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Ana González-pinto - One of the best experts on this subject based on the ideXlab platform.
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Epidemiology, Diagnosis and Management of Mixed Mania
CNS Drugs, 2007Co-Authors: Ana González-pinto, A. Aldama, Fernando Mosquera, Cristina González GómezAbstract:The presence of depressive symptomatology during acute Mania has been termed mixed Mania, dysphoric Mania, depressive Mania or mixed bipolar disorder. Highly prevalent, mixed Mania occurs in at least 30% of bipolar patients. Correct diagnosis is a major challenge. The DSM diagnostic criteria, the most widely adopted clinical convention, require a complete manic and complete depressive syndrome co-occurring for at least 1 week. However, recent alternative categorical and dimensional studies of manic phenomenology have shown that there are certain depressive symptoms or constellations that have special clinical importance when describing mixed states, such as depressed mood and anxiety symptomatology that do not overlap with manic symptoms. Patients with mixed Mania are over-represented in the subgroup with severe and treatment-resistant symptoms. The course and prognosis of mixed Mania are worse than that of pure manic forms in the medium and long term, with higher recurrence rates, higher frequency of co-morbid substance abuse and greater risk of suicidal ideation and attempts. Moreover, mixed manic episodes are usually associated with increased depression during follow-up, greater risk of rapid cycling course and higher prevalence of physical co-morbidities, principally related to thyroid function. All these factors are very relevant to selection of treatment. There are three crucial steps in the treatment of mixed Mania — making the correct diagnosis, starting treatment early, and considering not only the acute state but also maintenance treatment and the patient’s long-term outcome. Although challenging, acute mixed episodes are treatable. To date there have been no controlled studies devoted exclusively to treatment of mixed Mania, and the only controlled data available therefore derive from sub-analyses of randomised clinical trials. Both short-term and maintenance treatments of patients with mixed Mania requires experience and usually involves the combination of different treatments. As a general rule, there is some consensus about discontinuing antidepressants during mixed Mania. Olanzapine, aripiprazole or valproate semisodium (divalproex sodium) are first-line drugs for mild episodes; severe episodes of mixed Mania usually require treatment with a combination of valproate semisodium or lithium plus an antipsychotic, preferably an atypical agent. Carbamazepine is also useful for the treatment of mixed Mania. High-dose medications are sometimes needed to control the episode, and time to remission is usually longer than in pure Mania. Importantly, patients with mixed manic episodes have more adverse events of psychopharmacological treatment. In some cases, electroconvulsive therapy is required.
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Epidemiology, Diagnosis and Management of Mixed Mania
CNS Drugs, 2007Co-Authors: Ana González-pinto, A. Aldama, Fernando Mosquera, Cristina González GómezAbstract:The presence of depressive symptomatology during acute Mania has been termed mixed Mania, dysphoric Mania, depressive Mania or mixed bipolar disorder. Highly prevalent, mixed Mania occurs in at least 30% of bipolar patients. Correct diagnosis is a major challenge. The DSM diagnostic criteria, the most widely adopted clinical convention, require a complete manic and complete depressive syndrome co-occurring for at least 1 week. However, recent alternative categorical and dimensional studies of manic phenomenology have shown that there are certain depressive symptoms or constellations that have special clinical importance when describing mixed states, such as depressed mood and anxiety symptomatology that do not overlap with manic symptoms.
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Principal components of Mania.
Journal of affective disorders, 2003Co-Authors: A. Aldama, J Ballesteros, J L Pérez De Heredia, M Gutierrez, F Mosquera, Ana González-pintoAbstract:An alternative to the categorical classification of psychiatric diseases is the dimensional study of the signs and symptoms of psychiatric syndromes. To date, there have been few reports about the dimensions of Mania, and the existence of a depressive dimension in Mania remains controversial. The aim of this study was to investigate the dimensions of manic disorder by using classical scales to study the signs and symptoms of affective disorders. One-hundred and three consecutively admitted inpatients who met DSM IV criteria for bipolar disorder, manic or mixed were rated with the Young Mania Rating Scale (YMRS) and the Hamilton Depression Rating Scale (HDRS-21). A principal components factor analysis of the HDRS-21 and the YMRS was carried out. Factor analysis showed five independent and clinically interpretable factors corresponding to depression, dysphoria, hedonism, psychosis and activation. The distribution of factor scores on the depressive factor was bimodal, whereas it was unimodal on the dysphoric, hedonism and activation factors. Finally, the psychosis factor was not normally distributed. Patients of the sample were all medicated inpatients. Mania seems to be composed of three core dimensions, i.e. hedonism, dysphoria and activation, and is frequently accompanied by a psychotic and a depressive factor. The existence of a depressive factor suggests that it is essential to evaluate depression during Mania, and the distribution of the depressive factor supports the existence of two different states in Mania.
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Principal components of Mania.
Journal of Affective Disorders, 2002Co-Authors: Ana González-pinto, A. Aldama, J Ballesteros, M Gutierrez, J.l. Pérez De Heredia, Fernando MosqueraAbstract:Objective: An alternative to the categorical classification of psychiatric diseases is the dimensional study of the signs and symptoms of psychiatric syndromes. To date, there have been few reports about the dimensions of Mania, and the existence of a depressive dimension in Mania remains controversial. The aim of this study was to investigate the dimensions of manic disorder by using classical scales to study the signs and symptoms of affective disorders. Methods: One-hundred and three consecutively admitted inpatients who met DSM IV criteria for bipolar disorder, manic or mixed were rated with the Young Mania Rating Scale (YMRS) and the Hamilton Depression Rating Scale (HDRS-21). A principal components factor analysis of the HDRS-21 and the YMRS was carried out. Results: Factor analysis showed five independent and clinically interpretable factors corresponding to depression, dysphoria, hedonism, psychosis and activation. The distribution of factor scores on the depressive factor was bimodal, whereas it was unimodal on the dysphoric, hedonism and activation factors. Finally, the psychosis factor was not normally distributed. Limitations: Patients of the sample were all medicated inpatients. Conclusions: Mania seems to be composed of three core dimensions, i.e. hedonism, dysphoria and activation, and is frequently accompanied by a psychotic and a depressive factor. The existence of a depressive factor suggests that it is essential to evaluate depression during Mania, and the distribution of the depressive factor supports the existence of two different states in Mania.
John M. Davis - One of the best experts on this subject based on the ideXlab platform.
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A comparative evaluation of three self-rating scales for acute Mania
Biological Psychiatry, 2001Co-Authors: E. Altman, James L. Peterson, Donald Hedeker, John M. DavisAbstract:Abstract This study compared the performance of three self-rating Mania scales, The Internal State Scale (ISS), the Self-Report Manic Inventory (SRMI), and the Altman Self-Rating Mania Scale (ASRM), in a group of patients with acute Mania. Forty-four adult inpatients with bipolar disorder, manic or mixed, completed all scales shortly after admission, and 31 patients completed them again after 4–6 weeks of pharmacotherapy. Patients also were rated by clinicians on the Clinician-Administered Rating Scale for Mania (CARS-M). At baseline, scores on the ASRM and the ISS well-being subscale were significantly correlated with CARS-M scores. Posttreatment scores were significantly decreased for the ASRM, SRMI, and the ISS activation subscale. The sensitivities for each scale to correctly identify patients with acute symptoms was 45% for the ISS, 86% for the SRMI, and 93% for the ASRM. Specificities were 73%, 46.6%, and 33%, respectively. The ASRM and SRMI were more sensitive than the ISS in screening patients with acute Mania. All three measures were sensitive to treatment effects; however, the item content of the SRMI and the poor sensitivity of the ISS may limit their utility in inpatient settings.
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the altman self rating Mania scale
Biological Psychiatry, 1997Co-Authors: E. Altman, James L. Peterson, Donald Hedeker, John M. DavisAbstract:We report on the development, reliability, and validity of the Altman Self-Rating Mania Scale (ASRM). The ASRM was completed during medication washout and after treatment by 22 schizophrenic, 13 schizoaffective, 36 depressed, and 34 manic patients. The ClinicianAdministered Rating Scale for Mania (CARS-M) and Mania Rating Scale (MRS) were completed at the same time to measure concurrent validity. Test—retest reliability was assessed separately on 20 depressed and 10 manic patients who completed the ASRM twice during washout. Principal components analysis of ASRM items revealed three factors: Mania, psychotic symptoms, and irritability. Baseline Mania subscale scores were significantly higher for manic patients compared to all other diagnostic groups. Manic patients had significantly decreased posttreatment scores for all three subscales. ASRM Mania subscale scores were significantly correlated with MRS total scores (r = .718) and CARS-M Mania subscale scores (r = .766). Test-retest reliability for the ASRM was significant for all three subscales. Significant differences in severity levels were found for some symptoms between patient ratings on the ASRM and clinician ratings on the CARS-M. Mania subscale scores of greater than 5 on the ASRM resulted in values of 85.5% for sensitivity and 87.3% for specificity. Advantages of the ASRM over other self-rating Mania scales are discussed.
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depression during Mania treatment response to lithium or divalproex
Archives of General Psychiatry, 1997Co-Authors: Alan C. Swann, Charles L Bowden, Joseph R Calabrese, Frederick Petty, Steven C Dilsaver, Joyce G Small, David D Morris, John M. DavisAbstract:Background: Little information exists from controlled studies about clinical characteristics that predict treatment response in Mania. The presence of depressive symptoms during manic episodes may be associated with poor response to psychopharmacological treatments. This is an investigation of the relation between depressive symptoms and treatment response in acute manic episodes. Methods and Design: In a parallel-group, doubleblind study, 179 patients hospitalized for acute manic episodes were randomized to receive divalproex sodium, lithium carbonate, or placebo (ratio, 2:1:2). The study was carried out at 9 academic medical centers. Patients had comprehensive evaluations of behavior and symptoms before and during 3 weeks of treatment. The primary outcome measure, change in Mania factor scores derived from the Schedule for Affective Disorders and Schizophrenia: Change Version, was compared in pa- tients with and without depressive symptoms at baseline according to nurse- or physician-rated scales. Results: Depressive symptoms were associated with poor antimanic response to lithium and with better response to divalproex. This was not due to differences in overall severity of illness, substance abuse, gender, age, or history. Conclusions: These data suggest that even a modest level of pretreatment depression-related symptoms is a robust predictor of lithium nonresponse, and is associated with better response to divalproex. Although their overall efficacy in acute Mania is similar, lithium and divalproex may be most effective in clinically and biologically distinct groups of patients.
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efficacy of divalproex vs lithium and placebo in the treatment of Mania
JAMA, 1994Co-Authors: Charles L Bowden, Alan C. Swann, John M. Davis, Andrew M Brugger, Joseph R Calabrese, Philip G Janicak, Frederick Petty, Steven C Dilsaver, John A Rush, Joyce G SmallAbstract:Objective. —To compare the effectiveness of divalproex sodium with that of lithium and placebo in patients with acute Mania. Design. —Randomized, double-blind, parallel-group study of treatment outcomes in patients with manic-depressive illness. Patients. —A total of 179 hospitalized, acutely manic patients meeting the Research Diagnostic Criteria for manic disorder, approximately half of whom had been nonresponsive to lithium previously, were studied at nine university-affiliated hospitals. Interventions. —After a minimum 3-day washout period, random assignment for 21 days to divalproex, lithium, or placebo in a 2:1:2 ratio. Dosage of divalproex and lithium was increased if tolerated to a target concentration of 1041 μmol/L (150 μg/ mL) or 1.5 mmol/L (conventionally expressed as milliequivalents per liter), respectively. Main Outcome Measures. —Primary outcome measures were changes in the Mania Rating scale derived from the Schedule for Affective Disorders and Schizophrenia. Results. —Intent-to-treat analysis for efficacy was based on data from 68, 35, and 73 patients in the divalproex, lithium, and placebo groups, respectively. Groups were initially comparable except that all eight patients with four or more manic episodes in the previous year were in the divalproex group. In 30%, 33%, and 51% of the above groups, treatment was prematurely terminated due to lack of efficacy, with fewer premature terminations from divalproex than placebo (P=.017). The proportions of patients improving at least 50% were higher for divalproex and lithium groups than for the placebo group: 48% for divalproex (P=.004) and 49% for lithium (P=.025) vs 25% for placebo. Divalproex was as effective in rapid-cycling manic patients as in other patients. Conclusions. —Both divalproex and lithium were significantly more effective than placebo in reducing the symptoms of acute Mania. The efficacy of divalproex appears to be independent of prior responsiveness to lithium. (JAMA. 1994;271:918-924)
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efficacy of divalproex vs lithium and placebo in the treatment of Mania the depakote Mania study group
JAMA, 1994Co-Authors: Charles L Bowden, Alan C. Swann, John M. Davis, Andrew M Brugger, Joseph R Calabrese, Philip G Janicak, Frederick Petty, Steven C Dilsaver, A J Rush, Joyce G SmallAbstract:Objective To compare the effectiveness of divalproex sodium with that of lithium and placebo in patients with acute Mania. Design Randomized, double-blind, parallel-group study of treatment outcomes in patients with manic-depressive illness. Patients A total of 179 hospitalized, acutely manic patients meeting the Research Diagnostic Criteria for manic disorder, approximately half of whom had been nonresponsive to lithium previously, were studied at nine university-affiliated hospitals. Interventions After a minimum 3-day washout period, random assignment for 21 days to divalproex, lithium, or placebo in a 2:1:2 ratio. Dosage of divalproex and lithium was increased if tolerated to a target concentration of 1041 mumol/L (150 micrograms/mL) or 1.5 mmol/L (conventionally expressed as milliequivalents per liter), respectively. Main outcome measures Primary outcome measures were changes in the Mania Rating scale derived from the Schedule for Affective Disorders and Schizophrenia. Results Intent-to-treat analysis for efficacy was based on data from 68, 35, and 73 patients in the divalproex, lithium, and placebo groups, respectively. Groups were initially comparable except that all eight patients with four or more manic episodes in the previous year were in the divalproex group. In 30%, 33%, and 51% of the above groups, treatment was prematurely terminated due to lack of efficacy, with fewer premature terminations from divalproex than placebo (P = .017). The proportions of patients improving at least 50% were higher for divalproex and lithium groups than for the placebo group: 48% for divalproex (P = .004) and 49% for lithium (P = .025) vs 25% for placebo. Divalproex was as effective in rapid-cycling manic patients as in other patients. Conclusions Both divalproex and lithium were significantly more effective than placebo in reducing the symptoms of acute Mania. The efficacy of divalproex appears to be independent of prior responsiveness to lithium.
Dost Ongur - One of the best experts on this subject based on the ideXlab platform.
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diverse pathophysiological processes converge on network disruption in Mania
Journal of Affective Disorders, 2019Co-Authors: Ivy Lee, Kathryn Nielsen, Uzma Nawaz, Meihua Hall, Dost OngurAbstract:Abstract Background Neuroimaging of psychiatric disease is challenged by the difficulty of establishing the causal role of neuroimaging abnormalities. Lesions that cause Mania present a unique opportunity to understand how brain network disruption may cause Mania in both lesions and in bipolar disorder. Methods A literature search revealed 23 case reports with imaged lesions that caused Mania in patients without history of bipolar disorder. We traced these lesions and examined resting-state functional Magnetic Resonance Imaging (rsfMRI) connectivity to these lesions and control lesions to find networks that would be disrupted specifically by Mania-causing lesions. The results were then used as regions-of-interest to examine rsfMRI connectivity in patients with bipolar disorder (n = 16) who underwent imaging longitudinally across states of both Mania and euthymia alongside a cohort of healthy participants scanned longitudinally. We then sought to replicate these results in independent cohorts of manic (n = 26) and euthymic (n = 21) participants with bipolar disorder. Results Mania-inducing lesions overlap significantly in network connectivity. Mania-causing lesions selectively disrupt networks that include orbitofrontal cortex, dorsolateral prefrontal cortex, and temporal lobes. In bipolar disorder, the manic state was reflected in strong, significant, and specific disruption in network communication between these regions and regions implicated in bipolar pathophysiology: the amygdala and ventro-lateral prefrontal cortex. Limitations There was heterogeneity in the clinical characterization of Mania causing lesions. Conclusions Lesions causing Mania demonstrate shared and specific network disruptions. These disruptions are also observed in bipolar Mania and suggest a convergence of multiple disorders on shared circuit dysfunction to cause Mania.
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diverse pathophysiological processes converge on network disruption in Mania
bioRxiv, 2018Co-Authors: Ivy Lee, Kathryn Nielsen, Meihua Hall, Dost Ongur, Matcheri S KeshavanAbstract:Background: Neuroimaging of psychiatric disease is challenged by the difficulty of establishing the causal role of neuroimaging abnormalities. Lesions that cause Mania present a unique opportunity to understand how brain network disruption may cause Mania in both lesions and in bipolar disorder. Methods: A literature search revealed 23 case reports with imaged lesions that caused Mania in patients without history of bipolar disorder. We traced these lesions and examined resting-state functional Magnetic Resonance Imaging (rsfMRI) connectivity to these lesions and control lesions to find networks that would be disrupted specifically by Mania-causing lesions. The results were then used as regions-of-interest to examine rsfMRI connectivity in patients with bipolar disorder (n=16) who underwent imaging longitudinally across states of both Mania and euthymia alongside a cohort of healthy participants scanned longitudinally. We then sought to replicate these results in independent cohorts of manic (n=26) and euthymic (n=21) participants with bipolar disorder. Results: Mania-inducing lesions overlap significantly in network connectivity. Mania-causing lesions selectively disrupt networks that include orbitofrontal cortex, dorsolateral prefrontal cortex, and temporal lobes. In bipolar disorder, the manic state was reflected in strong, significant, and specific disruption in network communication between these regions and regions implicated in bipolar pathophysiology: the amygdala and ventro-lateral prefrontal cortex. Limitations: The was heterogeneity in the clinical characterization of Mania causing lesions. Conclusions: Lesions causing Mania demonstrate shared and specific network disruptions. These disruptions are also observed in bipolar Mania and suggest a convergence of multiple disorders on shared circuit dysfunction to cause Mania.
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antimanic treatment with tamoxifen affects brain chemistry a double blind placebo controlled proton magnetic resonance spectroscopy study
Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 2016Co-Authors: Bruce M. Cohen, Dost Ongur, Aysegul Yildiz, Burc Aydin, Necati Gokmen, Aysegul Yurt, Pembe Keskinoglu, Perry F RenshawAbstract:Abstract Background The antimanic efficacy of a protein kinase C inhibitor, tamoxifen, has been tested in several clinical trials, all reporting positive results. However, mechanisms underlying the observed clinical effects require further confirmation through studies of biological markers. Methods We investigated the effect of tamoxifen versus placebo on brain metabolites via a proton magnetic resonance spectroscopy study. Scanning was performed in 48 adult manic patients with bipolar disorder type I (mean Young Mania Rating Scale score of 37.8 ± 5.8) at baseline and after 3 weeks of double-blind treatment. We hypothesized that alleviation of manic symptoms would improve the levels of markers associated with brain energy metabolism (creatine plus phosphocreatine [total creatine (tCr)]) and neuronal viability ( N -acetylaspartate). Results The Young Mania Rating Scale scores decreased from 38.6 ± 4.5 to 20.0 ± 11.1 in the tamoxifen group and increased from 37.0 ± 6.8 to 43.1 ± 7.8 in the placebo group ( p p = .027). A significant correlation between the Young Mania Rating Scale score change and tCr percent change was observed in the whole group (Spearman rho = .341, p = .029). Levels of both tCr and N -acetylaspartate in the responder group were increased by 9.4% ± 15.2% and 6.1% ± 11.7%, respectively, whereas levels in the nonresponder group were decreased by 2.1% ± 13.2% and 6.5%± 10.5%, respectively ( p Conclusions Tamoxifen effectively treated Mania while increasing brain tCr levels, consistent with involvement of both excessive protein kinase C activation and impaired brain energy metabolism in the development of bipolar manic states.
Mauricio Tohen - One of the best experts on this subject based on the ideXlab platform.
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dissimilar morbidity following initial Mania versus mixed states in type i bipolar disorder
Journal of Affective Disorders, 2010Co-Authors: Ross J Baldessarini, Mauricio Tohen, Paola Salvatore, Harimandir K KhalsaAbstract:Background Mixed-states of bipolar disorders (BPD) may predict worse future illness and more depressive than manic morbidity, challenging a tendency to conflate mixed-states and Mania.
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olanzapine versus divalproex in the treatment of acute Mania
American Journal of Psychiatry, 2002Co-Authors: Mauricio Tohen, Lori L Altshuler, Robert W Baker, Carlos A Zarate, Trisha Suppes, Terrence A Ketter, Denai R Milton, R C Risser, J A Gilmore, Alan BreierAbstract:OBJECTIVE: The effects of olanzapine and divalproex for the treatment of Mania were compared in a large randomized clinical trial. METHOD: A 3-week, randomized, double-blind trial compared flexibly dosed olanzapine (5–20 mg/day) to divalproex (500–2500 mg/day in divided doses) for the treatment of patients hospitalized for acute bipolar manic or mixed episodes. The Young Mania Rating Scale and the Hamilton Depression Rating Scale were used to quantify manic and depressive symptoms, respectively. Safety was assessed with several measures. RESULTS: The protocol defined baseline-to-endpoint improvement in the mean total score on the Young Mania Rating Scale as the primary outcome variable. The mean Young Mania Rating Scale score decreased by 13.4 for patients treated with olanzapine (N=125) and 10.4 for those treated with divalproex (N=123). A priori categorizations defined response and remission rates: 54.4% of olanzapine-treated patients responded (≥50% reduction in Young Mania Rating Scale score), compare...
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Antidepressant-associated Mania: a controlled comparison with spontaneous Mania.
The American journal of psychiatry, 1994Co-Authors: Andrew L. Stoll, Pm. V. Mayer, Meridith L. Kolbrener, E. Goldstein, B. Suplit, J. Lucier, Bruce M. Cohen, Mauricio TohenAbstract:OBJECTIVE: Antidepressants have been associated with the induction of Mania and rapid cycling. This study examined whether antidepressant-associated manic states differ in any way from spontaneous Mania. METHOD: Forty-nine consecutive inpatients with antidepressant-associated manic states were compared with 49 matched inpatients with spontaneous Mania in a blind, retrospective chart review. RESULTS: Across virtually every clinical measure examined, the patients with antidepressant-associated manic states experienced milder and more time-limited manic episodes than the patients with spontaneous Mania. The patients with antidepressant-associated manic states were subject to frequent checking by nurses and hall restriction for a significantly shorter period of time than the patients with spontaneous Mania. The patients with antidepressant-associated manic states also had significantly less severe levels of delusions, hallucinations, psychomotor agitation, and bizarre behavior, according to a standard rating instrument, than the patients with spontaneous Mania. For further study the patients with antidepressant-associated Mania were divided into subgroups taking four individual classes of antidepressant drugs: tricyclics (N = 19), fluoxetine (N = 13), monoamine oxidase inhibitors (MAOIs) (N = 8), and bupropion (N = 6); three patients taking combinations of drugs were not included in these analyses. The patients with MAOI- and bupropion-associated Mania had a slightly lower overall rating of severity of psychopathology at admission than the subgroups with fluoxetine- and tricyclic-associated Mania. CONCLUSIONS: Antidepressant-associated Mania appears to be a milder and more time-limited syndrome than spontaneous Mania and may represent a distinct clinical entity. MAOIs and bupropion may be associated with milder manic states than either tricyclic drugs or fluoxetine. Language: en
Fernando Mosquera - One of the best experts on this subject based on the ideXlab platform.
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Epidemiology, Diagnosis and Management of Mixed Mania
CNS Drugs, 2007Co-Authors: Ana González-pinto, A. Aldama, Fernando Mosquera, Cristina González GómezAbstract:The presence of depressive symptomatology during acute Mania has been termed mixed Mania, dysphoric Mania, depressive Mania or mixed bipolar disorder. Highly prevalent, mixed Mania occurs in at least 30% of bipolar patients. Correct diagnosis is a major challenge. The DSM diagnostic criteria, the most widely adopted clinical convention, require a complete manic and complete depressive syndrome co-occurring for at least 1 week. However, recent alternative categorical and dimensional studies of manic phenomenology have shown that there are certain depressive symptoms or constellations that have special clinical importance when describing mixed states, such as depressed mood and anxiety symptomatology that do not overlap with manic symptoms. Patients with mixed Mania are over-represented in the subgroup with severe and treatment-resistant symptoms. The course and prognosis of mixed Mania are worse than that of pure manic forms in the medium and long term, with higher recurrence rates, higher frequency of co-morbid substance abuse and greater risk of suicidal ideation and attempts. Moreover, mixed manic episodes are usually associated with increased depression during follow-up, greater risk of rapid cycling course and higher prevalence of physical co-morbidities, principally related to thyroid function. All these factors are very relevant to selection of treatment. There are three crucial steps in the treatment of mixed Mania — making the correct diagnosis, starting treatment early, and considering not only the acute state but also maintenance treatment and the patient’s long-term outcome. Although challenging, acute mixed episodes are treatable. To date there have been no controlled studies devoted exclusively to treatment of mixed Mania, and the only controlled data available therefore derive from sub-analyses of randomised clinical trials. Both short-term and maintenance treatments of patients with mixed Mania requires experience and usually involves the combination of different treatments. As a general rule, there is some consensus about discontinuing antidepressants during mixed Mania. Olanzapine, aripiprazole or valproate semisodium (divalproex sodium) are first-line drugs for mild episodes; severe episodes of mixed Mania usually require treatment with a combination of valproate semisodium or lithium plus an antipsychotic, preferably an atypical agent. Carbamazepine is also useful for the treatment of mixed Mania. High-dose medications are sometimes needed to control the episode, and time to remission is usually longer than in pure Mania. Importantly, patients with mixed manic episodes have more adverse events of psychopharmacological treatment. In some cases, electroconvulsive therapy is required.
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Epidemiology, Diagnosis and Management of Mixed Mania
CNS Drugs, 2007Co-Authors: Ana González-pinto, A. Aldama, Fernando Mosquera, Cristina González GómezAbstract:The presence of depressive symptomatology during acute Mania has been termed mixed Mania, dysphoric Mania, depressive Mania or mixed bipolar disorder. Highly prevalent, mixed Mania occurs in at least 30% of bipolar patients. Correct diagnosis is a major challenge. The DSM diagnostic criteria, the most widely adopted clinical convention, require a complete manic and complete depressive syndrome co-occurring for at least 1 week. However, recent alternative categorical and dimensional studies of manic phenomenology have shown that there are certain depressive symptoms or constellations that have special clinical importance when describing mixed states, such as depressed mood and anxiety symptomatology that do not overlap with manic symptoms.
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Principal components of Mania.
Journal of Affective Disorders, 2002Co-Authors: Ana González-pinto, A. Aldama, J Ballesteros, M Gutierrez, J.l. Pérez De Heredia, Fernando MosqueraAbstract:Objective: An alternative to the categorical classification of psychiatric diseases is the dimensional study of the signs and symptoms of psychiatric syndromes. To date, there have been few reports about the dimensions of Mania, and the existence of a depressive dimension in Mania remains controversial. The aim of this study was to investigate the dimensions of manic disorder by using classical scales to study the signs and symptoms of affective disorders. Methods: One-hundred and three consecutively admitted inpatients who met DSM IV criteria for bipolar disorder, manic or mixed were rated with the Young Mania Rating Scale (YMRS) and the Hamilton Depression Rating Scale (HDRS-21). A principal components factor analysis of the HDRS-21 and the YMRS was carried out. Results: Factor analysis showed five independent and clinically interpretable factors corresponding to depression, dysphoria, hedonism, psychosis and activation. The distribution of factor scores on the depressive factor was bimodal, whereas it was unimodal on the dysphoric, hedonism and activation factors. Finally, the psychosis factor was not normally distributed. Limitations: Patients of the sample were all medicated inpatients. Conclusions: Mania seems to be composed of three core dimensions, i.e. hedonism, dysphoria and activation, and is frequently accompanied by a psychotic and a depressive factor. The existence of a depressive factor suggests that it is essential to evaluate depression during Mania, and the distribution of the depressive factor supports the existence of two different states in Mania.
