PCN 605 GCU Diagnosing Depressive Disorder or Cyclothymic Disorder Discussion

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1. What are some of the challenges in diagnosing an individual with persistent depressive disorder or cyclothymic disorder? Explain with examples.

2. Read the case study of “Jack” located in the Topic 4 materials and provide the appropriate DSM-5 diagnoses in descending order, from the dominant, to the least dominant. For each diagnosis you assign, provide an explanation of the diagnostic criteria you assessed to be compelling, as found in the DSM-5 diagnostic criteria monograph for each disorder.

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1. Read Chapters 6 and 7 in DSM-5 in Action. Dziegielewski, S. F. (2014). DSM-5 in action (3rd ed.). John Wiley & Sons. 2. Read pages 123-188 in the DSM-5. Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). (2013). American Psychiatric Publishing. 3. Read "Combining Medication Treatment and Cognitive-Behavior Therapy for Bipolar Disorder," by Basco, Ladd, Myers, and Tyler, from Journal of Cognitive Psychotherapy (2007). https://lopes.idm.oclc.org/login?url=https://search-proquestcom.lopes.idm.oclc.org/docview/89071100?accountid=7374 4. Explore the Diagnostic and Statistical Manual of Mental Disorders website. http://www.dsm5.org/Pages/Default.aspx 5. Read “Elevated Reward-Related Neural Activation as a Unique Biological Marker of Bipolar Disorder: Assessment and Treatment Implications” by Nusslock, Young, & Damme, from Behaviour Research and Therapy (2014). https://www-sciencedirectcom.lopes.idm.oclc.org/science/article/pii/S0005796714001405?via%3Dihub 6. Read "Predictors of Suicidal Ideation and Attempt Among Patients With Major Depressive Disorder at a Tertiary Care Hospital, Puducherry," by Lalthankimi, et al., from Journal of Neurosciences in Rural Practice (2021). https://lopes.idm.oclc.org/login?url=https://search.ebscohost.com/login.aspx?direct=true&db= a9h&AN=148381753&site=eds-live&scope=site&custid=s8333196&groupid=main&profile=eds1 7. Read “Differential Diagnosis of Bipolar Disorder and Major Depressive Disorder” by Hirschfeld, from Journal of Affective Disorders (2014). https://www-sciencedirectcom.lopes.idm.oclc.org/science/article/pii/S0165032714700047?via%3Dihub 8. Read “Diagnostic Utility of Worry and Rumination: A Comparison Between Generalized Anxiety Disorder and Major Depressive Disorder” by Yang, Kim, Lee, Lee, Yu, Jeon, & Kim, from Psychiatry and Clinical Neurosciences (2014). https://lopes.idm.oclc.org/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=a 9h&AN=97637640&site=ehost-live&scope=site 9. Read “Managing Major Depressive Disorder Through the Use of Adjunct Therapies” by Katzman, Psychiatry Research (2014). https://www-sciencedirectcom.lopes.idm.oclc.org/science/article/pii/S0165178114700010?via%3Dihub 10 Read “An Update on the Diagnosis and Treatment of Bipolar Disorder, Part 1: Mania” from Psychiatric Times (2015). https://lopes.idm.oclc.org/login?url=http://search.ebscohost.com/login.aspx?direct=true&d b=ofs&AN=112070371&site=ehost-live&scope=site 11 Read the “Case Study: Jack” document in preparation for this week’s discussion question. November 2015 All other clinicians either will receive a CME Attendance Certificate or may choose any of the types of CE credit being offered. PREMIERE DATE: November 20, 2015 EXPIRATION DATE: November 20, 2016 This activity offers CE credits for: 1. Physicians (CME) 2. Other An Update on the Diagnosis and Treatment of Bipolar Disorder, Part 1: Mania by Philip G. Janicak, MD and Joseph Esposito, MS, MD Dr Janicak is Director of the Transcranial Magnetic Stimulation Center at Edward/Elmhurst Healthcare and is on the faculty of the department of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine in Chicago; Dr Esposito is a First-Year Resident at the Delaware Psychiatric Center in New Castle, Del. I n this 2-part article, we consider bipolar disorder symptom manifestations in light of the changes in DSM-5. We review the management of acute mania and hypomania, as well as subsequent maintenance strategies. Throughout, we also consider the implications of course specifiers (eg, rapid cycling, mixed or psychotic features) for altering treatment approaches (Table 1). In Part 2 (December 2015 issue of Psychiatric Times) we will discuss the management of bipolar depression and cyclothymic disorder, the role of psychotherapy, and future directions. Diagnosis of bipolar disorder The lifetime prevalence of bipolar disorder is estimated to be 1.6%.1 This illness typically begins early in life and is characterized by acute exacerba- ACTIVITY GOAL This article reviews DSM-5 changes to symptom criteria for bipolar disorder. The primary focus is on the diagnosis and treatment of mania and hypomania. LEARNING OBJECTIVES At the end of this CE activity, participants should be able to: • Understand the various bipolar specifiers • Identify bipolar diagnostic categories • Identify FDA-approved indications for pharmacologic management of bipolar mania • Distinguish which intervention (pharmacotherapy or psychotherapy) is best for each patient TARGET AUDIENCE This continuing medical education activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders. CREDIT INFORMATION CME Credit (Physicians): This activity has been planned and implemented in accordance with the Essential Areas and policies of the 1511PT206973AJanicak_CME.indd 29 tions of mania, hypomania, and depression; a chronic, recurrent course with substantial interepisodic morbidity; an increase in other psychiatric (eg, substance abuse) and medical (eg, cardiovascular disease) comorbidities; and a heightened risk for suicide. As a result, bipolar disorder negatively affects functioning in multiple spheres of activity, health status, and quality of life. A manic episode experienced even once in a lifetime qualifies for a diagnosis of bipolar I disorder. While these patients may experience hypomanic and major depressive episodes as well, these are not required criteria. Despite this, depression typically is the more predominant mood disturbance. A diagnosis of bipolar II disorder requires both a hypomanic and a major depressive episode. It is important to emphasize that bipolar II is not a less severe form of bipolar I, but rather a distinct disease process that can be just as detrimental to psychosocial functioning, particularly in the depressive phase. While patients with bipolar I and bipolar II disorder may experience major depressive episodes and hypomania, bipolar II patients never experience mania. Bipolar disorder usually presents as discrete episodes. Thus, mania and hypomania often occur with a relatively sudden and recognizable change in behavior clearly out of character from the patient’s baseline mood state. While mania and hypomania share many of the same symptoms, a key difference is severity (Table 2). True mania must be present for at least 1 week Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of CME Outfitters, LLC, and Psychiatric Times. CME Outfitters, LLC, is accredited by the ACCME to provide continuing medical education for physicians. CME Outfitters designates this enduring material for a maximum of 1.5 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. (Please see Mania, page 30) Philip G. Janicak, MD, reports that he has received grant support from, and is on the speakers bureau for, Neuronetics Inc, Sunovion, and OrthoMcNeil/Janssen; he is also a consultant for Neuronetics Inc. Joseph Esposito, MS, MD, has no disclosures to report. Michael Gilin, MD, (peer/content reviewer) reports that he is on the speakers bureau for Otsuka. Note to Nurse Practitioners and Physician Assistants: AANPCP and AAPA accept certificates of participation for educational activities certified for 1.5 AMA PRA Category 1 Credit™. Applicable Psychiatric Times staff and CME Outfitters staff have no disclosures to report. DISCLOSURE DECLARATION It is the policy of CME Outfitters, LLC, to ensure independence, balance, objectivity, and scientific rigor and integrity in all of their CME/ CE activities. Faculty must disclose to the participants any relationships with commercial companies whose products or devices may be mentioned in faculty presentations, or with the commercial supporter of this CME/CE activity. CME Outfitters, LLC, has evaluated, identified, and attempted to resolve any potential conflicts of interest through a rigorous content validation procedure, use of evidencebased data/research, and a multidisciplinary peer-review process. Faculty of this CME/CE activity may include discussion of products or de­vices that are not currently labeled for use by the FDA. The faculty have been informed of their responsibility to disclose to the audience if they will be discussing off-label or investigational uses (any uses not approved by the FDA) of products or devices. CME Outfitters, LLC, and the faculty do not endorse the use of any product outside of the FDA-labeled indications. Medical professionals should not utilize the procedures, products, or diagnosis techniques discussed during this activity without evaluation of their patient for contraindications or dangers of use. The following information is for participant information only. It is not assumed that these relationships will have a negative impact on the presentations. Questions about this activity? Call us at 877.CME.PROS (877.263.7767) UNLABELED USE DISCLOSURE 11/2/15 9:52 AM 30 PSYCHIATRIC TIMES NOVEMBER 2015 CATEGORY 1 Mania Continued from page 29 with associated increases in energy or activity and marked functional impairment that results in a substantial loss of social and occupational functioning. Psychotic features may also be present in more severe episodes and often require hospitalization. Alternatively, hypomania should last at least 4 days with symptoms that are not as severe as mania in terms of social or occupational impairment. Psychotic features are never present in bipolar II patients, and hospitalization is a specific exclusion criterion. Per DSM-5, if either mania or hypomania presents with at least 3 criteria for a depressive episode, they would warrant a mixed specifier designation as well. Clarifying whether there has been a manic or hypomanic episode may be difficult. This is in part because patients may not consider hypomania or mild mania to be problematic. Clinicians need to carefully explore for possible past episodes, using collateral sources of information whenever possible. Screening instruments such as the Mood Disorders Questionnaire and the prospective Life Chart Method are also helpful.2,3 Cyclothymic disorder is characterized by at least 2 years (1 year in children and adolescents) of periodic hypomanic and depressive symptoms that are distinct from each other. Neither mood phase, however, ever meets the full criteria for a hypomanic or depressive episode. During this time, there are no periods of normal mood that last more than 2 months. These mood disturbances should also lead to problems in social or occupational functioning. Differential diagnosis Bipolar disorder can be difficult to distinguish from other psychiatric conditions because there is often substantial symptomatic overlap. Acute schizo- phrenia can mimic a more severe episode of mania and requires careful attention to the patient’s psychiatric history to help clarify the diagnosis. While similar symptoms may occur in both disorders, schizophrenia more commonly presents with hallucinations and fixed delusions. Schizoaffective disorder is distinguished from acute mania with psychosis by a period of psychotic symptoms that lasts at least 2 weeks in the absence of significant mood symptoms. Over the long-term course of schizoaffective disorder, however, there should be a substantial proportion of time (> 50%) when mood symptoms are present. MDD and bipolar depression are often clinically indistinguishable. MDD, however, involves only depressive episodes, whereas bipolar depression requires a history of mania or hypomania. Obtaining a thorough personal and family history, including premorbid functioning, may help clarify the diagnosis. Other disorders (eg, ADHD, conduct disorder, stimulant use) may also include certain symptoms of hypomania or mania and, to further complicate the diagnosis, often occur as comorbidities with bipolar disorder. Various substances, medications, and medical conditions can mimic the symptoms of bipolar disorder and have their own specific diagnostic categories. For example, manic or hypomanic symptoms due to the effects of cocaine would not be given a bipolar diagnosis unless the symptoms persisted well after the drug’s effects subsided. Table 3 lists and briefly describes DSM-5 categories for bipolar disorder. Management of bipolar mania and hypomania Treatment recommendations Several reviews, professional guidelines, pragmatic studies, and treatment algorithms serve as the basis for our suggested treatment approaches. The strategies recommended in these publications are based primarily on the strength of Table 1 – Bipolar specifiers Type Symptoms Comments With anxious distress Tenseness, restlessness, poor concentration due to worry, impending misfortune, fear of loss of control Number of symptoms: mild, 2; moderate, 3; moderate to severe, 4 or 5; severe, 4 or 5 with motor agitation With mixed features during mania or hypomania Manic or hypomanic episode plus depressed mood, decreased pleasure in activities, psychomotor retardation, fatigue, worthlessness or guilt, thoughts of death with or without a specific plan At least 3 symptoms present for the majority of the days during an episode With mixed features during a depressive episode Elevated mood, grandiosity, talkativeness, racing thoughts, increased goal-directed activity, risky behavior, decreased need for sleep At least 3 symptoms present for the majority of the days during an episode With rapid cycling Four or more mood episodes in the past 12 months Each episode must be separated by either a period of full remission or a switch to the opposite polarity With melancholic features Loss of pleasure in activities OR no reactivity to events that should be pleasurable AND 3 or more melancholic symptoms Melancholic symptoms: distinct quality of depression that is worse in the morning, early morning awakening, psychomotor changes, anorexia, weight loss, or excessive or inappropriate guilt With atypical features Mood reactivity AND at least 2 other symptoms Symptoms such as increased appetite or weight gain, hypersomnia, heavy feeling of the arms and legs, sensitivity to rejection With mood-congruent psychotic features Delusions or hallucinations Should be in line with what is expected for the current episode (eg, grandiosity during mania) With mood-incongruent psychotic features Delusions or hallucinations Should not fit with the current mood episode or are mixed with some congruent features With catatonia Catatonic features present for most of the episode May occur with mania or depression With peripartum onset Mood episode during pregnancy or up to 4 weeks after delivery Depressed episode may be associated with severe anxiety or panic attacks With seasonal pattern Mood episodes and remissions that only occur at a certain time of the year There is an absence of off-cycle episodes in at least the past 2 years and more seasonal episodes compared with non-seasonal episodes overall Adapted from DSM-5. 1511PT206973AJanicak_CME.indd 30 11/2/15 9:52 AM NOVEMBER 2015 PSYCHIATRIC TIMES CATEGORY 1 Table 2 – Mania and hypomania diagnostic criteria 31 Table 3 – Bipolar diagnostic categories Criteria Maniaa Hypomaniab Diagnosis Description Minimum timeframe for diagnosis 1 week 4 days Bipolar I disorder Number of symptoms for diagnosis At least 3 At least 3 Diagnosis requires at least 1 true manic episode with or without episodes of depression or hypomania Grandiosity Yes Yes Bipolar II disorder Decreased need for sleep Yes Yes More talkative Yes Yes Diagnosis requires at least 1 hypomanic episode AND 1 major depressive episode in the absence of any lifetime history of mania Flight of ideas Yes Yes Cyclothymic disorder Distractibility Yes Yes Increased goal-directed activity Yes Yes 2 years (1 in children and adolescents) of hypomanic and depressive symptoms that fall short of meeting DSM criteria for either mood state Risky behavior Yes Yes Marked impairment of social/occupational functioning Yes No Substance/medication-induced bipolar and related disorders A disturbance in mood that develops during or soon after substance intoxication or withdrawal Psychotic features Yes No May require hospitalization Yes No Bipolar and related disorders due to another medical condition The disturbance is a direct pathophysiological consequence of another medical condition Other specified bipolar and related disorders Symptoms that fall short of meeting criteria for bipolar I or II disorder (eg, short hypomanic episodes, belowcriteria hypomanic symptoms with major depression, hypomania without major depressive episode, cyclothymic symptoms occurring less than 2 years [1 in children and adolescents] ) Unspecified bipolar and related disorders Diagnosis used until a more specific diagnosis can be obtained (ie, limited information, emergency department setting) More severe. Less severe. Adapted from DSM-5. a b evidence from placebo- and/or active comparator-controlled trials involving various medications or psychotherapeutic approaches. In some cases, however, there is a lack of such data and information of lesser strength forms the basis for recommendations. In particular, guidelines for the management of certain patient subgroups (eg, rapid cyclers) are often based on results from fewer and less well-controlled trials. One additional caveat is that the preponderance of evidence derived from controlled trials is industry sponsored. Emergency interventions Manic patients who present with severe agitation or aggression may require immediate pharmacologic intervention to prevent harm to themselves and others. Second-generation antipsychotics are generally preferred over firstgeneration (typical) agents because of their lower short-term adverse effect burden. Benzodiazepines may also be used as adjuncts to quickly calm an agitated patient, to reduce the amount of antipsychotic required, or to prevent withdrawal symptoms when alcohol or other substances are involved. When possible, oral formulations should be offered initially and acute parenteral formulations reserved for those unwilling or unable to tolerate oral therapy.4 Alternatively, the combination of lower doses of haloperidol (eg, 2 to 5 mg) and lorazepam (eg, 2 mg) may be used either orally or parenterally. A recent study indicated that successful remission of postpartum psychotic mania may require combined treatment with lithium, an antipsychotic, and a benzodiazepine.5 In more emergent situations such as manic delirium, ECT can be life-saving.6 Stabilization strategies Once the safety of the patient and others is assured, attention turns to resolution of an acute episode (Figure). If the patient is currently taking an antidepressant, it should be discontinued (preferably by taper rather than by abrupt cessation) to prevent persistent manic symptoms and a greater risk for relapse. Most published strategies to manage acute, mild to moderate manic or mixed episodes (and to a lesser extent hypomania) recommend lithium, valproate, or a second-generation antipsychotic as first-line monotherapies. Of note, recent evidence supports lithium’s potential neuroprotective properties and lower non-suicide mortality risk compared with anticonvulsants.7,8 In patients with more severe symptoms, associated psychosis, or schizoaffective disorder, a second-generation antipsychotic alone or in combination with other mood stabilizers plus a benzodiazepine are usually recommended (eg, lithium or valproate plus an antipsychotic). Second-generation antipsychot- 1511PT206973AJanicak_CME.indd 31 Adapted from DSM-5. ics are usually preferred to first-generation antipsychotics to minimize adverse effects, particularly neuromotor; or to lithium, valproate, or carba­ mazepine during pregnancy. With insufficient benefit, clozapine as monotherapy or augmentation therapy may also be an alternative.9 Finally, ECT alone or combined with an atypical antipsychotic can control episodes of psychotic mania and severe refractory episodes, and constitutes a safer alternative during pregnancy.10,11 Lithium and valproate appear to be comparably effective in treating pure manic episodes, while valproate may be more effective for mixed or rapid cycling presentations.12 Carbamazepine with or without an antipsychotic is usually recommended as second-line therapy because it is limited by its adverse effect profile and the risk of significant interactions with other psychotropic and nonpsychotropic medications.12 In this context, oxcarbazepine—a structurally similar analog of carbamazepine—may be an alternative based on promising but limited data from preliminary studies, primarily because of its lower adverse effect profile and fewer drug interactions.13 Once the initial target dose or blood level is achieved, medication adjustments may be considered within 1 to 2 weeks if there is insufficient improvement. When feasible, dose adjustments of the initial medication(s) should be attempted before the addition of another medication to minimize adverse effects, drug interactions, and unnecessarily complicated treatment regimens—all of which may exacerbate adherence problems. At times, however, the combination of lithium plus valproate will more effectively control acute symptoms. This strategy is usually done in a sequential fashion rather starting both medications simultaneously. (Please see Mania, page 32) 11/3/15 9:45 AM 32 PSYCHIATRIC TIMES NOVEMBER 2015 CATEGORY 1 Mania Continued from page 31 Maintenance treatment The agent(s) used to successfully control a manic episode are typically continued for maintenance purposes. Thus, the most commonly recommended treatments mirror those used for acute management and include lithium, valproate, and second-generation antipsychotics. In addition, risperidone longacting injectable formulation (alone or in combination with lithium or valproate) may be considered for patients with a history of poor oral absorption or inadequate adherence. At times, combined treatments may enhance efficacy but often at the cost of a greater adverse effect burden. In this context, the results of the BALANCE study indicate that lithium alone is more likely to prevent relapse than valproate alone.14 However, it is unclear whether lithium alone is as effective in preventing relapse as the combination of lithium and valproate. In addition, psychotherapy to address residual mood symptoms and comorbid conditions such as substance use disorders is critical to achieving and maintaining a successful outcome. In the absence of persistent psychosis, adjunctive antipsychotics used for acute control may be slowly tapered after a reasonable period of mood stability is achieved. If benzodiazepines are used for acute stabilization, they should also be slowly discontinued when symptoms are resolved. Maintenance ECT may be continued after a successful acute treatment course at the lowest possible frequency, if symptoms are not adequately controlled with medication(s) and psychotherapy. Maintenance treatment should be continued for at least 6 to 12 months after complete remission of a manic episode before assessing the need for Figure. Treatment Strategy for Acute Mania Treatment strategy Clinical presentation Acute mild to moderate mania Start Lithium (0.8-1.2 mEq/L) or valproate (50-125 μg/mL) or second-generation antipsychotic; withdraw antidepressant if being used Insufficient response Moderate to severe episode; psychotic symptoms; primary mood stabilizer(s) insufficient Start Second-generation antipsychotic ± mood stabilizer ± benzodiazepine Insufficient response Poor oral absorption; inadequate adherence to oral medications Consider Risperidone long-acting injectable ± mood stabilizer ± benzodiazepine Insufficient response or intolerable adverse effects Mood stabilizer not tolerated May start Second-generation antipsychotic monotherapy ± benzodiazepine Insufficient response Prior nonresponse to lithium; rapid cycling; mixed state; medical contraindication to lithium; patient is not pregnant May start Valproate/carbamazepine ± antipsychotic ± benzodiazepine Insufficient response Combined mood stabilizers ± antipsychotic ± benzodiazepine Insufficient response Clozapine ± valproate or lithium Insufficient response Immediate danger (eg, manic delirium); previous good response to ECT; medical contraindication to pharmacotherapy; patient is pregnant May start ECT Insufficient response ECT plus second-generation antipsychotic Adapted from Janicak et al.1 1511PT206973AJanicak_CME.indd 32 11/2/15 9:52 AM NOVEMBER 2015 PSYCHIATRIC TIMES CATEGORY 1 ongoing treatment. Given the high relapse rates with discontinuation, however, it is generally recommended that maintenance therapy continue indefinitely. If lithium is discontinued, it should be done by a slow taper over several weeks to decrease the risk of relapse. Pharmacotherapy Lithium While lithium’s exact mechanism of action is unknown, its ability to modulate various aspects of brain chemistry is consistent with many current models of the pathogenesis of bipolar disorder. Lithium exerts multiple biochemical effects at a variety of targets owing to its relatively simple nature. Because of its similarity to other cations (eg, Na+, K+, Ca++, Mg+), lithium can alter ion channels and pumps in cell membranes. It is also implicated in the modulation of neurotransmitters and neuropeptides such as lithium-induced decreases in beta-adrenergic receptor number, beta-adrenergic activity through inhibition of thyroid hormone, dopamine receptor supersensitivity, and glutamate-mediated calcium signaling; and increases in serotonin release. In addition, lithium interacts with G-protein and second messenger systems leading to downstream effects on DNA transcription, which may serve to explain its long-term therapeutic effects. Neuroprotective properties such as increasing neuronal viability in the context of glutamate cytotoxicity and the expression of brain-derived neurotrophic factor are also associated with sustained lithium treatment.15 Lithium is rapidly absorbed in the gastrointestinal tract, is not protein bound, and distributes throughout total body water with peak serum concentrations at 1 to 2 hours after administration (4 to 5 hours for slow-release preparations). It has no metabolites and is almost entirely excreted by the kidneys. Its typical half-life in a healthy adult is about 24 hours, and steady- 33 state serum levels are usually achieved in 4 to 5 days. Lithium is usually started at 300 mg, 2 or 3 times daily, and gradually increased 300 to 600 mg every 1 to 5 days based on response to treatment, blood levels, and tolerability. Optimal dosing generally falls between 900 and 1900 mg daily to achieve a target serum concentration of 0.8 to 1.2 mEq/L. If dose adjustments are made, a lithium trough (10 to 12 hours after the last dose) level should be drawn 5 to 7 days after the change to properly reflect the new steady-state concentration. Lithium is contraindicated in patients with significant renal impairment, dehydration, and low sodium levels, because these states increase the likelihood of acute toxicity. Lithium should also be avoided in patients with significant cardiovascular disease because of its impact on the heart’s conduction system. Lithium is associated with a number of adverse effects even at therapeutic levels. Nausea is most commonly managed by encouraging food intake with each dose or the use of extended-release formulations. Tremor, which can also be an early sign of toxicity, may be managed by dividing doses and avoiding exacerbating factors such as anxiety, stress, and caffeine. Weight gain, loose stools, and cognitive impairment can also occur and may require dose adjustment. Renal function should be assessed once or twice a year because lithium may cause impairment with long-term use. Lithium also affects the thyroid and parathyroid glands, reducing thyroid hormone release and increasing parathyroid hormone activity. In the context of pregnancy, lithium is listed as a category D drug owing to the risk of cardiac defects such as Ebstein’s anomaly. During pregnancy (particularly the first trimester), the developing fetus should be closely monitored for cardiac defects. Doses will need adjustment, particularly near par(Please see Mania, page 34) Table 4 – FDA-approved indications for pharmacologic management of bipolar mania Bipolor mania Drug Acute Maintenance Usual dose range (mg) Lithium A A 600-2400 Usual therapeutic serum range: 0.8-1.2 mEq/L for acute mania; teratogenic potential; requires ongoing monitoring of weight, renal and thyroid function Divalproex A – 750-2000 Usual therapeutic serum range: 50-125 µg/L for acute mania; teratogenic potential; requires ongoing monitoring of weight, CBC count, LFTs, and menstrual history Divalproex ER A, B – 750-2000 Usual therapeutic serum range: 85-125 µg/L for acute mania; teratogenic potential; requires ongoing monitoring of weight, CBC count, LFTs and menstrual history Carbamazepine XR A, B – 800-1600 Possible therapeutic serum range: 4-12 µg/mL; requires ongoing monitoring of weight, CBC count, LFTs, electrolytes; several AEs; teratogenic potential and drug-interaction issues limit usefulness Chlorpromazine A – 200-800 Approval not based on present-day FDA criteria Olanzapine A, B, C, D A 5-20 Sedation; cardiometabolic AEs Risperidone A, B, C – 1-6 Neuromotor AEs; hyperprolactinemia Risperidone LAI A A,C 25-50a May resolve absorption and adherence issues; may be used as monotherapy or in combination with lithium or divalproex; hyperprolactinemia Quetiapine A, C, D C 400-800 Sedation and cardiometabolic AEs Quetiapine XR A, B, C C 400-800 Sedation and cardiometabolic AEs Ziprasidone A, B C 80-160 Cardiometabolic risks reduced Aripiprazole A, B, C, D, E A, C 5-30 Agitation/anxiety; akathisia; cardiometabolic risks reduced Asenapine A, B, C C 10-20 Sublingual formulation only Comments A, monotherapy; B, mixed states; C, adjunct to lithium or valproate; D, pediatric/adolescent; E, acute parenteral. CBC, complete blood cell; LFT, liver function test; ER, extended release; XR, extended release; AEs, adverse effects; LAI, long-acting injectable. a Every 2 weeks. 1511PT206973AJanicak_CME.indd 33 11/2/15 9:52 AM page PB) 34 PSYCHIATRIC TIMES NOVEMBER 2015 CATEGORY 1 Mania Continued from page 33 turition and postpartum because of changes in metabolism and fluid volumes. When neonates are breastfed while their mother is taking lithium, they should be assessed for lethargy, as well as growth and feeding problems. Valproate As with lithium, the mechanism of action for valproate as a mood stabilizer is not fully understood. Two actions that may be relevant include blockade of voltage-dependent sodium ion receptor channels and enhancement of gamma-aminobutyric acid activity by increasing its synthesis and release. Valproate is well absorbed with greater than 80% bioavailability after oral administration and may be administered after meals because food delays absorption, lessening adverse effects. It is highly protein bound and remains mainly in the extracellular fluid. Peak serum levels occur between 1 and 4 hours after administration, and half-life ranges between 6 and 16 hours. Valproate is metabolized by the liver and excreted through the kidneys. Valproate is usually started at a dose of 250 mg, 2 or 3 times daily, and titrated every few days until a dose of 1500 to 2500 mg/d is reached. Valproate can also be orally loaded at 20 to 30 mg/kg daily to more rapidly achieve therapeutic levels. Optimal therapeutic plasma levels of valproate generally fall between 50 and 125 µg/mL and should be checked 2 to 5 days after a dose increase, 12 hours after the last dose. Mania, hypomania, and mixed episodes can be managed initially with 1 of 3 strategies: lithium, valproate, or a second-generation antipsychotic either as monotherapy or in various combinations. Valproate can cause nausea, vomiting, hair loss, easy bruising, and tremor. Valproate-associated weight gain and insulin resistance can lead to metabolic syndrome. More rarely, it may cause liver toxicity, elevations in ammonium levels, pancreatitis, thrombocytopenia, and coagulation problems. It is contraindicated in persons with liver disease and those with mitochondrial disorders. Liver function tests should be performed before starting treatment and repeated during the first few months if indicated. In the context of pregnancy, valproate is listed as a category D drug because of a 9% risk of development of major malformations.16 Women of childbearing age should use adequate contraceptive methods while taking valproate and should receive folic acid. If pregnancy does occur, the patient should be switched to an alternative treatment and the fetus monitored for cardiac anomalies. Valproate also carries an increased risk of polycystic ovary syndrome, which is particularly relevant in women of childbearing age. Carbamazepine The hypothetical mechanism of action of carbamazepine in bipolar disorder may relate to its binding of sodium ion channels, enhancing the inactivated state and blocking the propagation of rapid action potentials. It is absorbed slowly, with peak serum levels occurring 6 to 8 hours after administration and a bioavailability of 85%, and is metabolized in the liver by cytochrome P450 (CYP450) 3A4. Its half-life during the initial stages of treatment ranges from 25 to 65 hours, but may decrease to 12 to 17 hours after several weeks owing to autoinduction. For this reason, serum levels should be measured at 3, 6, and 9 weeks after starting treatment. Oxcarbazepine is usually fully absorbed and not affected by food with peak serum concentrations achieved 4 to 6 hours after administration and a half-life of 8 to 12 hours. Oxcarbazepine also undergoes hepatic metabolism but is less likely to induce liver enzymes than carbamazepine. Carbamazepine is usually started at an oral dose of 400 to 600 mg daily with dose increases of 200 mg every 3 to 5 days until a clinical effect is achieved or adverse effects become intolerable. Although target serum levels 1511PT206973AJanicak_CME.indd 34 for patients with epilepsy typically range from 4 to 12 µg/mL, clinical response and tolerability should take priority over levels in those with bipolar disorder. Starting doses of oxcarbazepine are generally 300 to 600 mg daily, which can be increased by up to 600 mg per day weekly with a range of 300 to 3000 mg daily. Common adverse effects of carbamazepine include nausea, vomiting, headache, diarrhea, hyponatremia (possibly higher risk with oxcarbazepine), rash, pruritus, fluid retention, and low testosterone in males. More serious effects include Stevens-Johnson syndrome, agranulocytosis, and aplastic anemia, which often present within the first few months of treatment. Carbamazepine can lead to multiple clinically relevant drug interactions, primarily through CYP450 3A4 induction. Pharmacogenetic testing (eg, HLAB*1502, HLA-A*31:01) can prevent carbamazepine-induced hypersensitivity reactions (ie, Stevens-Johnson syndrome) in certain ethnic groups (eg, Han Chinese, Europeans). In the context of pregnancy, carbamazepine is labeled as a category D drug owing to an increased risk of spina bifida, craniofacial defects, cardiovascular malformations, developmental delays, and hypospadias. Women of childbearing age should use adequate contraceptive methods while taking carbamazepine and should receive folic acid. While carbamazepine enters the breast milk as its active metabolite and is detected in the serum of breastfed infants, it is generally thought to be safe. However, mothers are encouraged to discontinue breastfeeding if the neonate begins to experience related adverse events (eg, transient hepatic dysfunction). Oxcarbazepine is a category C drug found to cause adverse effects in animal studies, but with no specific malformations identified in humans. It is also transferred to newborns in small amounts through breast milk. Antipsychotics First-generation antipsychotics preceded the availability of lithium in the US by almost 20 years and were the mainstay of medication treatment for bipolar disorder during this period. Indeed, chlorpromazine still has an FDAapproved indication for this disorder. With the advent of lithium, however, the primary role of antipsychotics was to serve as adjunctive therapy for more severe episodes. With extended experience, lithium was found insufficiently effective and/or poorly tolerated in a substantial proportion of patients with bipolar disorder. This ushered in a series of studies with anticonvulsant agents and second-generation antipsychotics to ascertain their potential as alternative mood stabilizers. Theories on the mechanism of action of secondgeneration antipsychotics focus on their multiple neuroreceptor effects, particularly related to the dopamine and serotonin systems. A series of controlled trials considered olanzapine as either monotherapy or adjunctive therapy for bipolar disorder, particularly for acute mania. The consistently positive results with olanzapine led to studies with other secondgeneration antipsychotics. While the most common adverse effects of antipsychotics include neuromotor, sedative, hormonal, and metabolic complications, they vary substantially among the different agents. For example, haloperidol and risperidone can increase the risk of acute extrapyramidal side effects and hyperprolactinemia, while agents such as olanzapine and quetia­ pine may be more likely to cause sedation, weight gain, and related cardiometabolic effects. Table 4 lists the agents approved by the FDA for acute and maintenance treatment of mania and hypomania; phases of the illness for which antipsychotics have approved indication(s) as either monotherapy or adjunctive therapy; their usual dosing ranges; and other clinically relevant considerations. Conclusion The defining characteristic of bipolar disorder is the presence of mania or hypomania. Bipolar I disorder is primarily distinguished from bipolar II disorder by meeting the criteria for a full manic episode. Conversely, bipolar II disorder must meet criteria for both a hypomanic and a depressed episode. Cyclothymic disorder consists of more chronic mood disturbances that do not meet the full criteria for hypomania, mania, or depression. Treatment approaches depend on the illness phase and symptom severity. Mania, hypomania, and mixed episodes can be managed initially with 1 of 3 strategies: lithium, valproate, or a second-generation antipsychotic either as monotherapy or in various combinations. Short-term use of antipsychotics and/or benzodiazepines may also address associated symptoms (eg, agitation, psychosis, drug or alcohol withdrawal) during an acute exacerbation. Successful maintenance strategies usually require a combination of pharma- 11/2/15 9:52 AM 35 NOVEMBER 2015 PSYCHIATRIC TIMES w w w. psychi atr i cti mes. com CATEGORY 1 cologic and psychotherapeutic approaches customized to meet the needs of a given patient. Serotonin: How Psychiatry Got Over Its “High School Crush” Continued from page 28 References 1. Janicak PG, Marder SR, Pavuluri MN. Principles and Practice of Psychopharmacotherapy. 5th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2011:351-462. 2. Hirschfeld RM, Calabrese JR, Weissman MM, et al. Screening for bipolar disorder in the community. J Clin Psychiatry. 2003;64:53-59. 3. Denicoff KD, Leverich GS, Nolen WA, et al. Validation of the prospective NIMH-Life-Chart Method (NIMHLCM-p) for longitudinal assessment of bipolar illness. Psychol Med. 2000;30:1391-1397. 4. Yatham LN, Kennedy SH, Parikh SV, et al. Canadian Network for Mood and Anxiety Treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) collaborative update of CANMAT guidelines for the management of patients with bipolar disorder: update 2013. Bipolar Disord. 2013;15:1-44. 5. Bergink V, Burgerhout KM, Koorengevel KM, et al. Treatment of psychosis and mania in the postpartum period. Am J Psychiatry. 2015;172:115-123. 6. Jacobowski NL, Heckers S, Bobo WV. Delirious mania: detection, diagnosis, and clinical management in the acute setting. J Psychiat Pract. 2013;19:15-28. 7. Gerhard T, Devanand DP, Huang HM, et al. Lithium treatment and risk for dementia in adults with bipolar disorder: a population-based cohort study. Brit J Psychiatry. 2015;207:46-51. 8. Smith EG, Austin KL, Kim HM, et al. Mortality associated with lithium and valproate treatment of US Veterans Health Administration patients with mental disorders. Brit J Psychiatry. 2015;207:55-63. 9. Li XB, Tang YL, Wang CY, de Leon J. Clozapine for treatment-resistant bipolar disorder: a systematic review. Bipolar Disord. 27 Oct 2014; (Epub ahead of print). 10. Hirschfeld R. Guideline watch: practice guideline for the treatment of patients with bipolar disorder. 2005. http://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/bipolar-watch.pdf. Accessed September 29, 2015. 11. Medda P, Toni C, Giorgi M, et al. Electroconvulsive therapy in 197 patients with a severe, drug-resistant bipolar mixed state: treatment outcome and predictors of response. J Clin Psychiatry. 2015;76:1168-1173. 12. Grunze H, Vieta E, Goodwin GM, et al. The World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the biological treatment of bipolar disorders: update 2009 on the treatment of acute mania. World J Biol Psychiatry. 2009;10:85-116. 13. Kakkar AK, Rehan HS, Unni KE, et al. Comparative efficacy and safety of oxcarbazepine versus divalproex sodium in the treatment of acute mania: a pilot study. Eur Psychiatry. 2009;24:178-182. 14. Geddes JR, Goodwin GM, Rendell J, et al. Lithium plus valproate combination therapy versus monotherapy for relapse prevention in bipolar I disorder (BALANCE): a randomised open-label trial. Lancet. 2010;375:385-395. 15. Dwivedi T, Zhang H. Lithium-induced neuroprotection is associated with epigenetic modification of specific BDNF gene promoter and altered expression of apoptotic-regulatory proteins. Front Neuroscience. 2014;8:457. 16. Hernandez-Diaz S, Smith C, Shen A, et al. Comparative safety of antiepileptic drugs during pregnancy. Neurology. 2012;78:1692-1699. ❒ Post-tests, credit request forms, and activity evaluations must be completed online at www.cmeoutfitters.com/PT (requires free account activation), and participants can print their certificate or statement of credit immediately (80% pass rate required). This Web site supports all browsers except Internet Explorer for Mac. For complete technical requirements and privacy policy, visit www.neurosciencecme.com/technical.asp. CME POST-TEST PLEASE NOTE THAT THE POST-TEST IS AVAILABLE ONLINE ONLY ON THE 20TH OF THE MONTH OF ACTIVITY ISSUE AND FOR A YEAR AFTER. Need Additional CME Credit? Check Out These CME Activities— Hurry, Some Expire Soon! Understanding and Treating Delirium by Alan T. Bates, MD, PhD and Yesne Alici, MD This CME article reviews the pathophysiology and epidemiology of delirium and provides strategies for assessment, prevention, and management of this syndrome; expiration date: December 2015. http://www.psychiatrictimes.com/cme/understanding-and-treating-delirium The Dynamics of Psychosis: Therapeutic Implications by Brian V. Martindale, FRCP, FRCPsych A CME that covers contemporary ideas about psychotic conditions and clinical approaches for treatment; expiration date: January 2016. http://www.psychiatrictimes.com/cme/dynamics-psychosis-therapeutic-implications A Practical Update on Neuroimaging for Psychiatric Disorders by Robin Hurley, MD, FANPA, Shiv Patel, MD, DABR, and Katherine Tauber, PhD, FANPA Which neuroimaging test for which psychiatric patient—and when? What to ask the neuroradiologist? Expiration date: February 2016. http://www.psychiatrictimes.com/cme/practical-update-neuroimaging-psychiatric-disorders 1511PT206973AJanicak_CME.indd 35 nized the complexities of sorting out psychosocial causes from biological effects—which can in turn become new causes or predispositions. They wrote: . . . it is . . . conceivable that early experiences of the infant or child may cause enduring biochemical changes, and that these may predispose some individuals to depressions in adulthood. It is not likely that changes in the metabolism of the biogenic amines [dopamine, norepinephrine, and serotonin] alone will account for the complex phenomena of normal or pathological affect.11 The causal chain in the genesis of major depression is almost certainly long and complex—probably beginning with a genetic predisposition to depression, exacerbated by psychosocial stressors and losses, and worsened by dysfunctional personality traits and poor social supports. And while the “selfdefeating cognitions” posited by cognitive theorists may not be a proximal cause of depression, their presence may deepen or prolong the person’s depression.12 Recently, psychiatrists have also focused on socio-economic, educational, and cultural factors that contribute to the risk, and perhaps the onset, of clinical depression. In their recently released book, The Social Determinants of Mental Health, psychiatrists Michael T. Compton, MD, and Ruth S. Shim, MD,13 cite the following risk factors for depression: racial discrimination, poverty, unemployment, lack of social skills, reduced frustration tolerance and self-regulation, and food insecurity.14 All this is nothing radically new—it’s really an elaboration of the biopsychosocial model that has dominated academic psychiatry since the 1980s. Clearly, this multi-level model bears little resemblance to a simplistic chemical imbalance theory. And it gives the lie to those who claim that psychiatry has become reductionistic, hostile to the role of the “mind,” or void of psychodynamic understanding. On the contrary, this expanded biopsychosocial model opens the possibility for therapeutic interventions at several links in the causal chain. Thus, antidepressants—and perhaps, someday, anti-inflammatory agents—may ameliorate the biological components of depression, while psychotherapy reduces the experiential aspects of the illness, such as pathological guilt and self-loathing. In short, if serotonin was once American psychiatry’s “high school crush,” the field now appears wedded to a more mature model of biological and psychosocial understanding. Dr Pies is Editor in Chief Emeritus of Psychiatric Times and a Professor in the psychiatry departments at SUNY Upstate Medical University in Syracuse, NY and Tufts University School of Medicine in Boston. References 1. LeBano L. Inflammation, mood disorders, and disease model convergence. Psych Congress Network (interview with Dr Roger McIntyre). http://www.psychcongress.com/article/depression-inflammation-connectiondiabetes-and-disease-model-convergence-23649. Accessed September 11, 2015. 2. Pies R. Doctor, is my mood disorder due to a chemical imbalance? Psych Central. http://psychcentral.com/ blog/archives/2011/08/04/doctor-is-my-mood-disorder-due-to-a-chemical-imbalance/. Accessed September 11, 2015. 3. Pies R. Nuances, narratives, and the “chemical imbalance” debate. Psychiatric Times. April 11, 2014. http:// www.psychiatrictimes.com/couch-crisis/nuances-narratives-chemical-imbalance-debate. Accessed September 11, 2015. 4. American Psychiatric Association. Let’s talk facts: what is mental illness? 2005. https://www.cpp. edu/~healthcounseling/Documents/mental-illness-b1.pdf. Accessed September 11, 2015. 5. Understanding Science: How Science Really Works. http://undsci.berkeley.edu/article/howscienceworks_19. Accessed September 11, 2015. 6. Healy D. Serotonin and depression. BMJ. April 21, 2015. http://www.bmj.com/content/350/bmj.h1771. long. Accessed September 11, 2015. 7. Grohol JM. The problem with Google’s health knowledge graphs. Psych Central. http://psychcentral.com/blog/ archives/2015/08/21/the-problem-with-googles-health-knowledge-graphs/. Accessed September 11, 2015. 8. Gong Q, He Y. Depression, neuroimaging and connectomics: a selective overview. Biol Psychiatry. 2015;77:223-235. 9. Borchard T. Is the link between serotonin and depression a myth? Psych Central. http://psychcentral.com/blog/ archives/2015/09/01/is-the-link-between-serotonin-and-depression-a-myth/. Accessed September 11, 2015. 10. Raison CL, Miller AH. Role of inflammation in depression: implications for phenomenology, pathophysiology and treatment. Mod Trends Pharmacopsychiatri. 2013;28:33-48. 11. Schildkraut JJ, Kety SS. Biogenic amines and emotion. Science. 1967;156:21-37. 12. Ellis A, Harper RA. A Guide to Rational Living. Los Angeles: Wilshire Book Co; 1961. 13. Compton MT, Shim RS. The Social Determinants of Mental Health. Washington, DC: American Psychiatric Association Publishing; 2015. 14. Bailey RK. Book Forum. Review of The Social Determinants of Mental Health. Am J Psychiatry. 2015;172:913-914. ❒ 11/2/15 9:52 AM Copyright of Psychiatric Times is the property of UBM Medica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. Journal of Cognitive Psychotherapy: An International Quarterly Volume 21, Number 1 • 2007 Combining Medication Treatment and Cognitive-Behavior Therapy for Bipolar Disorder Monica Ramirez Basco, PhD University of Texas at Arlington Gretchen Ladd, PhD Cook Children's Medical Center Diane S. Myers, PhD David Tyler, MD University of Texas Southwestern Medical Center at Dallas Bipolar disorder (BPD) is a severe, recurrent psychiatric illness characterized by a chronic course of vacillating episodes of major depression and mania that impair functioning across many psychosocial domains (DSM–IV; DSM–IV-TR). Within each type of episode, changes occur in mood, cognitive processing, and regulation of vegetative functioning. Typical mood shifts include sadness (in depression) or euphoria (in mania). Either state can produce irritability, anxiety, and anger. In addition, both the process and the content of cognitive functioning are altered. Typical changes in process include decreased speed of thought in depression and increased speed of thought in mania. Content changes include negativity in depression and in mixed states, and grandiosity or paranoia in manic states. According to the cognitive-behavioral model of BPD (Basco & Rush, 2005), these changes in mood and cognition are accompanied by behavioral changes, typically increases in activity in mania and decreases in activity in depression. These behavioral changes, in turn, generally have a negative impact on the individual’s psychosocial functioning, such as slowed work productivity, neglect of household or family responsibilities, and reduced involvement in social activities, bring negative consequences to patients as well as those in their primary support groups. In mania, risk taking, disorganized behavior, sleep loss, and reduced medication adherence quickly exacerbate symptoms, reduce quality of functioning, and create significant psychosocial problems. BPD is sensitive to stress (Goodwin & Jamison, 1990). As symptoms alter functioning, new stressors are created as a consequence. Added stress exacerbates symptoms, and functioning may decline further. Keywords: cognitive therapy; bipolar; medication; noncompliance P atients suffering from BPD have often been ill for quite some time prior to accurate diagnosis and treatment. Given that many have already married and begun families at the time of symptom onset, it is no surprise that when adequate care is finally offered, the clinician © 2007 Springer Publishing Company 7 8 Therapy for Bipolar Disorder may need to spend as much time on marital and parenting issues as on medically treating the underlying disorder. Indeed, it is probably uncommon for purely medical management to suffice in any patient with newly diagnosed BPD. Early on in the treatment of a patient with BPD, medication management may have to take first priority, because the patient may simply be too ill to benefit from or tolerate psychotherapy. Patients with severe mania, those who cycle very rapidly, those with psychosis, and those with profound depression may require the improvement that comes from beginning a medication regimen and the stabilization and decrease in symptom intensity that usually follows. Once this is achieved, formal psychotherapy can begin. During this early phase, when the severity of symptoms may interfere with psychotherapy, much useful psychotherapeutic work can be done with patients’ families. Education about the disorder as well as support by the management team can help prepare the family for further psychotherapeutic work after the patient is stabilized. There is no absolute rule for when to begin psychotherapy. In general, manic or mixed patients need to be relatively free of intense psychotic symptoms and stable enough to tolerate 15–20 minutes of interaction without becoming agitated or irritable. Early in treatment with a very ill patient, the sessions may be quite brief. Some outpatients can benefit from several brief office visits during a week rather than one hour-long session. Some patients suffering from depression may benefit little from psychotherapy until psychosis and intense psychomotor retardation have improved. An example is Jim, who was referred for treatment in an effort to avoid rehospitalization. Jim had been hospitalized several weeks before and had been released once his suicidal ideation subsided. However, his depression continued to be so severe that it was difficult for him to make conversation or maintain eye contact. He was unable to sustain his energy to participate in full therapy sessions. Therefore, he was provided with brief supportive therapy until his cognitive functioning and energy improved. Those who have been ill for years with many failed trials of medications can present the greatest challenge. All medication trials must be reviewed in as much detail as possible with the patient and loved ones, as some useful medications may have been tried and discarded without sufficient reason. In addition, the long-term use of antidepressants may make it impossible to know if concurrent mood stabilizers were of value. Pharmacotherapy is obviously an essential component of the treatment of BPD. However, its efficacy is often limited by poor patient adherence. Research suggests a 40%–60% risk of nonadherence throughout the course of treatment for patients with BPD (Basco & Rush, 1995). Further, symptom breakthroughs commonly occur even in patients who take their medications as prescribed (Maj, Pirozzi, & Magliano, 1996). Often, symptom recurrence or relapse is foreshadowed by the early emergence of subsyndromal symptoms of depression and mania. If recognized, these early indicators can provide an opportunity for proactive intervention. COGNITIVE-BEHAVIOR THERAPY (CBT) FOR BIPOLAR DISORDER Several studies demonstrate that CBT is an effective complementary treatment to pharmacotherapy in BPD. The cognitive-behavioral formulation of BPD (Basco & Rush, 1996) focuses on an exacerbating cycle in which reactions to cognitive and affective symptoms decrease functioning and create psychosocial problems. Stress related to these psychosocial problems can cause symptoms to worsen. The goal of CBT in this context is to target cognitive, behavioral, and affective changes in depression and mania, and to help the patient effectively manage BPD by stopping the progression of episodes. One target of CBT in treating BPD is psychoeducation about the disorder, the pharmacological treatments, and the ways in which environmental factors and the patient’s behaviors and cognition affect the course of the illness. The second component of CBT is to help patients to develop an early warning system that allows them to anticipate the onset of depression or mania Ramirez Basco et al. 9 and to respond accordingly. The third element involves improving and maintaining adherence to pharmacological treatments, psychosocial interventions, and lifestyle modifications critical to managing the illness. These include stimulation reduction and good sleep hygiene. After progress has been made in expanding the patient’s knowledge about BPD, improving the patient’s ability to self-monitor symptoms, and increasing the patient’s adherence to prescribed treatment, the fourth piece of the intervention, cognitive and behavioral management of symptoms, can be conducted more effectively. The final goal of CBT is to teach patients methods for resolving and preventing common psychosocial problems associated with the disorder, including relationship-, financial-, and work-related difficulties (Basco, 2006; Basco & Rush, 2005). Several preliminary studies have demonstrated the feasibility and usefulness of CBT in treating BPD. However, most have studied CBT as an add-on to pharmacotherapy versus pharmacotherapy alone and, therefore, have generally not controlled adequately for attention and other nonspecific effects of psychotherapy. While the conclusions may seem promising, no definitive statements can be made about the efficacy of CBT in BPD. One of the first studies of CBT in BPD was conducted by Cochran (1984). She tested the effectiveness of six weeks of CBT plus pharmacotherapy against pharmacotherapy alone, by targeting attitudes that interfered with medication compliance during the maintenance phase of treatment. Outcome assessments, which consisted of a composite assessment of medication compliance, appointment attendance, and serum lithium levels, showed that the CBT plus pharmacotherapy group had better composite adherence scores than the control group, and the effect was still evident at 6 months post-treatment. The CBT plus pharmacotherapy group was less likely to terminate treatment against medical advice and had fewer hospitalizations and noncomplianceprecipitated affective episodes as compared to the control condition. The short-term nature of CBT interventions makes them attractive for treating patients in acute episodes and there is some evidence that the intervention can be delivered in a cost-effective group format. Patelis-Siotis et al. (2001) evaluated the efficacy of group CBT aimed at improving psychosocial functioning in patients with BPD. Forty-nine patients were placed in groups of 7–12 and given fourteen 2-hour sessions of group CBT. At baseline, patients were mildly depressed or euthymic and there was no significant change in symptoms from pre- to post-treatment. Study completers did, however, show significant improvements in psychosocial functioning. Though there was no control group in this study and patients were relatively asymptomatic, the results suggest that group CBT interventions may be beneficial for improving quality of life for bipolar patients and for maintaining stability in symptoms. Scott, Garland, and Moorhead (2001) tested a relapse-prevention-focused intervention with patients who were randomly assigned to CBT plus pharmacotherapy (n = 21) or medication alone (n = 21). Sixty percent of participants had comorbid personality disorders and several had a strong history of medication noncompliance, although all were actively treatment with pharmacotherapy at study enrollment. Relative to the control group, the therapy plus medication group showed significantly fewer symptoms and improved social functioning after 6 months of CBT. The control subjects were provided CBT after completion of a 6-month observation period to assess within-person changes. This group showed similar improvement in symptoms and functioning from pre- to post-CBT and had significantly fewer hospitalizations at 12 months post-treatment relative to their 6-month wait-list period prior to initiating CBT. Scott and colleagues (2006) were unable to replicate these positive results. Across five treatment sites, 253 patients with BPD were randomized to receive either 22 sessions of medication treatment as usual (TAU; n = 126) or CBT plus TAU (n = 127). TAU varied across the five sites, with some providing additional clinician contact time. Patients with more severe psychopathology, such as those with acute mania, borderline personality disorder, or rapid cycling BPD, and those current abusing illicit drugs were excluded from the sample. Some patients were not receiving medication treatment at the time of the trial. Contrary to their previous studies (e.g., Scott & Tacchi, 2002; Scott 10 Therapy for Bipolar Disorder et al., 2001), Scott and colleagues (2006) found no between-group differences in recurrence rate, level of medication adherence, or symptom control over the 18 months of follow-up. A post hoc analysis showed that patients in the CBT plus pharmacotherapy group with fewer than 12 lifetime episodes of illness had a longer time to first recurrence than those with more than 12 episodes. Given that the interepisode length often shortens with the duration of the illness (Goodwin & Jamison, 1990), their finding might reflect the greater chronicity and cyclicity of BPD over time. Still, this larger scale study calls into question the effect size of CBT interventions for BPD when added to pharmacotherapy. Lam et al. (2001) evaluated a 12–20 session adjunctive CBT intervention utilizing symptom management skills (n = 13) against standard outpatient medication treatment alone (n = 12) for patients in the maintenance phase of treatment. Relative to the control group, at post-treatment and 6-month follow-up, patients receiving CBT with their medication treatment had fewer bipolar episodes and better coping skills for prodromal symptoms, and were more adherent to pharmacotherapy. Lam et al. (2003) examined the effect of CBT on relapse prevention in patients reporting noncompliance with pharmacotherapy. Over a 12-month period, 103 participants were randomly assigned to medication management alone or to medication management with adjunctive CBT. Those in the CBT with medication group received 14 sessions during the first 6 months and 2 booster sessions in the second 6 months. They found that the CBT with medication group had significantly fewer bipolar episodes, fewer days in an episode, and fewer hospital admissions. Patients who received CBT along with medication also reported higher social functioning, fewer mood symptoms, and less fluctuation in manic symptoms. Lam et al. concluded that CBT is a useful treatment in preventing relapse in conjunction with mood stabilizers. At 18 months following completion of treatment, Lam, Hayward, Watkins, Wright, and Sham (2005a) found that that patients treated with CBT had fewer days in bipolar episodes relative to the control group and had better ratings of mood and better psychosocial functioning, and demonstrated better management of prodromal symptoms. However, there was no difference in relapse rates between groups at the 18-month follow-up. The cost-effectiveness of this intervention was also evaluated (Lam, Wright, & Kerr, 2005b). Relative to the control group, those receiving CBT in addition to medication had better clinical outcomes, but incurred similar treatment costs. Taking into consideration the value of symptom-free days, which allow for greater productivity, their analyses showed that CBT was a costeffective adjunctive intervention, particularly when the costs of CBT could be lessened. The presence of residual symptoms following an affective episode may increase the likelihood of relapse (Fava, 1999). Fava, Bartolucci, Rafanelli, and Mangelli (2001) conducted an uncontrolled study of the long-term efficacy of CBT aimed at reducing residual symptoms in 15 medicationcompliant patients with BPD who had relapsed while on lithium prophylaxis. Patients were treated in the acute phase with antidepressants or antipsychotics, which were tapered off as CBT began. Ten 30-minute CBT sessions were provided after symptom stabilization. A follow-up evaluation indicated a significant decrease in residual symptoms and a significant increase in the number of months before relapse following CBT, as compared to baseline levels. While all 15 patients had relapsed within 30 months of the initial lithium therapy and prior to beginning any psychosocial interventions, only 5 of these patients relapsed within 30 months after CBT was initiated. Without a control condition it is difficult to determine if the positive effect was due to CBT specifically or the nonspecific effects of psychotherapy, including attention and monitoring of symptoms. In a randomized controlled trial of 6 months of CBT plus treatment as usual with mood stabilizers versus medication alone in 52 individuals with BPD, Ball, Mitchell, Corry, Skillecorn, and Malhi (2006) found that CBT participants had significantly less severe depression and mania scores, improved attitudes, better self-control, better treatment adherence, and a lower relapse rate. A longer time before depressive relapse approached significance. The effect was strongest in the first 12 months of the intervention. However, the two groups had similar outcomes at 18 months. Their findings suggest that continuation and/or maintenance treatment may be needed to secure a more lasting effect. Ramirez Basco et al. 11 Bernhard et al. (2006) tested a cognitive-psychoeducational program for individuals with BPD and their family members. Sixty-two patients received fourteen 90-minute biweekly sessions, while their relatives (N = 49) participated in two 4-hour workshops, and both interventions focused on increasing the knowledge of BPD and its treatment. Although no control group was utilized, between-subject comparisons from pre- to post-treatment showed improvements in patients’ and relatives’ knowledge. Both groups rated the intervention as satisfactory. There was no change in subjective burden or expressed emotion at post-treatment. However, at the 12-month follow-up, relatives reported less of a burden and improvements in expressed emotion. In summary, research on CBT for BPD suggests that CBT can be beneficial in increasing medication adherence, in managing symptoms, in improving psychosocial functioning, and perhaps in reducing the risk of relapse when used in conjunction with pharmacotherapy. Unfortunately, studies to date have not controlled for attention and other nonspecific effects of psychotherapy. In addition, they have been limited by small sample sizes and stringent inclusion/exclusion criteria, as is common in psychotherapy development efforts. Patients with comorbid disorders and those with rapid cycling or mixed states were excluded in many studies thereby calling into question the generalizability of the findings. Nonetheless, these studies demonstrate the feasibility of CBT as an adjunct to medication treatment in patients with BPD. Whether CBT is delivered in an individual or a group format, it has the potential to complement and enhance the effectiveness of the pharmacological management of the disorder. CHALLENGES OF INITIATING TREATMENT FOR BIPOLAR DISORDER There are many challenges that face people who have BPD, beginning at the time of diagnosis and the initiation of medical treatment. Being unfamiliar with the symptoms of BPD, the experiences of mania and depression, especially in the presence of psychotic symptoms, can be overwhelming, confusing, and frightening. Depending on their knowledge and level of sophistication as well as the manner in which they came to the attention of clinicians, patients may be ready to understand and accept the diagnosis or may reject it outright. Psychotherapy can be particularly useful at this juncture in helping people to make sense of their experience, to understand the nature of their illness, and to cope with the distress associated with the treatment experience, often a first hospitalization, as well as the assignment of a diagnostic label such as BPD. To facilitate the initiation of pharmacotherapy, education about the illness and its treatment should be provided and reviewed periodically (Basco, 2006; Basco & Rush, 2005). Particularly useful is information about how a diagnosis was derived, what the treatment entails, and what the individual will need to do to engage in the treatment process. While generic information about BPD is useful, identification of the specific symptoms of depression or mania experienced by the patient may be more informative. The symptom summary worksheet method proposed by Basco and Rush (1996, 2005) can help patients to identify their specific symptoms of depression and mania and to contrast those symptoms with their normal or usual state. This exercise can also aid in the early detection of future episodes, if the patient and his or her family members or friends are vigilant in watching for changes from usual habits to symptomatic behaviors. Mood graphs can also be useful in sensitizing patients to fluctuations in affect and can help in monitoring the effects of pharmacotherapy. Generally, the initiation of medication treatment for BPD requires adjustments in the type, amount, and number of medications. Mood graphs can help patients and physicians track the effects of medication as these changes are made. Rather than relying on patients’ retrospective reports, mood graphs can more accurately reflect subjective experiences of symptom improvement or worsening that occur as the medication regimen changes. 12 Therapy for Bipolar Disorder Another challenge that can be addressed in psychotherapy is the emotional adjustment required to accept a diagnosis of BPD. In addition to realizing that he or she has a stigmatizing mental illness, the person may become aware that his or her life will not turn out as planned; that is, that lifelong medication will be needed to achieve mood stability. Loss of emotional and mental normalcy is as difficult a concept to accept as having a chronic physical illness. While the psychopharmacologist takes on the challenge of symptom stabilization, support from others who have been down this path, as in therapy or support groups, can facilitate acceptance of the illness and its treatment. Individual therapy can provide the extra time needed to process the emotions stimulated by the illness as well as the diagnostic and treatment experiences. CASE STUDY Albert is a 24-year-old, newly married, Caucasian male, who was brought to the attention of mental health professionals when he recently experienced an episode of mania. He had always been a very creative and outgoing person, the life of the party, and seemed to have more energy than his wife and his peers. His usual gregarious nature took a different turn after he started a new job at a city newspaper’s photojournalism desk. He began working the evening shift, covering accidents, fires, and burglaries. This was a significant change from his prior work taking photos of civic activities and other more mundane events. His new job was exciting and a bit overstimulating, making it hard for Albert to fall asleep at night. He would go to bed at midnight with his wife, but after tossing and turning for several hours, he would make his way to the living room to watch television, play video games, or listen to music until he could fall asleep. He tried to wake up early in the morning to spend time with his wife before she went off to work. Eventually, the sleep loss got the best of him and he became edgy, irritable, and unable to function well at work. People at work noticed his change in demeanor and suspected that he was using drugs. When his wife confronted him with this, Albert exploded at her and then drove off in his car. He was stopped by police some time later when he was found trying to get into the locked executive parking lot at the newspaper office. Uncertain if he was mentally ill or intoxicated, the police took him to a local emergency room and he was admitted to the psychiatric ward and diagnosed with mania. After a few days on the ward and the initiation of medication treatment, his mania lessened and he was able to sleep. His wife met with the attending psychiatrist, who explained the diagnosis and treatment. Albert had been told about his diagnosis of BPD, but he did not fully understand what it meant at the time. He was discharged and referred for follow-up medication treatment and for psychotherapy to learn more about the management of his illness. Albert was skeptical about the whole experience. He did not remember being manic and could only vaguely recall the events leading up to his admission to the hospital. He thought that it was all a big mistake and that he had been wronged by the police and the hospital. He did not like the medication he had been prescribed and didn’t want to keep taking it. He only agreed to see the therapist to please his wife. She also wanted to believe that nothing was wrong, but she had observed a change in Albert that did not make sense and she needed to know if it would happen again. Albert’s wife accompanied him to the first individual psychotherapy session. They discussed the nature of BPD and although Albert was not ready to accept it, he did acknowledge that something had happened to him that needed an explanation. He agreed to attend three additional sessions for the purpose of “getting to the truth” about what happened. During the course of these sessions, Albert was able to recall more and more Ramirez Basco et al. 13 about the changes he had experienced before going to the hospital. A review of Albert’s experiences with manic-like symptoms proved informative. The more he talked about his past, the more he was able to recall definite “up” periods, when he was more productive than usual, didn’t sleep as much, and had a lot of energy. The therapist’s process was to encourage the exploration of experiences with depression and mania without forcing the issue that BPD was the appropriate diagnosis. She asked the couple to think of alternative explanations for Albert’s experiences and asked them to consider how they might be able to tell the difference between normal ups and downs and BPD. Each alternative explanation was discussed and rejected by Albert until, by process of elimination, BPD became the working hypothesis to explain his symptoms. They all agreed that the true test of the diagnosis would be time. BPD tended to recur and if Albert had the illness, he would likely have another episode of depression or mania at some point in time. This prospect frightened Albert and his wife, but also motivated them to learn more about the illness and prepare for its possible return. The second part of therapy involved discussion of common precipitants of mania and depression, such as sleep loss and overstimulation, and precautions that could be taken to avoid them. To be successful in his job, Albert would have to be available to go after the big stories, even if they happened at night. He hated the idea of taking medication, but he was unwilling to go through another manic episode caused by sleep loss. So he agreed to take medication to help him fall asleep at night so that he would not run that risk. In addition, the therapist taught Albert some techniques for slowing his thoughts at night and relaxing his body so that he could more easily fall asleep. The final part of Albert’s therapy was to identify his specific signs and symptoms of depression and mania so that he and his wife would be able to see a recurrence as it developed. The symptom summary worksheet that lists the person’s unique changes in thoughts, actions, physical symptoms, and emotions that come with depression and mania was completed and a copy provided for Albert, his wife, the therapist, and Albert’s psychiatrist. If Albert or his wife noted any changes in his demeanor or habits, they were to review the list and call the doctor or therapist if more than one or two symptoms were emerging. When and if that occurred, Albert could be taught methods for containing his symptoms and reducing the risk of a complete relapse. Throughout this process and with his written consent, Albert’s therapist and psychiatrist discussed his progress. The therapist was able to relay information about Albert that helped the psychiatrist to confirm his diagnosis. In turn, the psychiatrist explained the medication treatment plan so that the therapist could help Albert maximize his adherence to treatment. Albert, his wife, the psychiatrist, and the therapist maintained open communication so they could function efficiently as a treatment team. MAINTENANCE PHASE TREATMENT Maintenance treatment of BPD often includes psychosocial interventions, such as group therapy or individual psychotherapy in combination with continued pharmacotherapy. Although most studies have examined interventions delivered during individual therapy, there have been some that support the efficacy of group-based interventions. One such model is used at the University of Texas Southwestern Medical Center at Dallas where psychiatrists and therapists (e.g., psychologists or social workers) function as cofacilitators in group psychotherapy. The aims of this treatment modality are to increase self-management skills, decrease episode frequency and severity, and improve overall quality of life while addressing medication issues, such as side effects and waning adherence. 14 Therapy for Bipolar Disorder The selection of individuals appropriate for group treatment is based upon joint assessment by the psychiatrist and therapist. Candidates for group therapy should have relative mood stability and not have active substance abuse or psychotic symptoms. Often a period of brief individual psychotherapy may precede inclusion in a group, to ensure a basic understanding of the illness and assess readiness for the group. The collaborative nature of the group allows the clinicians to model problem solving and open communication, providing a safe place to discuss functional, occupational, interpersonal, and psychosocial issues. Emphasizing enhanced symptom awareness and recognition; the role of lifestyle, stress, and illness management; and practical problem solving, communication, and anger management strategies, group members work together to identify environmental triggers, encourage self-monitoring of symptoms, and enhance awareness of personal illness patterns. Group maintenance psychotherapies for BPD, such as those evaluated by Cochran (1984) and Patelis-Siotis et al. (2001), can be also be facilitated solely by social workers, nurses, or other mental health professionals in a psychiatric clinic. In another treatment model, case managers in community mental health centers serve as communication links between patients, psychiatrists, and rehabilitation program staff. The multidisciplinary team approach developed by Mark Bauer and Linda McBride (2003), which utilizes a nurse case manager, is another model for supplementing pharmacotherapy with an adjunctive intervention aimed at improving compliance and early symptom detection, which leads to earlier medical intervention to prevent relapse. CONCLUSION Pharmacotherapy is the mainstay of treatment for BPD. However, the addition of psychotherapy in an individual or group format can enhance treatment adherence, teach coping skills, improve symptom detection early in the course of new episodes, and provide the education and support needed to ease adjustment to the illness and its treatment. Several studies have provided support for the efficacy of a multidisciplinary team approach to the treatment of this disorder. However, there is a need for randomized trials that control for the nonspecific effects of psychotherapy in a consistent manner. Clinically, an argument can be made for the combination of pharmacotherapy and psychotherapy in BPD to maximize the effectiveness of treatment. Therapists can facilitate communication between patient and physicians, reinforce the physician’s instructions, and troubleshoot adherence problems. Therapists can also help in the detection of relapse, as they may be able to see patients with greater frequency than the psychiatrist and can reinforce their relapse prevention plans. Also, when psychiatrists are trained in CBT they can provide psychotherapy along with medication as an integrated method of treatment. Therapeutic innovations in psychotherapy and psychopharmacology continue to evolve and refinements continue to be made. Clinicians no longer have to feel helpless in the face of this complicated and persistent mental illness. Most importantly, people with this illness are getting the message that they can be active participants in their care. REFERENCES American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text revision). Washington, DC: Author. Ramirez Basco et al. 15 Ball, J. R., Mitchell, P. B., Corry, J. C., Skillecorn, A., & Malhi, G. S. (2006). A randomized controlled trial of cognitive therapy for bipolar disorder: Focus on long-term change. Journal of Clinical Psychiatry, 67, 277–286. Ball, J., Mitchell, P., Malhi, G., Skillecorn, A., & Smith, M. (2003). Schema-focused cognitive therapy for bipolar disorder: Reducing vulnerability to relapse through attitudinal change. Australian and New Zealand Journal of Psychiatry, 37, 41–48. Basco, M. R. (2006). The Bipolar workbook: Tools for controlling your mood swings. New York: Guilford. Basco, M. R., & Rush, A. J. (1995). Compliance with pharmacotherapy in mood disorders. Psychiatric Annals, 25, 269–279. Basco, M. R., & Rush, A. J. (1996). Cognitive behavioral therapy for bipolar disorder. New York: Guilford. Basco, M. R., & Rush, A. J. (2005). Cognitive-behavioral therapy for bipolar disorder (2nd ed.). New York: Guilford. Bauer, M. S., & McBride, L. (2003). Structured group therapy for bipolar disorder: The life goals program. New York: Springer. Bernhard, B., Schaub, A., Kummler, P., Dittmann, S., Severus, E., Seemuller, F., et al. (2006). Impact of cognitive-psychoeducational interventions in bipolar patients and their relatives. European Psychiatry, 21, 81–86. Cochran, S. D. (1984). Preventing medical noncompliance in the outpatient treatment of bipolar affective disorders. Journal of Consulting and Clinical Psychology, 52, 873–878. Fava, G. A. (1999). Subclinical symptoms in mood disorders. Psychological Medicine, 29, 47–61. Fava, G. A., Bartolucci, G., Rafanelli, C., & Mangelli, L. (2001). Cognitive-behavioral management of patients with bipolar disorder who relapsed while on lithium prophylaxis. Journal of Clinical Psychiatry, 62, 556–559. Goodwin, R. K., & Jamison, K. R. (1990). Manic-depressive illness. New York: Oxford University Press. Lam, D. H., Bright, J., Jones, S., Hayward, P., Schuck, N., Chisholm, D., et al. (2001). Cognitive therapy for bipolar illness—A pilot study of relapse prevention. Cognitive Therapy and Research, 24, 503–520. Lam, D. H., Hayward, P., Watkins, E. R., Bright, K., & Sham, P. (2005a). Relapse prevention in patients with bipolar disorder: Cognitive therapy outcome after two years. American Journal of Psychiatry, 162, 324–329. Lam, D. H., Watkins, E. R., Hayward, P., Bright, J., Wright, K., Kerr, N., et al. (2003). A randomized controlled study of cognitive therapy for relapse prevention for bipolar affective disorder: Outcome of the first year. Archives of General Psychiatry, 60, 145–152. Lam, D. H., Wright, K., & Kerr, N. (2005b). Cost-effectiveness of relapse-prevention cognitive therapy for bipolar disorder: 30-month study. British Journal of Psychiatry, 186, 500–506. Maj, M., Pirozzi, R., & Magliano, L. (1996). Late non-response to lithium prophylaxis in bipolar patients: Prevalence and predictors. Journal of Affective Disorders, 39, 39–42. Patelis-Siotis, I., Young, T., Robb, J. C., Marriott, M., Bieling, P. J., Cox, L. C., et al. (2001). Group cognitive behavioral therapy for bipolar disorder: A feasibility and effectiveness study. Journal of Affective Disorders, 65, 145–153. Scott, J., Garland, A., & Moorhead, S. (2001). A pilot study of cognitive therapy in bipolar disorders. Psychological Medicine, 31, 459–467. Scott, J., Paykel, E., Morriss, R., Bentall, R., Kinderman, P., Johnson, T., et al. (2006). Cognitive-behavioural therapy for severe and recurrent bipolar disorders. British Journal of Psychiatry, 188, 313–320. Scott, J., & Tacchi, M. J. (2002). A pilot study of concordance therapy for individuals with bipolar disorders who are non-adherent with lithium prophylaxis. Bipolar Disorders, 4, 386–392. Correspondence regarding this article should be directed to Monica Ramirez Basco, PhD, 4104 Ambleside Ct., Colleyville, TX 76034. E-mail: MABasco@Comcast.net Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Psychiatry and Clinical Neurosciences 2014; 68: 712–720 doi:10.1111/pcn.12193 Regular Article Diagnostic utility of worry and rumination: A comparison between generalized anxiety disorder and major depressive disorder Min-Jeong Yang, MA,1† Bin-Na Kim, MA,1† Eun-Ho Lee, MA,2 Dongsoo Lee, Bum-Hee Yu, MD, PhD,1 Hong Jin Jeon, MD, PhD2 and Ji-Hae Kim, PhD1* MD, PhD,1 1 Department of Psychiatry, and 2Depression Center, Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea Aim: Although previous reports have addressed worry and rumination as prominent cognitive processes in generalized anxiety disorder (GAD) and major depressive disorder (MDD) and their distinct correlation with anxious and depressive symptoms, the differential association of worry and rumination with the diagnosis of GAD and MDD remains unclear. The purpose of this study was to investigate the distinct features of worry and rumination in factor structure and their predictive validity for the diagnosis of GAD and MDD. Methods: Four hundred and sixty-eight patients with GAD (n = 148) and MDD (n = 320) were enrolled and the diagnoses were confirmed with the Structured Clinical Interview for DSM-IV. Participants completed the Penn State Worry Questionnaire and Ruminative Response Scale and the severity of anxiety and depressive symptoms was assessed via clinician ratings. HE NOSOLOGIC RELATIONSHIP between generalized anxiety disorder (GAD) and major depressive disorder (MDD) has been a controversial topic, due to high rates of comorbidity and overlapping diagnostic criteria in the DSM-IV.1,2 In an extensive review, Hettema showed that overall lifetime T *Correspondence: Ji-Hae Kim, PhD, Department of Psychiatry, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul 135-710, South Korea. Email: jihae0931.kim@samsung.com † Both authors contributed equally to this article. Received 3 September 2012; revised 10 January 2014; accepted 11 April 2014. 712 Results: In joint factor analysis using the Penn State Worry Questionnaire and Ruminative Response Scale items, worry and rumination emerged as distinct factors. In logistic regression analyses, worry contributed to a higher probability of the diagnosis of GAD than rumination, as rumination did in MDD than worry. Conclusion: This is the first comprehensive study investigating the diagnostic utility of worry and rumination in a well-defined clinical sample of both GAD and MDD. Our results suggest that worry and rumination are distinct cognitive processes and play a differential role in the diagnosis of GAD and MDD, distinguishing them at the cognitive level. Key words: anxiety disorders, cognition, depressive disorder, depressive symptoms, differential diagnosis. comorbidities have been reported to be as high as 70–90% and that GAD has substantial overlap with MDD in the areas of genetics, childhood environment, demographics, and personality traits as well as shared pharmacologic efficacy of antidepressants.3 Despite high comorbidity and similarities between GAD and MDD, some evidence of differences and disorder-specific pathological processes has been reported.3,4 Among them, worry has been considered to be a key cognitive process that characterizes GAD, whereas rumination has traditionally been related to depression.5,6 Worry is defined as ‘a chain of thoughts and images, negatively affect-laden and relatively uncontrollable’7 and excessive and uncontrollable © 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology Psychiatry and Clinical Neurosciences 2014; 68: 712–720 Worry and rumination 713 worry is the cardinal diagnostic feature of DSM-IV GAD. Studies have pointed out that worry contributes to the maintenance and aggravation of anxiety by interfering with emotional processing.8 On the other hand, rumination is defined as ‘repetitively focusing one’s attention on one’s depressive symptoms and on the implications of these symptoms’ and has been found to be a salient cognitive feature of dysphoria, including MDD. Many studies have provided empirical support for the hypothesis that rumination prolongs and worsens depressed mood and predicts future depressive episodes.9 However, worry and rumination, although differing in degree, are prevalent in other disorders as well.10 Furthermore, due to apparent commonalities (e.g., repetitive thoughts in response to negative affect, maintenance or prolongation of pre-existing negative affect), the assertion of a distinctive role of the two constructs has been challenged. Accordingly, recent studies started to investigate the similarities and differences between worry and rumination and their relationship with anxious and depressive symptoms more systematically. Using structural equation modeling, Segerstrom et al.11 found that both worry and rumination loaded onto a latent variable labeled as ‘repetitive thought’ and specific factors of worry and rumination failed to differentially relate to anxiety and depression. Fresco et al.12 reported that worry and rumination are distinct factors in joint factor analysis; however, when their relations to symptoms were examined, both worry and rumination showed an undifferentiated pattern of strong associations with both anxiety and depression, consistent with the study by Segerstrom et al. On the other hand, other joint factor analysis studies controlling for the overlap between worry and rumination in analysis, demonstrated that worry and/or rumination have a differential association with anxiety and depression.13,14 In summary, results from previous studies converged on the conclusion that both worry and rumination are fairly similar, albeit not identical, cognitive processes, that impact anxiety and depression symptoms. However, methodological limitations prevent greater generalizability of previous findings to a clinical population. Most involved non-clinical student samples12–14 and in a study including a small clinical sample, the selection depended not on the structured clinical interview but on the self-referral problem.11 Also, whether worry and rumination are differentially related to the diagnosis of GAD and MDD has not been addressed and thus remains unclear, as previous studies focused only on symptom level in non-clinical samples. To date, no study examined whether two constructs can have differential value in diagnosis in a large patient sample diagnosed via formal structured diagnostic interview. As previous investigations recruited chiefly US or European participants, whether those results can be generalized to a Korean sample is another question that needs to be explored. Prevalence rates of MDD and GAD in East Asian countries, including South Korea, are reported to be lower than those in the West.15–17 Although explanations for such difference are relatively scant owing to the lack of enough crosscultural studies, different symptom phenomenology might be a factor. Koreans with MDD expressed more symptoms of ‘low energy’, ‘concentration difficulty’ or somatic symptoms and less symptoms of ‘depressed mood’.15 Nevertheless, this does not mean that the DSM criteria are invalid. The DSM MDD in Korea showed good internal consistency and discrimination, but showed a higher diagnostic threshold and different symptom presentations.15 With regard to GAD, even though the number and content of worry domains were reported to vary crossculturally, cross-cultural similarities in the Penn State Worry Questionnaire (PSWQ) scores indicate equivalent total level of worry across ethnic groups.16 In the present study, we used the DSM-IV criteria for diagnosis and PSWQ and Ruminative Response Scale (RRS) to assess worry and rumination, all of which are widely utilized measures worldwide and translated and validated in Korean. This study aims to replicate and integrate the current findings and to test the diagnostic utility of worry and rumination in well-defined GAD and MDD patient groups in South Korea. Specifically, we tested the following hypotheses. First, worry and rumination would load onto different latent variables in joint factor analysis, despite a significant correlation. Second, in logistic regression, worry would contribute to a higher probability of the diagnosis of GAD than rumination, while rumination would increase the probability of the diagnosis of MDD than worry. METHODS Participants Four hundred and sixty-eight Korean participants were enrolled at Samsung Medical Center (SMC) © 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology 714 M-J. Yang et al. Psychiatry and Clinical Neurosciences 2014; 68: 712–720 Table 1. Demographic variables in GAD and MDD (n = 468) Total sample Age (mean, SD) Sex Men Women Education Less than elementary school Less than high school Less than graduate school Socioeconomic status Low Below average Average Above average High Missing 49 (15.80) GAD (n = 148) 45.53 (15.15) MDD (n = 320) 50.60 (15.85) χ2 3.26 P † 0.001 162 (34.6%) 306 (65.4%) 55 (37.2%) 93 (62.8%) 107 (33.4%) 213 (66.6%) 1.05 0.592 76 (16.2%) 203 (43.4%) 189 (40.4%) 21 (14.2%) 72 (48.6%) 55 (37.2%) 55 (17.2%) 131 (40.9%) 134 (41.9%) 2.50 0.286 28 (6.0%) 64 (13.7%) 272 (58.1%) 73 (15.6%) 14 (3.0%) 17 (3.6%) 7 (4.7%) 21 (14.2%) 86 (58.1%) 27 (18.2%) 6 (4.1%) 1 (0.7%) 21 (6.6%) 43 (13.4%) 186 (58.1%) 46 (14.4%) 8 (2.5%) 16 (5.0%) 7.61 0.179 † Statistics for ANOVA. GAD, generalized anxiety disorder; MDD; major depressive disorder. between April 2006 and July 2011. The participants gave written informed consent before participating in the study, which was approved by the Institutional Review Board of SMC. With regard to the ethnicity, although different symptom presentation and relatively lower prevalence were reported in a Korean sample with either MDD or GAD, DSM MDD criteria and the core feature of GAD, which is worry, have been found to be reliable in a Korean sample.15,16 All participants, therefore, were diagnosed using the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I)18 carried out by a trained clinical psychologist. The primary inclusion criteria were the diagnoses of GAD and MDD. The inclusion criteria for MDD were patients with both single and recurrent episodes, while MDD patients with psychotic features or in full remission, and with comorbid anxiety disorders were excluded. In case of GAD, we decided to include GAD patients with comorbid MDD in order to increase the statistical power of the study, as excluding them would result in a much smaller sample size due to the high comorbidity of GAD and MDD. In order to control the severity of symptoms, we excluded the individuals with Hamilton Anxiety Rating Scale (HAM-A) score of less than 14 in the GAD group and the individuals with Hamilton Depression Scale (HAM-D) score of less than 17 in the MDD group.19,20 Of the enrolled 468 participants, 148 patients fulfilled the DSM-IV criteria for GAD, and 320 patients fulfilled the DSM-IV criteria for MDD. While there were no significant differences in sex, education level, and socioeconomic status, age was significantly different between the groups (Table 1). In logistic regression, we restricted the scope of analysis to the sample of GAD without MDD (n = 93) in order to make a clear comparison, while the MDD group (n = 320) was still composed of patients only diagnosed with MDD. This means that we excluded GAD patients with comorbid MDD from the GAD group, because these patients with both the diagnoses would confound the differential role of worry and rumination in binary prediction of GAD versus MDD and vice versa. Measures PSWQ The PSWQ is a 16-item self-report scale that assesses the generality, excessiveness, and uncontrollability of pathological worry.21 Items are rated on a five-point Likert scale and high score (range from 15 to 80) means a more frequent tendency to worry. Lim et al.22 validated the Korean version (Cronbach’s α = 0.92). The total PSWQ score is a sum of the scores of positively worded and reversed scores of negatively worded items. © 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology Psychiatry and Clinical Neurosciences 2014; 68: 712–720 Worry and rumination 715 ware.29 Statistical significance was defined at the 0.05 level, two-tailed. First of all, we performed the joint exploratory factor analysis using items from both the PSWQ and RRS. Maximum likelihood extraction with Quartimax rotation was chosen to allow for the anticipated correlation between factors. We adapted Thurstone’s criteria30 to define a well-loaded item, and the cleanest factor structure was determined if a factor included more than three items. The number of factors was determined by the Eigenvalues greater than 1.0, scree plot and interpretability of the factor.31 Afterwards, logistic regression analysis was conducted to identify the constructs prognostic of the diagnosis of GAD versus MDD and MDD versus GAD. Total PSWQ and RRS scores were entered simultaneously into an enter model and odds ratios (OR) were adjusted for HAM-A and HAM-D scores. RRS The RRS is a 22-item scale, a subscale of the original Response Style Questionnaire.23 Each item is rated on a four-point Likert scale with higher total score (range from 22 to 88) indicating more prominent rumination response style. Kim et al.24 showed good internal consistency, test–retest reliability (Cronbach’s α = 0.89 and 0.59, respectively) of the Korean version. HAM-A The HAM-A is a 14-item clinician rating scale, designed to measure the severity of anxiety symptoms.25 Items are rated on a four-point Likert scale and the total score ranges from 0 (remission) to 56 (moderate–severe). The psychometric properties of the Korean version have been demonstrated by...
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Case Study: Jack
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✓ Issues and challenges in diagnosing an individual with persistent depressive disorder or
cyclothymic disorder.
o Similar mania and depressive episode.
o Similar symptoms
✓ Case study: Jack
o Summary of the diagnosis based on DSM 5
o Analysis of his mental conditions from most dominant to least dominant.


CASE STUDY: JACK

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Case Study: Jack
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CASE STUDY: JACK

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Q.1
Persistent depressive disorder or cyclothymic disorders are both mood disorders that are
challenging to diagnose. Dysthymia and cyclothymia involve some symptoms of major depressive
disorder or manic depression (Dziegielewski, 2014). Therefore, it is possible to mistake these two
conditions for bipolar disorder and major depressive disorder because the symptoms cycle between
depression and mania. Howeve...

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New York University

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