Posted by jrbecker on February 11, 2005, at 12:16:18
In reply to Bipolar II Series -Antidepressnt-induced dysphoria, posted by jrbecker on February 11, 2005, at 12:14:46
Journal of Affective Disorders
Volume 84, Issues 2-3 , February 2005, Pages 209-217
Bipolar Depression: Focus on Phenomenology
doi:10.1016/j.jad.2004.05.004
Copyright © 2004 Elsevier B.V. All rights reserved.
Research report
Atypical depression: a variant of bipolar II or a bridge between unipolar and bipolar II?
Hagop S. Akiskala, , and Franco Benazzib, caInternational Mood Center, University of California at San Diego, V.A. Hospital, 3350 La Jolla Village Dr. 116-A, La Jolla, San Diego, CA 92161, USA
bE. Hecker Outpatient Psychiatry Center, Ravenna, Italy
cNational Health Service, Forli, ItalyReceived 10 February 2004; accepted 13 July 2004. Available online 10 February 2005.
Abstract
Background
Although increasing data link atypical depression (AD) to the bipolar spectrum, controversies abound about the extent of the overlap. In particular, the Columbia group, which has pioneered in providing data on operational clarity and pharmacological specificity of atypical depressions, has nonetheless consistently avoided studying its discriminatory validity from bipolar II (BP-II). Accordingly, we undertook a full scale validation of such a link in a large clinical sample of BP-II and unipolar (UP) major depressive disorder (MDD).
Methods
Consecutive 348 BP-II and 254 MDD outpatients presenting with major depressive episodes (MDE) were interviewed off psychoactive drugs with a modified Structured Clinical Interview for DSM-IV, the structured Family History Screen and the Hypomania Interview Guide. We used the DSM-IV criteria for “atypical features” specifier. Depressive mixed state was defined as ≥3 concurrent hypomanic signs and symptoms during MDE. Bipolar validators were age at onset, high depressive recurrence, depressive mixed state and bipolar family history (types I and II). Univariate and multivariate logistic regression were used to examine associations and control for confounding variables.
Results
Frequency of AD was 43.0% in the combined BP-II and MDD sample. AD, versus non-AD, had significantly higher rates of BP-II. AD was significantly associated with all bipolar validators, among which family history was the most robust. A dose–response relationship was found between number of atypical symptoms during MDE and bipolar family history loading. The association between bipolar family history and number of atypical symptoms remained significant after controlling for the confounding effect of BP-II. Bipolar family history was strongly associated with the atypical symptoms of leaden paralysis and hypersomnia.
Conclusion
These results confirm a strong link between AD and bipolar validators along psychopathologic and familial grounds. From a practical standpoint, AD is best viewed as a variant of BP-II. Clinicians confronted with MDE patients presenting with atypical features should strongly consider a BP-II diagnosis. In a more hypothetical vein, atypicality—or some associated features thereof—might serve as a nosologic bridge between UP and BP-II.
Keywords: Atypical depression; Bipolar II; Leaden paralysis; Hypersomnia
Article Outline
1. Introduction
2. Methods
3. Results
4. Discussion
References
1. Introduction
According to DSM-IV-TR (American Psychiatric Association, 2000), AD is not a distinct disorder but a specifier of the major depressive episode (MDE) of bipolar and major depressive disorders (MDD) (and dysthymia). DSM-IV-TR criteria for the “atypical feature” specifier require mood reactivity plus overeating or weight gain, oversleeping, leaden paralysis and interpersonal rejection sensitivity (at least two), and absence of melancholic or catatonic features. The diagnostic validity and optimal definition of AD is currently unclear. The diagnostic validity of the Columbia group's definition of AD (the basis of DSM-IV-TR criteria) is justified by treatment response studies (better to MAOIs than to TCAs, Quitkin et al., 2003) and on latent class analysis (Kendler et al., 1996 and Sullivan et al., 1998). This definition of AD is being increasingly questioned (Perugi et al., 1998, Perugi et al., 2003, Nierenberg et al., 1998, Posternak and Zimmerman, 2001, Posternak and Zimmerman, 2002, Angst et al., 2002, Benazzi, 2002a, Benazzi, 2002b and Parker et al., 2002). In particular, many studies supporting the diagnostic validity of atypical depression (AD) had the important limitation of insufficient attention paid to discriminatory validity from bipolar II (Horwath et al., 1992, Kendler et al., 1996, Rabkin et al., 1996, Levitan et al., 1997, Sullivan et al., 1998, Sullivan et al., 2002, Sotsky and Simmens, 1999, Williamson et al., 2000, McGrath et al., 2000 and Matza et al., 2003). Furthermore, key AD symptoms (oversleeping, overeating, weight gain) were found to be more characteristic of bipolar as compared with unipolar depression (Detre et al., 1972, Akiskal et al., 1983, Hantouche et al., 1998, Serretti et al., 1998 and Mitchell et al., 2001).
In a tertiary-care AD sample (Perugi et al., 2003), close links have been recently reported between AD and bipolar-II disorder (BP-II), and between these disorders and the (possible) bipolar traits of mood lability, interpersonal sensitivity and cyclothymic temperament. Follow-up, too, has shown a relationship between AD and BP-II (Ebert and Barocka, 1991). Cross-sectional studies have shown that DSM-IV AD is more common in BP-II (Perugi et al., 1998, Perugi et al., 2003, Benazzi, 2000, Agosti and Stewart, 2001 and Angst et al., 2003). The inclusion of BP-II in AD studies is important because BP-II is common (around 50%) among depressed outpatients (Akiskal and Mallya, 1987, Dunner and Tay, 1993, Hantouche et al., 1998, Perugi et al., 1998, Akiskal et al., 2000, Benazzi, 2000, Angst et al., 2002, Angst et al., 2003, Akiskal and Benazzi, 2003 and Benazzi, 2003a). In an Australian study, Parker et al. (2002) curiously focused on their inpatient psychiatric setting—which is not where atypical depressives ordinarily come for treatment. We therefore submit that the relationship between AD and the bipolar spectrum should be further investigated in non-tertiary care settings, which are more representative of usual clinical practice.
An important diagnostic validator for AD would be diagnostic stability over time, yet such has not been realized (Kendler et al., 1996, Levitan et al., 1997 and Angst et al., 2002). Finding more BP-II than MDD in AD is not by itself a strong validator of the bipolar nature of AD, as a significant percentage of AD is reported in MDD patients (Angst et al., 2003, Benazzi, 2002a and Benazzi, 2002b). Such diagnostic validators as family history, age at onset, gender, comorbidity, temperament, treatment response, outcome and putative biology are more relevant (Robins and Guze, 1970, Akiskal, 1980, Kendler, 1990, Kendler et al., 1996 and Kendell and Jablensky, 2003). According to Kendell and Jablensky (2003), finding a bimodal distribution (zone of rarity) of key symptoms between two related syndromes would support a categorical distinction. BP-II is the closest of the bipolar disorders to MDD. Atypical features were reported to be more common in BP-II versus MDD, but no zone of rarity in the distribution of atypical symptoms was found in a mixed BP-II and MDD sample (Benazzi, 2003b), a finding not supporting AD as a distinct disorder. The strongest validator of the bipolar nature of AD would be a shared bipolar diathesis (Perugi et al., 2003). Such familial validation can be further strengthened by a dose–response relationship between number of atypical symptoms present during depression and bipolar family history loading (Rothman and Greenland, 1998). The few studies on familial bipolarity in AD versus non-AD were based on nonbipolar samples of AD (Rabkin et al., 1996, Sullivan et al., 1998 and Matza et al., 2003). The only study including BP-II and MDD in an AD sample found more bipolar family history in BP-II AD (Perugi et al., 1998), but this study was conducted in a tertiary care center.
Our aim then was to test the relationship between AD and the bipolar spectrum, by studying its association with bipolar validators—particularly on the basis of familial grounds, in an outpatient private practice setting where the bulk of AD patients present for care.
2. Methods
The present analyses were designed by both authors, but data collection itself was accomplished in FB's private practice. The methods in this outpatient setting are detailed in previous reports (Benazzi and Akiskal, 2003, Akiskal and Benazzi, 2003 and Benazzi, 2003c). Patients were consecutive 348 BP-II and 254 MDD outpatients, presenting voluntarily for treatment of a MDE, assessed in the last 5 years. Sample features are presented in Table 1, whereby BP-II vs. MDD had significantly younger index age and age at onset, higher depressive recurrences, depressive mixed states, number of atypical symptoms, individual atypical symptoms and bipolar family history. Substance-related and borderline personality disorders—which are anyway quite rare in FB's private setting—were excluded. Patients had to be off psychoactive drugs for at least 2 weeks when presenting for treatment. During the assessment visit the following instruments were used:
(1) The Structured Clinical Interview for DSM-IV Axis I Disorders-Clinician Version (First et al., 1997) (SCID-CV, reported inter-rater reliability k=0.70–1.0) as modified by Benazzi and Akiskal (2003);
(2) The Global Assessment of Functioning Scale (GAF, in the SCID-CV) for index MDE severity;
(3) The structured Family History Screen (Weissman et al., 2000) for assessing bipolar disorders family history in probands' first-degree relatives;
(4) The Hypomania Interview Guide (Williams et al., 1994) to assess intra-MDE hypomanic symptoms. Often, family members or close friends supplemented clinical information during interview, increasing validity of BP-II diagnosis and family history (Akiskal et al., 2000 and American Psychiatric Association, 2000).
Table 1.
Sample features
Variables: mean (S.D.), % BP-II, n=348 MDD, n=254 T/X2, df=600, df=1 p
Index age, years 41.5 (13.2) 46.7 (14.7) 4.4 0.000
Age at onset first MDE, years 22.8 (10.7) 31.8 (13.8) 8.9 0.000
Index GAF 50.3 (9.3) 50.6 (9.6) 0.4 0.652
N atypical symptoms 2.8 (1.5) 2.1 (1.4) 6.3 0.000
Female gender 67.8 61.4 2.6 0.104
≥5 MDEs 80.1 57.8 35.2 0.000
Index MDE symptoms>2 years 38.5 35.8 0.4 0.502
Axis I comorbidity 53.7 46.8 2.7 0.095
Index psychotic features 8.0 8.6 0.0 0.787
Index melancholic features 12.0 14.1 0.5 0.448
Index atypical features 52.8 29.5 32.6 0.000
Index depressive mixed state 62.3 33.4 49.0 0.000
Bipolar (type I+II) family history 47.7 16.5 46.4 0.000Atypical symptoms
Mood reactivity 89.6 82.2 6.8 0.009
Increased weight 21.8 10.2 14.0 0.000
Increased eating 27.0 14.1 14.2 0.000
Increased sleep 37.6 24.0 12.5 0.000
Leaden paralysis 47.1 33.4 11.2 0.001
Interpersonal sensitivity 65.8 46.8 21.6 0.000
Bipolar II disorder versus major depressive disorder.
BP-II=bipolar II disorder, MDD=major depressive disorder, GAF=Global Assessment of Functioning Scale, MDE=major depressive episode.
Systematic interviews about history of hypo-manic episodes were routinely conducted after the diagnosis of MDE, before the assessment of study variables, thereby avoiding a possible bias. We also made appropriate modifications of the SCID-CV administered in semi-structured format (Dunner and Tay, 1993, Brugha et al., 2001, Simpson et al., 2002 and Benazzi, 2003c), focusing first on overactive behaviours before evaluating mood change (Benazzi and Akiskal, 2003). We have found that patients are more likely to remember euphoric and/or irritable mood after hypomanic behaviors are elicited (Benazzi and Akiskal, 2003). Despite this sequence in our procedures giving precedence to hypomanic behavior, the final diagnosis of BP-II always required eliciting recall of hypomanic mood change occurring at the time of the activated period. We used a 2-day minimum duration threshold for hypomania for BP-II diagnosis (Akiskal et al., 1977, Akiskal et al., 1978, Akiskal et al., 1979, Akiskal, 2000, Benazzi, 2001, Simpson et al., 2002, Dunner, 2003, Angst et al., 2003 and Judd et al., 2003). This lower cut-off for hypomania duration is unlikely to have led to overdiagnosing BP-II, as most BP-II in our study setting have hypomanias lasting more than 2 days (Benazzi and Akiskal, in press).
We used DSM-IV-TR diagnostic criteria for the atypical features specifier of the MDE: mood reactivity plus increased eating or weight, increased sleeping, leaden paralysis, interpersonal rejection sensitivity (at least two) and no melancholic or catatonic features. Atypical depression was defined as an MDE with this specifier.
Depressive mixed state was defined as ≥3 hypomanic signs and symptoms during an MDE, following Akiskal and Benazzi definition (2003). Other bipolar diagnostic validators were age at onset, depressive recurrences, bipolar (type I+II) family history, following previous reports (Robins and Guze, 1970, Akiskal, 1980, Kendler, 1990, McMahon et al., 1994, Ghaemi et al., 2002, Angst et al., 2003 and Akiskal and Benazzi, 2003). We conducted a dose–response relationship analysis (Rothman and Greenland, 1998) between the number of atypical symptoms and bipolar family history.
For pairwise comparisons of continuous variables we used the t-test and the chi-squared test for categorical variables. We also used univariate, multivariate and forward stepwise logistic regression to study associations and to control for confounding. STATA Statistical Software, Release 7, was used (Stata, College Station, TX, USA, 2001). P-values were two-tailed and α level was set at 0.05, given the exploratory nature of the study.
3. Results
Frequency of AD in the combined MDD and BP-II sample was 43.0% (259/602). AD, versus non-AD (Table 2), had significantly younger index age and age at onset, higher rate of BP-II, females, depressive mixed states, axis I comorbidity, fewer psychotic features and higher bipolar family history.
Table 2.
Comparison between AD and non-AD
Variables: mean (S.D.), % AD, n=259 Non-AD, n=343 T/X2, df=600, df=1 p
Index age, years 40.3 (12.9) 46.3 (14.3) 5.2 0.000
Age at onset first MDE, years 22.9 (10.7) 29.5 (13.7) 6.4 0.000
Index GAF 51.5 (8.0) 49.6 (10.3) 2.4 0.015
MDD 28.9 52.1 32.6 0.000
BP-II 71.0 47.8 32.6 0.000
Female gender 73.3 58.8 13.5 0.000
≥5 MDEs 74.9 67.6 3.7 0.052
Index MDE symptoms>2 years 41.6 34.1 3.6 0.057
Depressive mixed state 65.2 38.7 41.3 0.000
Axis I comorbidity 58.3 45.1 10.1 0.001
Index psychotic features 3.8 11.9 13.9 0.000
Bipolar (type I+II) family history 45.5 24.1 85.7 0.000
BP-II=bipolar II disorder, MDD=major depressive disorder, GAF=Global Assessment of Functioning Scale, MDE=major depressive episode.
Table 3 shows a dose–response relationship between number of atypical symptoms during the MDE (in the BP-II and MDD combined sample) and bipolar family history loading: the higher the bipolar family history loading, the higher was the number of atypical symptoms during MDE (chi-squared test for trend=21.9, df=1, p<0.0001).
Table 3.
Dose–response relationship between number of atypical symptoms during the MDE and bipolar family history in the entire 602 sample
Variables: % BP-FH MR IW IE IS LP IRS
MDE+0, n=29 27.5 0.0 0.0 0.0 0.0 0.0 0.0
MDE+1, n=141 21.9 78.0 0.0 0.0 1.4 6.3 14.1
MDE+2, n=161 26.7 89.4 0.6 3.1 13.0 26.0 67.7
MDE+3, n=117 41.0 98.2 6.8 10.2 39.3 65.8 80.3
MDE+4, n=72 51.3 97.2 34.7 47.2 75.0 70.8 75.0
MDE+5, n=53 41.5 100.0 73.5 94.3 75.4 77.3 79.2
MDE+6, n=29 48.2 100.0 100.0 100.0 100.0 100.0 100.0
MDE=major depressive episode, BP-FH=bipolar (type I+II) family history, MR=mood reactivity, IW=increased weight, IE=increased eating, IS=increased sleep, LP=leaden paralysis, IRS=interpersonal rejection sensitivity.
Chi-squared test for trend=21.9, df=1, p<0.0001.
Table 4 shows that, within the MDD subsample, MDD plus AD had a significantly higher bipolar family history loading and lower age at onset than MDD without AD.
Table 4.
Comparison of bipolar family history in the major depressive disorder group with (MDD+AD) and without (MDD-AD) depression with atypical features
Variables MDD+AD, n=75 MDD-AD, n=179 T/X2, df=252, df=1 p=0
Bipolar family history% 24.0 12.8 4.8 0.028
Age at onset first MDE, years, mean (S.D.) 25.8 (11.6) 34.4 (13.9) −4.7 0.000
The association between AD and bipolar validators was tested (Table 5) by univariate logistic regression. AD was significantly associated with all bipolar validators. In order to test which were the strongest bipolar validator predictors of AD and to control for confounding, multiple logistic regression was used (Table 6). All possible interactions were tested: These analyses showed that depressive mixed state, BP-II and bipolar family history were significant predictors. Logistic regression of bipolar family history versus number of atypical symptoms during the MDE gave an odds ratio (OR)=1.3, 95% CI=1.1–1.4, z=3.7, p=0.000. The same analysis, controlled for BP-II (a confounding factor as it was associated with both atypical features and bipolar family history), revealed an OR=1.1, 95% CI=1.0–1.3, z=2.4, p=0.013.
Table 5.
Univariate logistic regression of atypical depression versus bipolar diagnostic validators
Variables Odds ratio 95% CI
Age at onset 0.9 0.9–0.9**BP-II 2.6 1.9–3.7**
≥5 MDEs 1.4 0.9–2.0*
Depressive mixed state 2.9 2.1–4.1**
Bipolar (type I+II) family history 2.6 1.7–3.9**
CI=confidence interval, BP-II=bipolar II disorder, MDE=major depressive episode.
* Means p≤0.05.
** Means p≤0.01.
Table 6.
Multiple logistic regression of atypical depression versus all bipolar diagnostic validators
Variables Odds ratio 95% CI
Age at onset 0.9 0.9–0.9*BP-II 1.3 0.8–2.1
≥5 MDEs 0.9 0.2–2.9
Depressive mixed state 1.9 1.2–3.0**Bipolar (type I+II) family history 1.7 1.0–2.7*
CI=confidence interval, BP-II=bipolar II disorder, MDE=major depressive episode.
* Means p≤0.05.
** Means p≤0.01.
In order to find which were the atypical symptoms most strongly associated with bipolar family history, we resorted to forward stepwise multiple logistic regression of bipolar family history versus all the atypical symptoms. The only selected atypical symptoms were leaden paralysis, increased sleep and interpersonal sensitivity. Multiple logistic regression of bipolar family history versus these variables confirmed leaden paralysis OR=1.6, 95% CI=1.1–2.5, z=2.4, p=0.015, and increased sleep OR=1.6, 95% CI=1.0–2.4, z=2.1, p=0.029 as significant predictors.
4. Discussion
The rate of 43% of AD in MDD in our study is nearly identical to that of the Angst et al.'s (2002) community study and that found by Perugi et al. (2003) in a tertiary-care sample. Unlike these three studies, age at onset of AD versus non-AD was not significantly different in a unipolar sample (Asnis et al., 1995), and no gender differences were reported in several mainly MDD community samples (Horwath et al., 1992, Levitan et al., 1997 and Sullivan et al., 2002). In the latter community studies, which did not systematically assess BP-II and used an AD definition requiring only oversleeping and overeating, AD did not have a higher rate of bipolar I than non-AD. Since specialized experience in the diagnosis of BP-II improves its detection (Dunner and Tay, 1993, Brugha et al., 2001, Ghaemi et al., 2002, Simpson et al., 2002 and Benazzi, 2003c), nonclinician interviewers appear to have led to gross underestimates of this diagnosis in all of these AD studies.
Our comparison between AD and non-AD showed that AD had features reported in previous studies, such as young age at onset, higher rate of females, BP-II and depressive mixed states, as well as axis I comorbidity; these are in line with previous studies from both clinical and epidemiological settings (Perugi et al., 1998, Benazzi, 2000 and Angst et al., 2002). Most importantly, bipolar family history was more common in AD versus non-AD. These findings support a link between AD and the bipolar spectrum. This link was more strongly shown by the dose–response relationship found between number of atypical symptoms during depression and the bipolar family history loading. A dose–response relationship supports a causal link, according to Rothman and Greenland (1998). Furthermore, number of atypical symptoms and bipolar family history were closely associated even when controlling for the confounding effect of BP-II. The latter finding suggests that AD is not simply a subset of BP-II, that indeed it may have its own distinguishing features. The AD symptoms most strongly associated with bipolar family history were leaden paralysis and increased sleep. On the other hand, the fact that even in the MDD sample, AD had more bipolar family history than non-AD, suggests that AD could be a marker of the bipolar nature of a subgroup of MDD, thereby supporting a continuity between BP-II and MDD. The present results follow closely previous analyses (Benazzi, 2003b), showing lack of bimodality in the distribution of atypical symptoms between BP-II and MDD. More tersely stated, atypicality—or some features thereof—may represent a bridge in a spectrum subsuming BP-II and UP disorders. Such temperamental characteristics, as cyclothymia and interpersonal sensitivity (both of which were not measured in the present study) might, hypothetically, subserve the proposed relationship between UP, atypicality and soft bipolarity (Perugi et al., 2003). Quitkin (2002) has proposed that “despite aspects of the disorder resembling a maladaptive, persistent mode of behavior”, AD patients do respond to psychopharmacotherapy. This statement implies that the persistent maladaptive style is a trait affective measure. Whether this trait is best described as interpersonal sensitive anxiousness (Parker et al., 2002), trait mood lability (Akiskal et al., 1995 and Akiskal, 1996) or the related construct of cyclothymia (Perugi et al., 2003) is presently unknown. It is nonetheless likely that all three temperaments are interwoven concepts (Perugi et al., 2003 and Kochman et al., 2005), in press.
The findings of the present analyses must be placed in the context of methodological assets and limitations. Ours was a solo private practice in the outpatient setting. However, interviewer bias is unlikely, because study variables were part of a larger set of data systematically and routinely assessed during the first visit (for MDE) in all new patients during the last 5 years. The interview was conducted by a clinician (FB) studying and treating mood disorders for over two decades, using reliable and validated structured and semi-structured interviews, buttressed by information from key informants. All state-of-the-art instruments were administered in a systematic manner, in a very large clinical population. The finding of a high BP-II versus MDD ratio in the present analyses is due to the use of systematic methods for probing for hypomania (Benazzi and Akiskal, 2003). Finally, the rate of bipolar family history was in line with previous family history studies (Dunner, 2003 and Hirschfeld et al., 2003).
Studies from other research centers would be desirable to confirm, modify or extend our results. But for now, our data from psychopathologic and familial validation strategies strongly support the link between BP-II and atypical depression. The two affective subtypes, while not isomorphic, appear intimately linked diagnostically and probably by an underlying pathogenetic diathesis (Perugi et al., 2003). There is little justification, on clinical grounds, to diagnose atypical depression as a UP MDD preferentially over BP-II. Our data seem to also suggest that to the extent AD is related to BP-II, it might, phenomenologically, serve as a “proxy” for depressive mixed states. Alternatively, from a nosologic perspective, AD might be conceptualised as a bridge between UP and BP-II.
References
Agosti and Stewart, 2001 V. Agosti and J.W. Stewart, Atypical and non-atypical subtypes of depression: comparison of social functioning, symptoms, course of illness, co-morbidity and demographic features, J. Affect. Disord. 65 (2001), pp. 75–79. SummaryPlus | Full Text + Links | PDF (52 K)
Akiskal, 1980 H.S. Akiskal, External validating criteria for psychiatric diagnosis: their application in affective disorders, J. Clin. Psychiatry 41 (1980), pp. 6–14.
Akiskal, 1996 H.S. Akiskal, The prevalent clinical spectrum of bipolar disorders: beyond DSM-IV, J. Clin. Psychopharmacol. 16 (1996) (Suppl. 1), pp. 4S–14S. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Akiskal, 2000 H.S. Akiskal, Soft bipolarity: a footnote to Kraepelin 100 years later, Jpn. J. Psychopathol. 21 (2000), pp. 3–11.
Akiskal and Benazzi, 2003 H.S. Akiskal and F. Benazzi, Family history validation of the bipolar nature of depressive mixed states, J. Affect. Disord. 73 (2003), pp. 113–122. SummaryPlus | Full Text + Links | PDF (86 K)
Akiskal and Mallya, 1987 H.S. Akiskal and G. Mallya, Criteria for the “soft” bipolar spectrum: treatment implications, Psychopharmacol. Bull. 23 (1987), pp. 68–73. Abstract-EMBASE | Abstract-MEDLINE
Akiskal et al., 1977 H.S. Akiskal, A.H. Djenderedjian, R.H. Rosenthal and M.K. Khani, Cyclothymic disorder: validating criteria for inclusion in the bipolar affective group, Am. J. Psychiatry 134 (1977), pp. 1227–1233. Abstract-EMBASE | Abstract-PsycINFO
Akiskal et al., 1978 H.S. Akiskal, A.H. Bitar, V.R. Puzantian, T.L. Rosenthal and P.W. Walker, The nosological status of neurotic depression: a prospective three-to-four year examination in light of the primary-secondary and unipolar–bipolar dichotomies, Arch. Gen. Psychiatry 35 (1978), pp. 756–766. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Akiskal et al., 1979 H.S. Akiskal, M.K. Khani and A. Scott-Strauss, Cyclothymic temperamental disorders, Psychiatr. Clin. North Am. 2 (1979), pp. 527–554. Abstract-EMBASE
Akiskal et al., 1983 H.S. Akiskal, P.W. Walker, V.R. Puzantian, D. King, T.L. Rosenthal and M. Dranon, Bipolar outcome in the course of depressive illness: phenomenologic, familial, and pharmacologic predictors, J. Affect. Disord. 5 (1983), pp. 115–128. Abstract
Akiskal et al., 1995 H.S. Akiskal, J.D. Maser, P. Zeller, J. Endicott, W. Coryell, M. Keller, M. Warshaw, P. Clayton and F.K. Goodwin, Switching from unipolar to bipolar II: An 11-year prospective study of clinical and temperamental predictors in 559 patients, Arch. Gen. Psychiatry 52 (1995), pp. 114–123. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Akiskal et al., 2000 H.S. Akiskal, M.L. Bourgeois, J. Angst, R. Post, H.-J. Moller and R. Hirschfeld, Re-evaluating the prevalence and diagnostic composition within the broad clinical spectrum of bipolar disorders, J. Affect. Disord. 59 (2000) (Suppl. 1), pp. S5–S30. Abstract | PDF (1304 K)
American Psychiatric Association, 2000 American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders (Fourth edition), American Psychiatric Association, Washington, DC (2000) Text Revision (DSM-IV-TR).
Angst et al., 2002 J. Angst, A. Gamma, R. Sellaro, H. Zhang and K. Merikangas, Toward validation of atypical depression in the community: results of the Zurich cohort study, J. Affect. Disord. 72 (2002), pp. 125–138. SummaryPlus | Full Text + Links | PDF (109 K)
Angst et al., 2003 J. Angst, A. Gamma, F. Benazzi, V. Ajdacic, D. Eich and W. Rossler, Toward a re-definition of subthreshold bipolarity: epidemiology and proposed criteria for bipolar-II, minor bipolar disorders and hypomania, J. Affect. Disord. 73 (2003), pp. 133–146. SummaryPlus | Full Text + Links | PDF (106 K)
Asnis et al., 1995 G.M. Asnis, L.K. McGinn and W.C. Sanderson, Atypical depression: clinical aspects and noradrenergic function, Am. J. Psychiatry 152 (1995), pp. 31–36. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Benazzi, 2000 F. Benazzi, Depression with DSM-IV atypical features: a marker for bipolar II disorder, Eur. Arch. Psychiatry Clin. Neurosci. 250 (2000), pp. 53–55. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Benazzi, 2001 F. Benazzi, Is 4 days the minimum duration of hypomania in bipolar II disorder?, Eur. Arch. Psychiatry Clin. Neurosci. 251 (2001), pp. 32–34. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Benazzi, 2002a F. Benazzi, Can only reversed vegetative symptoms define atypical depression?, Eur. Arch. Psychiatry Clin. Neurosci. 252 (2002), pp. 288–293. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Benazzi, 2002b F. Benazzi, Should mood reactivity be included in the DSM-IV atypical features specifier?, Eur. Arch. Psychiatry Clin. Neurosci. 252 (2002), pp. 135–140. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Benazzi, 2003a F. Benazzi, Frequency of bipolar spectrum in 111 private practice depression outpatients, Eur. Arch. Psychiatry Clin. Neurosci. 253 (2003), pp. 203–208. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Benazzi, 2003b F. Benazzi, Bipolar II disorder and major depressive disorder: continuity or discontinuity?, World J. Biol. Psychiatry 4 (2003), pp. 166–171. Abstract-MEDLINE
Benazzi, 2003c F. Benazzi, Diagnosis of bipolar II disorder: a comparison of structured versus semistructured interviews, Prog. Neuro-psychopharmacol. Biol. Psychiatry 27 (2003), pp. 985–991. SummaryPlus | Full Text + Links | PDF (163 K)
Benazzi and Akiskal, 2003 F. Benazzi and H.S. Akiskal, Refining the evaluation of bipolar II: beyond the strict SCID-CV guidelines for hypomania, J. Affect. Disord. 73 (2003), pp. 33–38. SummaryPlus | Full Text + Links | PDF (65 K)
Benazzi and Akiskal, 2005 F. Benazzi and H.S. Akiskal, Setting the threshold for the duration of hypomania in the diagnosis of bipolar-II disorder, J. Affect. Disord. (2005) (in press).
Brugha et al., 2001 T.S. Brugha, R. Jenkins, N. Taub, H. Meltzer and P.E. Bebbington, A general population comparison of the Composite International Diagnostic Interview (CIDI) and the Schedules for Clinical Assessment in Neuropsychiatry (SCAN), Psychol. Med. 31 (2001), pp. 1001–1013. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Detre et al., 1972 T. Detre, J. Himmelhoch, M. Swartzburg, C.M. Anderson, R. Byck and D.J. Kupfer, Hypersomnia and manic-depressive disease, Am. J. Psychiatry 128 (1972), pp. 1303–1305. Abstract-MEDLINE | Abstract-PsycINFO
Dunner, 2003 D.L. Dunner, Clinical consequences of under-recognized bipolar spectrum disorder, Bipolar Disord. 5 (2003), pp. 456–464.
Dunner and Tay, 1993 D.L. Dunner and K.L. Tay, Diagnostic reliability of the history of hypomania in bipolar II patients and patients with major depression, Compr. Psychiatry 34 (1993), pp. 303–307. Abstract
Ebert and Barocka, 1991 D. Ebert and A. Barocka, The early course of atypical depression, Eur. Arch. Psychiatr. Neurol. Sci. 241 (1991), pp. 131–132. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
First et al., 1997 M.B. First, R.L. Spitzer, M. Gibbon and J.B.W. Williams, Structured Clinical Interview for DSM-IV Axis I Disorders-Clinician Version (SCID-CV), American Psychiatric Press, Washington, DC (1997).
Ghaemi et al., 2002 S.N. Ghaemi, J.Y. Ko and F.K. Goodwin, “Cade's disease” and beyond: misdiagnosis, antidepressant use, and a proposed definition for bipolar spectrum disorder, Can. J. Psychiatry 47 (2002), pp. 125–134. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Hantouche et al., 1998 E.G. Hantouche, H.S. Akiskal, S. Lencrenon, J.-F. Allilaire, D. Sechter, J.-M. Azorin, M. Bourgeois, J.-P. Fraud and L. Chatenet-Duchene, Systematic clinical methodology for validating bipolar-II disorder: data in mid-stream from a french national multi-site study (EPIDEP), J. Affect. Disord. 50 (1998), pp. 163–173. SummaryPlus | Full Text + Links | PDF (87 K)
Hirschfeld et al., 2003 R.M.A. Hirschfeld, J.R. Calabrese, M.M. Weissman, M. Reed, M.A. Davies, M.A. Frye, P.E. Keck, L. Lewis, S.L. McElroy, J.P. McNulty and K.D. Wagner, Screening for bipolar disorder in the community, J. Clin. Psychiatry 64 (2003), pp. 53–59. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Horwath et al., 1992 E. Horwath, J. Johnson, M.M. Weissman and C.D. Horning, The validity of major depression with atypical features based on a community study, J. Affect. Disord. 26 (1992), pp. 117–126.
Judd et al., 2003 L.L. Judd, H.S. Akiskal, P.J. Schettler, W. Coryell, J. Endicott, J.D. Maser, D.A. Solomon, A.C. Leon and M.B. Keller, A prospective investigation of the natural history of the long-term weekly symptomatic status of bipolar II disorder, Arch. Gen. Psychiatry 60 (2003), pp. 261–269. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Kendell and Jablensky, 2003 R. Kendell and A. Jablensky, Distinguishing between the validity and utility of psychiatric diagnoses, Am. J. Psychiatry 160 (2003), pp. 4–12. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Kendler, 1990 K.S. Kendler, Toward a scientific psychiatric nosology. Strengths and limitations, Arch. Gen. Psychiatry 47 (1990), pp. 969–973. Abstract-EMBASE | Abstract-MEDLINE
Kendler et al., 1996 K.S. Kendler, L.J. Eaves, E.E. Walters, M.C. Neale, A.C. Heath and R.C. Kessler, The identification and validation of distinct depressive syndromes in a population-based sample of female twins, Arch. Gen. Psychiatry 53 (1996), pp. 391–399. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Kochman et al., 2005 F.J. Kochman, E.G. Hantouche, P. Ferrari, S. Lancrenon, D. Bayart and H.S. Akiskal, The cyclothymic-sensitive temperament scale as a prospective predictor of bipolarity and suicidality in clinically depressed children and adolescents with major depressive disorder, J. Affect. Disord. (2005) in press.
Levitan et al., 1997 R.D. Levitan, A. Lesage, S.V. Parikh, P. Goering and S.H. Kennedy, Reversed neurovegetative symptoms of depression: a community study of Ontario, Am. J. Psychiatry 154 (1997), pp. 934–940. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Matza et al., 2003 L.S. Matza, D.A. Revicki, J.R. Davidson and J.W. Stewart, Depression with atypical features in the national comorbidity survey, Arch. Gen. Psychiatry 60 (2003), pp. 817–826. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
McGrath et al., 2000 P.J. McGrath, J.W. Stewart, M.N. Janal, E. Petkova, F.M. Quitkin and D.F. Klein, A placebo-controlled study of fluoxetine versus imipramine in the acute treatment of atypical depression, Am. J. Psychiatry 157 (2000), pp. 344–350. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
McMahon et al., 1994 F.J. McMahon, O.C. Stine, G.A. Chase, D.A. Meyers, S.G. Simpson and J.R. DePaulo, Influence of clinical subtype, sex, and lineality on age at onset of major affective disorder in a family sample, Am. J. Psychiatry 151 (1994), pp. 210–215. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Mitchell et al., 2001 P.B. Mitchell, K. Wilhelm, G. Parker, M.-P. Austin, P. Rutgers and G.S. Malhi, The clinical features of bipolar depression: a comparison with matched major depressive disorder patients, J. Clin. Psychiatry 62 (2001), pp. 212–216. Abstract-EMBASE | Abstract-PsycINFO
Nierenberg et al., 1998 A.A. Nierenberg, J.E. Alpert, J. Pava, J.F. Rosenbaum and M. Fava, Course and treatment of atypical depression, J. Clin. Psychiatry 59 (1998) (Suppl. 18), pp. 5–9. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Parker et al., 2002 G. Parker, K. Roy, P. Mitchell, K. Wilhelm, G. Malhi and D. Hadzi-Pavlovic, Atypical depression: a reappraisal, Am. J. Psychiatry 159 (2002), pp. 1470–1479. Abstract-EMBASE | Abstract-MEDLINE | Full Text via CrossRef
Perugi et al., 1998 G. Perugi, H.S. Akiskal, L. Lattanzi, D. Cecconi, C. Mastrocinque, A. Patronelli, S. Vignoli and E. Bemi, The high prevalence of “soft” bipolar (II) features in atypical depression, Compr. Psychiatry 39 (1998), pp. 63–71. SummaryPlus | Full Text + Links | PDF (787 K)
Perugi et al., 2003 G. Perugi, C. Toni, M.C. Travierso and H.S. Akiskal, The role of cyclothymia in atypical depression: toward a data-based reconceptualization of the borderline-bipolar II connection, J. Affect. Disord. 73 (2003), pp. 87–98. SummaryPlus | Full Text + Links | PDF (127 K)
Posternak and Zimmerman, 2001 M.A. Posternak and M. Zimmerman, Symptoms of atypical depression, Psychiatry Res. 104 (2001), pp. 175–181. SummaryPlus | Full Text + Links | PDF (73 K)
Posternak and Zimmerman, 2002 M.A. Posternak and M. Zimmerman, Partial validation of the atypical features subtype of major depressive disorder, Arch. Gen. Psychiatry 59 (2002), pp. 70–76. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Quitkin, 2002 F.M. Quitkin, Depression with atypical features: diagnostic validity, prevalence, and treatment, Prim. Care Companion J. Clin. Psychiatry 4 (2002), pp. 94–99.
Quitkin et al., 2003 F.M. Quitkin, P.J. McGrath, J.W. Stewart and D.F. Klein, A reappraisal of atypical depression, Am. J. Psychiatry 160 (2003), pp. 798–800. Abstract-PsycINFO
Rabkin et al., 1996 J.G. Rabkin, J.W. Stewart, F.M. Quitkin, P.J. McGrath, W.M. Harrison and D.F. Klein, Should atypical depression be included in DSM-IV?, DSM-IV Sourcebook vol. 2, American Psychiatric Association, Washington, DC (1996), pp. 239–260.
Robins and Guze, 1970 E. Robins and S.B. Guze, Establishment of diagnostic validity in psychiatric illness: its application to schizophrenia, Am. J. Psychiatry 126 (1970), pp. 983–987. Abstract-MEDLINE
Rothman and Greenland, 1998 K.J. Rothman and S. Greenland, Modern Epidemiology (2nd ed.), Lippincott Williams & Wilkins, Philadelphia (1998).
Serretti et al., 1998 A. Serretti, E. Lattuada, C. Cusin, F. Macciardi and E. Smeraldi, Analysis of depressive symptomatology in mood disorders, Depress. Anxiety 8 (1998), pp. 80–85. Abstract-EMBASE | Abstract-MEDLINE
Simpson et al., 2002 S.G. Simpson, F.J. McMahon, M.G. McInnis, D.F. MacKinnon, D. Edwin, S.E. Folstein and J.R. DePaulo, Diagnostic reliability of bipolar II diagnosis, Arch. Gen. Psychiatry 59 (2002), pp. 736–740. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Sotsky and Simmens, 1999 S.M. Sotsky and S.J. Simmens, Pharmacotherapy response and diagnostic validity in atypical depression, J. Affect. Disord. 54 (1999), pp. 237–247. SummaryPlus | Full Text + Links | PDF (138 K)
Sullivan et al., 1998 P.F. Sullivan, R.C. Kessler and K.S. Kendler, Latent class analysis of lifetime depressive symptoms in the national comorbidity survey, Am. J. Psychiatry 155 (1998), pp. 1398–1406. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO
Sullivan et al., 2002 P.F. Sullivan, C.A. Prescott and K.S. Kendler, The subtypes of major depression in a twin registry, J. Affect. Disord. 68 (2002), pp. 273–284. SummaryPlus | Full Text + Links | PDF (2977 K)
Weissman et al., 2000 M.M. Weissman, P. Wickramaratne, P. Adams, S. Wolk, H. Verdeli and M. Olfson, Brief screening for family psychiatric history. The family history screen, Arch. Gen. Psychiatry 57 (2000), pp. 675–682. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Williams et al., 1994 J.B.W. Williams, M. Terman, M.J. Link, L. Amira and N.E. Rosenthal, Hypomania Interview Guide (Including Hyperthymia). Current Assessment Version (HIGH-C). Clinical Assessment Tools Packet, Center for Environmental Therapeutics, Norwood, NJ (1994).
Williamson et al., 2000 D.E. Williamson, B. Birmaher, D.A. Brent, L. Balach, R.E. Dahl and N.D. Ryan, Atypical symptoms of depression in a sample of depressed child and adolescent outpatients, J. Am. Acad. Child Adolesc. Psych. 39 (2000), pp. 1253–1259. Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Text via CrossRef
Corresponding author. Tel.: +1 858 552 8585x2226; fax: +1 858 534 8598.
poster:jrbecker
thread:456267
URL: http://www.dr-bob.org/babble/20050207/msgs/456276.html