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Partial Validation of the Atypical Features Subtype of Major Depressive Disorder
Michael A. Posternak, MD;
Mark Zimmerman, MD
Arch Gen Psychiatry. 2002;59:70-76.
ABSTRACT
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Background Symptoms of the atypical features subtype of major depressive disorder
include mood reactivity, hypersomnia, hyperphagia, leaden paralysis, and rejection
sensitivity. This subtype was introduced into the mood disorders section of
the DSM-IV following a series of antidepressant trials
showing that such patients responded preferentially to monoamine oxidase inhibitors.
Studies aimed at validating the atypical features subtype have yielded inconsistent
results. Our study sought to reevaluate the validity of atypical depression
by examining the demographic and clinical features of a large cohort of depressed
patients who met DSM-IV criteria for atypical features.
Methods We evaluated 579 psychiatric outpatients with a current diagnosis of
major depressive disorder for the presence of atypical features. Detailed
demographic and clinical information was obtained for each patient through
semistructured interviews. Using the available literature, we made a series
of a priori hypotheses regarding how depressed patients with atypical features
(n = 130) would differ from those without atypical features (n = 449). In
addition, we tested the strength of the associations between each of the 5
atypical symptoms.
Results Although many of the predicted hypotheses were substantiated, an equal
number were not. Correlation analyses revealed modest associations between
several of the atypical symptoms, but mood reactivity was not associated with
any of the other symptom criteria.
Conclusion Our results provide partial support for the validity of the atypical
features subtype of major depressive disorder.
INTRODUCTION
ATYPICAL depression stands alone among the DSM-IV1 mood disorder subtypes as being born
out of the modern psychopharmacologic revolution. West and Dally2
first used the qualifier atypical to characterize
a cohort of depressed patients who appeared phobic, "overreactive," and "hysterical"
and exhibited prominent fatigue, reversed diurnal variation, initial insomnia,
and an absence of decreased appetite. Sargant3
added that such patients also tended to complain of severe lethargy, hypersomnia,
and irritability. Both sets of investigators believed that these patients
had good premorbid personalities but were now experiencing a chronic form
of depression. They also noted that such patients responded particularly well
to monoamine oxidase inhibitors (MAOIs) and less well to tricyclic antidepressants
and electroconvulsive therapy.
Quitkin et al4 subsequently argued that
these early investigators were actually describing 2 distinct subtypes. One
subtype included patients with panic disorder; the other, patients with hysteroid
dysphoria. The latter syndrome was characteristic of histrionic patients,
whose mood was described as "shallow" and excessively sensitive to both admiration
(mood reactive) and rejection (rejection sensitive). When depressed, such
patients purportedly displayed a propensity to oversleep and overeat. Although
the validity of hysteroid dysphoria was questioned by some,5-6
it was ultimately incorporated into the DSM-IV as
a depressive subtype by virtue of the preferential response such patients
showed for MAOIs rather than tricyclic antidepressants. In its current form,
the atypical subtype includes 5 features: mood reactivity plus at least 2
of the following 4 symptoms (hereafter referred to as atypical B symptoms):
hypersomnia, hyperphagia, severe lethargy (often described as a feeling of
"leaden paralysis"), and a pathological sensitivity to rejection and criticism.
The decision to include the atypical features subtype in the DSM-IV was controversial,7 in part because
studies that have examined the demographic and clinical features of patients
with atypical depression have frequently yielded contradictory results. For
example, the atypical features subtype has been associated with female sex
by some investigators8-11
but not others,12-14
younger age by some9, 12, 15
but not others,8, 13-14,16
bipolarity by some17-18 but not
others,13 greater anxiety by some9, 12, 19-21
but not others,11, 14, 16, 22
less severity by some11, 22 but
not others,8, 13, 23-24
a longer duration of illness by some8, 22, 25
but not others,13 a younger age of onset by
some12, 17, 22, 26
but not others,7, 23 higher rates
of recurrence by some12-13 but
not others,22 and more suicidality by some,12 but less suicidality by others.14-22
Integrating these results has been difficult because investigators have used
disparate criteria to define the atypical subtype and have often studied distinct
and highly selected populations of subjects.
In our study, we sought to assess and reevaluate the validity of the
atypical subtype by comparing the demographic and clinical features of depressed
patients with and without atypical features. Our analyses are based on data
collected from the Rhode Island Methods to Improve Diagnostic Assessment and
Services (MIDAS) project,27 which has overcome
many of the limitations of previous studies by (1) evaluating a large cohort
of unselected psychiatric outpatients; (2) abiding by the current DSM-IV formulation of atypical depression; (3) using semistructured
interviews conducted by researchers with extensive training to obtain diagnoses
on most major Axis I and Axis II disorders; and (4) obtaining extensive information
regarding baseline demographic and clinical features. Our study uses the results
from the first 579 patients who were evaluated in the MIDAS project and who
received a current diagnosis of major depressive disorder.
Because of the inconsistencies in the results of previous studies, there
is no straightforward way to generate hypotheses regarding how patients with
atypical features would be expected to differ from those without atypical
features. In reviewing the literature, therefore, we have given more weight
to the Columbia University (New York, NY) group's formulation of the disorder
because this group developed the current set of diagnostic criteria and demonstrated
the preferential MAOI response pattern.28-32
We tested the hypotheses that depressed patients with atypical features would
be more likely than nonatypical depressed patients to exhibit the following
characteristics: (1) female sex; (2) younger age; (3) a longer episode duration;
(4) a younger age at onset; (5) higher rates of bipolarity; (6) milder illness;
(7) greater comorbidity with panic attacks, agoraphobia, social phobia, hypochondriasis,
bulimia, and body dysmorphic disorder; (8) amphetamine abuse or dependence;
and (9) histrionic and avoidant personality disorders (PDs). In addition,
we predicted that reversed diurnal variation, an absence of psychomotor retardation,
an absence of guilt, irritability, and psychic anxiety would be more common
in this cohort. We also predicted that patients with atypical depression would
have more lifetime nonserious suicide attempts and fewer serious attempts
compared with patients who had nonatypical depression.
To test the internal consistency of the criteria set, we hypothesized
that patients who maintained mood reactivity would more frequently meet the
atypical B criteria threshold than those with an unreactive mood. We also
expected that each of the 5 atypical symptoms would be significantly correlated
with each other, and that hypersomnia and hyperphagia would be more strongly
correlated with the other atypical symptoms than would the nonatypical symptoms
of insomnia and decreased appetite.
Last, because some investigators have argued that mood reactivity plus
1 of 4 atypical B symptoms, or probable atypical depression, may better capture
the unique features of patients who respond preferentially to MAOIs,7, 9, 28-29,33-34
we sought to determine whether such a modification would be supported by our
data. If patients with probable atypical depression resemble those who meet
threshold criteria, we would expect the demographic and clinical features
of these 2 cohorts to be similar.
SUBJECTS AND METHODS
SUBJECTS
All subjects in our study were recruited from the Rhode Island Hospital
(Providence) Department of Psychiatry's outpatient practice. During their
initial telephone screen, all patients were invited to participate in an in-depth
diagnostic evaluation prior to meeting with their treating clinician (psychiatrist,
psychologist, or social worker). Only non-English-speaking patients and those
with evidence of cognitive impairment were excluded from the study. To date,
1130 patients have been evaluated. Of these, 579 (51.2%) were diagnosed as
having a current major depressive disorder and form the cohort of interest
for the study. The Rhode Island Hospital institutional review board approved
the research protocol, and all patients provided informed written consent.
METHODS
Consenting patients were interviewed at baseline using the Structured
Clinical Interview for DSM-IV (SCID).35
Diagnostic raters were PhD psychologists or college graduate research assistants
who had undergone extensive training, as described elsewhere.36
Mood reactivity was assessed according to the SCID by asking patients
whether they felt better, even temporarily, when something good happened.
Hyperphagia was defined as increased appetite nearly every day for at least
2 weeks or an increase in body weight of 5% or more. Hypersomnia was defined
as sleeping significantly more than usual. Leaden paralysis was considered
to be present when a patient acknowledged often having a heavy, leaden feeling
in the arms or legs. Rejection sensitivity was defined as a long-standing
pattern of interpersonal sensitivity (not limited to episodes of mood disturbance)
that caused significant social or occupational impairment. All 5 symptoms
were rated as being either present, absent, or subthreshold, and only the
first rating counted as being present. Reliability ratings for each of the
atypical symptoms were obtained from 24 joint interviews.  Values for
the atypical symptoms were as follows: mood reactivity, 0.83; hyperphagia,
1.0; hypersomnia, 0.90; leaden paralysis, 0.78; and rejection sensitivity,
0.75, indicating excellent interrater reliability.
The SCID was supplemented with questions from the Schedule for Affective
Disorders and Schizophrenia (SADS)37 to assess
the severity of symptoms during the week prior to the evaluation. From this,
we were able to obtain extracted 21-item Hamilton Depression Rating Scale
(HAM-D) scores following the algorithm developed by Endicott et al.38 Current social-functioning ratings were obtained
using the SADS item that rates the highest level of social relations during
the last 5 years. Baseline Clinical Global Impression–Severity (CGI-S)39 ratings and current Global Assessment of Functioning
(GAF)40 scores were also obtained for each
patient by the diagnostic interviewer. Personality disorder assessments were
incorporated into the protocol for only the last 530 patients; the first 600
patients did not undergo an Axis II diagnostic evaluation. Thus, PD diagnoses
were available for only 262 (45.3%) of the 579 patients with major depression.
Personality disorders were assessed using the Structured Interview for DSM-IV Personality.41
All diagnoses were made according to DSM-IV
criteria. Our analyses comparing depressed patients with and without atypical
features are based on current rather than lifetime diagnoses of affective
disorders. In comparing comorbidity rates, however, we used lifetime diagnoses.
Psychomotor retardation was rated by interviewer observation rather than patient
report. Prior suicidal behavior was analyzed based on the most serious lifetime
attempt. The determination of seriousness was made after assessing the method
and purpose of the attempt, the likelihood of rescue, and the seriousness
of injury.
STATISTICAL ANALYSES
We performed  2 and t tests
to analyze all categorical and continuous variables, respectively. Correlation
coefficients were obtained using the Spearman  because all variables
tested were dichotomous. For all hypothesized comparisons, statistical significance
was set at P<.05, and all tests were 2-tailed.
In addition, 34 tests were performed without an a priori hypothesis. For these
tests, the Bonferroni correction was used to adjust for chance positive findings.
Statistical significance in these analyses was set at P<.05 divided by 34, or P<.0015.
RESULTS
PREVALENCE OF ATYPICAL FEATURES IN MAJOR DEPRESSION
Of the 579 patients with a current major depressive disorder, 130 (22.5%)
met criteria for the atypical subtype. Rates of atypical symptoms in the 579
patients were as follows: mood reactivity, 71.7%; hypersomnia, 16.8%; hyperphagia,
21.8%; leaden paralysis, 28.0%; and rejection sensitivity, 40.9%. Symptom
rates in the 130 patients with atypical depression were 100% for mood reactivity,
36.2% for hypersomnia, 53.1% for hyperphagia, 60.8% for leaden paralysis,
and 75.4% for rejection sensitivity.
DEMOGRAPHIC AND CLINICAL FEATURES ASSOCIATED WITH ATYPICAL DEPRESSION
The demographic and clinical features of the 130 patients with atypical
depression were compared with those of the 449 patients with nonatypical depression
(Table 1). As predicted, atypical
depression was associated with female sex, a younger age at onset, and a longer
episode duration. Contrary to expectation, patients with atypical features
were not younger, the diagnosis was not more prevalent in patients with bipolar
disorder, and atypical depression was associated with a greater rather than
lesser severity of illness, both on HAM-D scores and CGI-S ratings.
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Table 1. Comparison of Demographic and Clinical Features of Depressed
Patients With and Without Atypical Features*
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Because this latter finding is contrary to the established opinion regarding
atypical depression, we further explored the relationship between severity
and atypicality. With a worsening of mood, as rated on the 6-point mood severity
item from the SADS, rates of hypersomnia (r = 0.11; P = .01), leaden paralysis (r
= 0.21; P<.001), and rejection sensitivity (r = 0.13; P = .009) all increased.
The percentage of patients who met criteria for atypical features also increased
with greater mood severity but not to a statistically significant degree (r = 0.07; P = .08), largely because
mood reactivity was inversely correlated with mood severity (r = -0.18; P<.001).
PRESENCE OF SYMPTOMS HYPOTHESIZED TO BE ASSOCIATED WITH ATYPICAL DEPRESSION
In comparing patients with atypical depression with those who had nonatypical
depression, the former cohort was more often rated as irritable (72.3% vs
62.1%; 21 = 4.5; P = .03)
and anxious (66.9% vs 55.0%; 21 = 5.9; P = .02). However, patients with atypical depression were no more likely
to display reversed diurnal variation (26.2% vs 30.5%; 21 = 0.9; P = .34), less likely to demonstrate
an absence of guilt (34.6% vs 45.4%; 21 = 4.8; P = .03), and more often rated as having psychomotor retardation
(40.0% vs 28.1%; 21 = 6.7; P = .009).
Rates of current suicidal ideation were nearly identical in both cohorts
(51.5% and 48.6%). Of the depressed patients with atypical features, 20% had
a history of a serious suicide attempt compared with 16.5% of nonatypical
depressed patients; rates of nonserious suicide attempts were likewise similar
between the 2 groups (8.5% and 10.9%, respectively). Thus, contrary to expectation,
patients with atypical depression were neither more prone to nonserious suicide
attempts nor less prone to serious ones.
COMORBIDITY IN PATIENTS WITH ATYPICAL DEPRESSION
Patients with atypical depression were significantly more likely to
have panic disorder with agoraphobia and social phobia but were not more likely
to have panic disorder without agoraphobia (Table 2). No differences were found in rates of other anxiety disorders
or substance use disorders, including amphetamine abuse or dependence. Lifetime
diagnoses of hypochondriasis (5.4% vs 1.6%; 21
= 6.2; P = .01) and body dysmorphic disorder (6.9%
vs 1.8%; 21 = 9.4; P =
.002) were more common in patients with atypical depression; bulimia was not
found to be more common (6.2% vs 2.7%; 21 = 3.7; P = .06).
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Table 2. Lifetime Comorbidity Rates in Depressed Patients With and
Without Atypical Features*
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Of the 579 depressed patients in our sample, 262 underwent an Axis II
evaluation. A dimensional analysis, which compares the number of DSM-IV criteria met for each PD, confirmed that histrionic and avoidant
traits were associated with atypical depression (F261 = 4.2; P = .04, and F261 = 35.2; P<.001, respectively). In fact, patients with atypical depression
had higher mean dimensional rating scores for each of the 10 PDs than patients
with nonatypical depression (Table 3).
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Table 3. DSM-IV Personality Disorder Dimensional
Scores in Depressed Patients With and Without Atypical Features*
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From a categorical standpoint, 100 (38.2%) of the 262 depressed patients
met the diagnostic threshold for at least 1 comorbid PD. Avoidant PD (but
not histrionic PD) was significantly associated with a greater likelihood
of having atypical features (21 = 20.1; P<.001). No other PDs were associated with the atypical subtype,
although some of the sample sizes were small (Table 4).
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Table 4. Comorbidity Rates in Depressed Patients With and Without Atypical
Features*
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CORRELATIONS AMONG ATYPICAL SYMPTOMS
We first evaluated whether the presence of mood reactivity was significantly
associated with having at least 2 of 4 atypical B symptoms. Of the 579 patients
diagnosed as having a current major depressive disorder, 415 (71.7%) were
mood reactive and 164 (28.3%) were mood nonreactive. Of the mood-reactive
patients, 130 (31.3%) met the atypical B criteria; 53 (32.3%) of the mood-nonreactive
patients also met the criteria. Thus, mood reactivity was not associated with
a greater likelihood of meeting the atypical B diagnostic threshold.
Next, we assessed the strength of association between the 5 atypical
symptoms (Table 5). Mood reactivity
was not correlated with any of the atypical B symptoms. Hyperphagia was significantly
associated with hypersomnia (r = 0.09; P = .03) as well as leaden paralysis (r =
0.10; P = .02), and leaden paralysis was significantly
associated with rejection sensitivity (r = 0.09; P = .03). No other symptom domains were significantly correlated.
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Table 5. Correlations Among Atypical Symptoms and Comparisons With
the Nonatypical Symptoms of Decreased Appetite and Decreased Sleep*
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To assess the discriminant validity of the atypical subtype, we compared
the strength of associations between hyperphagia and hypersomnia with the
remaining 3 atypical symptoms and contrasted these with the strength of associations
between the nonatypical symptoms of decreased appetite and insomnia. In making
these comparisons, only the previously mentioned associations reached statistical
significance. Hyperphagia was positively associated with each of the other
4 atypical symptoms (r = 0.04 to 0.10), whereas decreased
appetite was negatively correlated with them (r = -0.04
to 0.00). Hypersomnia was more strongly correlated with hyperphagia (r = 0.09) and rejection sensitivity (r = 0.02) than was insomnia (r = -0.02
for both); however, leaden paralysis was more strongly correlated with insomnia
(r = 0.06) than with hypersomnia (r = 0.01). These results suggest a positive but modest correlation
between the atypical B symptoms, and fairly good discriminant validity compared
with the nonatypical symptoms of decreased appetite and insomnia.
CATEGORIZING PATIENTS WITH PROBABLE ATYPICAL DEPRESSION
Probable atypical depression is defined as mood reactivity plus exactly
1 of 4 atypical B symptoms. Of the 449 patients who did not meet the full
criteria for atypical depression, 141 (31.5%) met the probable criteria for
this disorder. To determine whether these patients more closely resembled
those who met the full criteria or those with nonatypical depression, we performed
the following analysis: we compared the 141 patients with probable atypical
depression with both the 130 patients who had atypical depression and the
308 patients with nonatypical depression across each demographic and clinical
variable. Patients with probable atypical depression differed significantly
from those with threshold criteria on 7 variables. They were less severely
ill; had a shorter episode duration; had higher rates of comorbid social phobia;
had lower rates of borderline, narcissistic, and avoidant traits; and had
lower rates of avoidant PD. In contrast, patients with probable atypical depression
differed significantly from patients with nonatypical depression on only 1
variable: they were more likely to be female. Thus, our results suggest that
patients with probable atypical depression are distinct from those who meet
threshold criteria.
COMMENT
The ideal method for introducing a new diagnosis into the official nomenclature
is to postulate its features by drawing from clinical experience, establish
its boundaries through empirical research, test its reliability, and confirm
its validity. Rarely have psychiatric diagnoses followed this route, and atypical
depression is no exception. This condition is somewhat unique, however, because
it evolved largely from the results of psychopharmacology trials. Previous
studies attempting to validate the subtype by more traditional means had methodological
shortcomings and consequently have yielded inconsistent results. Because our
hypotheses were based on this inconsistent literature, it would have been
unrealistic to expect that all of the hypotheses would be confirmed. The degree
to which our results validate the subtype is therefore a matter of judgment.
Our most salient finding regards mood reactivity. Mood reactivity has
been considered an essential component of the atypical features subtype; of
the 5 atypical symptoms, it is the only one required to make the diagnosis.
Consistent with other reports,11, 14, 22, 32, 42-43
we did not find any evidence to suggest that mood reactivity is associated
with the atypical B symptoms. In some antidepressant trials, the presence
of mood reactivity has been shown to predict a preferential MAOI response,33, 44 whereas other studies have found
that it is not predictive34 or that mood unreactivity predicts a superior MAOI response.19, 22, 45
Of the remaining atypical symptoms, correlation analyses revealed significant
but modest associations. Although correlation coefficients of 0.09 to 0.10
account for only about 1% of the variance, the association between insomnia
and decreased appetite (r = 0.13) was only slightly
higher. This suggests that this level of correlation may be clinically meaningful.
Our analyses lend support to the discriminant validity of the subtype because
hyperphagia and hypersomnia were generally more closely correlated with the
remaining atypical symptoms than were the nonatypical symptoms of decreased
appetite and insomnia.
Three of the most commonly cited validators of atypical depression were
confirmed in our study: a preponderance of women, a younger age at onset,
and a longer duration of illness. Two other important validators were not
confirmed. Depressed patients with atypical features were not younger, and
they were found to be more rather than less severely depressed. Although psychopharmacologic
studies have consistently reported that patients with atypical depression
have a milder illness, these studies are vulnerable to sampling bias because
subjects with mild depression are invariably excluded from these trials. The
lower rates of severity found in these studies could also reflect the fact
that the HAM-D rating scale does not account for reversed neurovegetative
symptoms. In our study, a greater severity of illness in patients with atypical
depression was corroborated by lower baseline GAF scores and poorer social-functioning
ratings.
Our analysis of comorbid Axis I disorders confirmed that panic disorder
with agoraphobia, social phobia, hypochondriasis, and body dysmorphic disorder
were all associated with atypical depression, as predicted. Panic disorder
without agoraphobia was not associated with this condition. Although most
research assessing the predictive value of comorbid anxiety for MAOI response
rates in patients with atypical features has focused on the presence of comorbid
panic attacks,19-20,27, 29-30,42, 44, 46-47
our results suggest that the phobic element may be more relevant.
Despite the statistically significant findings, we would argue that
our results do not support a strong association between histrionic PD and
atypical depression because (1) personality traits were also found to be higher
in PDs that have not been postulated to be associated with atypical features;
(2) the mean ± SD number of DSM-IV histrionic
traits in the 54 patients with atypical depression was only 1.0 ± 1.2;
and (3) only 1.9% of the depressed patients with atypical features met the
criteria for histrionic PD. Our finding that avoidant PD is associated with
atypical depression is consistent with previous studies.21, 24
One possible explanation for this finding, however, is that rejection sensitivity
may be closely related to avoidant traits. If so, the comorbidity findings
could simply be a consequence of the overlapping nature of these constructs;
in fact, all of the comorbid conditions associated with the atypical features
subtype appear to have this phobic-hyperconscious element in common. To determine
whether the other atypical symptoms were independently associated with these
disorders, we reanalyzed our data set using a modified definition of atypical
depression that required mood reactivity plus 2 of 3 atypical B symptoms (excluding
rejection sensitivity). Of all the validators we assessed in this study, only
1 remained significantly associated with the atypical subtype: being female.
This suggests that the comorbidity findings may be a consequence of the fact
that rejection sensitivity is an element of most, if not all, of these disorders.
Two limitations of our study should be kept in mind. First, although
multiple raters were used to interview patients, the study was entirely carried
out at one site, and the results therefore warrant replication. Second, the
small sample sizes for conditions such as panic disorder without agoraphobia,
bipolar disorder, and certain PDs may have provided insufficient power to
detect real differences that might have been present; these analyses should
be interpreted cautiously.
We conclude that our results lend partial support for the validity of
the DSM-IV atypical features subtype. We could find
no evidence, however, to suggest that mood reactivity is a valid component
of the subtype, and this feature should perhaps be dropped from the diagnostic
criteria set. With MAOIs falling into disuse, it seems unlikely that more
pharmacologic trials will be performed to further address these issues. Thirty
years ago, using antidepressant response rates in probands and family members,
Pare and Mack48 suggested that certain patients
may have a distinct genetic makeup that predisposes them to respond to particular
antidepressants. Since then, little progress has been made in our ability
to profile specific antidepressant responders. It would be unfortunate if
the one instance in which a clear beneficial response pattern was known were
not more fully investigated to uncover any underlying clues that might be
available.
AUTHOR INFORMATION
Accepted for publication June 26, 2001.
Corresponding author and reprints: Michael A. Posternak, MD, Department
of Psychiatry and Human Behavior, Brown University School of Medicine, Rhode
Island Hospital, 235 Plain St, Suite 501, Providence, RI 02905 (e-mail: mposternak{at}lifespan.org).
From the Department of Psychiatry and Human Behavior, Brown University
School of Medicine, Rhode Island Hospital, Providence.
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