clinicians on the front line:active management of …€¦ · depression is a highly prevalent yet...

CLINICIANS ON THE FRONT LINE: ACTIVE MANAGEMENT OF

Depression and AnxietyIN PRIMARY CARE

Sponsored by Boston University School of Medicine Produced by Haymarket Medical

A SUPPLEMENT TO CORTLANDT FORUM JULY 2006

For additional information regarding an innovative

CME post-activity with 20 free CME credits,

See Back Cover

A CME/CE Activity

Release date: July 2006. Expiration date: July 31, 2007.

This activity is supported by an educational grant from Wyeth Pharmaceuticals.

CA-CF_Depress_DR_Rev 7/11/06 11:18 AM Page A1

2 JULY 2006

STATEMENT OF NEEDSDepression is a highly prevalent yet underdiagnosed and undertreated condition that has a significant impact on patients’ qual-ity of life in terms of suffering and functional impairment, disability, health risks, and lifespan; the prevalence of depression witha co-existing anxiety disorder is also quite high. Approximately half of all cases of depression are missed in primary-care prac-tice, and fewer than one quarter of patients who are diagnosed receive adequate care.1,2 Yet primary-care practice represents anideal setting for identification, since patients with depression are frequent users of general medical services.3

With proper skills and tools, depression can be reliably diagnosed and treated; full recovery can be expected for 50%-70% ofpatients.4 Anxiety disorders are highly treatable as well. With an understanding of symptoms and risk factors associated withdepression, along with a familiarity with brief, easy-to-use questionnaires, clinicians can improve their rate of diagnosis, result-ing in improved patient management. Current guidelines recommend either antidepressant medicine or psychotherapy as first-line treatment for mild to moderate Major Depressive Disorder and combined pharmacologic treatment and psychotherapy forsevere disease. Clinicians need to understand the various classes of available antidepressant medications so optimal treatmentmay be afforded to patients. This program will focus on improving the diagnosis, treatment, and long-term management ofpatients with depression and anxiety in the primary-care setting.

1. Schwenk TL, Evans DL, Laden SK, et al. Treatment outcome and physician-patient communication in primary care patients with chronic,recurrent depression. Am J Psychiatry. 2004;161:1892-1901.2. Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity SurveyReplication (NCS-R). JAMA. 2003;289:3095-3105.3. Lepine JP. The epidemiology of anxiety disorders: prevalence and societal costs. J Clin Psychiatry. 2002;14(suppl 63):4-8.4. Oquendo M, Liebowitz M. The diagnosis and treatment of depression in primary care: an evidence-based approach. Available at: http://www.medscape.com/viewprogram/4571_pnt. Accessed March 13, 2006.

LEARNING OBJECTIVESAfter completing this educational activity, participants should be able to:• Recognize obstacles and challenges to the optimal management of depression and anxiety• Identify patients who may be at risk for depression or anxiety in primary-care practice for whom further screening is appropriate• Incorporate screening tools for depression into the practice setting to improve detection rates of depression• Diagnose a greater number of patients with anxiety, depression, or a combination of both• Select the most appropriate treatment options for individual patients to improve remission rates and patients’ quality of life

AUDIENCEThe target audience includes primary-care physicians, nurse practitioners, and physician assistants.

Clinicians on the Front Line: Active Management of Depression and Anxiety in Primary Care

AUTHORSLarry Culpepper, MD, MPH (Course Director)Professor and ChairDepartment of Family MedicineBoston University School of MedicineBoston, MA

Catherine R. Judd, PA-C, MSParkland Health and Hospital SystemDallas, TXUniversity of Texas Southwestern Medical CenterDallas, TX

Mary D. Moller, DNP, ARNP, BC, CPRPClinical Director, Suncrest Wellness CenterNine Mile Falls, WAAdjunct Instructor of NursingWashington State University College of NursingSpokane, WA

Charles B. Nemeroff, MD, PhDReunette W. Harris Professor and ChairmanDepartment of Psychiatry & Behavioral SciencesEmory University School of MedicineAtlanta, GA

Mark H. Rapaport, MDChairmanDepartment of Psychiatry and Mental HealthThe Polier Endowed Chair in Schizophrenia andRelated DisordersCedars-Sinai Medical CenterVice Chair and Professor of PsychiatryUniversity of California, Los AngelesLos Angeles, CA

INDEPENDENT EDUCATIONAL REVIEWERDomenic A. Ciraulo, MDPsychiatrist-in-ChiefBoston Medical CenterProfessor and ChairmanDivision of PsychiatryBoston University School of Medicine Boston, MA

CA-CF_Depress_DR_Rev 7/11/06 11:18 AM

JULY 2006 3

DISCLOSURE STATEMENTBoston University School of Medicine asks all individuals involved in the development and presentation of Continuing MedicalEducation (CME) activities to disclose all relationships with commercial interests. This information is disclosed to CME activityparticipants. Boston University School of Medicine has procedures to resolve any apparent conflicts of interest. In addition, faculty members are asked to disclose when any discussion of unapproved use of pharmaceuticals and/or devices occurs.

Larry Culpepper, MD, MPH, is a consultant and is on the speakers’ bureau for AstraZeneca Pharmaceuticals, Forest Laboratories,Pfizer Inc., and Wyeth Pharmaceuticals.

Catherine R. Judd, PA-C, MS, is on the speakers’ bureau for Bristol-Myers Squibb Company and is on the advisory boards forAstraZeneca Pharmaceuticals and Eli Lilly and Company.

Mary D. Moller, DNP, ARNP, BC, CPRP, is on the speakers’ bureau for Wyeth Pharmaceuticals.

Charles B. Nemeroff, MD, PhD, received grant/research support from AstraZeneca Pharmaceuticals, Bristol-Myers SquibbCompany, Forest Laboratories, Janssen Pharmaceutica, Pfizer Inc., Wyeth Pharmaceuticals, AFSP, NARSAD, and NIMH; is a con-sultant for Abbott Laboratories, Acadia Pharmaceuticals, Bristol-Myers Squibb Company, Corcept Therapeutics, CypressBiosciences, Cyberonics Inc., Eli Lilly & Company, Forest Laboratories, GlaxoSmithKline, Janssen Pharmaceutica, OtsukaAmerica Pharmaceutical Inc., Pfizer Inc., Quintiles, UCB Pharma, and Wyeth Pharmaceuticals; is on the speakers’ bureaus forAbbott Laboratories, GlaxoSmithKline, Janssen Pharmaceutica, and Pfizer Inc.; has stock/is a shareholder with AcadiaPharmaceuticals, Corcept Therapeutics, Cypress Biosciences, and NovaDel Pharma, Inc.; and is on the Board of Directors ofNovaDel Pharma.

Mark H. Rapaport, MD, received grant/research support from Abbott Laboratories, AstraZeneca Pharmaceuticals, CorceptTherapeutics, Cyberonics, Inc., Forest Laboratories, GlaxoSmithKline, Janssen Pharmaceutica, Novartis Pharmaceuticals,Pharmacia-Upjohn, Pfizer Inc., Sanofi-Synthelabo, Solvay, Stanley Foundation, UCB Pharma, Inc., Wyeth Pharmaceuticals,NIMH, and NCCAM; is a consultant/lecturer for Cyberonics, Inc., Eli Lilly and Company, Forest Laboratories, GlaxoSmithKline,Janssen Pharmaceutica, Neurocrine Biosciences, Novartis Pharmaceuticals, Pfizer Inc., Roche Laboratories, Sanofi-Synthelabo,Solvay, Sumitomo, Wyeth Pharmaceuticals, NIMH, and NIDA; is on the speakers’ bureaus for Cyberonics, Inc., Eli Lilly andCompany, Forest Laboratories, GlaxoSmithKline, Janssen Pharmaceutica, Novartis Pharmaceuticals, and Pfizer Inc.; and hasstock/is a shareholder with Forest Laboratories.

Domenic A. Ciraulo, MD, received grant/research support from Alkermes, Inc., Bristol-Myers Squibb Company, Cephalon, Inc.,Lipha Pharmaceuticals Ltd., Ortho-McNeil Pharmaceutical, and UCB Pharma; and is a consultant for Alkermes, Inc.

The planning committee members (Julie White, MS, Boston University School of Medicine; Kathi Gannon, Haymarket Medical;and Sharon Barnett, Haymarket Medical), have no significant financial relationships to disclose.

Off-label discussion: Table 4 on page 13 contains the only off-label discussion of pharmacotherapy. The off-label uses are clear-ly indicated. This chart was developed by Dr. Rapaport and revised by Dr. Culpepper. For additional information, please refer tothe individual package inserts.

DISCLAIMER: THESE MATERIALS AND ALL OTHER MATERIALS PROVIDED IN CONJUNCTION WITH CONTINUING MEDICAL EDUCATIONACTIVITIES ARE INTENDED SOLELY FOR PURPOSES OF SUPPLEMENTING CONTINUING MEDICAL EDUCATION PROGRAMS FOR QUALIFIEDHEALTH-CARE PROFESSIONALS. ANYONE USING THE MATERIALS ASSUMES FULL RESPONSIBILITY AND ALL RISK FOR THEIR APPROPRIATEUSE. TRUSTEES OF BOSTON UNIVERSITY MAKE NO WARRANTIES OR REPRESENTATIONS WHATSOEVER REGARDING THE ACCURACY, COM-PLETENESS, CURRENTNESS, NONINFRINGEMENT, MERCHANTABILITY, OR FITNESS FOR A PARTICULAR PURPOSE OF THE MATERIALS. IN NOEVENT WILL TRUSTEES OF BOSTON UNIVERSITY BE LIABLE TO ANYONE FOR ANY DECISION MADE OR ACTION TAKEN IN RELIANCE ON THEMATERIALS. IN NO EVENT SHOULD THE INFORMATION IN THE MATERIALS BE USED AS A SUBSTITUTE FOR PROFESSIONAL CARE.

ACCREDITATIONBoston University School of Medicine is accredited by the Accreditation Council for Continuing Medical Education(ACCME) to provide continuing medical education for physicians.

Boston University School of Medicine designates this educational activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™.Physicians should only claim credit commensurate with the extent of their participation in the activity.

This program has been reviewed and is approved for a maximum of one hour of AAPA Category 1 (Preapproved) CMEcredit by the Physician Assistant Review Panel. Approval is valid for one year from the issue date of July 2006.Participants may submit the self-assessment at any time during that period.

This program was planned in accordance with AAPA’s CME Standards for Enduring Material Programs and for CommercialSupport of Enduring Material Programs.

This program has been approved for a maximum of 1.0 contact hour of continuing education by the American Academy of NursePractitioners. Program ID 0605202.

This activity has been reviewed and is acceptable for up to 1 Prescribed credit(s) by the American Academy of Family Physicians.AAFP accreditation begins 07/01/06. Term of approval is for one year(s) from this date, with option for yearly renewal.

Estimated time to complete this activity: 1.0 hour. Credit available through July 31, 2007.

Cover image: Photo Researchers Inc.

©2006 Trustees of Boston University

Produced by Haymarket Medical Continuing Education25 Philips Parkway, Suite 105Montvale, NJ 07645


4 JULY 2006

Depression and anxiety are the most com-mon psychiatric disorders seen in pri-mary-care practice;1 the symptoms ofboth are familiar to primary-care practi-

tioners. Unfortunately, fewer than 50% of the peo-ple who have depression actually ask for help,according to the National Mental HealthAssociation. This limits the help that health-careproviders can offer. The relatively high incidence ofdepression among patients seen in primary care isexemplified by the data in Figure 1. Compared witha community prevalence of 4%, the prevalence inprimary-care clinics is estimated at 5%-10%.2

Over the course of a person’s life, the probabil-ity of developing a major depressive disorder(MDD) in the United States is 17%. In a 2004study, the rates of MDD were highest (just over10% per year) in people aged 18-25 and aged 35-49.3 Almost 9% of persons aged 26-34 experiencedMDD; in the 50-64 age category, 7.6% of personsexperienced such an event. Persons older than 65(1.3%) were least likely to experience MDD. Thelifetime prevalence of social anxiety disorder(SAD), post-traumatic stress disorder (PTSD), gen-eralized anxiety disorder (GAD), panic disorder,

and obsessive compulsive disorder (OCD) are13.3%, 7.8%, 5.1%, 3.5%, and 2.5%, respectively.Alcohol dependence, which may complicate thecourse of anxiety and depression, has a lifetimeprevalence of 14.1%.2,4 Related anxiety disorders,including phobias, compulsions, and panic, arenot included in these figures and further increasethe prevalence of anxiety disorders.

The consequences of overlooking depressionin patients are serious because of the large num-ber of patients affected. Mood disorders are asso-ciated with increased morbidity and mortality.Coupled with the high prevalence of depressionand anxiety among patients in primary-carepractice is the fact that only about one third ofthese patients actually seek treatment for theirsymptoms. Of those who do seek medical help,two thirds see a primary-care clinician and halfof them receive a diagnosis of depression. Onlyabout 10% of patients are treated according tocurrent guideline recommendations.5,6

All primary-care practitioners should under-stand that depression is a potentially lethal ill-ness. About 8% of patients who are hospitalizedbecause of a suicide attempt eventually go on

Clinicians on the Front Line:Active Management of Depressionand Anxiety in Primary Care

Primary-care practitioners confront myriad issuesin managing their patients with depressionand/or anxiety. Understanding the scope and epidemiology of these disorders is essential tounderstanding their shared characteristics. Do wealways recognize these patients in practice?What are the barriers to diagnosis and treat-ment, and how can they be overcome? What arethe treatment options for these sometimes life-altering conditions, and how do we choose fromamong the many that exist?


JULY 2006 5

to commit suicide. For patients hospitalized formood disorders, the suicide rate is about 4%.7 Inone study, two thirds of patients who had com-mitted suicide had consulted a general practi-tioner in the month before they died.8 These dataunderscore the importance of primary-careproviders in the recognition and treatment ofpatients with depression.

The impact of anxiety should not be underes-timated, either. GAD, which has a lifetime preva-lence of 5.1%, has a significant impact in terms ofdirect and indirect costs.2,9 GAD has a negativeimpact on quality of life; functional and occupa-tional capacity; and ultimately, morbidity andmortality.10 The percentage of suicide attemptsexceeds 10%, emphasizing the fact that, likedepression, anxiety disorders are potentiallylethal illnesses.

When a patient’s impairment of role func-tioning is severe or when suicidality is present,the perceived need for treatment is high. In con-trast, patients with MDD, anxiety, or substanceabuse problems tend to view these illnesses ascharacter flaws or weaknesses rather than braindiseases. They neither perceive the need for helpnor seek help.11

The diagnostic criteria for MDD and GAD areshown in Tables 1 and 2.

COMORBID ANXIETY AND DEPRESSIONIn the primary-care population, depression andanxiety frequently coexist, with up to 50% ofpatients with depression also experiencing anxi-ety;12 conversely, approximately 39% of patientswith anxiety also experience depression.13

Remission rates are lower in patients withcomorbid anxiety and depression than inpatients who present with either condition alone.Few studies exist of patients with comorbid anxi-ety and depression because these patients are fre-quently excluded from clinical trials. The preva-lence of comorbidity of depression and anxietydisorders is illustrated in Figure 2.

Table 1. Diagnostic Criteria for Major Depressive Disorder (MDD)

According to DSM-IV, the diagnostic manual from theAmerican Psychiatric Association, MDD is present if:

Five (or more) of the following symptoms have beenpresent during the same 2-week period and at leastone of the symptoms is either (1) depressed mood, or(2) loss of interest or pleasure:1.Patient is depressed, sad, blue, tearful

2.Patient has lost interest or pleasure in things he or she previously liked to do

3.Patient’s appetite is much less or much greater than usual, and patient has lost or gained weight

4.Patient has a lot of trouble sleeping or sleeps too much

5.Patient is so agitated, restless, or slowed down that others have begun to notice

6.Patient is tired and has no energy

7.Patient feels worthless or excessively guilty about things he or she has done or not done

8.Patient has trouble concentrating, thinking clearly, or making decisions

9.Patient feels he or she would be better off dead and has thoughts of suicide

For a diagnosis of depression to be made:1.The symptoms must be severe enough to upset the

patient’s daily routine or to impact his or her work or interfere with relationships

2.The depression should not have a specific cause, like alcohol, drugs, medication side effects, or physical illness

3.The depression is not just a normal reaction to the death of a loved one

Source: Diagnostic and Statistical Manual of Mental Disorders. 4th edition(DSM-IV-TR [text revision]). Washington, DC: American Psychiatric Press; 2000.

Figure 1. Prevalence of depression in United States.

Source: Kessler RC, et al. Arch Gen Psychiatry. 1994;51:8-19.

25

20

15

10

5

0Poin

to

fPr

eval

ence

of

Maj

or

Dep

ress

ion

Community

4%

Primary-CareClinic

5%-10%

MedicalInpatientSetting

10%-14%

NursingHome

6%-25%


6 JULY 2006

RECOGNIZING THE PATIENT WITH DEPRESSION The recognition of patients at risk for depressionis an extraordinarily important responsibility ofthe primary-care provider. Numerous studies andsurveys of primary-care practices serving the gen-eral population have shown that a very large per-centage of patients with depression, includingmajor depression, are undiagnosed or misdiag-nosed in these settings, leading to increased mor-bidity and mortality. Knowing the risk factors for

depression and identifying the at-risk patient are crucial in the primary-care setting.

About one third of the risk for developingMDD is genetic, and about two thirds is environ-mental. In patients with bipolar disorder, thegenetic contribution is even higher. Therefore,obtaining the patient’s family history is crucial.The patient’s personal history of depression isalso important, since a previous episode increas-es an individual’s risk for a subsequent episode.

Women are approximately twice as likely asmen to develop depression. Although the rea-sons for the difference in gender susceptibilityare unclear, there is evidence to suggest that theincreased incidence is related to hormonal fac-tors, stress, and lifestyle. Life stressors are impor-tant risk factors for the development of depres-sion; individuals who have experienced adversechildhood experiences (ACEs), including child-hood trauma, neglect, sexual and/or physicalabuse, and parental loss at an early age, are atincreased risk for developing depression, asdemonstrated in a variety of studies.14,15

A number of other psychiatric and medicaldisorders increase the risk for depression, withanxiety disorders prominent among them.Alcoholism and other forms of substance abuseare associated with an increased risk for depres-sion; many patients undoubtedly use alcoholand drugs as a means of self-medication fordepressive symptoms. There are medical disor-ders with high rates of comorbid depression,including Parkinson’s disease, Alzheimer’s dis-ease, cardiovascular disorders, pancreatic cancer,and a variety of other malignancies. One quarterof women with breast cancer experience majordepression. Primary sleep disorders, especiallysleep apnea and narcolepsy, are also linked todepression in some patients. The known risk fac-tors for depression are summarized in Table 3.14,15

Data from Chapman et al demonstrated theeffects of ACEs on depression later in life.16 Theretrospective cohort study included more than9,400 adult members of an HMO-based primary-care clinic in San Diego. Participants completeda questionnaire about a variety of health issues,


Table 2. Diagnostic Criteria for Generalized Anxiety Disorder (GAD)

According to DSM-IV, the diagnostic manual from theAmerican Psychiatric Association, GAD is present if:• Excessive anxiety and worry (apprehensive expectation)

occurs more days than not for 6 months, about a number of events or activities (such as work or school performance)

• The patient finds it difficult to control the worry• The anxiety and worry are associated with three (or more)

of the following six symptoms (with at least some symp-toms present for more days than not for the past 6 months). Note: Only one item is required in children on most days for at least 6 months.n Restlessness, feeling ”keyed up,” or “on edge”n Fatigabilityn Difficulty in concentration or mind going blank n Irritabilityn Muscle tensionn Sleep disturbances (difficulty falling or staying asleep, or

restless, unsatisfying sleep)

The focus of the anxiety and worry is not confined to fea-tures of an Axis 1 disorder, ie, the anxiety or worry is notabout having a panic attack (as in panic disorder), beingembarrassed in public (as in social phobia), being contami-nated (as in obsessive-compulsive disorder), being awayfrom home or close relatives (as in separation anxiety disorder); gaining weight (as in anorexia nervosa), havingmultiple physical complaints (as in somatization disorder), or having a serious illness (as in hypochondriasis); and the anxiety and worry do not occur exclusively during post-traumatic stress disorder.

The anxiety, worry, or physical symptoms cause clinicallysignificant distress or impairment in social, occupational, orother important areas of functioning.

The disturbance is not due to the direct physiologic effectsof a substance (eg, a drug of abuse, a medication) or a gen-eral medical condition (eg, hyperthyroidism) and does notoccur exclusively during a mood disorder, a psychotic disor-der, or a pervasive developmental disorder.

Source: Diagnostic and Statistical Manual of Mental Disorders. 4th edition. (DSM-IV-TR [text revision]). Washington, DC: American Psychiatric Press; 2000.


JULY 2006 7

including recent bouts of depression, history ofabuse in childhood, and household dysfunction.ACEs included situations such as the incarcera-tion of a parent, loss of a parent, domestic vio-lence, and sexual or physical abuse.

In this group, the lifetime prevalence ofdepressive disorders was 23%. A history of child-hood emotional abuse increased the risk for life-time depressive disorders; the odds ratio was 2.7in women and 2.5 in men. When scores weregiven to help assess the impact of ACEs, a strong,dose-dependent relationship existed between the ACE score and the probability of life-time and recent depressive episodes (P <.0001).Investigators determined that the number of ACEshas a graded relationship to both lifetime andrecent depressive disorders and that exposure toACEs is associated with an increased risk ofdepressive disorders that persists for decades.These findings demonstrate the importance ofincluding questions about ACE history in patientsat risk for depression and recognizing and inter-vening promptly if a child may be affected by adeath, abuse, or other traumatic experience.16

DEPRESSION AND REPRODUCTIVE ISSUESSome mood disorders are often undiagnosed.Postpartum depression, for example, has an over-all prevalence of 10%.17 Certain subgroups are at

even greater risk; about 26% of adolescents whogive birth, particularly single mothers, have arisk of developing postpartum depression.18 Thiscondition is associated with an increased risk forsuicide. Obstetricians, the clinicians with whomnew mothers are most likely to have contactafter delivery, are likely to focus on issues such asepisiotomy healing and breastfeeding at the firstpostpartum visit and therefore may not inquireabout symptoms of depression. Besides being arisk factor for suicide, postpartum depression canimpede mother-infant bonding. Deficits in thisarea can result in negative outcomes for thechild, including an increased risk for anxiety anddepression in adulthood.19

Depressive disorder also occurs in somewomen after spontaneous abortion or miscar-riage, a phenomenon that is widely under-recog-nized. Janssen and colleagues demonstrated thatmore than 33% of the women in their cohortwho experienced a pregnancy loss were severelydepressed at some point during the 18 monthsfollowing the loss. The longer the duration ofpregnancy before the loss, the higher the risk ofdeveloping a depressive disorder.20 The messagefor primary-care practitioners is to treat a womanfor major depression if her reaction is moresevere or persists longer than expected after amiscarriage. Many of these women will notactively seek treatment for their symptoms;therefore, it is the responsibility of the primary-care clinician to ask about the symptoms.

DEPRESSION IN CHILDREN AND ADOLESCENTSAlthough some aspects of the treatment of chil-dren with depression are controversial, no one anylonger doubts the fact that children in all agegroups do become depressed. The prevalence of

Women are approximatelytwice as likely as men todevelop depression.

Figure 2. Differential diagnostic considerations in over-lapping anxiety and depression.

Weissman MM, et al. J Clin Psychiatry.1994;55(suppl):5-10. Wittchen HU, et al.Arch Gen Psychiatry. 1994;51:355-364. Kessler RC, et al. Arch Gen Psychiatry.1995;52:1048-1060. Magee WJ, et al. Arch Gen Psychiatry. 1996;53:159-168.Bleich A, et al. Br J Psychiatry. 1997;170:479-482.

SADGAD DEPRESSION

PanicDisorder PTSD

OCD


depressive disorders in children of various ages isestimated at 0.8% in preschoolers; 2.0% inschool-aged, prepubertal children; and 4.5% inadolescents (the rate of depression rises afterpuberty to the late teenage years).21

Diagnosing depression in children is a chal-lenge. Depressive disorders can be difficult to dif-ferentiate from behavioral disorders, and ofcourse, the two types of problems can coexist inthe same patient.15 Depression in adolescentsand children should be diagnosed and treated.Depressive disorders that begin before age 20 areassociated with recurrent mood disorders inadulthood.22 Nearly one third of adolescents whoare hospitalized with severe MDD eventuallydevelop bipolar disorder.23

DEPRESSION IN ELDERLY PATIENTS At the other end of the spectrum, the elderlyexperience a high incidence of depression;approximately 15% of those aged 65 years andolder are affected. The major social and demo-graphic risk factors for depression in the elderlyare generally similar to those in younger agegroups: women; the unmarried, particularly thewidowed; those with stressful life events; andthose who lack a supportive social network.Depression may mask cognitive impairment or acomorbid condition among members of this age

group, and comorbid somatic symptoms are alsocommon. Health-care practitioners and patientsneed to understand that depression is not a nor-mal part of aging; it needs to be identified so itcan be appropriately treated.

WHEN THE COMPLAINT IS SOMATICPrimary-care providers generally do an excellentjob of detecting depression or anxiety whenpatients specifically complain of emotional prob-lems. But more often than not, patients withmood disorders present to primary-care practi-tioners with somatic complaints. When a physi-cal or somatic symptom is the primary com-plaint, the correct diagnosis is made in only 50%of patients.24 The underlying etiology of physicalcomplaints may be difficult to identify in a largepercentage of patients.

Additionally, it may be difficult to determineif symptoms of depression are causally associatedwith or influenced by concomitant substanceabuse or legitimate use of prescription or over-the-counter medications. Similarly, it can be dif-ficult to determine if symptoms are linked insome way to a comorbid chronic disease. Anothercomplicating factor is that physical complaintsmay be amplified in the presence of depressionand anxiety disorders. Another obstacle to therecognition and diagnosis of mood disorders isthe clinician’s personal beliefs and biases; theremay be a belief that emotional or mood prob-lems are a normal response to stressors in thepatient’s life. When clinicians fail to find a causefor physical symptoms, it is often difficult tomove beyond a negative workup, particularly inthe primary-care setting. While clinicians areprimed to recognize and treat somatic complaints,they may overlook the psychiatric disorders thattrigger somatic complaints.24,25 Untreated, thesemood disorders can have a negative long-termimpact on morbidity and mortality associatedwith other chronic diseases.

The 2003 study of chronic painful physicalconditions (CPPCs) by Ohayon and Schatzbergunequivocally demonstrated the associationbetween pain and depression.26 Among 748 sub-

8 JULY 2006


Table 3. Risk Factors for Depression

• Family history of depressive disorders

• Personal history of a depressive episode(s)

• Female gender

• Life stressor (bereavement, chronic financial problems)

• Certain personality traits

• Loss of parents at an early age

• Childhood abuse

• Alcohol or other substance abuse

• Anxiety disorders

• Neurologic or medical disorders (Parkinson’s disease, Alzheimer’s disease, stroke)

• Primary sleep disordersSources: Hirschfeld RMA, Goodwin FK. In: The American Psychiatric Press Textbook of Psychiatry. 1987:403-441.Depression Guideline Panel. Depression in Primary Care: Volume 1. Detection andDiagnosis. 1993:1-65.


JULY 2006 9

jects who were diagnosed with MDD, 18.2% and28.9%, respectively, had a medical condition orCPPC and 14.5% suffered from both conditions.Fewer than 40% of these patients with MDD hadneither condition. In patients with only onedepressive symptom, almost 56% had neithercondition (Figure 3).26

Accumulating data demonstrate that thetreatment of depression is associated withdecreases in levels of perceived pain. Primary-care practitioners should consider the possibilityof depression in any patient with chronic pain inwhom there is no obvious medical source for thepain or in whom the pain seems out of propor-tion to the underlying physical pathology.

Patients with somatic complaints and mooddisorders are high utilizers of medical services.They are often considered to be the “problem”patients in primary-care practices because of theirfrequent telephone calls, multiple office visits,and numerous somatic complaints that requirephysical examinations and laboratory tests.When clinicians see these individuals as problemor frustrating patients, the stigma that can beassociated with depression, has been applied, rais-ing the barrier to detection and treatment.

OVERCOMING THE BARRIERSOnly a minority of patients with depressionundergo appropriate diagnostic workup andreceive appropriate treatment. A hypotheticalmodel, shown in Figure 4, demonstrates this

problem. Only about half of 100 depressedpatients were appropriately identified and diag-nosed. The failure to identify and diagnose sucha large portion of depressed patients is amplifiedby the fact that only about half of the patientswho are identified receive any treatment for their illness.29

The diagnosis of depression can be approached in different ways. The biomedicalexclusionary approach is common in primary-care practice, as well as in other fields of medi-cine. All the “rule-outs” are done on physicalexam, such as pain and various somatic com-plaints. In many cases, this can be a valid andhelpful approach. The practitioner must alsodetermine what medicines the patient is taking,including prescription, over-the-counter, andalternative or herbal products. An alternative,the mental health approach, examines the psy-chosocial aspects of the patient’s symptoms first.This approach is less common in primary carethan the biomedical exclusionary approach. Acombined approach addresses physical and men-tal health complaints simultaneously.

The differential diagnosis of depression maybe complex, whether the patient presents withdepression alone or with depression and comor-bid conditions such as anxiety or chronic pain.Psychiatric referral resources may also be inshort supply for some patients,30 and managed-care organizations may refuse to reimburse forfollow-up visits.31

Figure 3. Study of patients with chronic painful physical conditions showed the association between pain and depression.

Ohayon MM, Schatzberg, A. Arch Gen Psychiatry. 2003;60:39-47.

Medicalcondition

16.6%(n = 520)

Painful physical

condition18.3%

(n = 576)

9.3%(n = 292)

3,140 subjects with at least one depressive symptom

Methodology: Phone interviews using Sleep EVAL Expert System

Without medical condition and painful physical condition

55.8% (n = 1,752)

Medicalcondition

18.2%(n = 136)

Painful physical

condition28.9%

(n = 216)

748 subjects with major depressive disorder diagnosis

Without medical condition and painful physical condition

38.4% (n = 288)

14.5%(n = 108)

Adjusted odds ratio for major depression disorder: 1.0


10 JULY 2006

FACILITATING DEPRESSION SCREENINGWhat are the barriers to the diagnosis of depres-sion in primary care? The limited time allottedfor a typical office visit is an important impedi-ment that must be considered. Psychiatric assess-ment skills may be lacking in some primary-careproviders, and the staff may not have the time toadminister and help with screening tools that apatient might complete in the waiting room. Ifdepression screening is conducted during officevisits, it is helpful if the test is scored while thepatient is still in the office. In some systems,screening results in a brief interaction that canlead to future appointments being made.Depression questionnaires should be easilyadministered, quickly scored, and designed to betime-efficient for both patients and staff.

Patients themselves sometimes present diag-nostic barriers to depression. They often fail torecognize their own symptoms—guilt and/orsleep disturbances, for example—as signs ofdepression. Some feel guilty or stigmatized by thesymptoms or consider them signs of weakness.Others have difficulty reaching out for help;some are hesitant to intrude on a clinician’s timewith what they regard as a trivial or “soft” com-plaint, perhaps one that has been misdiagnosedin the past. Cultural influences vary in membersof different ethnic groups and may also affect apatient’s decision to seek help for depression.

Some practices offer screening questionnairesto new patients before their first visit, allowingtime before this visit for the results to be inter-preted; the clinician will initiate a discussionabout the results with the patient at the time ofthe visit. This approach has merit for newpatients, but the possibility of emergent depres-sion in established patients may still be over-looked. Health-care practitioners should ensurethat all patients in the practice, both new andexisting, are screened periodically for depression.

Various screening questionnaires and toolshave been devised for the detection of depres-sion among patients in primary-care practice.Too few, however, meet the requirements forsimplicity, ease of administration, and timelyadministration. The US Preventive Services TaskForce (USPSTF) recommends screening for de-pression in primary care if practices can activelymanage those patients who test positive.32 TheUSPSTF found that the following two simplequestions are about as effective for initial screen-ing as longer instruments:

1. Over the past few weeks, have you felt down, depressed, or hopeless?

2. Over the past few weeks, have you felt littleinterest in doing things?

If the response to either of these two ques-tions is positive, further investigation is recom-mended. This can be performed by using thePatient Health Questionnaire-9 (PHQ-9) oranother depression questionnaire or by conduct-ing a clinical interview.

The PHQ-933 was developed as a screeninginstrument and has good applicability in a clini-cal setting. Patients are asked whether they haveexperienced the following over a 2-week period:

1. Little interest or pleasure in things2. Feelings of depression or hopelessness3. Somnolence or insomnia4. Fatigue or lack of energy5. Poor appetite or overeating6. Negative feelings about themselves, or a


Figure 4. A study showing the unmet needs in the treatment of depression.

Source: Hirschfeld RM, Keller MB, Panico S, et al. JAMA. 1997;277:333-340.

Diagnosed with depressionNO50

YES50

100 DEPRESSED PATIENTS

Treated?NO25

YES25

Treated to remission of symptomsNO17

YES8


JULY 2006 11

perception that they have let people down7. Difficulty concentrating8. Slowness in movement or speaking that is

evident to others9. Restless or “fidgety” movements

10. Thoughts of self-harm or feelings that they would being better off dead.

A diagnosis of MDD should be consideredwhen five or more items have been present formost days over the past 2 weeks and at least oneof the first two items is present.

For patients in whom anxiety symptoms tendto dominate, administration of the PHQ-533 foranxiety may be helpful. Patients are asked toanswer these questions:

1. In the past 4 weeks, have you had an anxi-ety attack or suddenly felt fear or panic?

2. Has this ever happened before?3. Do some of these attacks come out of the

blue or in situations in which you didn’t expect to be nervous or uncomfortable?

4. Do these attacks bother you a lot? 5. Do you worry about having more attacks

like these?6. During your last bad anxiety attack, did

you have symptoms such as shortness of breath, sweating, heart racing or pounding,dizziness or faintness, tingling or numb-ness, or nausea or an upset stomach?

An anxiety disorder should be considered ifthree out of the five items are answered with aYes, and panic disorder should be specificallyconsidered if all are answered Yes.

Other factors should be taken into considera-tion, however, before a differential diagnosis ofdepression is made. Bipolar disorder should alsobe considered, as this psychiatric condition oftenpresents as unipolar depression initially. If sub-stance abuse is present, the determination needsto be made as to whether there is an independentdepression apart from the substance abuse. Ifbereavement is an issue, the clinician needs todetermine whether or not the depression associ-

ated with the bereavement has moved into MDD.In a patient with symptoms of MDD, subclin-

ical hypothyroidism can account for somedecreased energy and lack of interest in life, so athyroid function test may be in order. While nolaboratory testing is required as part of the assess-ment leading to a diagnosis of a depressive oranxiety order, other laboratory tests that shouldbe considered in patients with possible depres-sion are a complete blood count, blood ureanitrogen and creatinine, a serum toxicologyscreen, and an electrolytes screen, including cal-cium, phosphate, and magnesium.

TREATMENT AND LONG-TERM REMISSIONBefore beginning treatment for mood and/oranxiety disorders, several issues need to be dis-cussed with the patient. These include: Why isthe patient in the office? What does the patientwant and need from you? How does the patientconceptualize his or her condition? Does thepatient have a preference about the type of treat-ment that should be prescribed or the type oftreatment most likely to be effective? Is thepatient ready to do the work associated withrecovery from mood and anxiety disorders?

The initial intervention begins with reassur-ance and education. Most patients with depressionand/or anxiety benefit from the assurance thatthese are brain diseases—actual physical disordersthat are treatable. They need to be educated aboutthe frequency, course, and prognosis of the disor-der as well as the available treatment options andtheir possible side effects. Patients should be toldthat healing takes time and that treatment mustcontinue even after symptoms have resolved.

The initial intervention may also include a

Treatments must be individualized and modified according topatient response.


12 JULY 2006

quick, comprehensive, structured approach todetermine the symptoms that most concern thepatient. One aspect of the process can includequantification of the patient’s relevant targetsymptoms on a Likert Scale.

Constant communication between providerand patient is essential throughout treatment.Medicine is a mixture of art and science. Eachperson is unique, and treatments are individual-ized and modified according to the patient’sresponse. The first intervention may not be theideal one, but with time and collaborative effort,treatment may be successfully tailored to theindividual patient. Primary-care clinicians shouldensure that patients understand that recoveryfrom mood or anxiety disorders is not a passiveprocess; patients are in control of their treatment.Medications work only if patients take them asdirected. Therapy is effective only when patientsdo the work required by the therapy. Patients alsoneed to understand that a healthy lifestyle,including adequate sleep, nutrition, hygiene,physical activity, and stress reduction, is crucialto a good treatment outcome.

The intensity, frequency, and impairmentcaused by target symptoms are a critical focus ofprimary-care visits after the initial visit. At eachsubsequent visit, patients should be asked abouttheir medications; clinicians should not assumethat patients are taking recently prescribed medi-cines or even the medicines they were taking at aprior office visit. They need to be asked about sideeffects of medicines, particularly ones that maybe uncomfortable to discuss, such as sexual sideeffects. Patients may still, at each visit, needreminders that healing takes time and is often a

saw-toothed process, that is, two steps forwardand one step back. Stressful life events, for exam-ple, can slow recovery. Patients who have noticedsymptom improvements need to be reminded tocontinue taking the prescribed medication asdirected to ensure that their recovery is complete.

SELECTING A TREATMENT Treatment options for patients with mood disor-ders include psychotherapy, pharmacotherapy,combined psychotherapy and pharmacotherapy,and combination pharmacologic therapy. Whencomorbid conditions are present, more intensivetreatment is often required. This might take theform of more than one medication or moreintensive psychotherapy.

PSYCHOTHERAPEUTIC OPTIONS Of the available psychotherapeutic treatmentoptions, cognitive-behavioral therapy (CBT),alone or in combination with pharmacotherapy,has the best evidence in its favor. Components ofCBT typically include psychoeducation, self-monitoring of target symptoms, symptom management, cognitive restructuring, and expo-sure (when appropriate). Increasing evidencealso supports the use of interpersonal therapy,which may be a powerful and strong tool incombating mood disorders. Interpersonal thera-py is designed to improve the quality of thepatient’s interpersonal world by helping thepatient understand the underlying interpersonalthemes that appear to be involved in the onsetand maintenance of the psychiatric illness.

Psychodynamic therapy may be utilized inpatients with anxiety to help generate self-aware-ness. This approach may involve both uncover-ing and learning how to deal more effectivelywith unconscious conflicts. However, peer-reviewed evidence supporting this form of psy-chotherapy is scarce.34

The key components of CBT target maladap-tive chains of thoughts, feelings, and behaviors.Therapeutic maneuvers focus on teaching thepatient to monitor and correct catastrophicthought patterns. It has been established that


The key components ofCBT target maladaptivechains of thoughts, feelings, and behaviors.


CBT is biologically active and can produce alter-ations in cerebral blood flow in patients.35 CBTcan be an initial alternative to pharmacotherapyin patients with mood and anxiety disorders aswell as a replacement strategy. CBT is often com-bined with pharmacotherapy as adjuvant thera-py in patients with treatment-resistant depres-sion. CBT plus pharmacotherapy typically pro-duces a greater acute treatment response andgreater maintenance of treatment gains thaneither therapy used alone.36

In one study, investigators evaluated 158patients with recent MDD whose illness had par-tially remitted with antidepressant treatment thatconsisted of mean daily dosages equivalent to 185-mg amitriptyline or 30-mg fluoxetine.36 Patientsexperienced residual symptoms of 2 to 18 months’duration and were randomized to receive eitherpharmacologic therapy alone or pharmacologictherapy plus CBT for 16 sessions over 20 weeks.CBT reduced relapse rates for acute major depres-

sion and persistent severe residual symptoms inboth intent-to-treat and treated-per-protocol sam-ples. The relapse rate at 68 weeks was reduced sig-nificantly from 47% in the pharmacologic manage-ment control group to 29% with CBT plus pharma-cologic therapy (hazard ratio: 0.54; 95% confidenceinterval, 0.32-0.93; intent-to-treat analysis).36

THE PHARMACOLOGIC APPROACHThere is strong evidence for the efficacy of the SSRIsin treating depression and anxiety, but the sero-tonin-norepinephrine reuptake inhibitors (SNRIs),tricyclic antidepressants (TCAs), and monoamineoxidase inhibitors (MAOIs) are effective as well.37

Emerging evidence suggests that atypical antipsy-chotic agents may be useful when combined withantidepressants in patients with MDD and GAD.Anxiety disorders may also respond to combina-tions of these drugs (Table 4).37

SSRIsThe SSRIs include fluoxetine, paroxetine, esci-talopram, sertraline, citalopram, and fluvox-amine. These are considered first-line agents fordepression by many experts. The excellent side-effect profiles of these agents are probably due totheir specificity for the serotonin transporter.They all cause an increase in serotonin concen-trations in the synapse.

SNRIsThe SNRIs include venlafaxine and duloxetine.These agents work by blocking the serotonin andnorepinephrine transporters, leading to anincrease in serotonin and norepinephrine con-centrations in the synapse. There is some evi-dence that enhancing the activity of both sero-tonin and norepinephrine is more efficacious insome patients than enhancing serotonin activityalone in the treatment of depression.38,39

Atypical antidepressantsThis category includes bupropion, mirtazapine,trazodone, and generic nefazodone. The agents inthis class all have slightly different mechanismsof action. Mirtazapine and nefazodone enhance

JULY 2006 13

Table 4. Efficacy of Pharmacotherapy in Anxiety

Efficacy MDD PD GAD SAD PTSD

Effective SSRIs* SSRIs* SSRIs* SSRIs* SSRIs*

(>2 RCTs) SNRIs* SNRIs† SNRIs* SNRIs* TCAs†

TCAs* TCAs† TCAs†

BZD* BZD* BZD†

MAOIs* MAOIs† MAOIs† MAOIs†

mirtazapine*bupropion*nefazodone*

trazodone* trazodone†

buspirone†

AEDs† AEDs† AEDs†

*Indicated for the treatment of that specific disorder. †Off-label use.RCT= randomized controlled trial; SSRI = selective serotonin reuptake inhibitor;SNRI = serotonin norepinephrine reuptake inhibitor; TCA = tricyclic antidepres-sant; BZD = benzodiazepine; MAOI = monoamine oxidase inhibitor; AED =antiepileptic drug.

Adapted from: Lydiard RB. Textbook of Anxiety Disorders. Washington, DC:American Psychiatric Press, Inc.; 2002:348-361.


14 JULY 2006

the activity of norepinephrine and serotonin byblocking certain receptors in the brain; trazodoneappears similar but has little effect on norepi-nephrine. The mechanism of action of bupropionis obscure; it weakly inhibits the reuptake ofdopamine, serotonin, and norepinephrine.

Primary-care clinicians who treat patientswith mood or anxiety disorders must rememberthe so-called three Ds of treatment:

Dose: Sufficient intensityDuration: Adequate time allowed for responseDocument: Completion of therapeutic trials

When initiating treatment with an antide-pressant, the general approach is to start with alow dose and titrate based on side effects andefficacy. The right dose should provide efficacywith minimal or no side effects. Antidepressantmedications will not have maximum efficacyunless thyroid function is in the normal range.

Again, it may take several weeks to titrate thedosage in an individual patient to achieve maxi-mal efficacy along with minimal side effects.

Keller et al demonstrated that in patients withchronic depression, combined acute treatmentwas more effective than either psychotherapy orpharmacotherapy alone but that all three modal-ities were very useful.40 In this study, 681 adultswith chronic, nonpsychotic MDD were randomlyassigned to 12 weeks of outpatient treatmentwith nefazodone (maximum dose 600 mg daily),16 to 20 sessions of CBT, or both. At baseline, allpatients had scores of at least 20 on the HamiltonRating Scale for Depression, indicating clinicallysignificant depression. Remission was defined asa score of ≤ 8 at weeks 10 and 12. For patientswho did not achieve remission, a satisfactoryresponse was defined as a reduction in the scoreby at least 50% from baseline and a score of ≤ 15.Investigators who rated the scale were unaware ofthe patients’ treatment assignments.


Figure 5. Strategies for the treatment of major depression with comorbid anxiety in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial.

REMISSION

STAGE 1A – AUGMENTATIONPARTIAL RESPONSE

PARTIAL RESPONSE OR NONRESPONSE

STAGE 1Monotherapy

SSRI, venlafaxine XR,mirtazapine CONTINUATION

REMISSION

PARTIAL RESPONSE

ANY STAGE(S) CAN BE SKIPPED DEPENDING ON THE CLINICAL PICTURE

STAGE 4CONTINUATION

REMISSION

STAGE 2A – AUGMENTATIONPARTIAL RESPONSE


STAGE 2Monotherapy

SSRI, venlafaxine XR, mirtazapine,TCA

(class other than used in Stage 1)

CONTINUATION

BY STAGE 3 WE SUGGEST GETTING EXPERT CONSULTATION


STAGE 3Combination treatments

(eg, TCA+SSRI, bupropion SR+SSRI,

SSRI+trazodone)

SSRI = selective serotonin reuptake inhibitor. TCA = tricyclic antidepressant.

Greer TL, Trivedi MH. University of Virginia School of Medicine Reports on Psychiatric Disorders. 2005.Available at: www.utsouthwestern.edu/findfac/research/0,2357,52864,00.html. Accessed June 16, 2006.

Any algorithm medicationnot previously tried


JULY 2006 15

Of the 681 patients who participated in thestudy, 662 attended at least one treatment sessionand were included in the analysis of response.The overall rate of response (remission or satisfac-tory response) was 48% in both the nefazodonegroup and the psychotherapy group, comparedwith 73% in the combined-treatment group (P < .001 for both comparisons). Among the 519subjects who completed the study, the responserates were 55% in the nefazodone group and 52%in the psychotherapy group, compared with 85%in the combined-treatment group (P <.001 forboth comparisons). The rates of withdrawal weresimilar across the three groups.40

A stepwise approach to the treatment ofmajor depression with comorbid anxiety, a verycommon clinical presentation, is depicted inFigure 5.41 In keeping with the dictum of startingat a low dosage and proceeding carefully, Stage 1of treatment should consist of monotherapywith an SSRI or an SNRI. If the patient’s responseis partial or absent, augmentation therapy (stage1A) can be implemented. It is more likely, how-ever, that the provider will choose a differentagent from the same drug class or an agent froma different class altogether, such as an SNRI orTCA in patients for whom an SSRI has not shownefficacy (Stage 2). Data that may help the clini-cian decide between a different drug from thesame class or a drug from another class aresparse. If the patient still has not experiencedsufficient symptom relief or if side effects havebecome intolerable, combination treatmentsmay be useful (Stage 3). A typical Stage 3 regimenmight include a TCA plus an SSRI, an SSRI plustrazodone, or bupropion plus an SSRI. In mostcases, expert consultation is recommended whena patient requires Stage 3 or Stage 4 treatmentwith Stage 4 defined as “any algorithm medica-tion not previouly tried.”41

Whether the newer antidepressants (SSRIs,SNRIs, atypical antidepressants) should be usedin children and teenagers—and how they shouldbe used—remains a controversial issue. Manyspecialists who treat childhood and adolescentdepression believe that severe depression in

young patients requires prompt treatment,although data on the safety and efficacy of psy-chotherapy and pharmacotherapy are sparse inthis age group.

What is the best sequence of treatments in theweeks and months after the start of therapy? Oneof the key issues is a determination of when treatment adjustments are required. Typically,somatic symptoms improve in the first 2 to 4weeks, followed by improvements in the psychi-atric symptoms, including feelings of anxiety anddepression. If these are not markedly improvedby 4 to 6 weeks after the start of treatment, atreatment adjustment is warranted. The firstintervention is usually an increase in the dose,unless the patient is at the maximum dose or ifside effects prevent a dose increase. If side effectsare not a problem, it is possible to treat patientsat dosages higher than those approved by theFDA, especially when using SSRIs and SNRIs.

Augmentation may be another option, espe-cially if response has been good but completeremission has not been achieved. A switch to adrug from another class may also be useful. Inpatients with severe depression, either pharma-cotherapy or combined psychotherapy and phar-macotherapy is recommended due to the delayin improvement with psychotherapy alone.

Most guidelines and data now support continu-ing treatment for at least 6 to 9 months after apatient has achieved symptom remission followingthe first lifetime episode of MDD. At that point,treatment may be discontinued gradually. Forpatients who have had two episodes, some judg-ment is involved. If the episode of depression hasbeen severe or complicated by significant anxietyor substance abuse, or if the patient has been slowto respond to treatment, it may be necessary tomaintain pharmacotherapy indefinitely followingthe second episode. In contrast, if the patientresponded to the current treatment regimen rapid-ly and fully, treatment may be discontinued after 2to 3 years following the second lifetime episode.Certainly following a third episode, most specialistsin this field would consider treating patients indef-initely to prevent further relapse or recurrence.


16 JULY 2006

GETTING TO REMISSIONRemission of symptoms is the unambiguousestablished goal of acute-phase treatment; howev-er, symptom resolution occurs in only about onethird of patients who are treated with monother-apy. The percentage of patients who are treated andremain in remission (ie, who avoid relapse/recur-rence) over the long term is even lower.30

Chief among the barriers to remission are psy-chiatric and medical comorbidity, psychosocialstress, inherited vulnerability, and insufficienttreatment intensity. Health-care practitionerscannot change factors such as inherited vulnera-bility, and the ability to modify psychosocialstress is limited. Clinicians can, however, modifytreatment intensity and some aspects of comor-bid conditions, especially psychiatric ones.

Grilo and colleagues demonstrated that whenpatients with panic disorder lack confidence in agiven treatment, they tend to discontinue thetreatment.42 Two variables were independentlyassociated with increased dropout rates: lowerhousehold income and negative treatment atti-tudes. A trend toward higher dropout rates wasdemonstrated in patients who attributed theirpanic disorder to life stressors, as well as in olderpatients. Patients need to be educated; cliniciansalso need to match the patient’s requests fortreatment with the interventions that offer thebest chances of recovery. Understandingpatients’ belief systems, cultural notions, andperceptions of their illness is essential. Attentionto a patient’s literacy level is crucial when distrib-uting patient-education materials.

LONG-TERM APPROACHES Depression and anxiety are chronic diseasesrequiring long-term follow-up and treatment. As

patients move beyond the first weeks of treat-ment with a good response, the clinical focusshifts to concerns for long-term care. Goals oflong-term treatment of mood disorders include:

• Minimizing relapses and recurrences• Progressing from response to remission• Improving treatment adherence with anti-

depressant therapy and other medical and psychiatric treatments

• Minimizing and managing side effects of medications

• Slowing the progression of psychiatric and medical illnesses.

Clinicians must emphasize treatment adher-ence when counseling their patients. The impactof side effects may be minimized with simpleadjustments, such as taking a medication withfood or changing the time of day when the drugis taken. Sexual side effects might be managed bybetter timing the medication to correlate withthe time of sexual activity or by augmentingtherapy. In men, this might include treatmentwith an agent for erectile dysfunction.

An increasingly important aspect of long-term care in patients with depression is therecognition that treatment for MDD, in particu-lar, may have the potential to reduce the progres-sion of comorbid psychiatric or medical illnesses.Understanding of the interactions of depressionand conditions such as increased sympatheticnervous system tone and its possible impact oncardiovascular disease and diabetes is growing.The medical arena may be evolving into an erain which the treatment of depression becomesan essential part of risk-factor management forchronic medical illness.

Active management of the patient over thelong term is critical, and data are available from anumber of sources that identify groups that are athigh risk for early relapse. The likelihood ofrelapse during the first or second year after treat-ment increases as a function of the number ofprior episodes and the presence of residual symp-toms after treatment. In a study by Judd et al,


Active management of the patient over the long term is critical.


JULY 2006 17

researchers determined whether the level of recov-ery from a major depressive episode would predictthe duration of recovery in patients with unipolarmajor depression.43 Participants were categorizedat intake either as having residual depressivesymptoms or as asymptomatic. The two risk fac-tors associated with early relapse were recoverystatus (residual symptoms or asymptomatic) andhistory of recurrent depressive episodes.

The most compelling message of these data isthe greater propensity for relapse in patientswith residual symptoms than in their asymptom-atic counterparts. When the investigators con-trolled for the effect of recurrent MDD, patientswith unipolar major depression and residualsymptoms were more likely to experience relapseduring any given interval after recovery thanwere those with asymptomatic recovery.43 Themajority of patients who do not attain substan-tial elimination of symptoms are more likely toexperience relapse if not aggressively managedwith additional adjustments to the regimen.

CBT also has a marked impact on recovery interms of neurophysiology and brain receptordynamics. The efficacy of CBT is reflected in itsassociation over the long term with sustainingremission.44 The beneficial impact of CBT maynot be confined to depression, and long-termtreatment with CBT may also decrease the risk ofrelapse of accompanying anxiety disorders.45

From a practical standpoint, determining effec-tive ways to monitor treatment is important.Charting and medical recordkeeping can helpkeep track of important information; flowchartscan be very effective. One effective flow-chartingmethod is to simply identify the three or fourmost problematic symptoms for a particularpatient and chart them. Another is to identify thecore symptoms of depression, particularly thoseaffecting the patient at illness onset. Side-effectflow-charting also may be helpful, especially ifside effects have been an ongoing patient con-cern. Another approach is to identify the patient’skey functional impairments at the time of initialdiagnosis and again sometime during the first 2months of treatment. The return of various func-

tions is then charted over time. This can be impor-tant not only for the clinician but for the patientto emphasize the importance of treatment.

Clinicians should be familiar with the phas-es of depression treatment. One essential pointis that when treatment is effective and symp-toms are alleviated, patients move into a vul-nerable time that commonly occurs during thefirst weeks after the start of a response.Paradoxically, this is when the patient is likelyto stop treatment.46-48

To determine why patients prematurely stoptreatment for depression, 272 patients seen ingeneral practice who were taking antidepressantsfor MDD completed a compliance questionnairein a study by Demyttenaere and colleagues.49

Patients were telephoned monthly for up to 6months while they continued to take their med-ication. By the end of the study, 53% of patientshad discontinued their antidepressant medicineswithout consulting the clinician. The most com-mon reasons for stopping were that patients feltbetter, experienced adverse events, were afraid ofdrug dependence, felt uncomfortable takingmedication, thought the drug lacked efficacy, orbelieved that they should solve their problemswithout drugs.50

Coordinated care, which typically involves ateam approach, can be highly effective in improv-ing treatment outcomes. A case manager trackspatients in the practice, assesses their current sta-tus, determines the need for intervention, and pro-vides direct counseling support and referral to self-help or patient groups. The case manager also facil-itates access to psychiatrists for patients who needmore specialized attention because they have not

Coordinated care isassociated with significantimprovement comparedwith usual primary care.


18 JULY 2006

responded well to therapy or have responded buthave not achieved remission. This type of inter-vention can be helpful, for example, in treatingpanic disorder. In almost every cost corridor, coor-dinated care is associated with significant improve-ments compared with usual primary care.50

SUMMARYDepression and anxiety are common in primarycare. They frequently are undiagnosed and are asource of morbidity and mortality. Both condi-

tions increase the risk of suicide, increase the useof health-care resources, cause occupationalimpairment, and often become chronic. The jobof the primary-care clinician is to ensure thatpatients with depression and/or anxiety are rec-ognized and receive a targeted and complete diag-nostic evaluation and treatment with all availableand appropriate modalities. This usually includespharmacotherapy and CBT. Prevention of relapseand persistence of remission are dependent oncareful follow-up.


Mrs. M is a 45-year-old mother ofthree teenagers aged 13, 16, and18. She has been happily marriedfor 20 years; she does not work

outside the home. Mrs. M has a college degreeand worked part-time as an accountant for 6years after her youngest child started school. Shehad faithfully kept a daily exercise regimen forthose 6 years. One year ago, she started takingSt. John’s wort at night to help her sleep, andshe is still sleeping fitfully. For the last year, Mrs.M has been unable to work even part-timebecause of chronic fatigue, fear of failure, andproblems thinking clearly. She has been able toexercise only sporadically. Mrs. M has with-drawn from her usual social activities but stillhas a good relationship with her children andextended family.

PERTINENT HISTORY Mrs. M presented to the primary-care clinicianseeking treatment for what she perceived asdepression. She reported having mild postpar-tum depression after the birth of her third child12 years ago but did not report it to her physi-

cian. Six years ago, after starting back to work,she sought her first formal treatment from herprimary-care physician for a “low-grade” depres-sion. She was sequentially treated with three dif-ferent selective serotonin reuptake inhibitors(SSRIs) that only “helped some.” She wasswitched to mirtazapine, which “helped a littlemore.” She was able to continue to work part-time but has never really felt like her old self. Sherecently decided to stop the antidepressant med-ications she had been taking for 3 years. Now shefeels she may be premenopausal and is con-cerned because she has recently had thoughts ofsuicide. She has gained 15 pounds in the lastyear, even though she has a poor appetite.

PHYSICAL EXAM Mrs. M was 5’5” and weighed 160 pounds. Hervital signs included: temperature, 98.2º F; bloodpressure, 94/60 mm Hg; pulse, 88, regular sinusrhythm; and respirations, 18 breaths per minute.Her lungs were clear. Her skin color was pale andher eyes were dull, with periorbital edema notedbilaterally. Her hair was dull, and thinning of theeyebrows was noted. Mrs. M reported dry skin

CASE STUDY: A 45-Year-Old Mother With Chronic Depression and Fatigue


JULY 2006 19

and constipation. Her menstrual periods hadbeen irregular for the last year, and she experi-enced decreased libido. She was not a smoker butdrank six cups of strong coffee daily. She said shedid not like to drink water.

MENTAL STATUS EXAM Mrs. M presented in a calm and pleasant man-ner. Her affect was restricted, congruent, andonly minimally animated. She was able to initi-ate and maintain limited conversation with softspeech that was otherwise of normal rate,rhythm, pitch, and intensity. She was able toestablish and maintain intermittent periods ofnormal eye contact. Her hygiene and groomingwere casual. She did not report any history ofabuse or trauma. Mrs. M denied substancedependence or abuse and reported drinking twoto three glasses of wine weekly. She denied hav-ing psychotic symptoms; no formal thoughtdisorder was evident. Her cognitive functionswere slowed, but there was an adequate fund ofinformation. She reported loss of interest ineveryday life and trouble concentrating. Resultsfrom the Patient Health Questionnaire-9 con-firmed depressive patterns. Mrs. M reportedthinking about suicide but denied having anactual plan.

DIAGNOSTIC IMPRESSION AXIS I: 296.32 Major depression, moderate, withsuicidal ideation, no psychotic features. AXIS II: N/AAXIS III: Mild obesity, R/O 244.9 (acquiredhypothyroidism), R/O early menopauseAXIS IV: Problems with primary support group:N/AProblems related to the social environment:Has dropped out of her bridge clubEducational problems: N/AOccupational problems: Unable to maintainemploymentOther psychosocial/environmental problems:Unable to perform usual daily activitiesAXIS V: Current Global Assessment of Func-tioning: 55

TREATMENT The clinician made a decision to discontinueMrs. M’s St. John’s wort. Because of her priorpoor response to SSRIs and mirtazapine, a sero-tonin norepinephrine reuptake inhibitor was ini-tiated. Laboratory tests were ordered to evaluateMrs. M’s free T3 and free T4, in addition to hertotal T3 and total T4 plus thyroid-stimulatinghormone (TSH).51 Her results were as follows:TSH 3.25, free T4=.9, free T3=2.8, total T4=5.8,total T3=168. She was started on levothyroxine50 µg and will be monitored every month untilTSH is under 1.25, free T4=1.3, and free T3=3.2.52

The clinician also ordered a comprehensivemetabolic panel, complete blood cell count, uri-nalysis, lipid profile, and hormone panel. Mrs. Mwas asked to increase her water intake to at leastsix glasses daily and to begin to eliminate caf-feine. She was encouraged to walk 20 minutesdaily at moderate speed. She was counseled ondecreasing saturated fats in her diet and increas-ing fresh fruits and vegetables. Mrs. M was goingto be monitored on a weekly basis until the clini-cian determined she was stable. She was alsoreferred for counseling.

FOLLOW-UPMrs. M came for her weekly follow-up visits. Hervenlafaxine dose was increased by 37.5 mg week-ly until she stabilized at 150 mg daily in themorning. Her sleep normalized within 2 weeks.After 4 months of venlafaxine and thyroid sup-plementation, Mrs. M has been able to increaseher exercise to her previous level; her thyroidlevels have normalized at a dose of 100 µg oflevothyroxine without requiring T3 augmenta-tion. She is considering the possibility of lookingfor part-time work.

She has benefited from counseling, which sheis continuing on a weekly basis. After 4 weeks,she was able to reduce the visits to her clinicianto every 2 weeks. Now, after 4 months, she hasagain been able to decrease the frequency ofthese visits to once a month. After 6 months, itis anticipated that Mrs. M will be seen by her cli-nician for follow-up every 8 weeks.


20 JULY 2006


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5. Montano CB. Recognition and treatment of depression in a primarycare setting. J Clin Psychiatry. 1994;55(suppl):18-34.

6. Andersen SM, Harthorn, BH. The recognition, diagnosis, and treat-ment of mental disorders by primary care physicians. Med Care.1989;27:869-886.

7. Bostwick JM, Pankratz VS. Affective disorders and suicide risk: areexamination. Am J Psychiatry. 2000;157:1925-1932.

8. Andersen UA, Andersen M, Rosholm JU, Gram LF. Contacts to thehealth care system prior to suicide: a comprehensive analysis usingregisters for general and psychiatric hospital admissions, contacts togeneral practitioners and practicing specialists and drug prescriptions.Acta Psychiatr Scand. 2000;102:126-134.

9. Greenberg PE, Sisitsky T, Kessler RC, et al. The economic burden ofanxiety disorders in the 1990s. J Clin Psychiatry. 1999;60:427-435.

10. Massion AO, Warshaw MG, Keller MB. Quality of life and psychi-atric morbidity in panic disorder and generalized anxiety disorder. AmJ Psychiatry. 1993;150:600-607.

Ms. J is a 52-year-old woman who wasreferred to the psychiatric clinic byher obstetrician/gynecologist. Shewas having intense anxiety about

her menorrhagia; she was experiencing severecramping and was considering a hysterectomy.

Ms. J reported a lifelong history of anxietyand sensitivity to side effects of medications. Shehad a long past of being easily overwhelmed. Shereported the onset of full-fledged panic attacksover the last few months, which were character-ized by dizziness, weakness, shortness of breath,heart palpitations, numbness, tingling, feelingout of control, and shaking. These attacks, whichreached a crescendo after about 10–15 minutes,were spontaneous and came on in situationswhen she felt trapped, such as when driving orshopping or in social situations.

Ms. J did not have a history of depression anddenied feeling sad, blue, or anhedonic. Shedescribed her energy level as “fair” and has hadproblems falling asleep but not with early-morn-ing awakening. She reported having alwaysbruised easily but did not have any hematologicdisorders. The patient was so worried about havinga panic attack on the way to surgery that she was

having second thoughts about the hysterectomy,despite being repeatedly told that it was indicated.

TREATMENT Ms. J’s target symptoms included dizziness, pal-pitations, and shaking, since these were identi-fied by the patient as the most troubling. She wasinitially stabilized on clonazepam 2 mg at bed-time. She had almost immediate resolution ofthe full symptom attacks and, within 10 days,had only occasional limited symptom attacks.She had the hysterectomy, and after her initialpostoperative phase, sertraline 25 mg was initiat-ed. The dose was increased to 50 mg after 10 daysand stabilized over 30 days at 100 mg.Clonazepam was then tapered by 0.5 mg every 5days until the taper was complete.

FOLLOW-UPMs. J has remained free from panic attacks andhas been able to return to work. She is seen quar-terly for follow-up care and has resumed travel-ing, exercising, and participating in social activi-ties. She uses a modified form of bibliotherapy,based on resources from the Anxiety DisordersAssociation of America website. n

CASE STUDY: A 52-Year-Old Woman“Panicked” by Panic Attacks


JULY 2006 21

11. Mojtabai R, Olfson M, Mechanic D. Perceived need and help-seek-ing in adults with mood, anxiety, or substance use disorders. Arch GenPsychiatry. 2002;59:77-84.

12. Roy-Byrne PP, Katon W. Generalized anxiety disorder in primarycare: the precursor/modifier pathway to increased health care utiliza-tion. J Clin Psychiatry. 1997;58(suppl 3):34-48.

13. Judd LL, Kessler RC, Paulus MP, et al. Comorbidity as a fundamen-tal feature of generalized anxiety disorders: results from the NationalComorbidity Study (NCS). Acta Psychiatr Scand Suppl. 1998;393:6-11.

14. Hirschfeld RMA, Goodwin FK. In: The American Psychiatric PressTextbook of Psychiatry. Washington, DC. American Psychiatric Press.1987:403-441.

15. Depression Guideline Panel. Depression in Primary Care: Volume 1.Detection and Diagnosis. Clinical Practice Guidelines No. 5. 1993:1-65.

16. Chapman DP, Whitfield CL, Felitti VJ, et al. Adverse childhoodexperiences and the risk of depressive disorders in adulthood. J AffectDisord. 2004;82:217-225.

17. Stowe ZN, Nemeroff CB. Women at risk for postpartum-onsetmajor depression. Am J Obstet Gynecol. 1995;173:639-645.

18. Troutman BR, Cutrona CE. Nonpsychotic postpartum depressionamong adolescent mothers. J Abnorm Psychol. 1990;99:69-78.

19. Mian AI. Depression in pregnancy and the postpartum period: bal-ancing adverse effects of untreated illness with treatment risks. JPsychiatr Pract. 2005;11:389-396.

20. Janssen HJ, Cuisinier MC, Hoogduin KA, de Graauw KP. Con-trolled prospective study on the mental health of women followingpregnancy loss. Am J Psychiatry. 1996;153:226-230.

21. Weller EB, Weller RA. In: Psychiatric Disorders in Children andAdolescents. 1990:3-20.

22. Giles DE, Jarrett RB, Biggs MM, et al. Clinical predictors of recur-rence in depression. Am J Psychiatry. 1989;146:764-767.

23. Strober M, Carlson G. Bipolar illness in adolescents with majordepression: clinical, genetic, and psychopharmacologic predictors in athree- to four-year prospective follow-up investigation. Arch GenPsychiatry. 1982;39:549-555.

24. Kroenke K, Mangelsdorff AD. Common symptoms in ambulatorycare: incidence, evaluation, therapy, and outcome. Am J Med.1989;86:262-266.

25. Katon W, Von Korff M, Lin E, et al. Distressed high utilizers of med-ical care. DSM-III-R diagnoses and treatment needs. Gen HospPsychiatry. 1990;12:355-362.

26. Ohayon MM, Schatzberg AF. Using chronic pain to predict depres-sive morbidity in the general population. Arch Gen Psychiatry.2003;60:39-47.

27. Wise TN, Arnold LM, Maletic V. Management of painful physicalsymptoms associated with depression and mood disorders. CNS Spectr.2005;10(12 suppl 19):1-13.

28. Lin EH, Katon W, Von Korff M, et al. Frustrating patients: physi-cian and patient perspectives among distressed high users of medicalservices. J Gen Intern Med. 1991;6:241-246.

29. Hirschfeld RM, Keller MB, Panico S, et al. The National Depressiveand Manic-Depressive Association consensus statement on the under-treatment of depression. JAMA. 1997;277:333-340.

30. Tesar GE. Should primary care physicians screen for depression?Cleve Clin J Med. 2003;70:488-490.

31. Magruder KM, Norquist GS. Structural issues and policy in the pri-mary care management of depression. J Clin Psychiatry. 1999;60(suppl7):45-51; discussion 52-53.

32. Pignone MP, Gaynes BN, Rushton JL, et al. Ann Intern Med.2002;136:765-776.

33. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a briefdepression severity measure. J Gen Intern Med. 2001;16:606-613.

34. Lang AJ. Treating generalized anxiety disorder with cognitive-behavioral therapy. J Clin Psychiatry. 2004;65(suppl 13):14-19.

35. Linden DE. How psychotherapy changes the brain–the contribu-tion of functional neuroimaging. Mol Psychiatry. 2006;11:528-538.EPub. Available at: http://www.nature.com/mp/journal/v11/n6/full/4001816a.html. Accessed June 16, 2006.

36. Paykel ES, Scott J, Teasdale JD, et al. Prevention of relapse in resid-ual depression by cognitive therapy: a controlled trial. Arch GenPsychiatry. 1999;56:829-835.

37. Lydiard RB. In: Stein DJ, Hollander E, eds. The American PsychiatricPublishing Textbook of Anxiety Disorders. 1st ed. Washington, DC:American Psychiatric Association; 2002:348-361.

38. Sussman N. SNRIs versus SSRIs: Mechanism of action in treatingdepression and painful physical symptoms. Primary Care Companion. J Clin Psychiatry. 2003;5[suppl 7]:19-26.

39. Thase ME, Entsuah AR, Rudolph RL. Remission rates during treat-ment with venlafaxine or selective serotonin reuptake inhibitors. BrJ Psychiatry. 2001;178:234-241.

40. Keller MB, McCullough JP, Klein DN, et al. A comparison of nefa-zodone, the cognitive behavioral-analysis system of psychotherapy,and their combination for the treatment of chronic depression. N EnglJ Med. 2000;342:1462-1470.

41. Greer TL, Trivedi MH. Comorbid depression and anxiety: charac-teristics, functional consequences, and treatment considerations.University of Virginia School of Medicine Reports on PsychiatricDisorders. 2005. Available at: http://www.healthsystem.virginia.edu/internet/cme/brochures/Psych/uva-psych-dis-2-2-.pdf. Accessed March 31, 2006.

42. Grilo CM, Money R, Barlow DH, et al. Pretreatment patient factorspredicting attrition from a multicenter randomized controlled treat-ment study for panic disorder. Compr Psychiatry. 1998;39:323-332.

43. Judd LL, Akiskal HS, Maser JD, et al. Major depressive disorder: aprospective study of residual subthreshold depressive symptoms aspredictor of rapid relapse. J Affect Disord. 1998;50:97-108.

44. Fava GA, Rafanelli C, Grandi S, et al. Prevention of recurrentdepression with cognitive behavioral therapy: preliminary findings.Arch Gen Psychiatry. 1998;55:816-820.

45. Walker JR, Van Ameringen MA, Swinson R, et al. Prevention ofrelapse in generalized social phobia: results of a 24-week study inresponders to 20 weeks of sertraline treatment. J Clin Psychopharmacol.2000;20:636-644.

46. Streja DA, Hui RL, Streja E, McCombs JS. Selective contracting andpatient outcomes: a case study of formulary restrictions for selectiveserotonin reuptake inhibitor antidepressants. Am J Manag Care.1999;5:1133-1142.

47. Russell JM, Berndt ER, Miceli R, et al. Course and cost of treatmentfor depression with fluoxetine, paroxetine, and sertraline. Am J ManagCare. 1999;5:597-606.

48. Melfi CA, Chawla AJ, Croghan TW, et al. The effects of adherenceto antidepressant treatment guidelines on relapse and recurrence ofdepression. Arch Gen Psychiatry. 1998,55:1128-1132.

49. Demyttenaere K, Enzlin P, Dewe W, et al. Compliance with antide-pressants in a primary care setting, 1: Beyond lack of efficacy andadverse events. J Clin Psychiatry. 2001;62(suppl 22):30-33.

50. Katon WJ, Roy-Byrne P, Russo J, Cowley D. Cost-effectiveness andcost offset of a collaborative care intervention for primary carepatients with panic disorder. Arch Gen Psychiatry. 2002;59:1098-1104.

51. The American Association of Clinical Endocrinologists MedicalGuidelines, 2002. Available at: http://www.aace.com/pub/pdf/guide-lines/hypo_hyper.pdf. Accessed June 9, 2006.

52. Arem R. The Thyroid Solution: A Mind-Body Program for BeatingDepression and Regaining Your Emotional and Physical Health. New York:Ballantine Publishing; 1999.


22 JULY 2006


1. According to the diagnostic criteria for major depressive disorder (MDD), which condition must be present? A. Either suicidal ideation or depressed mood B. Either depressed mood or loss of interest or pleasureC. Either weight loss/gain or suicidal ideation D. Either sleep disturbances or loss of interest or pleasure

2. The prevalence of depression in the United States is highest in which setting?A. CommunityB. Primary-care clinicC. Medical inpatientD. Nursing home

3. Which of the following behaviors is most prominent in anxiety disorders?A. HypervigilanceB. IrritabilityC. Concentration problemsD. Muscle tension

4. Twenty-five percent of women with which of the following experience major depression? A. Postpartum depressionB. Pregnancy loss C. Breast cancerD. Any comorbid condition

5. Approximately one third of adolescents who are hospital-ized with severe MDD eventually receive a diagnosis of:A. Bipolar disorderB. Obsessive-compulsive disorderC. Attention-deficit/hyperactivity disorderD. Conduct disorder

6. The recommended duration of treatment to prevent relapse or recurrence for a patient who has experienced at least three episodes of MDD is:A. 6 monthsB. 1 yearC. 3 monthsD. Indefinitely

7. Which of the following statements is true about atypical antidepressant agents?A. They all have the same mechanism of action.B. They all have slightly different mechanisms of action. C. Three of them were recently removed from the market

because of an elevated risk of hepatic injury. D. They all have the net effect of decreasing levels of

serotonin and norepinephrine in the synapse.

8. Stage 1 of pharmacologic treatment for major depressionwith comorbid anxiety should consist of:A. A tricyclic antidepressant agent B. A monoamine oxidase inhibitorC. A selective serotonin reuptake inhibitor or a

serotonin/norepinephrine reuptake inhibitorD. A neuroleptic agent

9. When there are no limiting side effects in treating major depression with comorbid anxiety but a treatment ad-justment is warranted, the first intervention is usually to:A. Add another drug in the same classB. Switch to a drug in another classC. Reduce the dose intervalD. Increase the dose amount

10. Patients with which of the following are least likely to think they need help and also least likely to seek it?A. Substance disorderB. Anxiety disorderC. Mood disorder plus anxietyD. Mood disorder only

11. Of the following, the most important barrier to remission of depression and anxiety is:A. Psychiatric and medical comorbidityB. Lack of available effective treatmentsC. Age younger than 18D. Lack of available cognitive-behavioral therapies

12. In a coordinated-care model, which health-care profes-sional is responsible for tracking patients in the practice?A. PsychiatristB. Nurse practitionerC. Case manager D. Primary-care physician

CME/CE Post-TestOn the answer sheet on the following page, please darken the circle of the one answer to each question that is true.

To obtain credit, you must have 70 percent or more of the answers correct. For participants who pass the test, please allow 4 weeksafter returning the post-test and evaluation form to receive your certificate.

Completed answer sheets/program evaluations should be returned as indicated on the form. Credit is available through July 31, 2007.

Estimated time to complete: 1 hour


JULY 2006 23

1.

2.

3.

4.

5.

6.

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8.

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12.

A B C D A B C D A B C D

A B C D A B C D

A B C D A B C D

A B C D A B C D

A B C D

A B C D

A B C D

Answer Sheet and Program Evaluation

PLEASE PROVIDE THE ADDRESS TO WHICH YOU WOULD LIKE YOUR CERTIFICATE MAILED:

First Name Last Name M.I.

CHECK ONE o MD o DO o RN o NP o PA o Other:

Number & Street Address

City State ZIP Code

Phone Number ( ) Fax Number ( )

E-mail Address

I claim credits (Up to 1.0 AMA PRA category 1 credits/Up to 1.0 CE contact hours).

PROGRAM EVALUATION1. How would you rate this activity overall? (5 = excellent, 1 = poor. Please circle one.) 5 4 3 2 1

2. In your opinion, did you perceive any commercial bias? o Yes o NoIf yes, please explain:________________________________________________________________________________________________________________

3. Do you plan on making any changes in your practice as a result of this activity? o Yes o NoIf yes, please explain:________________________________________________________________________________________________________________

May we contact you in the future to determine if you made changes? o Yes o NoIf yes, please provide e-mail address:__________________________________________________________________________________________________

4. Do you feel each of the following objectives was met?

5. Do you feel that the information in this activity was based on the best evidence available? o Yes o NoIf no, please explain:________________________________________________________________________________________________________________

6. Please suggest topics for future activities._____________________________________________________________________________________________

7. Please rate the content of this activity (5 = excellent, 1 = poor. Please circle one.)

7a. Timely, up-to-date? 5 4 3 2 1

7b. Relevant to your practice? 5 4 3 2 1

8. Additional Comments:_______________________________________________________________________________________________________________

Please complete and return to Boston University School of Medicine, Office of Continuing Medical Education: E.DepressHay06Office of Continuing Medical EducationBoston University School of Medicine715 Albany Street, A-305Boston, MA 02118Phone: 617-638-4605Fax: 617-638-4905

Expiration Date: July 31, 2007.

Recognize obstacles and challenges to the optimal management of depression and anxiety o Yes o No o Partially o N/A

Identify patients who may be at risk for depression or anxiety in primary-care practice for o Yes o No o Partially o N/Awhom further screening is appropriate

Incorporate screening tools for depression into the practice setting to improve detection rates o Yes o No o Partially o N/Aof depression

Diagnose a greater number of patients with anxiety, depression, or a combination of both o Yes o No o Partially o N/A

Select the most appropriate treatment options for individual patients to improve remission o Yes o No o Partially o N/Arates and patients’ quality of life

ANSWER SHEET



PROGRAM DESCRIPTIONBoston University School of Medicine ContinuingMedical Education (BUSM CME), under the direction ofLarry Culpepper, MD, MPH, Professor and Chair, FamilyMedicine, and John Wiecha, MD, MPH, AssistantProfessor of Family Medicine, is sponsoring 2 VirtualCommunities of Practice (COP) during Fall 2006. Eachgroup will comprise 15-25 physicians, physician assis-tants, and nurse practitioners who are committed to mak-ing practice changes in the identification and manage-ment of the depressed patient. Enrollment is limited to 25individuals per group, and registration is on a first-come,first-served basis.

TARGET AUDIENCEPrimary-care physicians, nurse practitioners, and physi-cian assistants

EDUCATIONAL NEEDS ADDRESSEDAs with many chronic diseases, depression is a complexand challenging condition to effectively treat over thelong term. The likelihood of improving the managementof patients suffering from depression can be enhancedthrough changes in practice. The Boston UniversitySchool of Medicine Virtual Communities of Practice willenable each participant to have the opportunity to exam-ine his or her practice with the benefit of expert consulta-tion and peer interaction. This will result in the opportu-nity for individually tailored approaches to change.

LEARNING OBJECTIVESParticipants will:• Identify system barriers that exist in their practices that

inhibit the screening and successful case management of the depressed patient

• Develop and implement strategies to overcome the identified system barriers

• Manage the care of the depressed patient during the first 6–12 weeks of care, actively assessing the success ofselected interventions

• Transition the depressed patient from the acute to the chronic maintenance plan during the 6-to-12–week period of care

ACCREDITATIONBoston University School of Medicine is accredited by theAccreditation Council for Continuing Medical Education(ACCME) to provide continuing medical education forphysicians.

Boston University School of Medicine designates this edu-cational activity for a maximum of 20 AMA PRA Category 1Credit(s)™. Physicians should only claim credit commensu-rate with the extent of their participation in the activity.

GRANT SUPPORTThis program is supported by an educational grant fromWyeth Pharmaceuticals.

What will this require of you?• A commitment to yourself and your peers to be an

active participant in this program. The success of this program is dependent on regular participation and keeping up with the requirements of the activity.

• Approximately 2 hours per week during a 16-week period—September through November 2006—during which the following tasks must be completed: • Conduct a root-cause analysis to assess any

system/practice barriers to identifying and providing quality care for your patients with depression

• Review 5 charts to gather a “snapshot” of your current practice with depressed patients

• Create learning objectives based on a self-assessment of your learning needs

• Participate in four 1-hour teleconferences led by our faculty facilitator, during which you will review and discuss what each of you learned about your practice,discuss system/practice barriers, hear from faculty experts, and discuss what implications this informa-tion has for your practice. These teleconferences will occur in September and October 2006

• Use your COP team website to find forms, input data,access resources, and correspond with your peers andthe faculty

• Review 5 additional charts to gather a second “snap-shot” of your practice

• Reflect on the learning that has occurred as a result ofthis activity. You will be asked to report this to BUSMCME, as confirmation of your participation in this activity.

• Report on changes that you have made in your prac-tice as a result of this activity

• Complete an evaluation of this activity

What is in it for you?• Improved patient care, including better identification

of patients with depression and more effective manage-ment of patients under treatment for depression

• Better efficiency in your practice• Increased understanding of ways to improve office

systems in the care of chronically ill patients • Generation of practice-improvement data potentially

useful in earning quality-incentive payments from insurers

• Satisfaction in learning from and working with peers on an issue

• 20 CME credits

AN INVITATION TO JOIN A CME POST-ACTIVITY

Virtual Communities of Practice

If you would like to join our Virtual Communities of Practice, visit http://depression.haymarketmedical.com

EARN 20 FREE

CME CREDITS


clinicians on the front line:active management of …€¦ · depression is a highly prevalent yet...

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