Alternative Therapy Treatments for Depression and Anxiety


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This slide presentation is provided by Daniela White, M.D. Psychiatrist at Midtown TMS Treatment Center in Houston, Texas. with the latest in depression treatments.describes alternative treatments that are available besides the traditional pharmacological (medicine or prescription drug treatment. These alternative treatments, including TMS, are effective, evidenced based, treatment alternatives for treating depression, anxiety and other mood disorders.

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Alternative Therapy Treatments for Depression and Anxiety

  1. 1. Pharmacology and Beyond… MOOD DISORDERS © Daniela M. White, MD, 2011
  2. 2. GOALS OF THIS PRESENTATION  Create familiarity with the use of psychometric scales to help in the differential diagnosis of mood disorders  Formulate an integrative treatment, tailored to the individual needs of the patient  Provide understanding of the principles of newer treatments of depression (i.e.TMS)
  3. 3. STYLE OF THIS PRESENTATION  Created with the clinical approach in mind as a collection of clinical “pearls”  Suggests an open approach to a variety of treatment modalities  Open to discussion and questions, best at the end of it
  5. 5. AND LAST BUT NOT LEAST…  MOOD DISORDER NOS.  When nothing else fits, a diagnosis of mood disorder nos. is appropriate  Very helpful for the child and adolescent patients with ‘severe disturbance of temperament’ (a possible future diagnosis in DSM –V)
  7. 7. ESSENTIALS OF DIAGNOSIS  Sleep changes  Interest (loss of)  Guilt (worthlessness, regret)  Energy loss or fatigue  Concentration difficulties  Appetite changes  Psychomotor retardation or agitation  Suicidality
  9. 9. PHQ-9 AND QIDS-SR  Psychometric scales for depression  Help the patient to have an objective sense of their depression  Help us to evaluate the response to the treatment  Very useful for legal depositions
  10. 10. PHQ-9 AND QIDS-SR  PHQ-9 is a patient health questionnaire, comprising 9 questions.  Scoring helps differentiating between different degrees of severity of the depression  QIDS-SR – quick inventory of depressive symptoms, also allowing scoring and differentiating the degrees of depression
  11. 11. REMEMBER….IT’S NOT A BIPOLAR DISORDER IF ….  THERE IS NO HISTORY OF A MANIC OR HYPOMANIC EPISODE…  MDQ is a very handy tool for reviewing the manic/hypomanic symptoms
  12. 12. MDQ  Mood Disorder Questionnaire  Screening for bipolarity, especially sensitive for Bipolar I  13 items, reviewing symptoms of mania  7 items answered with yes , happening within the same period of time  Level of severity – moderate  Developed by Hirschfeld, MD
  13. 13. ONE MANIC OR HYPOMANIC EPISODE  Changes the diagnosis to a Bipolar Disorder  Changes the treatment  Changes the outcome
  14. 14. WHEN IN DOUBT:  ITS BETTER TO BE SAFE THEN SORRY  Is safer to err on the side of bipolar disorder (esp. in children and adolescents when the criteria are less well defined)  In doing so, explain your rationale to the caregivers  Finding the right medication can be a balancing act (unipolar vs. bipolar depression, side effects vs. therapeutic effects)
  16. 16. BIO-PSYCHO-SOCIAL MODEL  Represents factors that we need to be aware of in order to make an accurate diagnosis and treatment BEHAVIOR Coping illness COGNITIVE Appraisal Meaning perception SOCIO- CULTURAL Social support Customs values ENVIRONMENT Life events BIOLOGY Genetics; Biological response BIO- PSYCHO- SOCIAL
  17. 17. BIOLOGY OF DEPRESSION • Genetic predisposition (suggested by the familial nature of the depression or mood disorder) • Medical conditions: low vitamin D, low B12, hypothyroidism, autoimmune disorders; low testosterone, blood dyscresias ( anemia)
  18. 18. BIOLOGY OF DEPRESSION  Depletion of monoamine levels;  Abnormalities of intracellular signal transmission and/or gene expression;  Other neurotransmitters (GABA, glycine etc);  Hormones (thyroid and adrenal hormones);  Neuropeptides (CRH,endorphines,substance P)
  19. 19. NEUROENDOCRINE FACTORS  Abnormalities of the HPA axis (hypothalamic- pituitary-adrenal axis) : increased cortisol, increased ACTH  Most depressed patients are euthyroid; some have subclinical hypothyroidism ( more association with cognitive impairment)  BDNF( brain derived neurotropic factor) levels are decreased with stress
  20. 20. BRAIN IMAGING  Decreased left prefrontal cortex (PFC) blood flow and metabolism  Basal ganglia abnormalities  Increased amygdala activity  Abnormalities in hippocampus
  21. 21. NEURAL MODEL  Dysfunction of the DLPFC, limbic and striatal systems impair the modulation of the amygdala/hippocampal structures  Neuroimaging is not cost effective for the clinical practice, at this point (not used for diagnosis purposes)
  22. 22. PSYCHOLOGY OF DEPRESSION  Psychoanalytic and psychodynamic theories (depression as a result of loss, anger turned against self …)  Behavioral and cognitive theories ( cognitive distortions and misrepresentation of life events)
  23. 23. SOCIAL-ENVIRONMENTAL FACTORS ASSOCIATED WITH DEPRESSION  Life events ( death, divorce, loss of loved one, loss of career, change in career, job conflicts...)  Evaluate social network ( let’s not forget the social media…FB, twitter)  Evaluate spiritual or religious life, belief system  Family life, living situation, family diagram, family conflicts…  Military service  Hobbies, extracurricular activities  Exercise, nutrition, sleep habits
  24. 24. WHAT FOLLOWS NEXT?  How do we formulate treatment?  Following the same guidelines of the bio- psycho-social model…towards an integrative approach in psychiatry
  25. 25. INTEGRATIVE TREATMENT  Pharmacological (SSRI, SNRI, NRI, SSRI+ 5HT1 partial agonist, SSRI+ 5HT2 antagonism)  Biological treatments (TMS, light therapy)  Psychological treatment (various forms of therapy)  CAM (complementary and alternative medicine) including: -Meditation for stress management (yoga) -Dietary guidelines, exercise, nutritional supplements -Botanical remedies -Bibliotherapy ( effective treatment for mild moderate)
  26. 26. PHARMACOLOGICAL TREATMENT  Antidepressants (SSRI, SNRI, NRI, SSRI+5HT1 partial agonists)  Check for a family history of a good response to a particular antidepressant  What worked before will work again  Some patients are sensitive to the difference between brands and different generics
  27. 27. PHARMACOLOGICAL TREATMENT  Always optimize one medication before switching the class or augmenting  Discuss side effects ( patient education is very helpful to increase compliance)  Take into account patient’s financial concerns (increases compliance)  Discontinue medications that do not work to avoid unnecessary polypharmacy  More doses, less compliance
  28. 28. SSRIs  All of them in generic forms, including Lexapro;  Mostly helpful in depression with anxiety, obsessive features;  Less desirable for lethargic forms of depression;  Increased crave for carbohydrates, possible weight gain and sexual side effects;
  29. 29. SSRI’s continue..  Risk of SSRI induced apathy ( patients are not depressed anymore, just blah..)  Risk of SIADH – rare, but possible especially with polypharmacy  Possible drug-drug interactions with fluoxetine, paroxetine, less with escitalopram  Prozac FDA approved for child/adolescent depression
  30. 30. SSRI’S continues  Sertraline FDA approved for OCD in children and adolescent patients  Lexapro approved for GAD and depression in 10-13 years old  Discuss with patients and the families the black box warning ( suicide risk under age 24)  MDD could end with suicide, as an outcome to the lack of medical intervention
  31. 31. SNRI-Cymbalta, Effexor, Pristiq  Think about them like the broad range antibiotic…work on serotonin and norepinephrine  Cymbalta has equal action on both S and NE from a lower dose  Effexor and Pristiq tend to act more on NE as the dose escalates, at lower doses acts like SSRI (more or less)  Less apathy because of the NE component  Less sexual side effects because of NE component (especially with women)
  32. 32. SNRI continue  Risk of HTN with Pristiq, Effexor, less with Cymbalta  Less discontinuation syndrome with Cymbalta, because of the longer half-life time  Warnings for the Serotonin syndrome from the pharmacies and manufacturers
  33. 33. NRI –wellbutrin, aplenzin and generics  Great antidepressants, but not antianxiety medications  Rarely useful in anxious depressed patients, could increase the anxiety levels  No sexual side effects, no weight gain  Help with the SSRI induced apathy, because of the NE component.
  34. 34. TRAZODONE AND VIIBRYD  Practically weight neutral and not causing sexual side effects  Viibryd works as SSRI and partial 5HT1 agonist  Trazodone works as a SSRI and 5HT2 antagonism( SARI=serotonin antagonist-reuptake inhibition)  Oleptro (Trazodone –ER) helps with sleep, the formulation allows qhs dosing, less next day drowsiness then Trazodone-IR  Viibryd: absorption is increased with food ( also nausea, a main side effect is mitigated when given with food)
  35. 35. MIRTAZEPINE  Antagonism of pre-synaptic alpha2-receptors  Helps the depression associated with anxiety  Main side effects are weight gain and sedation; no sexual side effects  Has antiemetic properties  Could cause granulocitopenia (pay attention to increase frequency of sore throat complaints)
  36. 36. MOST COMMOM STRATEGIES  Augmentation with atypical antipsychotics (Abilify, Seroquel, Zyprexa)  Weight gain a possible side effect, as well as next day sedation; akathisia possible with Abilify  Fairly rapid response, within two weeks separation on MADRAS scales from placebo
  37. 37. Continue…  Thyroid, lithium augmentation ( needs TFT’s monitoring, and li levels)  Lithium shown as having antisuicidal properties, even at lower doses 300-600 mg/day  Lamictal augmentation, not as popular  Folate (Deplin) supplementation enhances the response to antidepressants  Buspar augmentation suggested by STAR -D  Pindolol augmentation also noted to increase the rate of response to antidepressants
  38. 38. QUESTIONS?
  39. 39. Best Practices Treatment Guideline for Depression Based on 2010 APA practice guidelines and NeuroStar TMS Therapy® indication for use. Adapted from: Practice Guideline for the Treatment of Patients with Major Depressive Disorder, 3rd Edition, APA (2010) 39 Unmet Medical Needs
  40. 40. BIOLOGICAL TREATMENTS TMS – the new kid on the block Light therapy
  41. 41. Transcranial Magnetic Stimulation (TMS)  The treatment coil produces MRI-strength magnetic field pulses.  Magnetic field pulses pass unimpeded through the cranium for 2-3 cm. and induce a small electric current.  Induced electric currents stimulate the firing of nearby neurons, causing the release of neurotransmitters and clinical effects. Faraday (1839) Experimental Research in Electricity. Vol 1; Barker (1991) J Clin Neurophysiol; Barker (1985) Lancet 41 A Proven Approach
  42. 42. TMS Requires a Neurostar Device Chair Computer system
  43. 43. TMS  Refer back to the APA 2010 guidelines  FDA clearance since 2008 for depressed patients who failed between 1-4 trials of antidepressants  Indicated before the atypical augmentation  Delivers treatment locally, therefore it has no systemic side effects
  44. 44. Treating the Brain as an Electrochemical Target Major brain regions known to be involved in mood regulation Amygdala Ventromedial Prefrontal Cortex Prefrontal Cortex Anterior Cingulate Gyrus Brain activity can be altered: • Chemically (eg, via drugs) or, • Electrically (eg, via TMS) – Drug action is anatomically diffuse and systemic – TMS is focused, non- invasive and non-systemic Pizzigalli (2011) Neuropsychopharmacology 44 A Proven Approach
  45. 45. TMS  One of the four types of neuromodulation  Other neuromodulation treatments: DBS, VNS, ECT  The only one that is not invasive  The patient is awake while receiving treatment
  46. 46. Activation of fronto-cingulate brain circuit following a course of TMS applied to the left dorsolateral prefrontal cortex in patients with Major Depression Targeted Effects on Mood Circuits in Brain Kito (2008) J Neuropsychiatry Clin Neurosci TMS Coil L L R R 46 A Proven Approach
  47. 47. TMS  Moving magnetic field creates electrical currents that penetrate thru DLPFC and reach hippocampal structures, targeting the amygdala  Locally depolarizes neurons and creates changes in the neurotransmitters at the postsynaptic levels
  48. 48. LIGHT THERAPY  Usually used to treat Seasonal Affective Disorder with specially build lamps  Parameters for use are 7000 lx intensity at 20 inches exposure, about 60 minutes, in the morning after arousal  Has been used in the treatment for unipolar depression in special population (pregnant and elderly patients)  Shows improvement compared to the placebo studies using blue or red light exposure
  49. 49. COMORBID MEDICAL PROBLEMS  Need to be addressed accordingly  Refer to a PCP and establish a good connection to help coordinate treatment (adequate treatment of HTN, obesity, diabetes, anemia, low testosterone levels)  Refer to a specialist for endocrine problems (hypothyroidism, adrenal insufficiency, hypogonadism)
  50. 50. CAM  Complementary and Alternative Medicine  Used in addition to conventional medicine  Represents a diverse set of therapies  Most commonly represented by the dietary supplements  Also includes: acupuncture, hypnosis, homeopathy, ayurveda yoga, meditation etc
  52. 52. NUTRITION- the minimum we could do  Ask about the number of meals and snacks per day  Ask about food preferences  Ask about illnesses that could require special diets or expose patients to certain nutritional deficits (malabsorption of B12, Folic acid)  Ask patients to keep a journal of their daily intake, of food and beverages (include water, soda and alcohol intake) for 3-5 days
  53. 53. NUTRITION-the minimum we could do  DIABETES patients could have hypoglycemic episodes that could cause palpitation and diaphoresis, irritability  ALCOHOL dependent patient could have B12, folic acid malabsorption – contributing to the depressive symptoms, lack of energy  Folic acid deficiency reduces the response to antidepressant ( less substrate for their action)
  54. 54. NUTRITION - supplements  If deficient in folic acid or B12, supplement with folic acid (OTC) or Deplin ( metfolate)  B12 injections and the nasal spray have a better absorption rate that the oral tablets  Sometimes blood levels are irrelevant, and a lot of physicians supplement based on the history of poor/inadequate nutrition  Encourage a balance diet, sometimes calculating the baseline metabolic rate help the patient to establish goals ( there are apps for that)  Vit D. deficiency-supplement with vit D
  55. 55. EXERCISE  Ask patient if exercise is part of their daily or weekly routine  Ask details about what the exercise involves  Playing drums, picking up the mail, or walking the dog doesn’t count as physical exercise  The minimum they could do is walking with a speed of 2 per 30 minutes, 4-5 times per week
  56. 56. EXERCISE-common chores examples  Washing and waxing a car for 45-60 min  Washing windows or floors for 45-60 min  Gardening for 30-45 min  Wheeling self in wheelchair for 30-40 min  Raking leaves for 30 min  Stair walking for 15 minutes  etc
  57. 57. EXERCISE-AT WORK  Stand instead of sitting when talking on the phone  Take the stairs instead of the elevators  Walk down the hall to talk to somebody then calling on the phone  Schedule exercise time and treat it like a business appointment
  58. 58. EXERCISE – overcoming barriers  Ask about physical exercise at every appointment  Discuss benefits of exercise for depression (augmentation value to antidepressants)  Recommend exercise as a prescription  Encourage patient to increase physical activity daily
  59. 59. EXERCISE – possible mechanisms  Elevations of endorphins in CNS  Changes in Serotonin and Norepinephrine  Increased levels of BDNF (Brain Derived Neurotrophic Factor)  Reduction of serum cortisol  Elevation of body temperature  Improved self-esteem  Distraction from daily stress  Induction of a relaxed state via biofeedback
  60. 60. YOGA  Can reduce depressive symptoms and induce remission  Questionable application in older or less fitted patients ( since the patients in the studies were young and relatively fit)  No safety issues or adverse events
  61. 61. MEDITATION  Is a complex mental process that involves changes in cognition, sensory perception, emotions, hormones and autonomic activity.  Likely affects different neurotransmitters systems, including dopamine, serotonin, glutamate.  The overall understanding of the biological mechanism in terms of the effects on body and brain is still limited.
  62. 62. MEDITATION  attempts to reach a subjective state characterized by a sense of no space, no time, no thought (i.e. thevada)  attempts to focus attention on a particular image, object, phrase, or word (tibetan buddhism)  focuses on whatever thought and feelings enter the mind (mindfulness meditation)  etc
  63. 63. GOALS of MEDITATION • Used in psychiatric and medical practices for stress management • Depression relapse prevention programs • Pain treatment • Eating disorders • etc
  64. 64. St. John’s wort  Hypericum perforatum)  Induces significantly higher remission rates than placebo in mild to moderate depression  900-1500 mg/day  Can affect blood levels of medications metabolized by Cyt P450  Mostly recommended for depressed patients who can’t tolerate SSRIs
  65. 65. SAMe  Metabolite involved in biosynthesis of norepinephrine, serotonin, dopamine  Shows greater efficacy then placebo  800-1600 mg/d  Can be used as an adjunctive treatment for incomplete response to standard treatment  Can be used as a complementary treatment to speed the onset of antidepressants
  66. 66. PUFA-polyunsaturated fatty acids  Most commonly known Omega 3 (EPA and DHA) come from fish oil  Most sources of Omega 6 come from cooking oil  The ratio between Omega 6 and Omega 3 is currently greater then 10:1 when “ man has evolved on a diet ratio of 1:1”  The change in ratio has been linked with a lot of health problems, including emotional problems
  67. 67. OMEGA 3-Dietary Recommendations  Two servings of fatty fish each week  One caps of most supplements has 180 mg of EPA and 120 mg of DHA  3 capsules per day are needed to reduce cardiac risk (900 mg )  Patients with cardiovascular disease have a higher incidence of depression  Depression studies used higher doses ( 1800-9000 mg of n-3)
  68. 68. HYPNOSIS  Is a social interaction in which one person, designated the subject , responds to suggestions offered by another person, designated the hypnotist, for experiences involving alterations in perceptions, memory and voluntary action.  Depends upon the dissociation from normal thought process and awareness, and a relative shift towards the unconscious process.
  69. 69. HYPNOSIS  Is rarely a therapy in itself but rather a vehicle for therapy when the unconscious mind would otherwise get in the way.  The hypnotist is guiding the patient to self- hypnosis.  Patient’s ability to do so depends on the relationship he has with the hypnotist.
  70. 70. HYPNOSIS APPLICATIONS  Ego strengthening  Anxiety  Depression  Stress reduction  Public speaking fear  etc
  71. 71. PSYCHOTHERAPY  Interpersonal psychotherapy- addresses interpersonal loses, social isolation, role transitions and disputes, deficits in social skills  Cognitive therapy- helps patients recognize and correct erroneous beliefs and maladaptive behaviors
  72. 72. PSYCHOTHERAPY  Marital and family therapy- reduces the risk of relapse in depressed patients who also have marital problems  Selection of the specific therapy is based on the patients needs and strengths
  73. 73. QUESTIONS?
  75. 75. BIPOLAR DISORDERS  I – episodes of mania cycling with depressive episodes  II- episodes of hypomania cycling with depressive episodes  Cyclothymia- hypomania cycling with less severe episodes of depression  MANIA WITHOUT DEPRESSION IS VERY RARE
  76. 76. MANIC EPISODE  Inflated self esteem/grandiosity  Decreased need for sleep  Talkativeness  Flight of ideas  Distractibility  Increased goal directed activity/agitation  Engaging in high risk activities
  77. 77. MDQ  Mood Disorder Questionnaire  Screening for bipolarity, especially sensitive for Bipolar I  13 items, reviewing symptoms of mania  7 items answered with yes , happening within the same period of time  Level of severity – moderate  Developed by Hirschfeld, MD
  78. 78. BIO-PSYCHO-SOCIAL MODEL  Represents factors that we need to be aware of in order to make an accurate diagnosis and treatment BEHAVIOR Coping illness COGNITIVE Appraisal Meaning perception SOCIO- CULTURAL Social support Customs values ENVIRONMENT Life events BIOLOGY Genetics; Biological response BIO- PSYCHO- SOCIAL
  79. 79. BIOLOGICAL FACTORS  BP has a strong genetic association, more then 2/3 of patients show family history of affective disorder  Neurotransmitters theories conceptualized depression and mania as two opposing poles  i.e.: less NE/S available in depression, more NE/S present in mania ( antidepressants increasing the levels of NE/S induce mania)
  80. 80. BIOLOGICAL FACTORS  Abnormalities in electrolyte distribution in affective disorders ( retention of sodium during intracellularly during depression)  The activity of sodium/potassium-activated ATP-ase is lower in the depressive phases  Lithium responders are reported to have lower erythrocyte Na/K ATPase
  81. 81. PSYCHOSOCIAL THEORIES  Same as in depression  More stressful life events precede earlier episodes  Early episodes increase the vulnerability for future episodes  Kindling- repeated episodes increase the severity and duration of the illness
  82. 82. PHARMACOTHERAPY of BIPOLAR DISORDER  Treatment of acute mania  Treatment of acute bipolar depression  Maintenance treatment of bipolar disorder
  83. 83. ACUTE MANIA  MOOD STABILIZERS  Typical (lithium carbonate, valproate, carbamazepine)  Atypical antipsychotics (all of them approved by FDA for antimanic properties except LATUDA (lurasidone)
  84. 84. MOOD STABILIZERS  First line-atypicals  Easier to use (no need for frequent monitoring of blood levels) and faster response  Less likelihood of toxicity (vs. lithium or carbamazepine)  Safer in overdose  Adverse effects include weight gain and possibility of metabolic syndrome (need monitoring of weight, lipid panel, VS)  All, but one FDA approved, for mania treatment  One approved for both mania and depression (Seroquel)
  85. 85. MOOD STABILIZERS  Traditional mood stabilizers tend to be added on to atypicals if failure to respond exist  LITHIUM levels need to be 0.6-1.2 mEq/L ( varies slightly with the laboratory used)  High potential of toxicity (with NSAIDS, dehydration and low salt–diet)  Monitor for side effects and the appearance of new ones during the treatment (signs of toxicity)  Still very reliable and the cheapest on the market
  86. 86. MOOD STABILIZERS  VALPROATE-750-2500 MG/DAY  Rapid oral loading at 15-20 mg /kg  Faster response then lithium  Risk of liver toxicity, need to check LFT  For women in child age bearing age, supplement with high doses of folic acid ( preventive of neural tubal defects)  Blood levels btw 50-120ug/ml  Increases levels of other medication by enzyme inhibition
  87. 87. MOOD STABILIZERS  CARBAMAZEPINE  Approved for mania in 2004  600-1800 mg /day  Blood levels of 4-12 ug/mL  Add high doses of folic acid for women with child bearing potential  Potential of blood dyscrasias ( check CBC)  Weight neutral is a great benefit  Decreases levels of other medications by enzymes induction
  88. 88. BIPOLAR DEPRESSION  Most antidepressants do not work, work for a short period of time or induce mania  Best treatment is a mood stabilizer (i.e.lithium, or atypicals with that indication-Seroquel, or Symbiax)  A combination of two mood stabilizers if one fails to induce response/remission  An antidepressant could be added as a third line  Lamictal or Ziprazidone low doses could also work ( not FDA approved)
  89. 89. OTHER TREATMENTS TMS, Light therapy, ECT All the other treatments discussed in the MDD treatment Therapy including the education about the disorder
  90. 90. MAINTENANCE TREATMENT OF BIPOLAR DISORDER  Prevention of recurrent episodes is the greatest challenge  Kindling will make future episodes more severe and more difficult to treat ( rapid cycling occurs later in the disorder
  91. 91. FDA Approved Agents for BD AGENT MANIA MAINTENANCE Aripiprazol Yes (2004) No Carbamazepine XR Yes (2004) No Divalproex Yes (1996) No Lamotrigine No Yes (2003) Lithium Yes (1970) Yes (1974) Olanzepine Yes (2000) Yes (2004) Risperidone Yes (2003) No Asenapine Yes (2009) No Quetiapine Yes (2004) No Ziprazidone Yes (2004) No
  92. 92. PRINCIPLES OF BD TREATMENT  Maintain dual focus: short term and prophylaxis  Mania as medical emergency: treat first, chemistries later  Load lithium and valproate; titrate lamotrigine  Retain lithium in treatment for antisuicidal and neuroprotective properties  Educate patient about the illness  Use regular visits  Contract with patient as needed for suicide and substance use avoidance
  93. 93. DYSTHYMIA  Depressed mood most of the day and present almost continuously  “ill humored” – term introduced in 1980  Used to be called-”depressive neurosis”  Pts. complain that they have always been depressed (early onset)  Low-grade chronicity for about 2 years  5-6 % in general population
  94. 94. BIO-PSYCHOSOCIAL MODEL  Biological Factors: similar to depression  Psychosocial Factors: – Personality and ego development culminating with difficulties adapting in adolescence – Early interpersonal disappointment leads to ambivalent love relationship as an adult – Disparity between actual and fantasized situations lead to diminished self-esteem – etc.
  95. 95. TREATMENT  Psychotherapy is considered the treatment of choice  Medications such as an NRI (bupropion) and SNRI (venlafaxine, duloxetine) are effective treatments  Exercise, healthy diet  Meditation  Supplements such as PUFA and Vit B12, folic acid (for documented deficiencies)
  96. 96. CYCLOTHYMIC DISORDER  A mild form of Bipolar Disorder II  Has episodes of hypomania and mild depression  Mostly agreed over a biological origin of the disorder  Some psychiatrists believe it’s just the result of a chaotic life
  97. 97. TREATMENT  Biological therapies – Mood stabilizers as the first line – Caution with antidepressant since the high risk of inducing a manic episode (40-50 % conversion) – Same guidelines for the dosing of mood stabilizers
  98. 98. TREATMENT  Psychosocial therapies  Increasing the awareness about the disorder  Family and group therapy to repair the damage caused by the disorder  CAM  Exercise  Dietary supplementation (PUFA)  Bibliotherapy (i.e. An Unquiet Mind)  Meditation  etc
  99. 99. MOOD DISORDER NOS  A very common diagnosis for children and adolescent psychiatry  Anytime there are difficulties in distinguishing between depression and mania and doesn't meet criteria for other diagnosis (different then the mixed episode when depressive and hypomanic symptoms coexist)  Use mood stabilizers as the first line treatment
  100. 100. QUESTIONS?