Antidepressant-induced Hypomania Research Articles

Retraction: Bipolar Affective Disorder: A Case of Antidepressant-Induced Hypomania.

[This retracts the article DOI: 10.7759/cureus.12399.].

P.3.007 - Antidepressant-induced hypomania in patients with major depression: evidence from the BRIDGE-II-MIX study

Wasted heat from exhaust gas and the other parts of vehicles such as brake discs can be a daily great source of energy for thermoelectric generators. Different features such as cross wind, vehicle speed, heat sink structure, number of brakes during driving and engine operation influence the temperature of exhaust and discs. Thus, measurement of vehicle’s wasted heat needs an accurate system. Hence, this paper suggests a flexible measurement system along with a reliable sensor which transfers data with high speed to a computer. The system measures temperature of heat resources during driving with considering the real conditions. The measurement system is located on different places of exhaust and brake discs. The transferred data is stored online in a computer for later applications including power and energy calculation of thermoelectric generators. Due to time consuming and difficulties of the measurements in all situations, an intelligent prediction algorithm is used to produce the extra data for various conditions. The applied intelligent method in the algorithm is adaptive neuro fuzzy inference system (ANFIS). The measured and estimated values are helpful to design an appropriate thermoelectric generator system and energy management in hybrid vehicles. In order to validate the results, an experimental prototype is built and used to compare the real data with theoretical one.

The prevalence of bipolar spectrum disorder in elderly patients with recurrent depression.

PurposeDespite a growing body of knowledge on bipolar spectrum disorder (BSD), relatively little is known about the clinical characteristics of BSD in elderly people. We investigated the prevalence of BSD in elderly patients with recurrent depression.Patients and methodsA total of 65 elderly outpatients (≥60 years of age) who met the Diagnostic and Statistical Manual of Mental Disorders IV criteria for recurrent major depressive disorder participated in the study. BSD was diagnosed according to the criteria developed by Ghaemi et al and the Mood Disorder Questionnaire (MDQ) was used to assess bipolarity.ResultsOf 65 subjects, eleven (16.9%) and 54 (83.1%) were diagnosed with BSD and unipolar depression, respectively. A total of 32.3% (n=22) had a positive screen for bipolar disorder, and we found a significant association between the BSD criteria and the criteria for a positive MDQ (P<0.001). Patients with BSD had a longer duration of illness (P=0.040) and more prior depressive episodes (P<0.001) than did those with unipolar depression. The BSD criteria of first-degree relative with bipolar disorder (P=0.030), antidepressant-induced hypomania (P=0.034), hyperthymic personality (P=0.001), and atypical depression (P=0.030) were highly associated with MDQ-positive patients.ConclusionOur results indicate that many depressed elderly patients have bipolar-related illness; moreover, some features of the depression are associated with bipolarity.

Antidepressant-induced mania or hypomania in DSM-5

To the Editor: In contrast to DSM-IV-TR, DSM-5 adds the note to the diagnostic criteria of manic episodes as follows: “A full manic episode that emerges during antidepressant treatment but persists at a fully syndromal level beyond the physiological effect of that treatment is sufficient evidence for a manic episode and, therefore, a bipolar I diagnosis” (American Psychiatric Association 2013). Also, hypomanic episodes have a similar note in DSM-5 (American Psychiatric Association 2013). These notes seem to widen the concept of bipolar disorder because patients developing mania or hypomania during antidepressant treatment beyond the physiological effect can be diagnosed as bipolar I or II in DSM-5 although they were diagnosed as suffering from substance-induced mood disorder in DSM-IV-TR. Back to DSM-III-R, manic episodes should have been diagnosed in cases that are apparently precipitated by antidepressants because DSM-III-R had a note that “somatic antidepressant treatment that apparently precipitates a mood disturbance should not be considered an etiologic organic factor” in the diagnostic criteria of manic episode (Goodwin and Jamison 2007). According to Dunner (a member of the DSM-IV task force), “There was a sense from the Task Force that bipolar conditions should not be over-diagnosed in the community. Therefore, hypomanic episodes occurring in response to treatment with antidepressant pharmacotherapy would not count toward the diagnosis of bipolar II. However, it is difficult to induce mania or hypomania in a true unipolar depression: “there is likelihood that patients who develop mania or hypomania in response to treatment are actually bipolar.” (American Psychiatric Association 1987). Thereafter, Chun and Dunner (2004) suggest that the rate of antidepressant-induced hypomania in major depressive disorder is very low and that antidepressant treatment cannot make a unipolar patient bipolar. Recently, Dumlu et al. (2011) confirmed that unipolar depression with a history of treatment-induced mania, bipolar I, and bipolar II clustered together in contrast to unipolar depression without manic switch. In this point, DSM-5 seems to be appropriately coming back to DSMIII-R. Nonetheless, beyond the physiological effect in the notes of DSM-5 should be deleted because patients who develop mania or hypomania in response to treatment may be actually bipolar (American Psychiatric Association 1987; Chun and Dunner 2004), and it seems difficult to determine whether manic or hypomanic state persists beyond the physiological effect in individual patients, inducing low reliability.

A comparison of clinical characteristics in bipolar I disorder and antidepressant-associated mania/hypomania

A comparison of clinical characteristics in bipolar I disorder and antidepressantassociated mania/hypomania Objective: Although hypomania/mania during antidepressant treatment is not rare, it is often neglected by clinicians. As a result of the recent developments in this topic, bipolarity is now accepted as a wide spectrum. Forty percent of the patients with bipolar disorder have been misdiagnosed or diagnosed in later stages of illness. There are no specific diagnostic criteria for antidepressant-induced hypomania/ mania. These patients have not been included in bipolar spectrum. In this study, we aimed to compare clinical features of BP I and antidepressant-induced hypomania/mania, and discussed bipolar spectrum disorders. Method: In this study, 84 consecutive patients who referred to outpatient unit were selected. Forty of the patients were diagnosed as antidepressant-induced mania or hypomania, and 44 of them as BP I disorder according to DSM-IV criteria. All patients were given SCID-I and a data form which included sociodemographic characteristics and clinical features. Results: The majority of the patients in both groups were female. The rate of major depression among the relatives of BP I group was significantly lower than antidepressant induced manic or hypomanic group. Antidepressant-associated mania or hypomania has been observed as a milder disorder compared to BP I. Conclusions: Our results suggest that antidepressant-associated mania or hypomania should be

Bipolarity in depressive patients without histories of diagnosis of bipolar disorder and the use of the Mood Disorder Questionnaire for detecting bipolarity

Objectives The present study was performed to evaluate the frequency of bipolar disorders among patients ( a) presenting with depressive episodes but ( b) who have never been diagnosed with bipolar disorder ( c) in routine clinical practice in Korean subjects and to identify which clinical features were helpful in discriminating bipolar patients from unipolar patients. In addition, authors assessed the practical use of the Mood Disorder Questionnaire (MDQ) to distinguish bipolar from unipolar disorder in these subjects and tested whether modifications of the MDQ scoring could improve its performance. Methods We evaluated consecutive patients who satisfied the inclusion criteria of a current depressive episode, plus at least one previous depressive episode. Subjects were interviewed for diagnosis using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders IV after completing the MDQ. To improve assessment of hypomania history, the interviewer made strenuous efforts to explore a possible history of hypomania, and patient-derived data were supplemented by information from family members or close relatives. Results Fifty-nine patients (53.2%) were classified as having bipolar disorder, leaving a group of 52 (46.8%) with unipolar depression. Among bipolar disorders, 1.8% (n = 2) had bipolar I disorder; 29.7% (n = 33), bipolar II disorder; 6.3% (n = 7), bipolar III disorder (history of antidepressant-induced hypomania without spontaneous hypomanic episode); and 15.3% (n = 17), bipolar disorder not otherwise specified (1-3 days brief hypomania). Postpartum depression (relative risk [RR] [95% confidence interval {CI}], 2.00 [1.23-3.24]), early age of onset (RR [95% CI], 1.85 [1.30-2.64]), mood lability (RR [95% CI], 1.85 [1.30-2.64]), brief depressive episode (RR [95% CI], 1.66 (1.16-2.37]), bipolar family history (RR [95% CI], 1.62 [1.08-2.43]), history of suicide attempt (RR [95% CI], 1.47 (1.05-2.04]), and alcohol problem (RR [95% CI], 1.45 (1.04-2.02]) were found to have higher risks for bipolar disorder among depressive subjects. We found that a modified scoring of the MDQ (ignoring question on functional impairment and co-occurrence of symptoms) yielded a sensitivity of 0.68 and a specificity of 0.63 for bipolar diagnosis, whereas the figures were 0.29 and 0.77, respectively, with the standard MDQ scoring. Conclusions The results of this study clearly indicate that a high frequency of bipolar disorders in depressive patients who have never been diagnosed with bipolar disorders and clinical features indicating bipolarity could help to differentiate bipolar subjects from unipolar subjects. Adapting the standard scoring, the MDQ showed limited use for detecting bipolar disorder; however, if the scoring modification is adapted, the MDQ can offer tolerable sensitivity.

Antidepressant-Induced Hypomania in Treatment-Resistant Depression

The authors propose that isolated treatment-associated hypomanic episodes in patients with chronic treatment-resistant major depressive disorder are not indicative of true bipolar depression. This proposal is in contrast to most studies that support the notion that antidepressant-induced hypomania reflects an underlying bipolar condition in such depressed patients. However, the patients described in the literature have not had treatment-resistant depression. Records of 146 patients with treatment-resistant major depression seen at a university-based tertiary referral center were reviewed for evidence of treatment-associated mania or hypomania. Treatment histories, clinical characteristics, and family histories of these patients were assessed. Of the 146 patients, 16 patients had evidenced treatment-induced hypomania or hypomanic-like episodes. The number of antidepressant trials these patients had received ranged from 2 to 13. The hypomanic episodes did not occur with the first antidepressant treatment trial except in one patient. All of the 16 patients had antidepressant treatment trials subsequent to the trial during which they experienced hypomania, but only one of them experienced further episodes of hypomania. In addition, only 1 of the 16 patients had a family history of bipolar disorder, a rate of bipolar family history that is considerably less than we have found among bipolar patients. These findings support the concept of antidepressant-induced hypomania presented in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, revised (DSM-IV-TR). However, we argue that this term should be restricted to patients with chronic treatment-resistant major depression who infrequently evidence mania or hypomania.

A Family Therapist's Guide to Bipolar III: Antidepressant-Induced Mania or Hypomania

This article explores the phenomenon of hypomania and mania induced by the treatment with antidepressants, sometimes called bipolar III. Family therapists need to be aware of this phenomenon because estimates are that between 3–10% of depressed individuals may be at risk for developing hypomania or mania when treated with antidepressants. The article discusses implications for family therapists, including their role in the prevention and early detection of antidepressant-induced mania or hypomania.

Frovatriptan-Induced Hypomania

Back to table of contents Previous article Next article LetterFull AccessFrovatriptan-Induced HypomaniaMichael S. Wilson, M.D., Michael S. WilsonSearch for more papers by this author, M.D., Louisiana State University, HSC, Department of PsychiatryNew Orleans, LAPublished Online:1 Aug 2005AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR There has been an ongoing debate in the literature about whether antidepressants can induce hypomania in patients with underlying bipolar disorder.1 There is, however, less knowledge about other medications inducing such changes. The following case is about how a medication belonging to the class of drugs, called the triptans, induced a hypomanic episode in a bipolar patient.Case ReportMr. A is a 51-year-old single, white male who was seen at an outpatient private psychiatry clinic. He was diagnosed with bipolar II disorder and maintained on lamotrigine 150 mg/day. The patient was last seen 3 weeks previously with a Young Mania Rating Scale (YMRS)2 of 7, with no hypomanic or mixed episodes in the previous 3 months. In that interim the patient was only taking lamotrigine and sumatriptan 50 mg as needed for migraine headaches as prescribed by his neurologist. Mr. A had few mood switches under the current medication regimen. Various prophylactic treatments for these migraine headaches had been tried in the past with either poor results or intolerable side effects.Mr. A was then started on frovatriptan 2.5 mg per day for migraine headache prophylaxis. Two days later the patient was seen in the psychiatry clinic. At that time Mr. A was very irritable, anxious, sleeping poorly, rapid speech, and frequently tangential with intermittent looseness of associations: with an YMRS score of 29. Mr. A denied any increase in stress in home, work, or social environments. With the patient’s permission, Mr. A’s radical change was discussed with his neurologist and it was agreed to try the following: immediately discontinue the frovatriptan and take olanzapine 2.5 mg as needed for sleep.The patient was seen 6 days later in the outpatient clinic. At this time he was less anxious, calmer, exhibited regular speech with goal direction, and was less agitated: his YMRS score was now 9. The patient reported not having taken any olanzapine. Another week later Mr. A was even calmer with a YMRS score of 6.A review of the available literature by the author was unable to elicit any other cases of a triptan causing irritability and/or hypomania. Mr. A’s reaction could be attributed to either the other triptans having a half-life ranging from 2–6 hours, while frovatriptan’s half-life is 25 hours causing it to more readily accumulate in the body—as it did after 3 days3 or could be caused by frovatriptan’s four times greater affinity for 5HT1B.4 If more reports of this adverse effect surface, it may become necessary to add frovatriptan to the antidepressants as possible causes of inducing mania/hypomania.References1 Chun BJ, Benjamin JDH, Dunner DL: A review of antidepressant-induced hypomania in major depression: suggestions for DSM-V. Bipolar Disord 2004; 6:32–42Crossref, Medline, Google Scholar2 Young RC, Biggs JT, Ziegler VE et al: A rating scale for mania: reliability, validity, and sensitivity. Br J Psychiatry 1978; 133:429–435Crossref, Medline, Google Scholar3 Elan Pharmaceuticals, Inc. Frova TM package insert, 2004Google Scholar4 Comer MB: Pharmacology of the selective 5-HT (1B/1D) agonist frovatriptan. Headache 2002; Suppl. 2:S47–53Google Scholar FiguresReferencesCited byDetailsCited Byブロー成形Seikei-Kakou, Vol. 19, No. 7 Volume 17Issue 3 August 2005Pages 430-431 Metrics PDF download History Published online 1 August 2005 Published in print 1 August 2005

Frovatriptan-Induced Hypomania

Back to table of contents Previous article Next article LetterFull AccessFrovatriptan-Induced HypomaniaMichael S. Wilson, M.D., Michael S. WilsonSearch for more papers by this author, M.D., Louisiana State University, HSC, Department of PsychiatryNew Orleans, LAPublished Online:1 Aug 2005AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR There has been an ongoing debate in the literature about whether antidepressants can induce hypomania in patients with underlying bipolar disorder.1 There is, however, less knowledge about other medications inducing such changes. The following case is about how a medication belonging to the class of drugs, called the triptans, induced a hypomanic episode in a bipolar patient.Case ReportMr. A is a 51-year-old single, white male who was seen at an outpatient private psychiatry clinic. He was diagnosed with bipolar II disorder and maintained on lamotrigine 150 mg/day. The patient was last seen 3 weeks previously with a Young Mania Rating Scale (YMRS)2 of 7, with no hypomanic or mixed episodes in the previous 3 months. In that interim the patient was only taking lamotrigine and sumatriptan 50 mg as needed for migraine headaches as prescribed by his neurologist. Mr. A had few mood switches under the current medication regimen. Various prophylactic treatments for these migraine headaches had been tried in the past with either poor results or intolerable side effects.Mr. A was then started on frovatriptan 2.5 mg per day for migraine headache prophylaxis. Two days later the patient was seen in the psychiatry clinic. At that time Mr. A was very irritable, anxious, sleeping poorly, rapid speech, and frequently tangential with intermittent looseness of associations: with an YMRS score of 29. Mr. A denied any increase in stress in home, work, or social environments. With the patient’s permission, Mr. A’s radical change was discussed with his neurologist and it was agreed to try the following: immediately discontinue the frovatriptan and take olanzapine 2.5 mg as needed for sleep.The patient was seen 6 days later in the outpatient clinic. At this time he was less anxious, calmer, exhibited regular speech with goal direction, and was less agitated: his YMRS score was now 9. The patient reported not having taken any olanzapine. Another week later Mr. A was even calmer with a YMRS score of 6.A review of the available literature by the author was unable to elicit any other cases of a triptan causing irritability and/or hypomania. Mr. A’s reaction could be attributed to either the other triptans having a half-life ranging from 2–6 hours, while frovatriptan’s half-life is 25 hours causing it to more readily accumulate in the body—as it did after 3 days3 or could be caused by frovatriptan’s four times greater affinity for 5HT1B.4 If more reports of this adverse effect surface, it may become necessary to add frovatriptan to the antidepressants as possible causes of inducing mania/hypomania.References1 Chun BJ, Benjamin JDH, Dunner DL: A review of antidepressant-induced hypomania in major depression: suggestions for DSM-V. Bipolar Disord 2004; 6:32–42Crossref, Medline, Google Scholar2 Young RC, Biggs JT, Ziegler VE et al: A rating scale for mania: reliability, validity, and sensitivity. Br J Psychiatry 1978; 133:429–435Crossref, Medline, Google Scholar3 Elan Pharmaceuticals, Inc. Frova TM package insert, 2004Google Scholar4 Comer MB: Pharmacology of the selective 5-HT (1B/1D) agonist frovatriptan. Headache 2002; Suppl. 2:S47–53Google Scholar FiguresReferencesCited byDetailsCited Byブロー成形Seikei-Kakou, Vol. 19, No. 7 Volume 17Issue 3 August 2005Pages 430-431 Metrics PDF download History Published online 1 August 2005 Published in print 1 August 2005

The high prevalence of bipolar spectrum disorders in young adults with recurrent depression: toward an innovative diagnostic framework

Background: Young adults with early-onset major depressive disorder (MDD) may be at high risk of progression to bipolar disorder. Although hypomanic symptoms are common in young people with depression, many do not reach the strict DSM-IV and ICD-10 criteria for hypomania. We used an emerging innovative framework for bipolar spectrum to evaluate this question. Methods: Consecutive referrals to a psychiatric outpatient clinic at a university health service were assessed for recurrent episodes of depression. DSM-IV diagnoses were based on a SCID-1 interview. We used two approaches to delineate bipolar spectrum. The first focused on bipolar spectrum disorder (BSD, as defined by Ghaemi et al. [Can. J. Psychiatry 47 (2002) 125]), and the second on a symptoms perspective based on MDD with a history of hypomanic symptoms, using a 15-point hypomanic symptoms checklist with a cut-off ≥8 or more symptoms (modified from J. Affect. Disord. 73 (2003) 39 and J. Affect. Disord. 73 (2003) 73). Data were also obtained on family history of affective disorder, course and number of episodes of depression, symptom severity, psychosocial functioning, suicidality and deliberate self-harm, and drug and alcohol use. Results: High rates of bipolar and bipolar spectrum disorder were identified. Under DSM-IV, 14 subjects (16.1%) had bipolar affective disorder and 73 subjects (83.9%) had recurrent MDD. Depending on the method used to diagnose bipolar spectrum, between 47.1% and 77.0% of the total cohort could be so diagnosed. Hypomanic symptom counts, irrespective of duration, yielded the highest estimates for bipolar spectrum. High rates of pharmacological hypomania were also identified: 12 subjects (16.4%) with recurrent MDD group reported this, and all could be diagnosed with bipolar spectrum. Limitations: The reliability of using the 15-point hypomanic scale for the diagnostic assignments was not tested. All subjects were recruited from a university health service and, given the affluence of their parents, findings may not generalise to other populations. Most importantly, because bipolar family history and pharmacological hypomania were part of the diagnostic criteria of the BSD group, they could not be used as external validators for Ghaemi's BSD construct. Conclusions: Bipolar disorders emerge as extremely common in this cohort of young adults with recurrent depression. Antidepressant-induced hypomania and high scores on a hypomanic symptoms checklist help to identify patients who are likely to have a bipolar spectrum illness, but who do not meet DSM-IV criteria for bipolar disorder. This is a preliminary study, and further evidence from external validating strategies are needed to verify the bipolar status of these patients in a larger and unselected cohort representing a broader socio-economic demographic profile.

A review of antidepressant-induced hypomania in major depression: suggestions for DSM-V.

To determine if the classification of 'antidepressant-induced hypomania' in DSM-IV is supported by available data. We reviewed the available scientific literature to examine the incidence of mania and hypomania in non-bipolar patients who were treated with antidepressants. Eighty-nine per cent of studies of antidepressants in major depressive disorder patients reported no cases of treatment-induced hypomania. No instances of treatment-induced hypomania were reported in three large studies of patients with chronic forms of depression. The rate of antidepressant-induced hypomania in major depressive disorder is within the rate of misdiagnosis of bipolar depression as unipolar. Depressed patients who experience antidepressant-associated hypomania are truly bipolar.

P.1.139 How accurate can we predict antidepressant-induced hypomania?

P.1.139 How accurate can we predict antidepressant-induced hypomania?

A Genetic Marker for Antidepressant-Induced Hypomania?

The use of antidepressants in patients with bipolar mood disorders is complicated by our current inability to predict whether the antidepressant is likely to induce mania or mood cycling. This comparison of 27 patients with bipolar I or II disorder and with histories of mania or hypomania while taking …