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Ask the Expert: Depression Presenter: Kenneth J. Herrmann, MD NAMI Conference Spring 2014.

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Presentation on theme: "Ask the Expert: Depression Presenter: Kenneth J. Herrmann, MD NAMI Conference Spring 2014."— Presentation transcript:

1 Ask the Expert: Depression Presenter: Kenneth J. Herrmann, MD NAMI Conference Spring 2014

2  Medical School at Chicago Medical School  Internship, residency in general psychiatry, fellowship in child and adolescent psychiatry at the University of Iowa  Formerly, Medical Director of Youth Services at the Mental Health Center of Dane Co.  Psychiatric Consultant, Psychiatric Services SC,  Past Vice-President, Board of Directors NAMI WI  Principal, My World Defense, A Healthcare Security Company, Kenneth J Herrmann M.D.

3  Irritable/Depressed mood, diminished pleasure/interest  Weight changes of greater than 5% in one month  Insomnia or hypersomnia  Psychomotor agitation or retardation  Fatigue or loss of energy, poor concentration  Feelings of worthlessness, suicidal thoughts, guilt Diagnosis of Major Depressive Disorder

4  Genetic factors  Personality and environmental factors  Biochemical abnormalities Etiology of Depression

5 Depression -Duration average of 7 1/2 months -44% in remission within 6 months of Dx -92% recovered by 1 ½ years -72% recurrence within five years Prognosis - Adolescence

6  Depression: -2% of children in general population -7% depression in children admitted to Hospital -40% children in ped neuro clinics with headaches=depression -4.7% ages 14-16 (3.3% dysthymia) (as age increases female rates increase) -one in five adolescents by age 20 -Lifetime: Males 12% Females 25% EPIDEMIOLOGY

7  Age at onset is decreasing  Incidence is increasing Trends for Affective Disorders

8  Substance Use  Prematurity  Family History  Head Injury Risk Factors For Mood Disorders

9  Hard to recruit for certain disorders  FDA requirements for drug approval  Funding  Exclusion criteria  Dropout rates  Liability  Time from idea to publication Limitations of Current Research

10  Moderate to severe depression  Fluoxetine alone or in combo with CBT  13 academic and community sites in the US  12-17 yrs old  Combined > mono  42 week total study time  Study start 7/98, completed 3/04 Arch. Gen. Psychiatry 10/07 The Treatment for Adolescents with Depression Study (TADS)

11 Thinking Outside the Box?

12  ? Adequate information  ? Diagnosis  Increase in antidep. use / decrease in suicides over 10 years prior to warning FDA warnings and the Antidepressants

13 CONCLUSIONS: In both the United States and the Netherlands, SSRI prescriptions for children and adolescents decreased after U.S. and European regulatory agencies issued warnings about a possible suicide risk with antidepressant use in pediatric patients, and these decreases were associated with increases in suicide rates in children and adolescents. Gibbons etal. Am J. Psychiatry 9/07

14 Diagnostic Accuracy is Most Important

15  Elevated, expansive or irritable mood  Inflated self-esteem or grandiosity  Decreased need for sleep  More talkative (distractible)  Flight of ideas or racing thoughts  Increase in activity  Foolish indulgencies Mania/Bipolar Affective Disorder (BPAD)

16  Grandiosity  Inappropriate sexual interest  Psychotic symptoms  “ Ultrarapid ” cycling Characteristics of BPAD in Children

17 … you felt so good or so hyper that other people thought you were not your normal self or you were so hyper that you got into trouble? … you were so irritable that you shouted at people or started fights or arguments? … you felt much more self-confident than usual? … you got much less sleep than usual and found you didn’t really miss it? … you were much more talkative or spoke much faster than usual? … thoughts raced through your head or you couldn’t slow your mind down? Mood Disorder Questionnaire Hirschfeld et al. Am J Psychiatry. 2000;157:1873-1875. Has there ever been a period of time when you were not your usual self and…

18 … you were so easily distracted by things around you that you had trouble concentrating or staying on track? … you had much more energy than usual? … you were much more active or did many more things than usual? …you were much more social or outgoing than usual; for example, you telephoned friends in the middle of the night? … you were much more interested in sex than usual? … you did things that were unusual for you or that other people might have thought were excessive, foolish, or risky? … spending money got you or your family into trouble? Mood Disorder Questionnaire (cont ’ d) Hirschfeld et al. Am J Psychiatry. 2000;157:1873-1875.

19 Depression  Adolescents 30% BPAD switch Irritability  Adults 10% switch Sadness

20 Depressive symptoms were predominant Over the long term, patients with bipolar I disorder spent nearly half of their time symptomatically ill Depression accounted for 31.9% of the time Patients experienced manic symptoms 9.3% of the time Depression (but not mania) predicted greater future illness burden Judd et al. Arch Gen Psychiatry. 2002;59:530-537. Long-term Frequency of Depressive Symptoms (Percent of Follow-up Weeks) Patients with bipolar I disorder experienced mood symptoms nearly half of the time during a 12.8-year follow-up period.

21 Age of Onset (Pooled Data N=1,304) Goodwin F, Jamison K. Manic Depression. New York: Oxford University Press; 1990.

22  Acute onset  Hypersomnic retarded depression  Psychosis  Postpartum onset  Family history  Antidepressant Hypersomnia Predictors of BPAD Outcome

23 Treatment for Depression

24  Cognitive Behavioral Therapy (CBT)  Dialectical behavior therapy (DBT)  Mindfulness Non-Medical Txment of Depression


26 NEUROTRANSMITTER EFFECTS OF ANTIDEPRESSANTS  NE5-HT DA  Bupropion SR   SSRIs  Venlafaxine   Nefazodone  Mirtazapine   Desipramine  Richelson. J Clin Psychiatry. 1994

27  Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 2010 The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity

28  Bupropion  Serotonin (re)-uptake inhibitors  TCA ’ s (Tricyclic Antidepressant)  Others: Nefazodone, Trazadone, Mirtazapine, Venlafaxine, duloxetine MAOI ’ s (including Selegiline (Emsam patch))  ECT  Trancranial Magnetic Stimulation (TMS) Somatic Depression Treatment

29  Vilazodone (Viibryd): diarrhea, nausea or vomiting, and trouble sleeping, increases serotonin.  Vortioxetine (Brintellix): nausea, constipation, and vomiting, increases serotonin  Levomilnacacipran (Fetzima): nausea or vomiting, constipation, sweating, increased heart rate, erectile dysfunction, and palpitations, increases serotonin and norepinephrine. Newer Antidepressants

30  Comorbidities: anxiety, subst. abuse,  Compliance  Formulary (preferred drug list)  Medical legal  Indication (“Off Label?”)  Side Effects Things to consider with meds

31 Treatment: Lamotrigine (Lamictal)  Positives: Once a day dosing possible No Blood tests Few complaints of SE ’ s  Negatives Long time to get up to good dose Rash ?

32 Neuroleptics (antipsychotics) Mood Disorders (primarily BD) Schizophrenia/Schizoaffective Some Sxs of PTSD

33  WBC monitoring  Constipation  Dizziness  Sedation  Miracle Clozapine

34  Wgt neutral?, EPS, Nonsedating, Agitation  FDA approved ABILIFY® (aripiprazole) for the acute treatment of manic and mixed episodes, maintenance treatment of manic or mixed episodes, and as add-on treatment to lithium or valproate, associated with Bipolar I Disorder, with or without psychotic features, and schizophrenia in pediatric patients (10 to 17 years old). Refractoy DepressionABILIFY Aripiprazole (Abilify)

35 Treatment: Risperidone (Risperdal)  Positives: No blood tests Once a day dosing Fast Shotgun FDA approved Risperdal (risperidone) for the treatment of schizophrenia in adolescents, ages 13 to 17, and for the short- term treatment of manic or mixed episodes of bipolar I disorder in children and adolescents ages 10 to 17.  Negatives: Prolactin Some reports of mania induction Weight gain Sedation NMS Tardive dyskinesia Diabetes risk

36 Treatment: Olanzapine (Zyprexa)  Positives: No blood tests Once a day dosing Data FDA indication Fast Shotgun  Negatives: Sedation Weight gain Diabetes risk

37  Wgt neutral  Sedating vs activating  Efficacy? Ziprasidone (Geodon)

38  Midrange sedation  Midrange wgt gain  Diabetes risk  Refractory Depression  Bipolar Depression Quetiapine (Seroquel)

39 Treatment: Lithium  Positives: Low suicide rates FDA approved 12yrs and older Long history of use Once a day dosing Cheap Negatives: Narrow therapeutic window Fluid balance issues Monitoring (thyroid & kidney) Acne Weight

40  Lurasidone (Latuda): (Bipolar Depression)Once a day, with food, sedation and EPS  Asenapine (Saphris): Once a day, disolves in mouth- some find unpleasant taste  Iloperidone (Fanapt) Twice a day The 3 Newest

41  SADS  Hospice family members Buproprion For Prevention of Depressive sx ’ s

42  ADHD: stimulants, bupropion, ?modafinil  Anxiety: (OCD too) gabapentine, tiagabine, SSRI, TCA  Depression: ECT, additional mood stabilizer (lamotrigine), antidepressant if we must  Fatigue: modafinil, stimulants  Insomnia: benzodiazepines, neuroleptics, mirtazepine, trazadone  Mania: mood stabilizer, neuroleptic Combined therapy: symptoms/ co- occurring conditions

43 Neurotrophic Effects of Mood Stabilizers? MRI studies “ …revealed that chronic lithium significantly increases total grey mattervolume in the human brain of patients with manic- depressive illness. Neuroprotective? “ …lithium and valproate have recently been demonstrated to robustly increase the expression of the cytoprotective protein bcl-2 in the central nervous system. ” Husseini et. al. The Good News

44  “Your doctor may use cytochrome P450 tests (CYP450 tests) to help determine how your body processes (metabolizes) a drug. Our bodies contain numerous P450 enzymes to process medications. Because of inherited (genetic) traits which cause variations in these enzymes, medications affect each person differently.” From a Mouth Swab

45 Genetic Testing

46  Earlier Identification and Aggressive Txmnt  Increase focus on primary and especially secondary Prevention  Neurotransmitter and enzyme specific treatment.  More delineation of “ Normal ” behavior and it ’ s relationship to our genes.  More Exploration of Combined Therapy  Remission not just response Future Trends Summary

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