1. A Modern Epidemic: Depression and Anxiety
Larry J. Witmer, D.O.
C.O.R.E. Clinical Professor
of Family Medicine
UH Aurora Family Medicine

2. Objectives
Review the definition and diagnostic signs and symptoms of GAD/MDD
Review HAMD scale for depression
Review prevalence and comorbidities of GAD/MDD
Review neurobiology of GAD/MDD
Discuss effective medical, non-medical, and alternative management of GAD/MDD
THE HAMILTON RATING SCALE FOR DEPRESSION

3. DEPRESSION

7. DSM-IV Definition of Depression (“SIG E CAPS”)
Sleep disturbance that includes insomnia or hypersomnia
Interest diminished or lack of pleasure in almost all activities most of the day, nearly every day
Guilt or feelings of worthlessness
Energy is lacking nearly daily

8. DSM-IV Definition of Depression (“SIG E CAPS”)
Concentration lacking with a diminished ability to think, or indecisiveness
Appetite change or unintentional weight loss or gain (≥5% of body weight in a month)
Psychomotor agitation or retardation
Suicidal ideation that can include recurrent thoughts of death

10. Diagnosing Depression
Major Depression (> 2 weeks)
Minor Depression (> 2 weeks)
Dysthymia (> 2 years)
≥5 depressive symptoms, including depressed mood or inability to experience pleasure, causing significant impairment in social, occupational, or other important areas of functioning
2 to 4 depressive symptoms, including depressed mood or inability to experience pleasure, causing significant impairment in social, occupational, or other important areas of functioning
3 or 4 dysthymic symptoms, including depressed mood, causing significant impairment in social, occupational, or other important areas of functioning
Dysthymia-classified as a type of affective disorder or mood disorder that often resembles a less severe, yet more chronic form of major (clinical) depression. However, persons with dysthymia may also experience major depressive episodes at times
chronic disturbance in mood involving depressed mood for at least two years. Less intense than major depression. Characterized by a depletion of usual coping strategies and the tendency to feel worse as the day progresses, most likely due to inability to cope with accumulated stressors

11. Depression – The Physical Presentation
Somatic symptoms frequently accompany depression
Depressed patients can present with ONLY somatic symptoms
90% depressed patients report comorbid anxiety symptoms

12. Depression – The Physical Presentation
In primary care, physical symptoms are often
the chief complaint in depressed patients
In a New England Journal of Medicine study, 69% of diagnosed depressed patients reported unexplained physical symptoms as their chief compliant1
N = 1146 Primary care patients with major depression
Reference:
Simon GE, et al. N Engl J Med. 1999;341(18):

13. Depression Assessment Tools
Patient Administered
Beck Depression Inventory-II (BDI-II)
Inventory of Depressive Symptomatology (IDS)
Quick Inventory of Depressive Symptomatology (QIDS)
Zung Self-Rating Depression Scale (SDS)
Physician Administered
Hamilton Rating Scale for Depression (HAMD)
Montgomery-Asberg Depression Rating Scale (MADRS)
Cornell Dysthymia Rating Scale (CDRS)
Center for Epidemiologic Studies Depression Scale (CES-D)
Depression Assessment Tools
Several depression screening instruments are available; the US Preventive Services Task Force has recommended that clinicians use the tests with which they are most comfortable and familiar.
To facilitate informed decision-making with regard to the selection of screening tools, the following section will briefly review the psychometric properties of several depression scales. The scales presented have been selected on the basis of their longstanding use in depression research, as well as their clinical utility.
Reference
U.S. Preventive Services Task Force. Ann Intern Med. 2002;136:
Whooley MA, et al. J Gen Intern Med. 1997:12:

14. The Hamilton Rating Scale for Depression
17-item and 14-item versions of symptoms covering:
depressed mood, feelings of guilt, suicide,
early insomnia, middle insomnia, late insomnia, difficulty with work & activities
psychomotor retardation, agitation, psychological
anxiety, somatic anxiety, change in appetite,
somatic symptoms (backache, headache, muscle aches, heaviness in limbs)
loss of energy, genital symptoms
loss of weight, insight, diurnal variation

15. The Hamilton Rating Scale for Depression
Scoring is on a 3-point to a 5-point scale; add all items for a total score
The higher the score, the worse the depression:
10 to 13 = mild
14 to 17 = mild to moderate
>17 = moderate to severe

16. Depressive illness is the most prevalent psychiatric disorder, and is associated with substantial morbidity and mortality. In the National Comorbidity Survey, the 12-month and lifetime prevalence rates for major depression were estimated to be 10.3 percent and 17.1 percent, respectively.
More recent data from the National Comorbidity Survey Replication study confirmed the earlier findings, with estimated 12-month and lifetime rates of depression estimated to be 6.6 percent and 16.2 percent, respectively.
References
1. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S, Wittchen HU, Kendler KS. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry. 1994;51:8-19.
2. Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, Rush AJ, Walters EE, Wang PS; National Comorbidity Survey Replication. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA. 2003;289:

17. ANXIETY

18. DSM-IV Definition of Anxiety
Persistent worry that is excessive and that the patient finds hard to control
work responsibilities, money, health, safety, car repairs, and household chores
3 of 6 symptoms usually present
High levels of muscle tension
Irritability
Difficulty concentrating
Sleep disturbances
Restlessness
Easily fatigued

19. DSM-IV Definition of Anxiety
Interference with work, family life, social activities, or other areas of functioning
Worry is out of proportion in its duration or intensity to the actual likelihood or impact of the feared situation or event
Frequently develop stress related physical illnesses such as:
IBS
TMJ
Bruxism (grinding teeth during sleep)
HTN

21. Onset of Anxiety
Insidious onset that can begin relatively early in life, although it can be precipitated by a sudden crisis at any age above 6-7 years of age
Many will say that they cannot remember a time in their lives when they were not worried about something
Not unusual for people to develop GAD in their early adult years or even later in reaction to chronic stress or anxiety-producing situations

22. Onset of Anxiety
Disorders typically develop in childhood or adolescence
By the age of 16 years, approximately 10% of young people will have an anxiety disorder of some type, with most occurring in females
Those who already have comorbid social anxiety disorder and MDD are nearly 9x more likely to have a recurrence of MDD and are 6x more likely than the general population to attempt suicide
157th Annual Meeting of the American Psychiatric Association
Conference Dates: to Location: New York, NY,USA

23. Anxiety Incidence rising in the U.S.
Worse over past several years due to economy
One of the most common mental health problems
Significant public health implications
Frequency with which they occur
Persistence of some associated conditions
Disability associated with them
Anxiety disorders are These disorders have significant public health implications because of the frequency with which they occur, the persistence of some of the conditions, and the disability associated with them.
Patients with anxiety disorders are at increased risk for comorbid depression
patients with certain chronic medical conditions are at increased risk for anxiety disorders.
Experimental models of early anxiety show that the offspring of animals who were "stressed" during pregnancy have persistently elevated, and measurable, levels of anxiety. These models mirror certain anxiety disorders in humans.
An understanding of the neurotransmitters involved in promoting anxiety can lead to a better understanding of the role of anxiolytic therapy and may also lead to more targeted treatments.

24. The average age of onset of major depressive disorder is the late 20s, but the disorder may begin at any age.
Results from epidemiological surveys consistently suggest that GAD typically begins between late teens and late 20s. Only a small number of first onsets occur subsequent to the mid-30s, but there is an increase in prevalence later in life (35-45 years of age).
Epidemiologic data suggest that first onset of social phobia occurs in childhood or adolescence. Onset of the disorder after the age of 25 is not common.
References
1. American Psychiatric Association. Practice Guideline for the Treatment of Patients with Major Depressive Disorder, 2nd Edition. Arlington, VA: American Psychiatric Association; 2000.
2. Wittchen HU, Zhao S, Kessler RC, Eaton WW. DSM-III-R generalized anxiety disorder in the National Comorbidity Survey. Arch Gen Psychiatry. 1994;51:
3. Schneier FR, Johnson J, Hornig CD, Liebowitz MR, Weissman MM. Social phobia: comorbidity and morbidity in an epidemiologic sample. Arch Gen Psychiatry ;49:

25. Prevalence estimates from the National Comorbidity Survey (NCS) suggest that anxiety disorders are the most common psychiatric diagnoses among the general population. Data from this epidemiologic study show that the 12-month and lifetime prevalence rates for any anxiety disorder (defined as panic disorder, agoraphobia, social anxiety disorder, simple phobia, and generalized anxiety disorder) are 17.2 percent and 24.9 percent, respectively.
Generalized anxiety disorder (GAD) was reported in the NCS study to have 12-month and lifetime prevalence rates of 3.1 percent and 5.1 percent, respectively, although the true rate of clinically significant GAD may be somewhat higher, due to evolving diagnostic criteria.
References
1. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S, Wittchen HU, Kendler KS. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry. 1994;51:8-19.
2. Wittchen HU, Zhao S, Kessler RC, Eaton WW. DSM-III-R generalized anxiety disorder in the National Comorbidity Survey. Arch Gen Psychiatry. 1994;51:

26. Comorbidity and Its Relevance
Depression comorbid with Anxiety
Mask GAD symptoms
Hamper GAD diagnosis and treatment
Exacerbate GAD symptoms

27. Comorbidity of GAD/MDD
Psychiatric comorbidity is a concern because it is associated with greater functional impairment and more extensive utilization of health services
People with comorbid anxiety and depression are slower to respond to both psychotherapy and pharmacologic intervention
157th Annual Meeting of the American Psychiatric Association
Conference Dates: to Location: New York, NY,USA

28. When anxiety and depression coexist, the anxiety disorder is more likely to precede the first episode of major depression, Indeed, in the NCS data, most cases of lifetime major depression were secondary, occurring in individuals with another primary disorder, of which anxiety disorders were the most common.
Comorbidity of anxiety and depression is associated with a poorer course of illness than either disorder alone. Comorbid illness tends to be of greater severity and persistence, with greater levels of functional impairment.
References
1. Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, Rush AJ, Walters EE, Wang PS: The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R). JAMA 2003; 289(23):

29. Both major depression (MDD) and generalized anxiety disorder (GAD) are associated with considerable functional impairment and disability. Co-morbid depression and GAD tends to result in greater levels of disability, as measured by the proportion of patients who report one or more days of disability in a 30 day period. Patients experience diminished functioning both at work and socially, with many reporting moderate or severe social disability.
Reference
1. Wittchen H.U. Generalized anxiety disorder: prevalence, burden, and cost to society. Depress Anxiety ;16:

30. Neurobiology of Depression and Anxiety

31. Serotonin5HT and NorepinephrineNE in the brain
Limbic System
Prefrontal Cortex
Serotonin and Norepinephrine in Depression1
Serotonin and norepinephrine are believed to be key neurotransmitters in the etiology of depression
From the raphe nuclei and locus ceruleus, 5-HT and NE, respectively, send projections up to the prefrontal cortex and limbic system where emotional depressive symptoms are thought to be mediated.
Additionally, there are also 5-HT and NE-rich tracts into the spinal cord, which are thought to modulate pain perception.
1. Adapted from Stahl SM. J Clin Psych. 2002; 63:
Locus Ceruleus (NE Source)
Raphe Nuclei (5-HT source)
Cooper JR, Bloom FE. The Biochemical Basis of Neuropharmacology

32. The neurotransmitter pathway
It’s not all in your head
Dysregulation of Serotonin (5HT) and Norepinephrine (NE) in the brain are strongly associated with depression
Dysregulation of 5HT and NE in the spinal cord may explain an increased pain perception among depressed patients1-3
Imbalances of 5HT and NE may explain the presence of both emotional and physical symptoms of depression.
Descending Pathway
Descending
Pathway
Ascending
Pathway
Ascending Pathway
Adapted from References:
Stahl SM. J. Clin Psych. 2002;63:
Verma S, et al. Int Rev Psychiatry. 2000;12:
Blier P, et al. J Psychiatry Neurosci. 2001;26(1):37-43.

34. Neurobiology
One hopeful aspect of the treatment of anxiety disorders is that some antidepressant treatments, which may be used in patients with comorbid anxiety and depression, promote neurogenesis
Primates have reduced levels of neurogenesis throughout life, so the neurogenic potential of certain therapies has implications for the treatment of anxiety

35. There are at least two sides to the neurotransmitter story
Functional domains of Serotonin and Norepinephrine1-4
Serotonin (5-HT)
Norepinephrine (NE)
Depressed Mood
Anxiety
Irritability
Thought process
Sex
Appetite
Aggression
Concentration
Interest
Motivation
Some symptoms (e.g. appetite, attention) seem to be mediated more by one neurotransmitter than the other. Some other symptoms (e.g. anxiety) seem to be mediated by either. There are other symptoms (e.g. aches and pain) that seem to be mediated more consistently by a combination of both the neurotransmitters.
Vague Aches and pain
Both serotonin and norepinephrine mediate a broad spectrum of depressive symptoms
References:
Adapted from: Stahl SM. In: Essential Psychopharmacology: Neuroscientific Basis and Practical Applications: 2nd ed. Cambridge University Press 2000.
Blier P, et al. J Psychiatry Neurosci. 2001;26(1):37-43.
Doraiswamy PM. J Clin Psychiatry. 2001;62(suppl 12):30-35.
Verma S, et al. Int Rev Psychiatry. 2000;12:

36. Neurobiology of Anxiety and Depression
Summary:
Anxiety disorders commonly lead to MDD and MDD is frequently comorbid with GAD
Functional anatomy of anxiety and depression involves (among others) the interaction between multiple areas of the brain which are complex for which studies continue
Neurochemistry of GAD/MDD involves brainstem 5-HT and NE systems

37. Optimal Treatment of Depression and Anxiety
Medications
Psychotherapy
Alternative and complementary therapies
Several alternative and complementary therapies have been found helpful in treating patients with generalized anxiety disorder. These include One herbal remedy that has been used in clinical trials for treating GAD is passionflower (Passiflora incarnata). One team of researchers found that passionflower extract was as effective as oxazepam(Serax) in relieving anxiety symptoms in a group of 36 outpatients diagnosed with GAD according to DSM-IVcriteria. In addition, the passionflower extract did not impair the subjects' job performance as frequently or as severely as the oxazepam.

38. The goals of antidepressant treatment are to reduce depressive symptoms and restore patients to wellness, or at least premorbid levels of functioning. The goal during longer term treatment is to keep patients well, preventing relapses and recurrences of depressive illness.
A number of treatment modalities are available for the management of patients with depression, including pharmacotherapy, psychotherapy, electroconvulsive therapy (ECT), or a combination of treatments. Psychotherapy alone tends to be used for patients with less severe forms of depression, and there are data to suggest that the combination of psychotherapy and pharmacotherapy is superior to either treatment by itself.
Selection of an initial treatment should be influenced both by clinical factors (such as severity of illness) and other factors such as patient preference and previous response to treatment. For patients with moderate to severe depression, antidepressant medication generally is prescribed, unless ECT is planned.
References
1. Practice guideline for the treatment of patients with major depressive disorder (revision). American Psychiatric Association. Am J Psychiatry Apr;157(4 Suppl):1-45.
2. Schulberg HC, Katon W, Simon GE, Rush AJ. Treating major depression in primary care practice: an update of the Agency for Health Care Policy and Research Practice Guidelines. Arch Gen Psychiatry 1998;55:

39. Despite the highly treatable nature of depressive disorders, it is estimated that no more than half of those with major depression actively seek and receive adequate treatment. Among the reasons for underdiagnosis of depression are that patients’ somatic complaints may mask their depression, and comorbid conditions are more readily identified. Additionally, patients may be reluctant to volunteer information or may even deny their feelings of being depressed. Increased vigilance for depressive symptoms among primary care providers and the use of structured interviews may improve the diagnosis of depression.
Even when depression is diagnosed and an antidepressant medication is prescribed, the patient may not receive adequate treatment. Among all patients starting treatment with antidepressants, the response rate is only about 50%, meaning that about half the time a patient will require some change to or addition of another treatment. Additional factors such as the delayed onset of antidepressant response and side effects that are difficult to tolerate may discourage patients from adhering to a treatment regimen. Other limitations of currently available medications include the potential for pharmacokinetic or pharmacodynamic interactions with other drugs or food, and with certain drugs there is substantial toxicity in overdose.
Efforts to develop new and better drugs for the treatment of depression are directed at overcoming these limitations. Among the strategies now being employed is the development of single-isomer drugs that may be more effective, safer and more easily tolerated than compounds derived through conventional chemical syntheses. Escitalopram is one such example of a single-isomer antidepressant.
References
1. Druss BG, Hoff RA, Rosenheck RA. Underuse of antidepressants in major depression: prevalence and correlates in a national sample of young adults. J Clin Psychiatry ;61:
2. Hirschfeld RM, Keller MB, Panico S, Aarons BS, Barlow D, Davidoff F, Endicott J, Froom J, Goldstein M, Gorman JM, Marek RG, Maurer TA, Meyer R, Phillips K, Ross J, Schwenk TL, Sharfstein SS, Thase ME, Wyatt RJ. The National Depressive and Manic-Depressive Association consensus statement on the undertreatment of depression. JAMA ;277:
3. Gumnick JF, Nemeroff CB. Problems with currently available antidepressants. J Clin Psychiatry ;61(suppl 10):5-15.

40. Major depressive disorder and generalized anxiety disorder are relapsing, chronic conditions that require long-term treatment.
References
1. Geddes JR, Carney SM, Davies C, et al. Relapse prevention with antidepressant drug treatment in depressive disorders: a systematic review. Lancet. 2003;361:
2. Rynn MA, Brawman-Mintzer O. Generalized anxiety disorder: acute and chronic treatment. CNS Spectr. 2004;9:

41. In clinical trials, about 50% to 70% of patients respond to antidepressants for the treatment of major depressive disorder, but many fail to remit. Perhaps 25% to 35% experience full remission.
In clinical trials in GAD, about 50 to 60% of patients respond to antidepressant treatment, but only about one third of patients achieve remission.
References
1. Nierenberg AA and Wright EC. Evolution of remission as the new standard in the treatment of depression. J Clin Psychiatry ;60(suppl 22):7-11.
2. Yonkers KA, Dyck IR, Warshaw M, Keller MB. Factors predicting the clinical course of generalised anxiety disorder. Br J Psychiatry ;176:

42. Traditionally, the 17-item Hamilton Rating Scale for Depression (HAMD) has been used to assess clinical response in major depressive disorder. More recently the Montgomery-Asberg Depression Rating Scale (MADRS) has gained acceptance as a reliable measure of depressive symptomatology.
The Hamilton Rating Scale for Anxiety (HAMA) is a common rating scale for GAD.
Reference
1. Ballenger JC. Clinical guidelines for establishing remission in patients with depression and anxiety. J Clin Psychiatry ;60(suppl 22):

43. The symptoms of major depression typically develop over days to weeks, although prodromal symptoms that do not meet the diagnostic threshold may occur over the preceding several months or years. In other cases, a major depressive disorder may develop suddenly. If untreated, a depressive episode typically lasts 6 months or longer.
Treatment of depression consists of an acute phase (6-12 weeks), during which improvement of depressive symptoms is monitored and then remission is induced; a continuation phase (4-9 months), during which remission is preserved; and a maintenance phase (≥ 1 year), during which the susceptible patient is protected against the recurrence of subsequent major depressive episodes.
Relapse — the reappearance of symptoms of depression during the acute or continuation phases — can occur before the patient has recovered fully from the index episode of depression, whereas “recurrence” describes the onset of a new episode of depression, after the patient has been well for 6 to 12 months. Although some people have only a single episode of major depressive disorder, it is estimated that from 50% to 85% of those who have one such episode eventually will have another.
Reference
1. Frank E, Prien RF, Jarrett RB, Keller MB, Kupfer DJ, Lavori PW, Rush AJ, Weissman MM. Conceptualization and rationale for consensus definitions of terms in major depressive disorder. Remission, recovery, relapse, and recurrence. Arch Gen Psychiatry ;48:

44. Importance of Long Term Treatment
33% of patients discontinue therapy within the first month
44% of patients discontinue therapy within the first 3 months
Masand, Clin Ther. 2003; Hamilton, Br J Clin Pharmacol
Discontinuation of antidepressant treatment prior to complete symptom resolution is common.
This slide set will review the long-term safety and efficacy of escitalopram in the treatment of major depressive disorder and generalized anxiety disorder and help physicians understand how to best treat their patients to achieve remission.
References
1. Masand PS. Tolerability and adherence issues in antidepressant therapy. Clin Ther. 2003;25:
2. Hamilton M. The clinical distinction between anxiety and depression. Br J Clin Pharmacol. 1983;15 Suppl 2:165S-1659S.

45. SSRI Treatment for MDD and GAD
Depression
Citalopram (Celexa)
Escitalopram (Lexapro)
Venlafexine (Effexor)
Duloxetine (Cymbalta)
Paroxetine (Paxil)
Fluoxetine (Prozac)
Sertraline (Zoloft)
Vilazodone (Viibryd)
Fluvoxamine (Luvox)
Anxiety
Escitalopram (Lexapro)
Venlafexine (Effexor)
Paroxetine (Paxil)
Fluoxetine (Prozac)
Sertraline (Zoloft)

46. The efficacy of citalopram, duloxetine, escitalopram, fluvoxamine, fluoxetine, paroxetine, sertraline and venlafaxine in the prevention of depression recurrence has been demonstrated in positive placebo-controlled studies.
GAD is not a recurring condition, and therefore is not included on this slide.
References
1. Hochstrasser B, Isaksen PM, Koponen H, Lauritzen L, Mahnert FA, Rouillon F, Wade AG, Andersen M, Pedersen SF, Swart JC, Nil R. Prophylactic effect of citalopram in unipolar, recurrent depression: placebo-controlled study of maintenance therapy. Br J Psychiatry. 2001;178:
2. Kornstein SG, Bose A, Li D. Maintenance treatment with escitalopram prevents recurrence of depressive episodes. Presented at the 157th Annual Meeting of the American Psychiatric Association, May 1-6, 2004, New York, NY.
3. Terra JL, Montgomery SA. Fluvoxamine prevents recurrence of depression: results of a long-term, double-blind, placebo-controlled study. Int Clin Psychopharmacol. 1998;13:55-62.
4. Montgomery SA, Dufour H, Brion S, Gailledreau J, Laqueille X, Ferrey G, Moron P, Parant-Lucena N, Singer L, Danion JM. The prophylactic efficacy of fluoxetine in unipolar depression. Br J Psychiatry ;3(suppl):69-76.
5. Franchini L, Gasperini M, Perez J, Smeraldi E, Zanardi R. Dose-response efficacy of paroxetine in preventing depressive recurrences: a randomized, double-blind study. J Clin Psychiatry. 1998;59:
6. Keller MB, Kocsis JH, Thase ME, Gelenberg AJ, Rush AJ, Koran L, Schatzberg A, Russell J, Hirschfeld R, Klein D, McCullough JP, Fawcett JA, Kornstein S, LaVange L, Harrison W. Maintenance phase efficacy of sertraline for chronic depression: a randomized controlled trial. JAMA. 1998;280:
7. Montgomery SA, Entsuah R, Hackett D, Kunz NR, Rudolph RL; Venlafaxine 335 Study Group. Venlafaxine versus placebo in the preventive treatment of recurrent major depression. J Clin Psychiatry. 2004;65:
8. Stein MB, Pollack MH, Bystritsky A, Kelsey JE, Mangano RM. Efficacy of low and higher dose extended-release venlafaxine in generalized social anxiety disorder: a 6-month randomized controlled trial. Psychopharmacology (Berl). 2005;177:
9. Montgomery SA, Entsuah R, Hackett D, Kunz NR, Rudolph RL; Venlafaxine 335 Study Group. Venlafaxine versus placebo in the preventive treatment of recurrent major depression. J Clin Psychiatry. 2004;65:
10. Simon JS, Aguiar LM, Kunz NR, Lei D. Extended-release venlafaxine in relapse prevention for patients with major depressive disorder. J Psychiatr Res. 2004;38:

47. Few get long-term treatment in the real world
Is there a need to protect patients from treatments only proven to have short-term efficacy?
Effective medications are frequently discontinued over relatively short time periods
Most patients using medications long-term are those who responded acutely and either perceive continued benefit or have suffered recurrence when attempting to taper
Few get long-term treatment in the real world
Lack of efficacy
Discontinues after
acute response
Unable to tolerate
Continues long-term
treatment
Based on Altshuler et al. AJP. 2003

48. Patients who present with any one of the following are at risk for depressive recurrence and physicians should consider them to be candidates for maintenance treatment:
Residual symptoms
More than three prior depressive episodes
Chronic depression
Family history of mood disorders
Comorbidities
Reference
1. Nierenberg AA, Petersen TJ, Alpert JE. Prevention of relapse and recurrence in depression: the role of long-term pharmacotherapy and psychotherapy. J Clin Psychiatry ;64(suppl 15):13-17.

49. Alternative and complementary therapies of MDD/GAD
Hypnotherapy/music therapy
Osteopathic manipulative therapy
2001 JAOA study in postpartum women, 8 weeks of OMT revealed 100% improvement with follow up evaluation
Ayurvedic medicine
Holistic system of healing which evolved in ancient India some years ago focusing on life energies and balance
Yoga
Religious practice
Guided imagery meditation

50. Alternative and complementary therapies of MDD/GAD
In the United States, over 40% of consumers used a complementary therapy over the course of the last year
Biofeedback and relaxation techniques to lower physiologic arousal
Massage therapy, hydrotherapy, shiatsu, and acupuncture have been reported to relieve muscle spasms or soreness
An herbal remedy that has been used in clinical trials for treating GAD is passionflower (Passiflora incarnata)

51. Alternative and complementary therapies of MDD/GAD
St. Johns Wort
May be effective in helping to support depressed mood and mood fluctuations by maintaining the balance of Serotonin, Norepinephrine, Dopamine and GABA
Zinc
An essential mineral found in almost every cell
Depression may be connected with low blood-zinc levels
Studies involving zinc supplementation in depressed patients suggest that zinc has a strong anti-depressant activity

52. Alternative and complementary therapies of MDD/GAD
Electroconvulsive Therapy (ECT)
Procedure in which electric currents are passed through the brain, intentionally triggering a brief seizure
Cause changes in brain chemistry that can quickly reverse symptoms of certain mental illnesses
Valerian Root
Direct sedative effect on the Central Nervous System
Used as a calming agent to reduce headaches, nervousness and insomnia

53. Summary
“SIG E CAPS” mnemonic to help interview those patients you suspect may have depression
90% of patients with MDD will have underlying GAD
5HT and NE are thought to be integral in pathway that leads to symptoms related to GAD/MDD
Many medical and non medical therapies available that should include psychotherapy
Ensure compliance with routine follow up visits as this can hamper efficacy of therapy

54. REFERENCES