Recurrent Major Depressive Episodes Research Articles

Managing Depression During the Menopausal Transition

The menopausal transition is associated with both first onset of depression and recurrent depression. Risk factors include vasomotor symptoms, a history of premenstrual dysphoria, postpartum depression, major depression, and sleep disturbances. Hormone replacement therapy, complementary and alternative medicine approaches, and counseling implications for assessment, education, advocacy, and self-care are discussed. ********** Women are diagnosed with depression at nearly twice the rate as men are (American Psychiatric Association [APA], 2000), a trend that begins in puberty (APA, 2000) and levels off after menopause (Bebbington et al., 2003). Without question, rates of depression in women are higher during their reproductive years. Although the connections between depression and premenstrual syndrome and the postpartum period are recognized and included in the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-IV-TR; APA, 2000), no such recognition exists for depression during the menopausal transition. Failing to recognize a potential biological component of a disorder and instead emphasizing psychosocial or intrapsychic factors can lead to treatment that is ineffective, if not harmful. Therefore, the purpose of this article is threefold: to discuss hormonally based factors associated with depression during the menopausal transition; to review the benefits and risks of hormone replacement therapy (HRT), selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and complementary and alternative medicine (CAM) approaches to treat depression; and to offer strategies for assessment, advocacy, and intervention. THE MENOPAUSAL TRANSITION AND RISK OF DEPRESSION Efforts to understand possible relationships between depression and reproductive cycles in women consistently point to a strong connection between the menopausal transition and increased occurrences of depression. In a critical review of the research literature, Soares and Zitek (2008) concluded that the menopausal transition seems to present a unique period in which some women are more vulnerable to initial onset or recurrent depressive symptoms and major depressive episodes. Similarly, Schmidt (2005) affirmed that research studies indicate a relationship between perimenopause (the early and late stages of the menopausal transition) and the onset of depression, a relationship that did not extend to the postmenopausal stage. Deecher, Andree, Sloan, and Schechter (2008) likewise concluded that clinical studies show an increase in major depressive disorder during perimenopause compared with such occurrences during premenopause or postmenopause. The authors found that this increased risk was present even in perimenopausal women who had no prior history of major depressive disorder. Findings from longitudinal studies illustrate these conclusions. Results from the Seattle Midlife Women's Study, a prospective study that followed women for approximately fourteen years, showed that the late menopause transition stage was significantly related to depressed mood (Woods et al., 2008). Results were similar for cohorts from another prospective study, the Penn Ovarian Aging Study, an ongoing longitudinal study (as cited in E. W. Freeman et al., 2004). An examination of a 4-year cohort from this study showed that depressive symptoms increased during the menopausal transition and decreased in postmenopause (E. W. Freeman et al., 2004). E. W. Freeman, Sammel, Lin, and Nelson (2006) examined another cohort over an 8-year period from the Penn Ovarian Aging Study. They found that a woman was 4 times more likely to have high depression scores and 2 1/2 times more likely to be diagnosed with depressive disorder when she was in the menopausal transition compared with her premenopausal period. Although no direct associations have been identified in the research between depression during the menopausal transition and specific levels of hormones (e. …

Cognitive style, personality and vulnerability to postnatal depression

Only some women with recurrent major depressive disorder experience postnatal episodes. Personality and/or cognitive styles might increase the likelihood of experiencing postnatal depression. To establish whether personality and cognitive style predicts vulnerability to postnatal episodes over and above their known relationship to depression in general. We compared personality and cognitive style in women with recurrent major depressive disorder who had experienced one or more postnatal episodes (postnatal depression (PND) group, n=143) with healthy female controls (control group, n=173). We also examined parous women with recurrent major depressive disorder who experienced no perinatal episodes (non-postnatal depression (NPND) group, n=131). The PND group had higher levels of neuroticism and dysfunctional beliefs, and lower self-esteem than the control group. However, there were no significant differences between the PND and NPND groups. Established personality and cognitive vulnerabilities for depression were reported by women with a history of postnatal depression, but there was no evidence that any of these traits or styles confer a specific risk for the postnatal onset of episodes.

PW01-30 - Increased scores on the hypomania check list-32 and on the mood disorder questionnaire in treatment-resistant depression: polish TRES-DEP study

ObjectiveAn undiagnosed bipolarity may be one of the reasons connected with treatment resistance in major depressive disorder. In recent years, the tools have been introduced helping to assess the bipolarity such as the Hypomania Checklist (HCL-32) and the Mood Disorder Questionnaire (MDQ). The objective of the study was to compare scores of bipolarity measured with these scales between patients with treatment-resistant and treatment non-resistant depression within the framework of all-Poland multi-center study TRES-DEP.MethodsOne-thousand and fifty-one patients recruited from 150 outpatient psychiatric clinics in Poland and fulfilling DSM-IV criteria for single or recurrent major depressive episode were studied. Five-hundred and sixty-nine patients were identified as having treatment-resistant depression on account of non-obtaining remission in recent depressive episode after minimum of two courses of adequate treatment with antidepressant drugs. They were compared with 482 patients with non-treatment-resistant depression. All patients were assessed using the structured demographic and clinical data interview, as well as the Polish version of HCL-32 and MDQResultsPatients with treatment-resistant depression scored significantly higher compared with non-resistant depression both on HCL-32 and MDQ (11.9+8.3 vs 8.5±7.7 and 4.3±3.5 vs 2.7±2.9, respectively). Independent risk factors of treatment resistance were scoring of14 or higher on HCL-32, and 6 or higher on MDQ.ConclusionsHigher scoring by patients with treatment-resistant depression on both HCL-32 and MDQ may suggest a possible association between bipolarity and worse response to antidepressant drugs in patients with major depressive disorder.

Management of seasonal affective disorder

Low mood associated with a certain season (usually winter) is very common. For example, in the UK, up to 6% of adults have “recurrent major depressive episodes with seasonal pattern”,...

Attachment and social adjustment: Relationships to suicide attempt and major depressive episode in a prospective study

ObjectiveTo study two aspects of interpersonal function – attachment security and social adjustment – in relation to suicide attempt and major depressive episode (MDE) during naturalistic follow-up of up to one year after presentation with MDE. Method136 adults who presented with a DSM-IV MDE completed the Adult Attachment Scale and the Social Adjustment Scale-Self Report at study entry. Based on follow-up interviews at three months and one year, we used survival analysis to investigate the relationship of scores on these measures with time to a suicide attempt and time to recurrent MDE. ResultsLess secure/more avoidant attachment predicted increased risk of suicide attempt during the 1-year follow-up (Wald χ2=9.14, df=1, p=0.003, HR=1.16, 95% CI=1.05 to 1.27). Poorer social adjustment predicted increased risk of recurrent MDE (Wald χ2=6.95, df=1, p=0.008, HR=2.36, 95% CI=1.25 to 4.46), and that in turn increased the risk of a suicide attempt (z=4.19, df=1, p<0.001, HR=17.3, 95% CI=4.6 to 65.5). ConclusionsAvoidant attachment in the setting of major depressive disorder is a potential therapeutic target to prevent suicidal behavior. Enhancing social adjustment may reduce relapse in major depressive disorder and thereby reduce risk of a suicide attempt. Study limitations include small sample size and use of a self-report attachment scale.

P01-269 Augmentation of zonisamide in poor or non-responder patients treated with duloxetine for single or recurrent unipolar major depressive episode

Objectives:The aim of our ongoing study is to investigate the effectiveness of Zonisamide augmentation to Duloxetine in partial and non-responder patients in course of Unipolar Major Depressive Episode.Method:35 outpatients will be enrolled in a 12-weeks open-label study including both genders, 18 to 65 years old subjects. Unipolar Major Depressive Episode diagnosis will be performed at screening time using “Structured Clinical Interview for DSM-IV-Axis-I Disorders- Italian 1996 version” (SCID-I, First et al., 1996) and by a ≥14 total score for the “Quick Inventory of Depressive Symptomathology-Self Rated” (QIDS-SR, Rush et al., 2003). Patients will be repeatedly evaluated during the course of the study using a wide range of mood and anxiety rating scales and monitoring biomarkers such as electroretinogram b-wave amplitude, interleukins, flogosis and BDNF factors etc. At week 6, Duloxetine partial/non responders will be augmetated to Zonisamide and further evaluations of mentioned markers will be repeated. A “Fisher-test” or χ² analysis will be performed at the end of the study. Expected p will be ≤ 0,005.Hypothesis:We expect Zonisamide augmentation to be an effective treatment for SNRI-resistant Major Depression.

Seasonal Affective Disorder: A Clinical Update

Seasonal affective disorder (SAD) consists of recurrent major depressive episodes in the fall/winter with remissions in spring/summer. A Medline search was conducted to identify studies relating to clinical management of SAD using the Medical Subject Heading, seasonal affective disorder, and key words, depress* and season*, focusing on studies published in the past 10 years. The Cochrane library of systematic reviews was also searched for relevant studies. A careful history is important to make the diagnosis and differentiate SAD from other similar conditions such as subsyndromal SAD and atypical depression. Seasonal patterns with winter worsening are also recognized in "nonseasonal" depression as well as many other psychiatric conditions, and comorbidity with SAD is common. The pathophysiology of SAD seems to be heterogeneous as research on circadian, neurotransmitter function and genetic hypotheses have shown discrepant results. A dual vulnerability model with differential loading on separate seasonal and depression factors has been proposed to explain these findings. Recent systematic reviews have shown that light therapy is an efficacious and well-tolerated treatment for SAD. There is also evidence for efficacy of pharmacotherapy to treat and prevent SAD. Clinical studies show equal effectiveness with light and antidepressants, so patient preference should be considered in the selection of initial treatment. Dawn stimulation, negative air ions, exercise and cognitve behaviour therapy are under investigation and may also be helpful treatments for SAD. SAD is a common condition with significant psychosocial impairment. Clinicians should be vigilant in recognizing seasonal patterns of depressive episodes because there are effective, evidence-based treatments for SAD.

Long-Term and Preventative Treatment for Seasonal Affective Disorder

Recurrent major depressive disorder with regular seasonal patterns, commonly known as seasonal affective disorder (SAD), has evoked substantial research in the last two decades. It is now recognised that SAD is a common condition with prevalence rates between 0.4% and 2.9% of the general population, and that patients with SAD experience significant morbidity and impairment in psychosocial function. There is good evidence that bright light therapy and antidepressant medications are effective for the short-term treatment of SAD; however, given that SAD is characterised by recurrent major depressive episodes, long-term and maintenance treatment must be considered. Unfortunately, there are few studies of longer term (>8 weeks) and maintenance (preventative) treatments for SAD. The weight of evidence suggests that light therapy usually needs to be continued daily throughout the winter season because of rapid relapse when light is stopped too early in the treatment period. However, some studies support the use of antidepressants to continue the response from a brief (1-2 weeks) course of light therapy early in the depressive episode, as soon as the first symptoms emerge in autumn. Only small studies have examined preventative treatment (before onset of symptoms) with light therapy, all of which have methodological limitations. The best evidence for preventative treatment in SAD comes from antidepressant studies. Three large, randomised, placebo-controlled studies have shown that preventative treatment with bupropion XL reduces the recurrence rate of depressive episodes in patients with SAD. Given the limitations in the evidence base and the inconsistent recurrence rate of winter depressive episodes, clinical recommendations for long-term and preventative treatment must individualise treatment choices and weigh potential benefits against possible adverse effects.

Are the vulnerability effects of personality and psychosocial functioning on depression accounted for by subthreshold symptoms?

Previous studies could not evaluate adequately the extent to which deviant levels of personality measures and psychosocial functioning found before and after a major depressive episode (MDE) should be attributed to subthreshold depressive symptoms. Our aim is to investigate whether pre- and post-MDE personality alterations and psychosocial disability truly reflect vulnerability, or whether they can be accounted for by the presence of subthreshold depressive symptoms. Data were derived from the Netherlands Mental Health and Incidence Study, a prospective general population study with three waves. Psychopathology was measured with the Composite International Diagnostic Interview (CIDI). Course of depressive symptoms was assessed with the Life Chart Instrument in a cohort of 195 respondents with a new or recurrent MDE between waves 2 and 3. Personality and psychosocial functioning were assessed with, respectively, four and two different measures. Alterations in measurements of personality and psychosocial functioning were present before onset and after remission of an MDE. Most pre- and postonset alterations occurred in the presence of subthreshold depressive symptoms. But even without these subthreshold symptoms, some alterations in measurements of personality and psychosocial functioning were found before and after an MDE. Depressive complaints between waves 2 and 3 were retrospectively assessed, and only a limited set of brief questionnaires was used to assess personality styles and psychosocial functioning. It is unlikely that the pre- and post-MDE alterations in personality and psychosocial functioning observed in earlier studies are entirely due to subthreshold depressive symptoms. This suggests that a depressive episode is interwoven in a long-standing and enduring pattern of mild personality deviance and limitations in psychosocial functioning.

A comparison of the familiality of chronic depression in recurrent early-onset depression pedigrees using different definitions of chronicity

BackgroundThe study of chronicity in the course of major depression has been complicated by varying definitions of this illness feature. Because familial clustering is one component of diagnostic validity we compared family clustering of chronicity as defined in the DSM-IV to that of chronicity determined by an assessment of lifetime course of depressive illness. MethodsIn 1750 affected subjects from 652 families recruited for a genetic study of recurrent, early-onset depression, we applied several definitions of chronicity. Odds ratios were determined for the likelihood of chronicity in a proband predicting chronicity in an affected relative. ResultsThere was greater family clustering of chronicity as determined by assessment of lifetime course (OR=2.54) than by DSM-IV defined chronic major depressive episode (MDE) (OR=1.93) or dysthymic disorder (OR=1.76). In families with probands who had preadolescent onset of MDD, familiality was increased by all definitions, with a much larger increase observed for chronicity by lifetime course (ORs were 6.14 for lifetime chronicity, 2.43 for chronic MDE, and 3.42 for comorbid dysthymic disorder). Agreement between these definitions of chronicity was only fair. LimitationsThe data used to determine chronicity were collected retrospectively and not blindly to relatives' status, and assessment of lifetime course was based on global clinical impressions gathered during a semi-structured diagnostic interview. Also, it can be difficult to determine whether individuals with recurrent major depressive episodes who frequently experience long periods of low grade depressive symptoms meet the strict timing requirements of DSM-IV dysthymic disorder. ConclusionsAn assessment of lifetime symptom course identifies a more familial, and thus possibly a more valid, type of chronic depression than the current DSM-IV categories which are defined in terms of particular cross-sectional features of illness.

Bipolar II Disorder: Current and Future Treatment Options

Bipolar II (BPII) disorder is a significant public health problem in the United States, and there is a dearth of studies of effective treatment modalities to deal with the recurrent major depressive episodes that accompany the disorder. This review attempts to summarize available data on agents useful in treating patients with the disease. English language controlled clinical trials involving BPII patients obtained from an extensive Medline search were critically reviewed. Agents that have potential utility in the treatment of BPII are profiled, based on their efficacy in bipolar I (BPI) or unipolar depression. The most efficacious agents are likely those with bimodal stabilizing properties, such as lithium, carbamazepine, and quetiapine. In fact, on the strength of favorable efficacy data obtained in patients with major depressive symptoms accompanying bipolar disorder, quetiapine recently became the first agent to be indicated by the FDA for monotherapeutic use in the treatment of bipolar depression, including BPII depression. Aside from the aforementioned agents, lamotrigine also shows promise in the treatment of BPII.

Propagation of major depressive disorder: Relationship between first episode symptoms and recurrence

Major depressive disorder is a highly recurrent disorder, with long-term estimates of recurrence ranging as high as 80%. The impact of first episode depressive symptoms on later recurrence has not been previously examined. The present study sought to identify risk factors for recurrent major depressive episodes by investigating first episode symptoms. It was predicted that the presence of depressed mood and sleep disturbance in the first episode would increase the likelihood of recurrence. Four hundred eighty-seven randomly selected community participants who met DSM-III-R criteria for at least one major depressive episode were assessed twice during adolescence and once in young adulthood. We examined the association between first major depressive episode symptoms and the presence of a recurrent episode. Recurrence was significant predicted by the presence of depressed mood and increased appetite at episode 1. A nonsignificant trend suggested that female gender may also be associated with recurrence. First episode depressed mood, increased appetite, and female gender may serve as specific risk factors for recurrence. The centrality of depressed mood to major depressive disorder is highlighted.

Increased Serum Levels of 8-Hydroxy-2′-Deoxyguanosine in Clinical Depression

We sought to understand the pathophysiological effects of depression by examining group differences in serum levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of oxidative damage. Our sample consisted of 169 participants. Eight-four of these participants met diagnostic criteria for clinical depression. The 85 participants in our comparison group were matched on age, gender, and ethnicity to the depressed group. 8-OHdG was measured by enzyme-linked immunosorbent assay. After adjusting for age, gender, race/ethnicity, years of education, daily smoking, average number of alcoholic drinks per week, average amount of physical activity per week, and body mass index, participants in the depressed group had significantly higher levels of oxidative DNA damage compared with participants in the control group. Pairwise comparisons showed that participants with major depression had significantly higher levels of 8-OHdG than control subjects and marginally higher levels of 8-OHdG compared with those with minor depression. Furthermore, participants with recurrent episodes of depression had more oxidative damage than participants with single episodes, who in turn had more damage than healthy control subjects. Finally, participants with recurrent episodes of major depression had more DNA damage than other depressed participants, who in turn had more damage than healthy control subjects. Our findings suggest that increased oxidative damage may represent a common pathophysiological mechanism, whereby depressed individuals become vulnerable to comorbid medical illness.

A Patient with a Resistant Major Depression Disorder Treated with Deep Brain Stimulation in the Inferior Thalamic Peduncle

The present report explored the effect of electrical stimulation on the inferior thalamic peduncle in a patient with resistant major depression disorder (MDD). This report refers to a 49-year-old woman with a history of recurrent episodes of major depression for 20 years (12 episodes and 2 hospitalizations), fulfilling Diagnostic and Statistical Manual of Mental Disorders, 4th edition, revised, criteria for MDD; in addition, the patient met criteria for borderline personality disorder and bulimia. Her longest episode of depression with suicidal ideation began 5 years before surgery. The patient's symptom array responded poorly to different combinations of antidepressants, cognitive therapy, and electroconvulsive therapy, which induced improvement only for short periods of time. Immediately before surgery, her Global Assessment of Functioning score was 20 and her Hamilton Depression Scale score ranged from 33 to 42. The patient was proposed for surgery for MDD. The patient had bilateral eight-contact electrodes stereotactically implanted for stimulation of areas at and around the inferior thalamic peduncle. Electrode position was corroborated by unilateral electrical stimulation searching for recruiting responses and regional direct current shifts in the electroencephalogram. Recording electrodes were replaced by tetrapolar electrodes for deep brain stimulation and connected to an internalized stimulation system for continuous bipolar stimulation at 130 Hz, 0.45 milliseconds, 2.5 V. Bimonthly follow-up included psychiatric and neuropsychological evaluations performed over the course of 24 months. After 8 months of ON stimulation, the patient entered a double-blind protocol with stimulators turned OFF. Improvement of depression measured by the Hamilton Depression Scale score was evident after initial placement of electrodes without electrical stimulation. Depression relapsed partially at the end of the first week. Electrical stimulation further improved depression, normalizing depression scores and neuropsychological performance. Patient depression scores ranked between 2 and 8 during 8 months of ON stimulation without antidepressant medication. After stimulation was turned OFF, spontaneous fluctuations in patient symptoms reflected by Hamilton Depression Scale and Global Assessment of Functioning scores were documented; these fluctuations disappeared after stimulation was turned on by Month 20. Complicated patients with comorbid conditions are common referrals to psychosurgery services. In this report, we present promising results of electrical stimulation of the inferior thalamic peduncle to treat recurrent unipolar depression in a patient with MDD and borderline personality disorder who responded poorly to treatment.

Successful Maintenance Electroconvulsive Therapy for More Than Seven Years

We report on a patient with recurrent major depressive episodes with psychotic features who was successfully treated with maintenance electroconvulsive treatment (M-ECT) over a long period without the need for concurrent treatment with an antidepressant or mood stabilizer. She started ECT in 1996 and has received M-ECT for more than 7 years. To date (2005), she has received 244 treatments. After 5 admissions in nearly 4 years, involving 29 months in hospital, she has not needed any further psychiatric admission for 7 1/2 years since the start of the M-ECT. Her depression has been in complete remission for nearly 6 years, with the exception of one mild-to-moderate nonpsychotic depressive episode lasting for 2 months. The patient exhibited slight cognitive deficits but had no subjective complaints before ECT, and her cognitive deficits did not worsen after the initial ECT. Thus M-ECT does not appear to cause cognitive deterioration. M-ECT is being continued on the patient's request.

Symptoms in Recurrent Episodes of Major Depression- Are they similar or Different?

Symptoms in Recurrent Episodes of Major Depression- Are they similar or Different?

Lithium and ECT – Concurrent use still demands attention: Three case reports

Bipolar disorders as well as recurrent major depressive episodes can be most effectively treated with electroconvulsive therapy (ECT). Since continuation/maintenance ECT is not well established, prophylactic therapy in recurrent illnesses is more commonly carried out using antidepressive medication alone or more often in combination with lithium. In case of relapse the clinically important question of discontinuation of lithium versus the concurrent use of ECT and lithium may arise. The safety of concurrent use has also to be balanced when lithium treatment is started within an ECT course. Since recent studies have reported no negative interactions with concurrent use, we here report three cases (one case of a prolonged seizure, a serotonin syndrome and a focal seizure) of severe lithium-induced side effects while patients underwent ECT without complications and lithium serum levels were still subtherapeutic. Clinical consequences are discussed and disturbances of the blood–brain barrier system as a speculative cause are hypothesized taking previous studies, animal studies and an additional reported clinical case into account.

Hippocampal Volume and First Major Depressive Episode After Cancer Diagnosis in Breast Cancer Survivors

Patients experiencing their first major depressive episode after receiving a diagnosis of cancer are frequently seen in clinical oncology settings; however, little is known about the neurobiological basis of the first episode. In previous studies, a smaller hippocampus than in healthy comparison subjects has been observed in patients with a history of recurrent and prolonged major depressive episodes. The purpose of the present study was to investigate whether there is an association between hippocampal volume and a first major depressive episode after cancer diagnosis in cancer survivors. The subjects were 68 female cancer survivors who had undergone breast cancer surgery 3 or more years earlier (mean interval=4.3 years, SD=0.9). The hippocampal volume and delayed recall function of the 17 cancer survivors who had their first major depressive episode after receiving their cancer diagnosis and the 51 with no history of major depressive episode at any time during their lives were measured by magnetic resonance imaging and the Wechsler Memory Scale-Revised, respectively. The mean duration of the major depressive episode after cancer diagnosis was 11.9 weeks (SD=14.2). There were no significant differences in left or right hippocampal volume or in delayed recall function between the cancer survivors with and without a major depressive episode after cancer diagnosis. First major depressive episodes after cancer diagnosis in female cancer survivors do not appear to be associated with hippocampal volume. However, a longitudinal study with healthy comparison subjects is needed to draw a definite conclusion.

Bipolar Spectrum Disorder: A Pilot Study

Objective: To assess depressive features of a proposed definition of bipolar spectrum disorder (BSD). Methods: Thirty-six patients with bipolar disorder type I or II were compared to 37 patients with unipolar major depressive disorder through patient interview and chart review. Results: Univariate analysis suggests that 7 of 12 (recurrent major depressive episodes, brief major depressive episodes, atypical depressive symptoms, early age of onset, family history of bipolar disorder, antidepressant tolerance, and antidepressant-induced mania) features of major depressive episodes were more likely to occur in bipolar versus unipolar patients. After adjustment in a multivariable regression model, however, the five most powerful predictors of bipolar disorder were brief major depressive episodes, early age of onset, antidepressant- induced mania, postpartum depression, and atypical depressive symptoms. Conclusions: This preliminary study supports the idea that bipolar disorder is characterized by some depressive features less likely to be found in unipolar depression. Further prospective study needs to be conducted comparing BSD with unipolar depression.

Bipolar II or Unipolar Depression: Pharmacologic Considerations

This column offers a question-and-answer forum to help nurses maintain their knowledge of advances in prescribing and psychopharmacology, and implications for safe psychiatric care. Send your questions related to prescribing psychotropic medications to the Editor, Mary Paquette, at mary@artwindows.com. ********** Question: One of my clients presented with symptoms of major depression. I prescribed one of the novel antidepressants. During a case conference, I was asked if bipolar (BP) II had been ruled out, because the client developed hypomania shortly after initiation of antidepressant treatment. Please discuss treatment considerations for the client with BP II depression. Deborah Antai-Otong responds: Historically, BP II has been underused and misdiagnosed as unipolar major depressive disorder. Both the client and clinician have missed or minimized hypomania or mild mania if it occurred in clients with atypical depression. Differences between BP II depression and unipolar depression include lower age at onset, more atypical features, more recurrences, and higher heritability in the former (Benazzi, 1999; Rush, 1998). Additional differences between bipolar II and unipolar depression include a higher prevalence of and natural history of depressive mixed states in bipolar II, which is rare in unipolar major depression. Clinical implications from these differences are that monotherapy with antidepressants in BP II depression worsen depressive mixed states, and clients seem to respond better to mood stabilizers (Benazzi & Akiskal, 2001). By definition, clients with BP II have recurrent major depressive episodes with a lifelong history of one or more hypomanic episodes of at least 4 days duration, and never mania (American Psychiatric Association [APA], 2000; Cassano et al., 1999). In contrast, symptoms of unipolar major depression occur without a history of hypomania or mania. An estimate of lifetime prevalence of BP II ranges from 0.3% to 2.0% and is more commonly found in women than in men (APA, 1994, 2000). BP II depression seems more resistant to conventional treatment than BP I (history of mania). Depressive states account for high morbidity and are strongly linked with suicidal behavior and sustained psychosocial impairment, placing a tremendous toll and burden on clients and families, and economic cost to society (APA, 2000; Rush, 1998; Woods, 2000). A major challenge for psychiatric nurses is making an accurate diagnosis of BP II and implementing appropriate treatment. Predictably, a misdiagnosis of unipolar disorder often results in inappropriate treatment, such as monotherapy with an antidepressant, which induces mood instability in the absence of more suitable pharmacotherapy with mood stabilizers and atypical antipsychotics (Akiskal et al., 2000). Assessment and Diagnosis Considerations A complete psychiatric and medical workup must be performed to determine the diagnosis. A complete physical includes: * Vital signs * Complete blood count with differential * Chemistry profile ('include serum electrolytes, glucose, hepatic, renal, and thyroid panels) * Pregnancy test (when appropriate) * Urinalysis * Urine drug screens * 12-lead electrocardiogram (Suppes & Dennehy, 2002) The psychosocial evaluation includes a comprehensive mental status examination, and suicide and homicide assessment. It must include information about history of symptoms, to include age of onset, length of mood cycle, history of rapid cycling (e.g., 3-4 cycles within 12 months); frequency of hypomania; and questions such as Have you ever had a time in your life when you had a lot of energy, did not need a lot of sleep and felt creative? Clients with BP II infrequently consider their hypomanic symptoms to require treatment. Normally, they seek treatment during a depressive episode. …