The Sleep of Patients With
Obsessive-Compulsive Disorder
Thomas R. Insel, MD; J. Christian Gillin, MD; Angela Moore, MSW;
Wallace B. Mendelson, MD; Richard J. Loewenstein, MD; Dennis L. Murphy, MD
\s=b\ Fourteen patients with obsessive-compulsive disorder
(OCD) were studied with all-night sleep EEG recordings. Nine
of these patients reported abnormal sleep patterns before the
polygraphic study. Analysis of the sleep records disclosed
significantly decreased total sleep time with more awakenings,
less stage 4 sleep, decreased rapid-eye-movement (REM)
efficiency, and shortened REM latency compared with those of
a group of age- and sex-matched normal subjects. These
abnormalities generally resembled those of an age-matched
group of depressed patients, although significant differences
remained. These findings suggest that such sleep abnormali-
ties as shortened REM latency may not be entirely specific for
primary affective illness. They also point to a possible bio-
logical link between OCD and affective illness.
(Arch Gen Psychiatry 1982;39:1372-1377)
Obsessive-compulsive
uncommon
thoughts, ideas, images,
disorder (OCD) is a severe and
illnesscharacterized by recurrent
or behavior that the patient resists
and recognizes as ego dystonic. The etiology and treatment
of this disorder have confounded psychiatrists for nearly a
century. Although the classic symptoms of this disorder,
such as washing and checking rituals, have traditionally
been interpreted psychologically, the syndrome has been
conspicuously unresponsive to psychodynamic treat-
ments.1,2 Investigators of various persuasions have thus
sought to find some "constitutional" element that would
explain the disorder. Janet,3 for instance, described the
disorder as a form of psychasthenia. Anna Freud4 spoke of a
"constitutional increase in the intensity of the anal-sadistic
tendencies." Neuropsychological data have implicated fron-
tal lobe dysfunction in OCD.5 Furthermore, recent thera-
peutic success with the tricyclic antidepressant,
clomipramine, has led to a "serotonin hypothesis" modeled
on the amine hypotheses of affective illness."
In an effort to extend these psychobiological approaches
to the disorder, we studied the sleep of obsessional patients
with all-night EEG recordings. While to the best of our
knowledge there have been no previous comprehensive
studies ofthe sleep of patients with OCD, several investiga-
tors9"11 have reported sleep abnormalities in depressed
patients, a group that shares several clinical features with
obsessive-compulsive patients.12 The clinical affinity of the
two disorders suggested to us the importance of studying
Accepted for publication April 15, 1982.
From the Clinical Neuropharmacology Branch (Drs Insel and Murphy)
and the Biological Psychiatry Branch (Drs Gillin, Mendelson, and Loewen-
stein), National Institute of Mental Health, and the Laboratory of Neuro-
sciences, National Institute of Aging (Ms Moore), Bethesda, Md. Dr Gillin is
now with the University of California, San Diego.
Reprint requests to Clinical Neuropharmacology Branch, National Insti-
tute of Mental Health, National Institutes of Health Clinical Center,
10/3D41, Bethesda, MD 20205 (Dr Insel).
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the sleep of obsessional patients to investigate biological
similarities as well.
METHODS
Patients were referred from across the country to an extensive
research program on OCD at the Clinical Center of the National
Institutes of Health, Bethesda, Md. At the time of admission, in
addition to a psychiatric interview (which elicited subjective
reports of sleep disturbance) and physical examination, collateral
information was obtained from the patients' families and from case
records of previous hospitalizations. During a two-week drug-free
assessment period, patients received routine clinical chemistry
tests, thyroid function studies, a 16-channel EEG, projective
psychological tests, and a battery of obsessional and other psychi-
atric rating inventories.
The final diagnosis was made by one of us (T. R. I.), using the data
from two psychiatric interviews as well as the results of the
assessment battery to establish that each patient satisfied both
Research Diagnostic Criteria (RDC)13 and DSM-IIP4 require-
ments for OCD. The DSM-III requires either obsessions (recur-
rent, persistent ideas, thoughts, images, or impulses that are ego
dystonic) or compulsions (repetitive and seemingly purposeful
behaviors that are performed according to certain rules or in a
stereotyped fashion) that are a significant source of distress to the
individual and are not due to another mental disorder. Ten of our
patients complained chiefly of obsessional fears or doubts that led
to checking rituals. Eight patients had a chief complaint of washing
rituals resulting from contamination fears. All the patients had
been ill for at least one year (mean duration of illness, 12 years).
Scores on the Leyton Obsessional Inventory for symptoms (mean,
28.8), resistance (mean, 40.4), and interference (mean, 44.8) scales
were comparable to those described by Cooper16 in a study
distinguishing obsessional neurotics from housewives with obses-
sional traits and normal subjects.
In no case was the obsessional disorder secondary to affective
illness or schizophrenia. Several patients did have affective symp-
toms. In these cases, the Schedule for Affective Disorders and
Schizophrenia16 was administered to refine the diagnosis. Seven
patients would have satisfied the DSM-III criteria for major
depressive disorder, but in each case the affective symptoms were
described by the patient as explicitly resulting from a loss of
functioning due to specific rituals or obsessions. These patients
were thus classified as having a secondary depression. Two pa-
tients in whom the affective symptoms had become autonomous
(ie, no longer related to the obsessional symptoms) and one patient
with hallucinations were excluded from this study.
In all, 18 patients met the criteria for OCD. Four, all with
cleaning rituals, refused to participate in the sleep study because
of concerns with contamination. Of the remaining 14 (eight men, six
women), the mean age was 35 years, with an age range of from 18 to
71 years. All participants agreed not to nap during the course of the
study.
Patients were studied in their hospital beds on our clinical
research unit. No patient received active medication during the
three weeks before the sleep study. In seven cases, the subjects
had been taking placebo capsules. Each of these seven had begun
receiving placebo several days before the sleep study as part of a
six-month study of drug response.
Between two and four all-night tracings of the EEG electromyo-
 Table 1.Sample Characteristics
Primary
Obsessive- Primary
Compulsive Affective
Disorder Normal Disorder
No._14_14_14
M/F ratio_8/6_8/6_7/7
Age,yr
Mean SE_36.4 + 4.24 35.1 3.81 35.23.47
Range_18-71_23-68_21-61
Hamilton Depression
Scale state mean 17.96(n 13)
=
... 31.40(n 10)*
=

*P<.01, Student's f test.

gram, and electro-oculogram were recorded for each subject

(sample total, 46). Each night's record was scored manually using
standard criteria.1' Sleep onset was defined as the first minute of
stage 2 or rapid-eye-movement (REM) sleep, followed by at least
eight minutes of sleep in the subsequent nine minutes. The REM
efficiency, expressed as a percentage, was calculated by dividing
the actual minutes of REM time in an REM period by the total
duration of the REM period. An individual mean was then calcu-
lated from the REM efficiency of each REM period during the
night. The REM architecture was investigated by two variables.
One method for describing REM distribution across the night in
each individual correlated REM period length with all previous
non-REM (NREM) time for each night (rREM.NREM). This measure
has been previously used by Vogel et al18 in a study of depressives.
If the duration of successive REM periods increased across the
night, as is normally the case, one should see a positive correlation.
If the proportion of REM sleep was unusually high early in the
night, a low or negative correlation should result. For the calcula-
tion of rREM.NREM, nights with fewer than three REM periods were
excluded from analysis. A group value was obtained by calculating
the mean of the individual correlation coefficients. As a second
approach to REM architecture, we tabulated REM activity, REM
time, and REM density (REM activity/REM time) for each REM
period during the night. Only the second night of recording was
used for these measures of the efficiency and distribution of REM,
as this was the one postadaptation night for which data were
available on all subjects.
During the week of the sleep recordings, all patients except one
were rated (without knowledge of the sleep results) on the 24-item
Hamilton Depression Scale,19 an obsessional subscale derived from
the Comprehensive Psychiatric Rating Scale,6 and the anxiety
subscale from the Global National Institute of Mental Health
Scales.19 For one patient, these scales were not completed during
the week of the sleep study, so he was later excluded from
correlations of sleep data with rating scale scores.
For purposes of comparison, we contrasted the findings in the
patients with OCD with those in normal and depressed subjects
previously studied in our laboratory.20 These subjects were se-
lected by matching for age and sex without reference to the sleep
data. As Table 1 indicates, the age means for the three groups were
nearly identical. Sex matching, less important than age,21 was off
by one subject in the depressed group. For ten of the age-matched
depressed control subjects, we had Hamilton Depression Scale
scores (including the three additional items) from the week of their
polygraphic sleep studies. This group appeared to be significantly
more depressed than our OCD sample (Table 1).
For both depressed and normal control groups, sleep records had
been collected and scored in an identical fashion, except that
adaptation night (ie, first night polygraphically recorded) data
were not available for scoring. The subsequent two nights were
used for comparisons with the OCD data.
Adaptation effects for the subjects with OCD were analyzed by a
two-tailed t test for paired data comparing nights 1 and 2. First-
night records were not scorable in two of the subjects with OCD,
reducing the sample size to 12. The mean for the postadaptation
nights was calculated for each of 18 sleep-recording variables in all
subjects. Again, statistical significance was determined by a two-
Hours
Fig 1.Top, Sleep pattern of 34-year-old male normal subject.
Bottom, Sleep pattern of 30-year-old subject with obsessive-com-
pulsive disorder shows reduced rapid-eye-movement (REM) la-
tency (RL), reduced stage 4 sleep, and interruptions of early REM
sleep. His primary symptom was checking, and his Hamilton
Depression Scale score was 13. A indicates awake, SL, sleep
latency.
tailed t test for paired data comparing patients with OCD with
normal subjects and then patients with OCD with depressed
patients. In this case, however, as the OCD data were used twice,
Bonferroni t statistics were used to render a more conservative
interpretation of the level of significance.22 In addition, we calcu-
lated linear regression coefficients for seven sleep variables
v rating scores on the depression, obsessional, and anxiety inven-
tories for each of the patients with OCD.
RESULTS
Subjective Findings
Of the 14 patients with OCD studied, nine reported sleep
disturbances in the initial psychiatric assessment. In seven pa-
tients, this was characterized as difficulty getting to sleep as well
as awakenings during the night. Two others reported hypersom-
nia, with 12 hours of sleep per night in each case. Five patients had
no symptoms related to sleep, although one of these had an earlier
history of somnambulism. Several subjects described their awak-
enings or difficulty falling asleep as specifically related to obses-
sional worries, eg, arising during the night to check that gas jets or
water faucets were off. One patient linked the onset of his checking
rituals (needing to resolve visually ambiguous stimuli) to imagery
that began during sleep. He would awaken with a need to "resolve
uncertainty" about the shape of a door frame or the color of a fabric
and would spend much of the morning struggling with this
dilemma. Later, this patient recovered completely with tra-
nylcypromine, a drug that presumably acts like other monoamine
oxidase inhibitors to powerfully suppress REM sleep.23
Another aspect of the subjective sleep complaints related to the
study itself. For many of the patients, particularly those with

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 Table 2.Sleep Variables (Mean : SE) Obtained in Obsessive-Compulsive Patients, Normal Subjects,
and Depressed Patients
Obsessive-
Compulsive Normal Depressed
Patients Subjects Patients
(N 14)
=
(N 14)
=
(N 14)
=

Totalrecording period, min 418.27.0 439.1 7.3* 435.6 + 8.2

Sleep continuity
Sleep latency, min 32.53.0 28.8 6.7 40.87.4
Total sleep time, mln 330.9 12.6 382.6 + 8.6* 335.1 14.4
Sleep efficiency, % 79.22.7 87.2 1.8 77.53.0
Early morning awakening, mln 16.54.5 9.53.1 18.84.9
Awake-movement time, min 40.1 8.4 18.3 + 3.1* 38.29.3
Sleep architecture
Stage 1, min 21.1 2.4 13.5 1.6* 7.81.8t
Stage 1, % 6.60.9 3.60.5t 2.50.6f
Stage 2, min 194.87.9 225.28.3* 209.97.0
Stage 2, % 58.91.2 58.8 1.7 64.0 + 2.9
Stage 3, min 26.93.9 30.4 3.3 13.33.7*
Stage 3, % 8.01.2 7.8 + 0.8 3.51.0*
Stage 4, mln 12.54.2 31.86.3t 19.25.9
Stage 4, % 3.41.1 8.31.6f 5.1 1.5
Delta, % 11.61.6 16.9 + 2.2* 8.8 2.3
Rapid eye movement (REM), % 22.81.2 20.71.3 24.8 1.4
REM measures
REM latency, mln 48.48.8 80.85.5* 47.3 5.1
REM density 1.680.12 1.690.14 2.20.18
REM efficiency, %+ 83.77.9 90.47.2* 88.511.9
rfor REM time/sum previous non-REMJ ,37.16 .32 + 15
. .09.15
No. of REM periods 3.80.2 3.8 + 0.1 3.9 0.3
Total REM time, min 75.73.9 82.02.9 85.27.2
*P<.05, Bonferroni t statistics for paired data comparing obsessive-compulsive patients with either normal subjects or depressed patients.
tP<.01.
tSecond night only.

cleaning rituals, the sleep-recording procedures were a source of
considerable stress. Two patients refused to allow recordings in
their regular hospital bed for fear of contamination. Others in-
sisted that they shower just before and just after the sleep
recordings. One patient who reluctantly consented to the sleep
study withdrew after two nights amid intense preoccupations that
the electrode headset had contaminated her bed.
Objective Findings
Theanalysis sleep EEGs generally corroborated the sub-
of
jective complaints of restless, fragmented sleep (Fig 1). As Table 2
shows, the patients with OCD differed from their matched normal
subjects on eight of 17 sleep variables (total recording period, the
18th variable, was not a sleep variable). Specifically, the patients
with OCD had shorter total sleep, more awakenings, almost twice
as much stage 1 sleep, less stage 2 sleep, less than half the amount
of stage 4 sleep, an overall decrease in the percent of delta sleep,
and nearly a 50% reduction in REM latency compared with the
normal subjects. The REM efficiency, a measure of the fragmenta-
tion within REM periods, was also reduced in the subjects with
OCD. Sleep efficiency was reduced, but not to a significant level (i
=
2.50, P<.06). Compared with the age-matched depressed sub-
jects, the patients with OCD differed on only two of the 17
variables. In this comparison, the patients with OCD had more
stage 1 and stage 3 sleep. In addition, there was a tendency (t
=
2.40, P-C.07) for patients with OCD to have lower REM density
than depressed patients.
The correlation of REM to previous NREM sleep was equivalent
for subjects with OCD and normal subjects but slightly higher in
subjects with OCD than in the depressed group. Tabulating REM
differences between groups, but there was a tendency for REM
activity and REM density to be greater in depressed subjects,
especially early in the night. Curiously, both subjects with OCD
and depressed subjects followed a pattern of increasing REM time
until the fourth REM period, when REM time declined. In
contrast, the normal subjects showed a progressive increase in
REM time across all four REM periods.
Adaptational effects, analyzed only for the patients with OCD,
were marked for REM latency but not significant for other
variables (Table 4). The REM latency from the first night of
recording was nearly double that seen on the second night, thus
approximating the REM latency in the normal subjects from the
postadaptation nights.
A few representative sleep variables were chosen for correlation
with rating data (Table 5). Sleep continuity (sleep efficiency and
awake-movement time) showed a positive correlation with depres-
sion and anxiety rating scale scores; however, only the correlation
with depression scores reached the P<.05 level of significance.
Obsessional ratings, while not correlated with measures of sleep
continuity, showed a trend toward an inverse relationship with
stage 4 sleep and a positive correlation with REM density. Of
interest, REM latency was not correlated with any of the three
rating scales.
We further divided our obsessional sample into two subgroups
on the basis of the initial clinical assessment: seven with affective
symptoms (mean age, 39.9 years; mean Hamilton Depression Scale
score, 23.4) and seven without significant affective symptoms
(mean age, 30.3 years; mean Hamilton Depression Scale score,
11.7). The differences between these two subgroups were signifi-
cant for depression ratings ( 4.06, P<.005), but not for age or
=

time across one night (Table 3) demonstrated no significant obsessional ratings (although the more depressed subgroup was

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 Table 3.Distribution of Rapid-Eye-Movement (REM) Table 5.Correlation Coefficients From Sleep
Time, REM Activity, and REM Density Across REM Periods Variables v Behavioral Ratings for 13
in Night 2 (Mean SE) Obsessive-Compulsive Patients
Obsessive- Comprehensive
Compulsive Normal Depressed Hamilton Psychiatric Rating Global
_Patients_Subjects Patients Depression ScaleObsessional Anxiety
Scale Subscale Scale
REM period 1 (n 14)
=
(n 14)
=
(n 14)
=

Time, min_16.82.5_14.53.2 19.52.6 Sleep efficiency -.56* .38 -.50t

Activity, units 28.66.2 24.1 7.1_40.710.0 Awake-movement
time .55* + .37 + .53t
Density*_1.560.13 1.21 0.14 1.880.21 +

REM period 2 (n 14)

=
(n 14)
=
(n=14) Stage 1 -.34 -.25 .37
Time, min_17.62.9_19.52.9 26.24.3 Stage 4 .37 50t -.31
Activity, units 28.36.2_31.85.6_49.99.0 Rapid-eye-movement
(REM) latency -.09 .31 -.01
Density_1.560.18 1.660.22 1.94 0.14 +

REM density + .36 + .49t + .27

REM period 3 (n 12)
=
(n=14) (n=14)
REM efficiency + .04 .17 -.04
Time, min_26.25.2 24.62.2 31.1 3.4
Activity, units 41.19.8 47.27.7 62.49.31 *Ps.05.
Density_1.570.22 1.820.18 2.000.22 tPs.10.
REM period 4 (n 8)
=
(n 9)
=
(n 7)
=

Time, min_17.42.3 30.55.6 20.35.9

Activity, units 34.1
5.9_45.711.3 39.0+14.4
Density 1.91 0.14 1.92 0.31 1.77 0.28
*REM actlvity/REM time.

Table4.Comparison of Nights 1 and 2 for 12

Obsessive-Compulsive Patients (Mean SE)
Sleep Variable_Night 1_Night 2_P*
Totalsleep time, min 338.0 21.0 331.6 17.7 NS
Sleep efficiency, %_82.4 + 3.3 76.2 4.0_NS +

Awake-movement
time, min_34.78.3 46.514.0 NS
Stage 1, %_6.5 + 1.5 6.61.4 NS
Stage 4, %_3.1 1.3_2.8 1.2 + NS OCD Normal OCD Normal
Delta, %_10.1 1.8_9.3 1.6_NS (Secondary (Nondepressed)
Rapid-eye movement Depressed)
(REM) latency, min 80.9 13.4 45.412.3 <025
Total REM time, min 81.910.5 82.5 + 6.6 NS Paired r= 1.97 Paired / = 2.24
One-tailed P < .05 One-tailed P < .05
*Level of significance of f statistic for paired data, d/=1l.
(n =
7) (n 7)
=

Fig 2.Mean rapid-eye-movement latency for depressed and

somewhat more obsessive). Both of these subgroups showed statis-
tically significant reductions in REM latency compared with age-
matched normal subjects, although among the patients with OCD
(Fig 2), the REM latency of the depressed subgroup was lower. The
difference between the depressed and nondepressed subgroups
was not statistically significant.
COMMENT
These subjective and objective descriptions suggest that
sleep is markedly abnormal for obsessive-compulsive pa-
tients. Earlier clinical descriptions have not mentioned
sleep as impaired in this disorder,24 although a recent report
of preliminary findings in a small group of obsessional
adolescents described similar abnormalities of sleep effi-
ciency, total sleep time, and REM latency.26 Both our
patients' subjective reports and their EEG records dis-
closed a pattern of shallow, interrupted, inefficient, and
shortened sleep. These results as well as the shortened
REM latency suggest that the sleep of patients with OCD
has many similarities to that of patients hospitalized with
primary depression. While the study was not directly
designed to formally compare depressed patients and pa-
tients with OCD, it appears that they differed from each
other in relatively few wayspatients with OCD had more
stage 1 and 3 sleep and tended to have less REM density
early in the night.
nondepressed subgroups of patients with obsessive-compulsive
disorder (OCD) and for age-matched normal subjects. Difference
between OCD subgroups was not significant.
We considered that these findings might reflect several
methodological problems in the study. One difficulty, for
instance, was the variability of sample size. Two of the
patients with OCD refused further sleep recordings after
the second night. Thus, for these two, only a single
postadaptation night was available for comparison with
normal and depressed subjects. To check on the validity of
our findings, we reanalyzed each of the abnormal sleep
variables for this one postadaptation night in all patients
with OCD and normal subjects. Results were similar
though not identical. On this single-night comparison,
REM latency, stage 1 sleep, stage 4 sleep and awake-
movement time continued to be significantly abnormal
(P<.05); total sleep and sleep efficiency showed a trend
toward being reduced in the subjects with OCD (P<.10);
and delta sleep was no longer remarkable.
Another problem was the use of placebo in half of the
patients with OCD. Placebo effects in insomniacs are well
known.26 The direction of these effects is opposite to the
findings in our patients; we considered, however, that the

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 use of placebo might have limited the validity of treating all
of the patients as a single group. For this reason, we
compared patients with OCD who were receiving placebo
with those not receiving placebo. No differences were
apparent on total sleep time, sleep efficiency, stage 1, stage
4, REM sleep, or REM latency. Awake-movement time was
greater in subjects not taking placebo. Comparing just the
patients receiving placebo with matched normals continued
to demonstrate differences in awake-movement time, stage
4 sleep, and REM latency. Patients not receiving placebo
had analogous mean differences from matched normals in
awake-movement time ( + 21.0 minutes) and REM latency
( 22 minutes), but greater variance reduced the statistical
significance of these differences. These seven patients not
-
receiving placebo therapy did have significant increases in
stage 1 sleep. In a related study of 13 obsessional subjects, a
spectrum of clinical variables (eg, mood, obsessions, anx-
iety) did not change during four weeks of placebo therapy
(our unpublished data), also suggesting the validity of
combining the patients with OCD as a group for analysis.
The sleep latencies of all three groups of patients are
prolonged beyond those in previous reports.11 Although this
may partly reflect our definition of sleep onset, a review of
individual data disclosed that one normal subject was a
clear outlier, with a sleep latency of 106 minutes. The mean
for the other 13 normal subjects was 22.7 minutes, which
was almost statistically shorter (P<.07) than that in the 13
matched subjects with OCD.
The reduction of REM efficiency in patients with OCD
was consistent with the general fragmentation of sleep and
the increase in stage 1 sleep. Reduced REM efficiency could
reflect either a decrease in REM time (ie, actual number of
minutes with REM during an REM period) or an increase in
the duration of the REM periods (REM time plus interven-
ing NREM or wakefulness). As REM time was not signifi-
cantly reduced in the subjects with OCD, an increase in the
intrusion of NREM or awake time must have contributed to
the lowering of REM efficiency. This fragmentation of REM
might correspond to the subjective reports of obsessions
intruding into sleep, leading to brief awakenings. Unfor-
tunately, we did not record sleep mentation reports. The
only relevant evidence we have, our correlational data
(Table 5), showed no relationship between severity of obses-
sions and REM efficiency. There is, however, another
aspect of REM efficiency that deserves mention. This sleep
variable previously has been found to be reduced in absti-
nent alcoholics27 and bipolar (more than unipolar) depres-
sives.28 In both of these earlier studies, REM efficiency was
linked to serotonin particularly because 5-hydroxytryp-
tophan, a serotonin precursor, normalized the reduced
REM efficiency of alcoholics.27 Recent pharmacologie stud-
ies of OCD have likewise focused on the serotonergic
system, as clomipramine, a tricyclic antidepressant that
powerfully inhibits neuronal reuptake of serotonin, has
been shown to be effective in this syndrome, which
heretofore had been refractory to medications.68 While the
links must still be considered very tentative, it may be that
the reduction in REM efficiency is another indicator of the
involvement of the serotonergic system in OCD.
It was surprising to find a reduction of REM latency in
the subjects with OCD compared with normal subjects. As
this abnormality has previously been most closely associ-
ated with primary affective illness, we considered the
possibility that our patients with OCD, many of whom were
depressed, might be suffering from primary rather than
secondary depressions. Two approaches using our rating
scale data, however, suggest that the severity of depressive
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symptoms did not account for the short REM latency. First,
depressive symptoms were not significantly correlated
with REM latency (Table 5). Second, when we divided our
sample into depressed and nondepressed subgroups, there
were nonsignificant differences in REM latency between
the two groups, although both values were significantly
shorter than that of age-matched normal subjects (Fig 2).
It appears that although the patients with OCD showed a
reduction in REM latency that was equal in magnitude to
that of patients with affective disorder, there were some
subtle differences that warrant emphasis. For instance,
Kupfer29 has shown that for patients with affective illness,
there is a significant negative correlation between the
length of REM latency and clinical ratings of depression.
Such a correlation was absent in the patients with OCD.
Furthermore, in patients with primary affective disorder,
REM latency is reduced on the first as well as subsequent
nights of laboratory sleep.30 In contrast, the patients with
OCD showed a normal REM latency on the first night.
Curiously, a similar "first-night effect" for REM latency has
previously been reported for patients with secondary de-
pressions.30
Recent formulations of the REM abnormalities in affec-
tive illness have stressed not only the reduction of REM
latency (which is technically an NREM measure), but also
an increase in REM density and an inversion of the normal
REM distribution such that more REM time occurs early in
the night.18,31 On these two latter variables, the patients
with OCD did not so closely resemble patients with affec-
tive illness. The REM density was lower in the patients with
OCD compared with the depressed patients, although this
difference did not quite reach statistical significance. Al-
though there is no generally accepted scheme for describing
REM distribution, the percentage of REM time in the first
REM period and rREM_NREM are two variables that have been
previously reported as abnormal in patients with primary
affective illness when compared with insomniacs.18 The
subjects with OCD had 22.9% of their REM time in the first
REM period. This value lies between the normal value of
20.2% and the corresponding value in the depressed sub-
jects of 23.9%. On the correlational measure, the subjects
with OCD appeared to be closer to the normal subjects,
although the variance in each group was high. It appears,
then, that on both the percentage of REM time in the first
REM period and the correlation of REM with previous
NREM, the subjects with OCD cannot be distinguished
from either normal subjects or patients with primary
depression. The present analysis did not address whether
our primary depressives could indeed be separated from
age-matched normal controls on these measures.
Short REM latencies have been described in other psy-
chiatric entities using earlier diagnostic categories. Early
articles reported this finding in small samples of schizo-
phrenics;3234 however, these reports were later contested on
the diagnostic grounds that many of these patients may
have been schizoaffective.35 Patients with subaffective dys-
thymia,36 anorexia nervosa37 (some of whom were later
diagnosed as depressed), and normal aging38 all may show
reduced REM latencies. Depressed subjects continue to
show even briefer REM latencies with age.21 Whether REM
latency is specific for some common element in all of these
syndromes remains conjectural. While the patients with
OCD showed very weak correlations between REM latency
and clinical ratings, it may be that weekly ratings are less
important for such a correlation than the state of the patient
just before sleep. This possibility, which is entirely hypo-
thetical, was suggested to us because the two subjects with
 OCD who had the longest REM latencies seemed the least
apprehensive about the sleep study. Future attempts at
correlating sleep measures to clinical variables might be
improved by the use of ratings just before sleep. Other
variables, such as the time of going to sleep39,40 or a history of
prior REM deprivation,41 will also need to be specified as
these factors can influence REM latency.
In addition to the sleep findings, the patients with OCD
shared some other similarities with those with primary
affective disorder. For instance, one patient had a history 12
years earlier of a circumscribed episode of major depressive
disorder without obsessive symptoms. Three patients had
family histories of affective disorder in first-degree rela-
tives; one had a family history of alcoholism. Moreover, as
part of another study in a larger sample of patients, ten of
the patients with OCD were given the dexamethasone
suppression test, which is purported to be of diagnostic
value in primary depression42 and major depressive disor-
der.43 Four of these patients showed no suppression, approx-
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