Bipolar disorder, a serious illness resulting in significant psychosocial morbidity and excess mortality, has been reported to be frequently underdiagnosed. However, during the past few years we have observed the emergence of an opposite phenomenon--the overdiagnosis of bipolar disorder. In the present report from the Rhode Island Methods to Improve Diagnostic Assessment and Services (MIDAS) project, we empirically examined whether bipolar disorder is overdiagnosed.
Seven hundred psychiatric outpatients were interviewed with the Structured Clinical Interview for DSM-IV (SCID) and completed a self-administered questionnaire, which asked the patients whether they had been previously diagnosed with bipolar or manic-depressive disorder by a health care professional. Family history information was obtained from the patient regarding first-degree relatives. Diagnoses were blind to the results of the self-administered scale. The study was conducted from May 2001 to March 2005.
Fewer than half the patients who reported that they had been previously diagnosed with bipolar disorder received a diagnosis of bipolar disorder based on the SCID. Patients with SCID-diagnosed bipolar disorder had a significantly higher morbid risk of bipolar disorder than patients who self-reported a previous diagnosis of bipolar disorder that was not confirmed by the SCID (p < .02). Patients who self-reported a previous diagnosis of bipolar disorder that was not confirmed by the SCID did not have a significantly higher morbid risk for bipolar disorder than the patients who were negative for bipolar disorder by self-report and the SCID.
Not only is there a problem with underdiagnosis of bipolar disorder, but also an equal if not greater problem exists with overdiagnosis.
"Diagnostic challenges can emerge, particularly in the context of BD II and BPD . Specifically, some authors have proposed that BPD may be a misdiagnosis in patients with bipolar spectrum conditions   , while others argue that BPD would be better conceptualized as an atypical variant of a mood disorder      . Contemporary diagnostic manuals including DSM-5 describe these disorders as distinct entities in separate sections of the manual, with clear differences in terms of prevalence, outcomes and course of illness [2,42–44]. "
[Show abstract][Hide abstract] ABSTRACT: Objectives: Clinical studies suggest a high co-morbidity rate of borderline personality disorder (BPD) with bipolar disorder (BD). This study examines the prevalence and correlates of BPD in BD (I and II) in a longitudinal population-based survey.
Methods: Data came from Waves 1 and 2 (Wave 2: N = 34,653, 70.2% cumulative response rate; age ≥ 20 years) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Lay interviewers conducted in person interviews using the Alcohol Use Disorders and Associated Disabilities Interview (AUDADIS-IV), a reliable diagnostic tool of psychiatric disorders based on DSM-IV criteria. Subjects with BD I (n = 812), BD I/BPD (n = 360), BD II (n = 327) and BD II/BPD (n = 101) were examined in terms of sociodemographics, mood, anxiety, substance use and personality disorder co-morbidities and history of childhood traumatic experiences.
Results: Lifetime prevalence of BPD was 29.0% in BD I and 24.0% in BD II. Significant differences were observed between co-morbid BD I/II and BPD versus BD I/II without BPD in terms of number of depressive episodes and age of onset co-morbidity, and childhood trauma. BPD was strongly and positively associated with incident BD I (AOR = 16.9; 95% CI: 13.88-20.55) and BD II (AOR = 9.5; 95% CI: 6.44-13.97).
Conclusions: BD with BPD has a more severe presentation of illness than BD alone. The results suggest that BPD is highly predictive of a future diagnosis of BD. Childhood traumatic experiences may have a role in understanding this relationship.
"The patterns may help identification of TRD patients and “short-cut” patients to effective treatment approaches, thus avoiding “serial antidepressant non-response.” Thirdly, we advance the case that TRD responds pharmacologically more like “bipolar” vis-à-vis “unipolar” depression (Angst et al., 2010; Li et al., 2012) although this approach is not without contrary evidence (Healy, 2006; Zimmerman et al., 2008). Finally, we propose a rationale for TRD that invokes the necessity of “stacking” medications, akin to treatment-resistant hypertension or diabetes, balancing the risk of polypharmacy versus continued symptomatology. "
[Show abstract][Hide abstract] ABSTRACT: First-line treatment of major depression includes administration of a selective serotonin reuptake inhibitor (SSRI), yet studies suggest that remission rates following two trials of an SSRI are less than 50%. The authors examine the putative biological substrates underlying “Treatment Refractory Depression (TRD)” with the goal of elucidating novel rationales to treat TRD. We look at relevant articles from the preclinical and clinical literature combined with clinical exposure to TRD patients. A major focus was to outline pathophysiological mechanisms whereby the serotonin (5-HT) system becomes impervious to the desired enhancement of 5-HT neurotransmission by SSRI’s. A complementary focus was to dissect neurotransmitter systems, which serve to inhibit the dorsal raphe. We propose, based on a body of translational studies, TRD may not represent a simple 5-HT deficit state but rather an excess of midbrain peri-raphe 5-HT and subsequent deficit at key fronto-limbic projection sites, with ultimate compromise in 5-HT-mediated neuroplasticity. Glutamate, 5-HT, noradrenaline and histamine are activated by stress and exert an inhibitory effect on 5-HT outflow, in part by “flooding” 5-HT1A autoreceptors by 5-HT itself. Certain factors putatively exacerbate this scenario- presence of the short arm of the serotonin transporter gene, early life adversity and comorbid bipolar disorder- each of which has been associated with SSRI-treatment resistance. By utilizing an incremental approach, we provide a system for treating the TRD patient based on a strategy of rescuing 5-HT neurotransmission from a state of SSRI-induced dorsal raphe stasis. This calls for “stacked” interventions, with an SSRI base, targeting, if necessary, the glutamatergic, serotonergic, noradrenergic and histaminergic systems, thereby successively eliminating the inhibitory effects each are capable of exerting on 5-HT neurons. Future studies are recommended to test this biologically based approach for TRD.
"Stewart and El-Mallakh (2007)  Outpatients from a substance abuse treatment program DSM-IV criteria Only 42.9% of patients diagnosed with BD actually met diagnostic criteria Goldberg et al. (2008)  Dual diagnosis inpatients SCID Only 33% of patients diagnosed with BD actually met criteria for that condition. Misdiagnosis associated with cocaine and polysubstance abuse Zimmerman et al. (2008)  O u t p a t i e n t s S C I D Clinician-based diagnosis of BD: PPV of 37% and NPV of 95% Ruggero et al. (2010)  O u t p a t i e n t s S C I D 40% of patients with borderline personality disorder mistakenly diagnosed with BD Zimmerman et al. (2010)  O u t p a t i e n t s S C I D Patients overdiagnosed with BD were significantly more likely to receive disability payments Chilakamarri et al. (2011)  "
[Show abstract][Hide abstract] ABSTRACT: Bipolar disorder (BD) is considered one of the most disabling mental conditions, with high rates of morbidity, disability, and premature death from suicide. Although BD is often misdiagnosed as major depressive disorder, some attention has recently been drawn to the possibility that BD could be overdiagnosed in some settings. The present paper focuses on a critical analysis of the overdiagnosis issue among bipolar patients. It includes a review of the available literature findings, followed by some recommendations aiming at optimizing the diagnosis of BD and increasing its reliability.
The Scientific World Journal 11/2013; 2013:297087. DOI:10.1155/2013/297087 · 1.73 Impact Factor
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