and any were ‘present’ in 80% and ‘intense’ in
sub-scale. There was no difference on the 49%
49% of cases. Seventy-three per cent re- Alcohol and drugs
BDI score (t (t¼770.48, P¼0.63)0.63) but ported symptoms of depersonalisation and Of the participants who answered ques-
there was a trend for slightly higher BAI derealisation, 21% reported depersonalisa- tions relating to alcohol and illicit drug
anxiety scores (t
(t¼1.7,
1.7, P¼0.09)
0.09) in the non- tion symptoms only and 6% reported use (n
(n¼154),
154), six reported being previously
interviewed group. There were no derealisation symptoms only. treated for alcohol misuse (one current)
430
D E P E R S ON A L I S AT I ON D I S O R D E R
and eight for drug misuse (two current). to date. The results both complement and (1997) we found that depersonalisation
Forty-six people said that they had used enhance those of earlier reports (Simeon disorder tends to run a chronic and
illegal drugs in the past, with the majority et al,
al, 1997; Lambert et al,
al, 2001a
2001a). unremitting course (see Appendix).
reporting cannabis use only (n (n¼20)
20) and
the remainder LSD, ecstasy, cocaine and Limitations Depersonaliation and derealisation
various combinations of drugs. Forty parti-
The main limitation of this study was the Seventy-three per cent of participants re-
cipants reported using illicit drugs and 28
criterion used to detect depersonalisation: ported symptoms of both depersonalisation
using alcohol just before the initial onset
61% of the sample underwent a full psychi- and derealisation, the latter as a single
of depersonalisation; the role of drugs
atric examination whereas the remainder phenomenon being rare (see also Sedman,
and alcohol in depersonalisation will be
were assessed on the basis of completed 1966). The majority of participants were
reported separately.
questionnaires (supplemented by a tele- designated as having a clinical diagnosis
phone interview in some). However, of ‘primary depersonalisation disorder’
Family history there were no significant differences (DSM–IV depersonalisation disorder). The
There was a suggestive family history between the two groups on a number of main symptoms focused on emotional and
(first- or second-degree relative) of demographic and clinical variables. In addi- sensory/perceptual disturbances such as
depersonalisation disorder in 10% of tion, this sample was not epidemiologically self-reported ‘flattening or blunting of
cases. For all participants (n
(n¼204),
204), 30% based. Various biases will have affected affect’, ‘feeling as if the world and/or the
reported a history of some psychiatric self- and practitioner referrals. The option self was unreal’ or ‘like seeing the world
disorder in a first-degree relative. The of contact through the internet may have through a goldfish bowl’. This supports
largest single diagnostic category was biased the sample towards relatively high the placing together of depersonalisation
depression (28%), followed by alcohol educational attainment and perhaps male and derealisation as in the ICD–10 classifi-
misuse (15%) and panic (14%). gender (Senior et al,
al, 1997) and less depres- cation and not their separation as in the
sion (Lambert et al, al, 2000), although a DSM–IV. Pure derealisation does exist
Anxiety and depression similar gender ratio was reported by and may well have a distinct neurophysio-
Simeon et al (1997) in the USA, whose logical basis because it resembles the
The mean BAI score was 21.1 (s.d.¼12.2)
(s.d. 12.2)
clinic attracts patients via ‘media advertise- syndrome of visual hypoemotionality
and the mean BDI score 22.0 (s.d.¼11.5)
(s.d. 11.5)
ments’. Furthermore, family and past psy- (Sierra et al,
al, 2002a
2002a). However, current
for the entire sample. The BAI scores
chiatric history were based on self-report and previous work have failed to show
correlated significantly (r
(r¼0.25–0.41;
0.25–0.41; all
and an unstructured clinical interview any clinical factors unique to ‘idiopathic’
P50.05), as did the BDI scores (r (r¼0.35–
0.35–
without independent corroboration. derealisation (Lambert et al,
al, 2000).
0.52; all P50.01), with all sub-scale
scores from the DES. We used BDI and
BAI scores to define operationally both Clinical course Associations: other psychiatric
primary and secondary depersonalisation. There was no uniform pattern to the mode disorders
One-way ANOVA showed that partici- of onset. Sudden onset did not appear to Clues to aetiology come from some of the
pants scoring in the ‘normal’ range (0–11) mark out a distinct subgroup. Depersonal- clinical associations. Just under half of all
on both the BAI and BDI had significantly isation disorder tended to occur around participants reported ‘seeing flashes of
lower mean scores on all sub-scales of 23 years of age (range 4–69), which is light’, suffered from tinnitus and/or
the DES (except DES–Amnesia, which somewhat later than Simeon et al’s al’s 1997 migraine. Patients with migraine have been
was generally low) than all other groups. series but similar to older series (e.g. Sed- noted to experience symptoms of deperso-
Out of the 19 with no depression or an- man, 1966). With our larger sample we nalisation, suggesting that this association
xiety, seven (37%) scored more than the were able to separate an early-onset group may not be due to chance (Lambert et al, al,
DES–Taxon cut-off of 13 and may be (5–16 years) who appeared to have a more 2002). Indeed, such an association (38%)
said to have ‘pure depersonalisation’. severe disorder in that they were more was noted by Shorvon et al in 1946. No
Their mean (s.d.) DES–Taxon score com- likely to report higher depersonalisation cases of temporal lobe disorder were un-
pared with the remaining 185 subjects disorder symptomatology and greater levels covered, although further specific tests such
was 12.0 (12.1) v. 39.7 (21.5); F 5.54; of anxiety and depression (see also Brauer as electroencephalography and magnetic
P50.001. Out of 57 with no or minimal et al,
al, 1970). They also endorsed a question resonance imaging were not carried out
depression or anxiety (scores of 418 on regarding hallucinations of voices. How- (see Lambert et al,
al, 2002). Trauma (includ-
the BAI and BDI, respectively), 22 ever, it is reassuring that in most cases ing physical/sexual abuse) was recorded as
(38.6%) had ‘pure depersonalisation’. several years had passed without any a contributing factor in 14% of cases com-
suggestion of a psychotic illness developing. pared with the 43% reported by Simeon
DISCUSSION These phenomenological differences et al (1997) who had been subjected to
between early and late onset were not childhood abuse including domestic
Depersonalisation disorder is probably not accounted for by a greater use of illicit violence. Again, specific study of such ante-
as rare as is commonly assumed. We have drugs or alcohol underlying the psychiatric cedents may be worthwhile. Factors that
amassed over 200 cases, slightly more diagnosis. Depersonalisation symptoms were identified by some to improve deper-
men than women, from a single clinic over in general appear to improve with age sonalisation, such as diet, exercise, alcohol
4 years – the largest cohort of people with (Sedman, 1966), but in line with classical and fatigue, were listed by others as
depersonalisation/derealisation described descriptions and Simeon et al’s al’s findings worsening the condition.
4 31
B AK ER E T AL
The main risk factor was a past (and behaviours (Simeon & Hollander, 1993), Case 3
family) psychiatric history, although this cognitive and behavioural avoidance of A 29-year-old female sales manager with deperso-
was non-specific. Half of the sample potential exacerbating factors or, instead, nalistion disorder for 6 months who is married with
reported being diagnosed formally with feelings of hopelessness. Differing apprai- a family business.
one or more psychiatric disorders (besides sals currently are being explored through Onset and attribution Current episode: gradual on-
depersonalisation disorder), the most the development of theoretical cognitive– set following recent marriage. Previous episode:
common being depression and/or anxiety behavioural models, and in practice using acute onset at age 20 years following a prolonged
(Dixon, 1963). The majority of participants a variety of therapeutic techniques includ- period of stress (duration of disorder¼5
disorder 5 years).
reported having ‘panic attacks’ (Cassano et ing ‘attention training’ (Senior et al, al, Subjective description ‘I don’t know who I am ^ of
al,
al, 1989; Segui et al,
al, 2000), prompting a re- 2001). In view of the chronicity and persis- course I am **** but I feel like a robot, like I am lis-
evaluation of Roth’s ‘phobic anxiety– tence of the condition, research into its tening to someone else talking, like I am looking at
depersonalisation syndrome’ concept aetiology and possible treatments, both myself from the outside, but it is not another voice
or body ^ it is mine, it is me, it just doesn’t feel like
(Roth, 1959), generalised anxiety, low or pharmacological and psychological, is
it. . . I spend all day trying to figure it out. Maybe I
flat mood (Ackner, 1954; Brauer et al, al, urgently required. am too analytical. Nothing makes it better but being
1970; Sedman, 1970) as well as symptoms with other people makes it worse.’
specific to depersonalisation disorder. ACKNOWLEDGEMENT Diagnosis The disorder is episodic and becoming
Other comorbid diagnoses were not
chronic. There was no previous psychiatric diagnosis.
made using a structured clinical interview The authors acknowledge the support of the
but scores on the BAI and BDI will enable Pilkington FamilyTrusts.
Case 4
comparison with other case series. Corre-
A 54-year-old married female barrister with deper-
lations between depersonalisation-specific APPENDIX
sonalistion disorder for 30 years.
symptoms from the DES were highest with
depression ratings, suggesting a degree of
Brief presentation of six ‘typical’ Onset and attribution Unsure of onset. Patient
overlap. On the other hand, it has been
cases of depersonalisation disorder recalls feeling the disorder all of her life.
shown that prognosis of anxiety disorder, The following case descriptions are anonymised, Subjective description ‘I feel nothing ^ never have.
reconstructed vignettes incorporating statements When my children were born ^ nothing. I am not
particularly panic, is worsened if accompa-
similar to those made by individuals from the sample sure what love is, I have been married 30 years, it
nied by depersonalisation (Segui et al, al, studied. drives my husband mad when I talk about it. I just
2000). The reasons why some people devel-
feel nothing ^ not pain, not anxiety, not happiness.
op depersonalisation as a complication of I am not depressed ^ I am nothing.’
Case 1
another neurotic disorder deserves further
A 26
26-year-old
-year-old male student with depersonalistion Diagnosis The disorder is constant and chronic,
investigation.
disorder for 9 years who failed to complete his stu- with a previous psychiatric diagnosis of depression.
Clearly, the clinical distinction between dies owing to illness.
primary and secondary depersonalisation
Onset and attribution Acute onset following illicit Case 5
seems easy to make but is not absolute.
drug use at a party. Believes that cannabis was A 40
40-year-old
-year-old divorced male with depersonalistion
We were able to extract a small group
‘spiked’ with unknown chemical. disorder for 2 years who is unemployed.
who had no symptoms of either depression
or anxiety, more than one-third of whom Subjective description Reported feeling emotionally Onset and attribution Gradual onset over 6 months
numb and cut-off from other people. Visual distur- for two separate episodes. Both episodes attributed
scored above a validated cut-off for deper-
bance of ‘hands and feet appearing to increase and to unhappy relationships.
sonalisation disorder. Links with anxiety decrease in size when I stare at them’. Said that he
and depression appear to be stronger than Subjective description ‘These feelings are unbear-
felt ‘as if I am living in a film ^ it’s all black and white
‘dissociation’, given the low scores on am- able. It is like walking around with a goldfish bowl
and 2D. I know that it is not real but that is how it
on your head. . . I can’t drive, can’t work.Y
work.You
ou try tak-
nesia items in the DES (Dubester & Braun, feels’.
ing photos when everything you look at feels . . . like
1995). Many authorities regard ‘amne- Diagnosis The disorder is constant and chronic. it is the wrong colour and depth is all wrong . . .
sia’ – recurrent discontinuities in conscious Previous psychiatric differential diagnoses were of When you try and tell people they think you’re mad.’
awareness – as the hallmark of dissociation anxiety, panic, depression and schizophrenia.
Diagnosis The disorder is constant and chronic
(Putnam et al,
al, 1996). The relatively low le-
within each episode. There was a previous diagnosis
vel of childhood abuse in this cohort again Case 2 of anxiety and depression.
supports a separation from other dissocia- A 30 -year-old male journalist with depersonalistion
tive disorders, as does the lack of significant disorder for 15 years. Case 6
female preponderance in this and other
Onset and attribution Acute onset following alcohol A 28-year-old male, unemployed shop assistant with
series (Shorvon et al,al, 1946; Simeon et al,al, binge at a party when aged 15 years. Patient believes depersonalistion disorder for 4 years.
2001). All in all, these clinical features that parental abuse was a contributing factor.
Onset and attribution Gradual onset over several
favour placing depersonalisation disorder
Subjective description ‘I’m Unreal and truly alone ^ months with each separate episode becoming more
with anxiety and mood disorders (as in like an outsider looking in. . .When I walk down the intense. No attribution made or significant life events
the ICD–10) rather than with dissociative street I feel as if I am swaying and the pavement is reported.
disorders (as in the DSM–IV). moving. I feel as if I can’t connect normally to people
Subjective description ‘This sounds mad but I am not
Comorbidity may arise from attempts on a mental level. I just don’t feel anything ^ I think
me. I look in the mirror and I don’t see me. I don’t
to cope with depersonalisation, such as I have gone mad.’
know who it is that I see and I don’t know where
anxious or obsessive ‘checking’ of symp- Diagnosis The disorder is constant and chronic, the real me has gone. Logically that cannot be the
toms change leading to compulsive with a previous psychiatric diagnosis of depression. case, but that is how it feels. I spend all day checking
432
D E P E R S ON A L I S AT I ON D I S O R D E R
433