 |
|
Autonomic Response in Depersonalization Disorder
Mauricio Sierra, MD, PhD;
Carl Senior, PhD;
Jeffrey Dalton, MSc;
Michael McDonough, MD;
Alison Bond, MD;
Mary L. Phillips, MD;
Anne M. O'Dwyer, MD;
Anthony S. David, MD
Arch Gen Psychiatry. 2002;59:833-838.
ABSTRACT
| |
Background Emotional-processing inhibition has been suggested as a mechanism underlying
some of the clinical features of depersonalization and/or derealization. In
this study, we tested the prediction that autonomic response to emotional
stimuli would be reduced in patients with depersonalization disorder.
Methods The skin conductance responses of 15 patients with chronic depersonalization
disorder according to DSM-IV, 15 controls, and 11
individuals with anxiety disorders according to DSM-IV,
were recorded in response to nonspecific elicitors (an unexpected clap and
taking a sigh) and in response to 15 randomized pictures with different emotional
valences: 5 unpleasant, 5 pleasant, and 5 neutral.
Results The skin conductance response to unpleasant pictures was significantly
reduced in patients with depersonalization disorder (magnitude of 0.017 µsiemens
in controls and 0.103 µsiemens in patients with anxiety disorders; P = .01). Also, the latency of response to these stimuli
was significantly prolonged in the group with depersonalization disorder (3.01
seconds compared with 2.5 and 2.1 seconds in the control and anxiety groups,
respectively; P = .02). In contrast, latency to nonspecific
stimuli (clap and sigh) was significantly shorter in the depersonalization
and anxiety groups (1.6 seconds) than in controls (2.3 seconds) (P = .03).
Conclusions In depersonalization disorder, autonomic response to unpleasant stimuli
is reduced. The fact that patients with depersonalization disorder respond
earlier to a startling noise suggests that they are in a heightened state
of alertness and that the reduced response to unpleasant stimuli is caused
by a selective inhibitory mechanism on emotional processing.
INTRODUCTION
DEPERSONALIZATION disorder is characterized by persistent or recurrent
episodes of "detachment or estrangement from one's self."1
The individual may feel like an automaton, or there may be the sensation of
being an outside observer of one's own mental processes.1
Many patients have a subjective absence of emotional feelings despite apparently
normal emotional expression.2
In contrast to the subjective nature of depersonalization, some early
work3 suggested that patients with depersonalization
may have an underactive sympathetic nervous system. For example, while measuring
the skin conductance (SC) of a patient with anxiety, Lader and Wing4 reported a dramatic change in the SC tracing from
the typical low-resistance, fluctuating pattern usually associated with anxiety
to a high-resistance, nonfluctuating pattern at the onset of a depersonalization
episode. These changes were also accompanied by a decline in pulse rate.4 A similar pattern was later reported by Lader5 in a second patient with ongoing depersonalization.
When the patient reverted to her previous anxious state, the SC changed to
extreme activity.
Using forearm blood flow as an index of sympathetic autonomic function,
Kelly and Walter6 found that 8 "depersonalized
patients" had the lowest basal recordings compared with patients with a range
of psychiatric disorders and controls. The finding that a high proportion
of patients with depersonalization disorder have high levels of anxiety7 renders the previous studies counterintuitive. Other
conditions accompanied by high levels of anxiety, such as posttraumatic stress
disorder, panic disorder, and obsessive-compulsive disorder (OCD), have hyperactive
skin conductance responses (SCRs).8-11
A recent model of depersonalization proposed that emotional numbing
and reduced autonomic responses might be accounted for by inhibition of the
amygdala and related limbic structures by the prefrontal cortex.2
This putative inhibitory mechanism could be a component of a hard-wired protective
response in the brain. The evolutionary benefits of such a mechanism would
be to enhance chances of survival during life-threatening situations by suppressing
disorganizing levels of fear while maintaining vigilant alertness.2, 12 A prediction stemming from this model
is that people with depersonalization disorder will have attenuated SCRs to
emotionally unpleasant stimuli. This model also predicts that the state of
heightened alertness will generate normal or heightened SCRs to nonspecific
stimuli ("physical stimuli") in patients with depersonalization disorder.
To test these predictions, we compared SCRs to neutral and emotional
visual stimuli in 15 patients with chronic depersonalization disorder, 15
controls, and 11 patients with anxiety disorders. The study was approved by
the ethics committee of the Institute of Psychiatry and Maudsley Hospital,
London, England.
PARTICIPANTS AND METHODS
PARTICIPANTS
Fifteen patients with a DSM-IV diagnosis of
depersonalization disorder were recruited from the Depersonalization Disorder
Clinic at Maudsley Hospital.13 The diagnosis
of depersonalization disorder was ascertained by means of a semistructured
interview using the Present State Examination14
by an experienced psychiatrist (M.S.) and by scores above the cutoff point
of 70 on the Cambridge Depersonalization Scale.15
All patients had chronic and continuous (as opposed to intermittent) depersonalization
disorder of durations ranging from 2 to 15 years. No patients were taking
any medication at the time of the study, and they were all medication free
for 2 months or longer. Patients with comorbid psychiatric or neurologic conditions
or substance or alcohol abuse were excluded by means of a thorough standard
psychiatric interview.
Eleven patients meeting DSM-IV criteria for
anxiety disorders (5 with OCD; 6 with panic disorder with agoraphobia) were
recruited from the Behavioral Psychotherapy Unit at Maudsley Hospital. Patients
were diagnosed by experienced clinicians by means of a thorough standard clinical
interview. In addition to the exclusion criteria applied to patients with
depersonalization disorder, care was taken to exclude "washers" in the OCD
sample, as frequent washing could affect SCRs. Two patients with OCD were
receiving medication (40 mg of fluoxetine hydrochloride and 50 mg of sertraline
hydrochloride). These 2 were not outliers on any of the psychophysiologic
measurements and, hence, were retained for the data analysis.
Fifteen controls were selected from staff members and students at the
Institute of Psychiatry, King's College. All controls denied a personal history
of mental illness and scored below the cutoff points on the administered scales.
No controls were taking any medication.
The 3 groups were matched for sex and age because these 2 variables
affect electrodermal activity.16 All participants
were paid for their participation in the study and provided written informed
consent.
STIMULI
Fifteen pictures selected from the International Affective Picture System
(IAPS)17 were used. Three groups of 5 pictures
were selected by valence: neutral (IAPS numbers 1670, 7160, 7150, 7100, and
7830) pleasant (IAPS numbers 1463, 1610, 1710, 1352, and 2530), and unpleasant
(IAPS numbers 3060, 9320, 6570, 6370, and 1930).
The pictures were randomized and arranged in counterbalanced order in
2 blocks. Each block was allocated randomly to roughly half of each group.
Pictures were presented on a color television placed 1.5 m from the participant.
Each picture was shown for 30 seconds, followed by a 30-second interstimulus
interval when the monitor screen was blank. Before presentation of the stimuli,
2 neutral pictures (IAPS numbers 7170 and 7050) were presented to facilitate
habituation to the projection system.
During the 30-second interval between pictures, participants were asked
to rate the picture they had just seen on the dimensions of valence (positive
to negative) and arousal (excited to calm) using the Self-Assessment Manikin,
an affective rating system devised by Lang.18
Ratings of valence on the Self-Assessment Manikin are indicated by 5 graphic
depictions of the manikin with facial expressions ranging from a severe frown
(most negative) to a broad smile (most positive). For arousal, the manikin
varies from a state of low to high agitation. The participant can select any
of the 5 figures, or boxes in between, on a 9-point rating scale for each
dimension. Ratings are scored such that 9 represents a high rating on each
dimension (ie, high pleasure or high arousal) and 1 represents a low rating
on each dimension.18
PROCEDURE
Skin conductance was recorded using standard silver–silver chloride
electrodes 0.5 cm in diameter. Electrodes were attached to the distal phalanges
of the first and second digits of the nondominant hand. Skin conductance was
measured using a constant voltage (0.6 V) SC module (SC4; Contact Precision
Instruments, Cambridge, Mass) attached to a personal computer. Water soluble
jelly (KY Jelly; Johnson & Johnson, Slough, England) was used as an electrolyte.
The SC signal was sampled at 100-millisecond intervals. Only deflections greater
than or equal to 0.04 µsiemens were computed. The timing of the stimuli
presentation was synchronized to the SC recording program.
Before the galvanic skin resistance (response) measurements, all participants
completed the following self-rating scales: the Beck Depression Inventory,19 the Spielberger trait and state scales,20
and the Cambridge Depersonalization Scale.15
To standardize the dermo-gel-electrode interface, participants were
requested to wash their hands using a nonabrasive soap (Ivory soap) as recommended
by Cacioppo and Tassinary.21 Participants were
then led into the testing room (adjacent) and sat on a comfortable chair.
After the electrodes had been placed there was a 5-minute habituation period
during which participants were asked to sit quietly, relax, and move as little
as possible. Two minutes of baseline SC were then recorded, during which there
were no stimuli and participants were instructed not to move or talk.
Two nonspecific elicitors of SCR, a hand clap (delivered about 30 cm
from the participant's left ear without warning) and a deep inhalation by
the participant, were used to assess the integrity of the dermoelectrical
system. These 2 stimuli were delivered 30 and 45 seconds (clap followed by
sigh) after a 2-minute baseline recording. These stimuli have been shown to
reliably elicit SCRs from healthy individuals.21-22
Participants were then told that a series of slides was going to be shown
on the television screen and they were instructed to look at each of them
carefully. During each interstimulus interval, participants were asked to
provide verbal ratings on valence (how pleasant the picture was) and arousal
(how "agitated" or moved the participant felt by the picture). For reference
purposes, an enlarged Self-Assessment Manikin was placed below the television
screen. All testing was restricted to afternoon hours (2 PM–5 PM), as
time of testing can be a source of confounding effects.16
DATA ANALYSES
Skin conductance levels and nonspecific fluctuations exceeding 0.04
µsiemens were counted during a 2-minute baseline recording. Amplitude
was defined as the highest deflection (phasic increase in conductance) from
baseline initiated 1 to 4 seconds after slide onset and exceeding 0.04 µsiemens.
For stimulus presentation, SCR magnitude (mean value of amplitude computed
across all stimulus presentations, including those without a measurable response)
was obtained. A log transformation (log[SCR + 1]) was used to normalize the
magnitude data. Because magnitude has the potential disadvantage of confounding
frequency and amplitude, which do not always covary, an SCR probability was
computed as a measure of response frequency above a threshold regardless of
amplitude (number of responses above 0.04 µsiemens per total number
of presentations).23 Response latencies (temporal
interval between stimulus onset and SCR initiation) were computed for all
responses occurring 1 to 4 seconds after onset of the stimulus. In addition
to the previous measurements, baseline mean conductance level (during the
initial 2 minutes) and number of nonspecific responses (ie, deflections occurring
>4 seconds after stimulus onset) during each epoch were counted.
Statistical analysis was performed using a software program (SPSS version
8; SPSS Inc, Chicago, Ill). Analysis of variance was used throughout, accompanied
by post-hoc analysis (Scheffé test). An   .05 was considered
statistically significant, and all significance tests were 2-tailed. For the
purpose of hypothesis testing, comparison of magnitudes to stimuli across
groups and response latency (Figure 1)
constituted the primary outcome variables. All other analyses were regarded
as exploratory.
|
|
|
|
Skin conductance response (SCR) magnitude to stimuli across groups.
Because the range of SCR amplitudes can vary across participants, responses
are standardized as range-corrected scores (for each participant, SCR magnitudes
were computed as a proportion of that participant's largest response).
|
|
|
RESULTS
The 3 groups did not differ significantly by age (F2,33 =
0.11; P = .89) or sex (F2,33 = 0.035; P = .96). Mean global scores on the Beck Depression Inventory
and the Spielberger scales (state and trait) did not differ significantly
between individuals with depersonalization disorder and those with anxiety
disorders; controls had significantly lower scores on these scales. Global
scores on the Cambridge Depersonalization Scale were significantly higher
for patients with depersonalization disorder than for controls and those with
anxiety disorders (Table 1).
|
|
|
|
Table 1. Global Scores on Administered Scales and Demographic Data*
|
|
|
No difference was found in the ratings for valence between patients
with depersonalization disorder and the other 2 groups. However, 1-way analysis
of variance revealed significant differences in the arousal ratings across
groups (F2 = 4.9; P = .01), with depersonalized
patients revealing lower scores for the unpleasant pictures than the other
2 groups (Scheffé, P<.05).
There was a difference in the mean [SD] resting baseline level of SC
across groups (F2 = 6.468; P = .004) (Table 2). The greatest difference (Scheffé, P<.05) was found between patients with depersonalization
disorder (1.8 [0.89] µsiemens) and those with anxiety disorders (4.1
[1.8] µsiemens). Controls had an SC intermediate to that in the other
2 groups (2.65 [1.8] µsiemens). The mean (SD) number of nonspecific
deflections during the 2-minute baseline recording showed a similar pattern,
with the lowest number in the depersonalization group (1.3 [1.8]) followed
by the control (1.5 [2.8]) and anxiety (4.0 [3.1]) groups. However, these
differences did not reach statistical significance (F2 = 2.4; P = .10).
|
|
|
|
Table 2. Skin Conductance Responses (SCRs), Latencies, and Subjective
Ratings to Administered Stimuli*
|
|
|
SKIN CONDUCTANCE RESPONSE
The magnitudes of SCRs to the unpleasant, pleasant, and neutral pictures
for each of the 3 groups are shown in Figure
1. Because responses to the startle noise (hand clap) did not differ
significantly from those to the sigh (F2,32 = 0.33; P = .76), both were collapsed into a single variable (physical stimulus).
There were no significant differences in the responses to the physical stimuli
across groups (F2,33 = 1.5; P = .36).
Because we predicted an interaction between type of emotional stimuli
and participant group (ie, a disproportionately lower response to unpleasant
stimuli in depersonalized patients), a mixed 2-factor analysis of variance
was used. It revealed a main effect for group (F1,32 = 14.6; P = .001) and a main effect for valence (F2,31
= 8.49; P = .001). There was also a significant group
x valence interaction (F2,32 = 3.8; P
= .03). Simple effects analyses showed that the 3 groups differed significantly
in their SCRs to unpleasant stimuli (F2 = 4.13; P = .02), with patients with depersonalization disorder having significantly
lower SCRs than controls and those with anxiety disorders (Scheffé, P<.05).
The group with depersonalization disorder also had a significantly lower
probability of response to the unpleasant stimuli (F2 = 7.4; P = .002), the differences being significant with controls
and the anxiety group (Scheffé, P<.05).
Although amplitude and SCR probability seemed to be lower for the pleasant
and neutral pictures in the depersonalization group, the difference did not
reach statistical significance (F2 = 0.03; P = .95).
Although our findings are consistent with the predicted lack of an SCR
to unpleasant stimuli, they also show a trend suggesting generalized hyporesponsiveness.
The SCRs to pleasant and neutral stimuli did not differ significantly across
groups, but there was a significant main effect of group, that is, lower responses
from patients with depersonalization disorder. Potentially, therefore, the
interpretation of a specific effect for unpleasant stimuli might be contaminated
by a floor effect arising from the reduced responses of the depersonalization
group overall. Consequently, we carried out a supplementary analysis using
range-corrected scores as suggested by Lykken and Venables24;
it expresses each SCR as a proportion of that participant's largest response.
These range-corrected means are shown in Figure 1. With this transform, genuine differences between SCRs
to unpleasant and neutral pictures were still evident as a group x valence
interaction (F2,32 = 3.7; P = .046). A
valence main effect (F2,64 = 14.03; P<.001)
and a group main effect (F2,32 = 3.73; P
= .043) were still found. This shows that even when the range of responses
is corrected, patients with depersonalization disorder still show a marked
reduction in their SCRs to unpleasant stimuli.
The fact that in our set of pictures those with negative valence also
had the highest arousability makes it difficult to know whether the reduced
responses seen in the depersonalization group were arousal or valence determined.
To address this problem, we compared a subset of 2 pleasant pictures (IAPS
numbers 1463 and 2352) and 2 unpleasant pictures (IAPS numbers 9330 and 6570)
with equivalent arousal ratings. The greatest difference between groups was
with the unpleasant pictures, but the difference did not reach statistical
significance (F2 = 1.8; P = .09).
LATENCY OF SCR
Analysis of variance for latency of SCR onset to type of stimuli revealed
a main effect for type of stimuli (physical and emotional: F1,21
= 18.14; P = .001) and for group (F1,21
= 5.5; P = .001). There was also an interaction between
type of stimuli (physical stimuli included) and group (F2,21 =
4.3; P = .03). Post hoc analyses revealed that depersonalized
patients had a longer latency to unpleasant pictures than did patients with
anxiety disorders (Scheffé, P<.05). Also,
depersonalized patients and those with anxiety disorders had a significantly
shorter latency to physical stimuli than controls (Scheffé, P<.05).
COMMENT
To our knowledge, this is the first study to explore SCRs to emotional
stimuli in depersonalization disorder. The study has several limitations,
including the relatively small sample sizes (in particular that of the anxiety
group). In addition, the anxiety group was not ideal in that it included patients
with 2 different disorders (panic disorder and OCD) that may differ in physiologic
response. However, because the aim of the study was to compare patients with
depersonalization disorder, controls, and patients with high levels of anxiety
regardless of nosologic status, this might not constitute a serious drawback.
Another limitation comes from the fact that the loudness of the clap and the
depth of the sigh (physical stimuli) were not rigorously controlled, and,
hence, these measures might have introduced a greater source of error than
the pictures.
Our findings show that, as predicted by Sierra and Berrios,2 depersonalization disorder seems to be associated
with reduced autonomic responding to aversive stimuli. In fact, there is no
differential responding by patients with depersonalization disorder to unpleasant
pictures compared with pleasant and neutral pictures. The absence of any differential
SCR to these types of emotional stimuli is striking; higher amplitude SCRs
to unpleasant stimuli were found in controls and those with anxiety disorders.
Standardizing the data to an index of response (as opposed to raw amplitude
measurements) did not abolish the findings, suggesting that these are not
due to a floor effect caused by a generalized dampening of SCRs. Rather, our
findings suggest that the SCR abnormalities in depersonalization disorder
have tonic and phasic components. Thus, the reduced baseline SC and fewer
nonspecific fluctuations suggest the presence of an inhibitory mechanism,
which tonically inhibits sympathetic outflow. This finding is in line with
that reported by Kelly and Walter,6 who found
marked low baseline forearm blood flow in depersonalized patients.
However, the fact that patients with depersonalization disorder showed
differential responses to the unpleasant stimuli suggests that phasic inhibitory
mechanisms are also at play. Patients with depersonalization disorder not
only had fewer measurable responses to the unpleasant pictures, but when they
showed a response, it had significantly lower amplitude. Also in favor of
a selective inhibitory mechanism is the finding that patients with depersonalization
disorder had a longer SCR latency to unpleasant stimuli but not to pleasant,
neutral, or physical stimuli. That these findings were selective to the unpleasant
pictures (an effect that was still observable after controlling for arousability)
implies that an adequate appraisal of valence is taking place. Indeed, subjective
ratings for valence did not differ across groups; therefore, the ability to
judge the emotional meaning of complex scenes is preserved in depersonalization
disorder. However, these patients rated the unpleasant pictures as less arousing,
thus paralleling the psychophysiologic data. In this regard, studies25 with healthy subjects (using IAPS pictures and the
Self-Assessment Manikin) have found that SCRs mainly correlate with subjective
arousal as opposed to valence.
The fact that there were no differences across groups to the physical
stimuli further suggests that SCRs are not indiscriminately reduced in depersonalization
disorder. Moreover, patients with depersonalization disorder and those with
anxiety disorders had quicker responses (shorter latency) to the nonspecific
stimuli than controls. The SCR to an unwarned stimulus, such as a clap, is
a component of the startle response, which is increased in anxiety disorders
and posttraumatic stress disorder and probably reflects a heightened state
of alertness.26 Indeed, levels of anxiety as
measured by self-rating scales were raised in patients with depersonalization
disorder and in those with anxiety disorders.
Taken as a whole, these results suggest the simultaneous existence of
inhibitory and facilitatory mechanisms on specific components of autonomic
activity. Thus, patients with depersonalization disorder in common with those
with anxiety disorders have similarly high anxiety ratings and SCRs (shorter
latency of response) to nonspecific stimuli, suggestive of a state of heightened
arousal. However, only patients with depersonalization disorder show a marked
diminution and delay in response to unpleasant pictures. These findings are
compatible with the model proposed by Sierra and Berrios,2
which postulates the simultaneous existence of an inhibitory mechanism on
emotional response and an excitatory mechanism leading to a state of heightened
alertness.
In the face of increased arousal (as suggested by the amplitude and
latency responses to the physical stimuli), a reduction in SCR amplitude and
increased response latency to the unpleasant pictures lends empirical support
to the notion that depersonalization is the manifestation of a protective,
functional response of the nervous system intended to deal with life-threatening
situations. However, the emergence and persistence of this response in a nonthreatening
situation would result in an extremely strange experience, namely, the sudden
onset of lack of emotional feelings, things looking devoid of emotional coloring
but with improved sensory definition. Moreover, it is suggested that a state
of heightened alertness in the absence of autonomic arousal might be conducive
to a state of heightened self-observation, which is a common feature of depersonalization
disorder. From a nosologic standpoint, the marked psychophysiologic differences
between patients with depersonalization disorder and those with anxiety disorders
lend support to the view that depersonalization disorder is a valid entity
in its own right. This notwithstanding, it is interesting that alexithymia
and antisocial personality disorder (conditions thought to be unrelated to
depersonalization) have recently been found to have similar psychophysiologic
features as those found in this study. Thus, subjects with high scores on
the Toronto Alexithymia Scale produce fewer specific SCRs to emotional visual
stimuli regardless of category.23 Similar findings
have been reported in individuals with "developmental" antisocial personality
disorder.27 Although alexithymia and antisocial
personality disorder seem to share with depersonalization disorder abnormalities
in the experiencing of emotions, there are clear phenomenologic differences.
For example, patients with sociopathic behavior seem to have a selective deficit
in the experiencing of empathy and fail to react autonomically to pictures
conveying distress but not to fearful or otherwise unpleasant pictures.27 Moreover, unlike patients with depersonalization
disorder, those with antisocial personality disorder have high levels of impulsivity
and make overt displays of lack of empathy.28
Patients with depersonalization disorder, in contrast, complain of subjective
emotional deficits despite normal behavioral expression.2
Patients with alexithymia seem to have difficulty differentiating and expressing
emotions verbally, which is thought to give rise to physiologic arousal and
a negative subjective state. Unlike patients with depersonalization disorder,
alexithymic patients have greater tonic electrodermal activity and report
more arousal and displeasure in general than controls.29
In conclusion, our findings support the view that depersonalization
disorder is characterized by reduced emotional reactivity to emotional stimuli.
Further work in this area should help in understanding this distressing disorder
and the interplay between affect and cognition.
AUTHOR INFORMATION
Submitted for publication December 7, 2000; final revision received
September 17, 2001; accepted October 12, 2001.
This study was supported by the Col WW Pilkington Will, Cecil Pilkington,
and AP Pilkington Pilozzo Charitable Trusts, United Kingdom.
Corresponding author and reprints: Mauricio Sierra, MD, PhD, Institute
of Psychiatry, 103 Denmark Hill, London SE5 8AZ, England (e-mail: M.Sierra-Siegert{at}iop.kcl.ac.uk).
From the Institue of Psychiatry, King's College, London University,
London, England. Dr Senior is now with the National Institute of Mental Health,
Bethesda, Md.
REFERENCES
| |
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition. Washington, DC: American Psychiatric Press; 1994.
2. Sierra M, Berrios GE. Depersonalization. Biol Psychiatry. 1998;44:898-908.
FULL TEXT
| PUBMED
3. Roth M, Argyle N. Anxiety panic and phobic disorder: an overview. J Psychiatr Res. 1988;22(suppl 1):33-54.
4. Lader MH, Wing L. Physiological Measures, Sedative Drugs and Morbid
Anxiety. London, England: Oxford University Press; 1966. Maudsley Monographs
No. 14.
5. Lader MH. The Psychophysiology of Mental Illness. London, England: Routledge & Kegan Paul; 1975.
6. Kelly DHW, Walter CJS. The relationship between clinical diagnosis and anxiety, assessed by
forearm blood flow and other measurements. Br J Psychiatry. 1968;114:611-626.
FREE FULL TEXT
7. Simeon D, Gross S, Guralnik O, Stein DJ, Schmeidler J, Hollander E. Feeling unreal. Am J Psychiatry. 1997;154:1107-1113.
ABSTRACT
8. Pitman RK, Orr SP, Shalev AY, Metzger LJ, Mellman TA. Psychophysiological alterations in post-traumatic stress disorder. Semin Clin Neuropsychiatry. 1999;4:234-241.
PUBMED
9. McFall ME, Murburg MM, Ko GN, Veith RC. Autonomic responses to stress in Vietnam combat veterans with posttraumatic
stress disorder. Biol Psychiatry. 1990;27:1165-1175.
FULL TEXT
| PUBMED
10. Roth WT, Wilhelm FH, Trabert W. Autonomic instability during relaxation in panic disorder. Psychiatry Res. 1998;80:155-164.
FULL TEXT
|
ISI
| PUBMED
11. Hoehn-Saric R, McLeod DR, Zimmerli WD, Hipsley PA. Symptoms and physiologic manifestations in obsessive compulsive patients
before and after treatment with clomipramine. J Clin Psychiatry. 1993;54:272-276.
PUBMED
12. Noyes R, Kletti R. Depersonalization in response to life-threatening danger. Compr Psychiatry. 1977;18:375-384.
FULL TEXT
|
ISI
| PUBMED
13. Phillips ML, Sierra M, Hunter E, Lambert MV, Medford N, Senior C, David AS. A depersonalisation research unit: progress report. Psychiatr Bull. 2001;25:105-108.
FREE FULL TEXT
14. Wing JK, Cooper JE, Sartorius NT. The Description and Classification of Psychiatric
Symptoms: An Instruction Manual for the PSE and CATEGO Program. Cambridge, England: Cambridge University Press; 1974.
15. Sierra M, Berrios GE. The Cambridge Depersonalization Scale: a new instrument for the measurement
of depersonalization. Psychiatry Res. 2000;93:153-164.
FULL TEXT
| PUBMED
16. Venables PH, Mitchell DA. The effects of age, sex and time of testing on skin conductance activity. Biol Psychol. 1996;43:87-101.
PUBMED
17. Lang PJ, Bradley MM, Cuthbert BN. International Affective Picture System (IAPS): Instruction
Manual and Affective Ratings: Technical Report A-4. Gainesville: Center for Research in Psychophysiology, University
of Florida; 1999.
18. Lang PJ. Behavioral treatment and bio-behavioral assessment: computer applications. In: Sidowski JB, Johnson KH, Williams EA, eds. Technology in Mental Health Care Delivery Systems. Norwood, NJ: Ablex;
1980:119-137.
19. Beck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for measuring depression. Arch Gen Psychiatry. 1961;4:561-571.
20. Spielberger CD, Gorsuck R, Lushene RE. The State-Trait Anxiety Inventory-Y Form. Palo Alto, Calif: Consultants Psychologists Press; 1977.
21. Cacioppo JT, ed, Tassinary LG, ed. Principles of Psychophysiology. Cambridge, England: Cambridge University Press; 1991.
22. Schneider RE, Fowles DC. A convenient, non-hydrating measurement of electrodermal activity. Psychophysiology. 1978;15:483-486.
PUBMED
23. Roedema TM, Simons RF. Emotion-processing deficit in alexithymia. Psychophysiology. 1999;36:379-387.
FULL TEXT
|
ISI
| PUBMED
24. Lykken DT, Venables PH. Direct measurement of skin conductance: a proposal for standardization. Psychophysiology. 1971;8:656-672.
ISI
| PUBMED
25. Lang PJ, Greenwald MK, Bradley MM, Hamm AO. Looking at pictures: affective, facial, visceral, and behavioral reactions. Psychophysiology. 1993;30:261-273.
ISI
| PUBMED
26. Howard R, Ford R. From the jumping Frenchmen of Maine to post-traumatic stress disorder:
the startle response in neuropsychiatry. Psychol Med. 1992;22:695-707.
ISI
| PUBMED
27. Blair RJ, Jones L, Clark F, Smith M. The psychopathic individual: a lack of responsiveness to distress cues? Psychophysiology. 1997;34:192-198.
ISI
| PUBMED
28. Blair RJ. A cognitive developmental approach to morality: investigating the psychopath. Cognition. 1995;57:1-29.
FULL TEXT
|
ISI
| PUBMED
29. Friedlander L, Lumley MA, Farchione T, Doyal G. Testing the alexithymia hypothesis. J Nerv Ment Dis. 1997;185:233-239.
ISI
| PUBMED
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati  Twitter
What's this?
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Cerebral and autonomic responses to emotional facial expressions in depersonalisation disorder
Lemche et al.
Br. J. Psychiatry 2008;193:222-228.
ABSTRACT
| FULL TEXT
Understanding and treating depersonalisation disorder
Medford et al.
Adv. Psychiatr. Treat. 2005;11:92-100.
ABSTRACT
| FULL TEXT
Depersonalisation disorder: clinical features of 204 cases
BAKER et al.
Br. J. Psychiatry 2003;182:428-433.
ABSTRACT
| FULL TEXT
|
