Over one-third of bipolar disorder (BD) patients do not receive adequate provision or continuity of maintenance treatment during their first follow-up maintenance phase, indicate study findings.

Studies investigating maintenance treatment in BD have lacked agreement on how the longitudinal treatment phases should be defined, thus presenting inconsistent results.

Erkki Isometsä (Helsinki University Central Hospital, Finland) and co-authors say that their study is “one of the first to investigate maintenance treatment received using life chart methodology, with the possibility of reporting longitudinal patterns of maintenance treatment.”

For the study, the researchers assessed the adequacy of pharmacologic treatment received by 154 BD patients who had taken part in the Jorvi Bipolar Study during the first maintenance phase (at least 2 weeks) after the index episode. Treatment information was collected in interviews and using psychiatric records and adequate maintenance-hase pharmacotherapy was based on published treatment guidelines, where patients had to be treated with lithium, valproate, carbamazepine, or olanzapine. Monotherapy with lamotrigine was defined as adequate in bipolar II disorder.

Overall, 63.0% of patients experienced depression prior to the maintenance phase, which lasted on average 220 days.

Adequate maintenance treatment was received by 69.3% of all patients during the time indicated and by 77.9% of patients with a clinical diagnosis of BD (n=129).

Furthermore, adequate treatment was received by 75.3% of patients for some time, but only by 61.0% of all patients throughout the maintenance phase. Again, a higher proportion of patients with a clinical BD diagnosis (72.1%) received treatment throughout the maintenance phase than did patients diagnosed with BD II (47.0%).

Most patients (81.0%) with adequate maintenance treatment some time during the maintenance phase received it throughout the phase, and nearly all patients (91.4%) with adequate maintenance treatment when the maintenance phase began received adequate treatment when the phase ended or follow-up was finished.

Logistic regression analysis revealed that a clinical diagnosis of BD was the most important predictor for adequate maintenance treatment throughout the first follow-up maintenance phase (odds ratio [OR]=106.5), followed by treatment in hospital during the episode before the maintenance phase (OR=11.1), rapid cycling (OR=3.4), and absence of comorbid personality disorders (OR=0.37 for any personality disorder).

“Further longitudinal effectiveness studies are needed to assess strategies to enhance the adequacy of interventions during the continuation and treatment phases in patients with bipolar disorders,” conclude Isometsä and team in the Journal of Affective Disorders.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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Study findings highlight the need for clinicians to recognize comorbid eating disorders in patients with bipolar disorder.

M Fornaro (University of Genoa, Italy) and colleagues found that one in three women with bipolar disorder had at least one eating disorder. Also, the presence of comorbid eating disorders may influence both the clinical characteristics and course of bipolar disorder.

The researchers assessed the prevalence of comorbid DSM-IV-defined anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) in 148 women with a lifetime history of bipolar I disorder, bipolar II disorder, and/or cyclothymia.

In all, 46 (31%) of the patients reported a lifetime history of at least one eating disorder. AN was the most common, affecting 23 (15.5%) patients, followed by BED and BN, which affected 21 (14.2%) and eight (5.4%) patients, respectively. Six (4.1%) patients reported multiple lifetime eating disorders.

As expected, the researchers found that body mass index was highest in patients with BED and lowest in patients with AN.

Fornaro et al also note in the Journal of Affective Disorders that “the presence of BED among bipolar disorder patients has relevant clinical and therapeutic implications.”

They explain: “In these patients the use of anti-dopaminergic drugs may induce weight gain not only by an appetite increase, but also favoring impulsive eating.”

The type of eating disorder did not influence clinical characteristics such as diagnostic distribution, psychotic and melancholic features, suicidal thoughts and attempts, hospitalization, seasonal pattern, post-partum onset, or premenstrual dysphoria.

The researchers suggest that the female-only sample and the small number of women with eating disorders may have affected the ability of the study to detect group differences.

However, women with comorbid BED were more likely than women with comorbid AN and those without eating disorders to experience rapid cyclicity (42.9% versus 32.0% and 18.6%, respectively) and comorbid drug abuse (28.5% versus 16.0% and 20.7%, respectively).

“Our results prompt for the recognition of [eating disorder] comorbidity among bipolar spectrum patients, indicating that BED and AN may influence in different extents both clinical characteristics and course of the illness,” says the team.

“Focusing on a ‘BED versus non-BED’ distinction, potentially relevant therapeutic implications should also be taken into account.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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Research findings suggest that there are unique neural mechanisms mediating face??”emotion processing deficits in patients with attention deficit/hyperactivity disorder (ADHD), bipolar disorder, and severe mood dysregulation.

Diagnosing these three psychiatric illnesses is difficult because deficits in emotion processing and hyperarousal symptoms are clinical features common to all three conditions, note Melissa Brotman (National Institute of Mental Health, Bethesda, Maryland, USA) and colleagues.

Evidence of unique neural mechanisms mediating face??”emotion processing deficits could therefore assist in the differential diagnosis of bipolar disorder, ADHD, and severe mood dysregulation in children, they say.

The researchers used functional magnetic resonance imaging (fMRI) to examine blood-oxygen-level-dependent (BOLD) signal in the amygdala of 43 children with bipolar disorder, 18 with nonirritable ADHD, and 29 children with chronic irritability known as severe mood dysregulation, and 37 mentally healthy children. The children were aged between 8 and 17 years.

During imaging, the children were shown pictures of adult faces, displaying neutral expressions. The children viewed the faces passively and were then asked to rate the perceived threat (how hostile is this face?) and subjective fear (how afraid are you of this face?) associated with the faces.

The results, published in the American Journal of Psychiatry, show that patients with bipolar disorder and those with severe mood dysregulation were more afraid of neutral faces than healthy individuals, while there was no difference for children with ADHD. There were no group differences with regard to hostility ratings.

Moreover, patients with severe mood dysregulation showed left amygdala hypoactivity when completing subjective fear ratings of neutral faces relative to mentally healthy children and those with bipolar disorder or ADHD.

In contrast, children with ADHD showed left amygdala hyperactivity relative to the other three groups when rating subjective fear of neutral faces.

Amygdala activity in children with bipolar disorder did not differ significantly from that in mentally healthy children.

“These findings suggest that there may be functional differences among ADHD, bipolar disorder, and severe mood dysregulation patients, despite the presence of overlapping behavioral deficits and clinical symptoms,” say Brotman et al.

In a related editorial, Mary Phillips, from University of Pittsburgh Medical Center in Pennsylvania, USA, said the findings “highlight the future promise of neuroimaging to identify biomarkers of psychiatric illnesses in youth.”

She added: “Further studies are clearly needed to elucidate whether functional abnormalities in key neural circuitry in emotion processing and emotion regulation, including not only the amygdala but also other neural regions interconnected with the amygdala, can accurately differentiate between bipolar disorder and other psychiatric illnesses in youth.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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Mental Health America is applauding legislation introduced by a bipartisan group of U.S. Senators to establish national centers of excellence for the treatment of depression and bipolar disorders.

The centers will create a national network to help diagnose people in need and improve access to evidence-based, quality care.

The bill, called the “ENHANCED Act” was introduced by U.S. Senators Debbie Stabenow (D-Mich.), George Voinovich (R-Ohio), Sherrod Brown (D-Ohio), and John Kerry (D-Mass.). Senator Kay Bailey Hutchison (R-Tex.) is also a co-sponsor.

The legislation is based on efforts catalyzed by the University of Michigan Depression Center with 15 other leading academic medical centers across the nation. Joining together, these universities created a network of depression centers positioned to take academic research and translate it into practice, standardize diagnoses, treat early and more effectively, and prevent recurrences of depression and bipolar disorders.

In a letter to Stabenow applauding her leadership in crafting the bill, Mental Health America said:

“These centers are especially critical at this time given the strong evidence that economic uncertainty and recession increase the rates of psychiatric symptoms and demand for services. Depression is associated with poorer health outcomes and higher health care costs. Rates of depression and suicide-already at a staggering level of nearly 33,000 persons a year (roughly twice the number of homicides)-tend to climb during times of economic tumult. Our nation must prioritize the integration and coordination of mental health with general health care.” (View the full letter PDF)

The ENHANCED Act of 2009:

- Creates a national network with a pathway for developing and expanding up to 30 depression centers of excellence to increase access to the most appropriate and evidence-based depression care.

- Develops evidence-based treatment standards, clinical guidelines, and protocols to improve accurate and timely diagnosis of depression and bipolar disorders.

- Expands multidisciplinary, translational, and patient-oriented research by fostering the collaboration of academic and community-based service centers.

- Establishes a sustainable national resource for public and professional education and training, to advance knowledge and eradicate the stigma associated with depression and mood disorders.

Mental Health America looks forward to working with the Senate sponsors to win enactment of the legislation.

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Current cigarette smoking is a predictor for current and 9-month suicidal ideation and behavior in bipolar disorder (BD) patients, suggest US study results.

Studies have shown that BD patients are four times as likely to have nicotine dependence than the general population. Furthermore, cigarette smoking in BD individuals has been associated with suicidal behavior, although the precise relationship between the two remains unclear.

To investigate, Michael Ostacher (Harvard Medical School, Boston, Massachusetts) and colleagues examined the association between smoking, suicidality, and prospective suicide attempts in 116 BD patients over a 9-month period.

In total, 27% of patients were smokers who showed significantly higher rates of lifetime substance abuse disorders (61% vs 33%), were younger (37.3 vs 46.7 years), and had an earlier age of BD onset (14.4 vs 18.4 years) compared with non-smokers.

Current smoking was associated with higher baseline and 9-month follow-up Suicide Behaviors Questionnaire (SBQ) scores after adjusting for smoking status, gender, anxiety comorbidity, recovery status, age at first episode, and lifetime substance abuse.

However, this association was not significant after adjusting for impulsivity, using Barratt Impulsiveness Scale scores, suggesting that “the link between suicide may in part be explained by impulsivity, although power was limited by the relatively small number of smokers, and SBQ scores were higher in this model,” say the researchers.

Overall, eight (7%) patients attempted suicide between baseline and 9-month follow-up, with smokers 5.25-fold more likely to attempt suicide than nonsmokers (16.1% vs 3.5%).

“While the predictive value of smoking in and of itself for the identification of patients with BD at risk for suicide is small, it may be a useful addition to other clinical risk factors in a comprehensive assessment of suicide risk,” say the researchers.

They call for further research to better understand the link between smoking and elevated suicidality in BD, “with attention to personality characteristics, impulsivity, and the effect of periods of fluctuating nicotine use, withdrawal, and discontinuation.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2009

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Postpartum bipolar II disorder may be mistakenly diagnosed as major depressive disorder, say Canadian and US scientists who make recommendations as to how patients should be treated.

Bipolar postpartum depression is commonly overlooked and mistaken for unipolar major depression. However, while bipolar I disorder is a reliable and relatively stable diagnosis, bipolar II disorder is less easily diagnosed and may be dismissed as a milder form of bipolar I disorder.

To examine the detection, diagnosis, and treatment of bipolar II postpartum depression Verinder Sharma, from the University of Western Ontario in London, Canada, and colleagues conducted a search of the PubMed database and reference lists for relevant articles published between 1998 and 2009.

Estimates of the prevalence of hypomania in non-clinical populations ranged from 9.6% to 20.4% on day 3 postpartum, at an average of approximately 15.0%. Furthermore, almost 20% of patients with hypomanic symptoms at day 3 postpartum developed postpartum depression in one study, with a significant proportion diagnosed with bipolar II disorder or bipolar disorder not otherwise specified (NOS).

Crucially, the team says in the Journal of Affective Disorders that, although there are formal rating scales for assessing bipolar spectrum disorder and unipolar postpartum depression, there are no validated instruments for screening, diagnosing, or monitoring bipolar disorder during pregnancy or postpartum, with even the Highs scale not validated as a diagnostic instrument.

There have only been three randomized controlled trials and six open-label studies of the pharmacologic treatment of postpartum depression, and three studies of the treatment of bipolar disorder during postpartum depression.

While the evidence suggests that postpartum bipolar depression should follow the same guidelines as for non-puerperal bipolar depression, the team says there is a lack of evidence-based treatment options. Women should be monitored closely, they argue, and prophylactic treatment may be considered.

The researchers conclude: “The lack of data on postpartum bipolar II and bipolar disorder NOS is surprising given the high prevalence of hypomanic symptoms immediately after delivery, the unique pharmacologic challenges posed by bipolar depression, and the heightened risk for suicide associated with bipolar spectrum disorder. and illness course that are commonly used to establish the bipolar diathesis of a clinical condition.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2009

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Mutations in the dystrobrevin binding protein 1 gene (DTNBP1) are associated with bipolar disorder, say European researchers in findings that reinforce the genetic overlap between schizophrenia and bipolar disorder.

As there is evidence to suggest a degree of overlap in genetic susceptibility between schizophrenia and bipolar disorder, the DTNBP1 gene, which has been linked to schizophrenia, has come under scrutiny for its potential associations with bipolar disorder.

To investigate further, Darya Gaysina, from King’s College London, UK, and colleagues genotyped 515 bipolar disorder patients and 1316 ethnically matched healthy controls for eight single nucleotide polymorphisms (SNPs), conducting an association analysis in 452 bipolar disorder patients and 956 controls.

The results, published in the American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics, showed that two SNPs ??” rs760761 and rs3213207 ??” were significantly associated with bipolar disorder, at odds ratios of 1.26 and 1.41, respectively, although only the former survived Bonferroni correction with borderline significance.

Furthermore, the G-C-G haplotype of the combined SNPs rs16876571-rs2619539-rs3213207, and the G-C-G-T haplotype of the combined SNPs rs16876571-rs2619539-rs3213207-rs760761, were significantly associated with bipolar disorder.

“Our results are consistent with previous studies in terms of a general association between the DTNBP1 and bipolar disorder,” the researchers conclude.

“They also provide additional molecular genetic evidence that a portion of the genotypic overlap between schizophrenia and bipolar affective disorder is attributable to this gene.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2009

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Study results suggest that anxiety state and trait are heritable and share some genetic factors in bipolar disorder (BD), with trait anxiety showing a stair-step distribution in family members based on their genetic proximity to the affected individual.

“If this trait is proven to be an endophenotype, it will be of help in diagnosing and treating bipolar I patients in a more reliable and biologically valid manner than our current classification allows,” say Javier Contreras (University of Texas Health Science Center at San Antonio, Texas, USA) and colleagues.

The localization of genes that predispose to BD has been difficult as some of these genes may be transmitted without expression of the categorical clinical phenotype.

“One strategy to overcome this obstacle is the use of quantitative endophenotypes, as has been done for other medical disorders,” explain the researchers in the Journal of Affective Disorders.

Contreras and team therefore computed heritability and genetic correlation of the state and trait scale from the Anxiety State and Trait Inventory in 30 bipolar I extended families, with an average family size of 10 members, and 20 unrelated healthy controls from a Costa Rican sample.

Of the 300 individuals from the extended families, 63 had BD type I, 74 major depressive disorder, 101 had no axis I disorder, with the remainder presenting other disorders.

The study showed that anxiety symptoms were underdiagnosed, with 14.4% meeting criteria for a DSM-IV categorical anxiety diagnosis compared with 26.0% of 274 individuals with no categorical anxiety diagnosis that were over the 75th percentile of the anxiety trait scale.

“This finding strongly encourages the use of anxiety quantitative measures in psychiatric genetics research,” says the team.

Patients with BD showed the highest trait anxiety scores, followed by relatives with other psychiatric disorders, healthy relatives, and healthy unrelated controls. The researchers note that although both state and trait showed significant heritability, state was less heritable and stable.

Furthermore, only anxiety trait showed normal distribution in healthy individuals, current mood status independence, and significant liability for BD type I.

“Further research is needed to evaluate if anxiety traits are specially related to bipolar I disorder in comparison with other traits such as anger, attention, or response inhibition deficit, pathological impulsivity or low self-directedness,” conclude the researchers.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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Older bipolar disorder patients have a similar cognitive profile to that of younger patients with the disease, say Swiss scientists, who suggest that processing speed and episodic memory are two core deficits in elderly patients.

Previous studies have indicated that bipolar disorder patients have impairments in processing speed, working memory, episodic memory, and executive function. However, these investigations have largely focused on young and middle-aged patients and all have shown that the severity of cognitive deficits increase with illness duration.

To examine cognitive deficits in older patients, Christophe Delaloye, from University Hospitals of Geneva in Chêne-Bourg, and colleagues administered a comprehensive neuropsychological battery to 22 euthymic elderly bipolar disorder patients with an average age of 68.45 years and 22 gender-, age-, and education-matched controls.

In comparison with controls, bipolar disorder patients were found to have significantly slower processing speed, lower working memory scores, lower episodic memory scores, and verbal fluency scores, at r-value effect sizes of 0.44, 0.44, 0.48, and 0.38, respectively.

There were no significant differences between the two groups in terms of executive function, and duration of illness had no impact on cognitive performance.

Processing speed was found to explain 19% of the variance in working memory scores, 14% of the verbal fluency composite scores, and 23% of the variance in episodic memory scores in hierarchical regression analysis. After controlling for processing speed, only episodic memory had a persistent group effect, explaining 10% of the variance in scores.

The team writes in the journal Bipolar Disorders: “Euthymic elderly BD patients had reduced performance in measures of processing speed, working memory, verbal fluency, and episodic memory compared to controls. This pattern of cognitive deficits is largely comparable to the one reported in younger BD cohorts.

“Moreover, the length of illness was not associated with cognitive performance in our elderly BD group, suggesting that longstanding BD is not associated with an increase in cognitive decline.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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The auditory event-related P300 amplitude appears to be an endophenotype for schizophrenia, but it is also affected in bipolar disorder patients and may be a marker for psychosis in general, conclude UK researchers.

Decreased P300 positive event-related potential component amplitude, which requires the detection of rare target stimuli, is associated with alcoholism and schizophrenia, and studies have shown that the potential is genetically influenced. However, such studies have different and more complex tasks than those used in clinical studies.

Patricia Bestelmeyer, from the University of Glasgow, and colleagues therefore initially examined the genetic influence on the P300 potential in 14 pairs of healthy monozygotic twins and 14 pairs of healthy dizygotic twins. The team measured the P300 amplitude response to one auditory and one visual paradigm, each of which consisted of 150 stimuli in two blocks, with oddball stimuli appearing at a probability of 20%.

Participants made significantly more errors when reacting to visual than to auditory stimuli on univariate analysis, while a mixed design analysis of variance showed that individuals reacted significantly faster to oddball trials. On multivariate analysis, there were no significant effects of zygosity for reaction time and error rate.

The results, published in the journal Psychiatry Research, indicate that the auditory P300 amplitude was significantly intraclass correlated in monozygotic twins, and the correlation was significantly larger than that seen in dizygotic twins. No significant correlations were seen for auditory P300 latency, or for visual P300 amplitude or latency.

In a second experiment, the team used the same paradigms, procedure, recording condition, and analysis to study visual and auditory P300 in 21 schizophrenia patients, 19 bipolar disorder patients, and 35 healthy unmedicated controls.

Healthy controls made significantly fewer errors in response to auditory stimuli than schizophrenia patients but not compared with bipolar disorder patients. In contrast, healthy controls reacted significantly faster to oddball stimuli than individuals from both patient groups, a pattern that was repeated with standard stimuli. In response to visual stimuli, the only significant difference was between healthy controls and bipolar disorder patients on reaction times, with the former being faster.

Interestingly, while schizophrenia and bipolar disorder patients had significantly lower auditory P300 amplitudes than controls, there were no significant differences between patient groups. A similar pattern was seen for visual P300 amplitudes the centro-parietal electrode site (Pz), although the reduction in bipolar disorder patients versus controls had only a non-significant trend for difference. There were no significant differences in auditory or visual P300 latencies.

The team concludes: “Taken together, our findings imply that the auditory P300 amplitude at Pz may be an endophenotype for psychosis in general rather than specifically for schizophrenia.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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