This slide presentation is provided by Daniela White, M.D. Psychiatrist at Midtown TMS Treatment Center in Houston, Texas. http://danielawhite-md.com/ 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.

1. Pharmacology and
Beyond…
MOOD DISORDERS
© Daniela M. White, MD, 2011

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. 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

4. MOOD DISORDERS by DSM-IV TR
 MAJOR DEPRESSIVE DISORDER
 DYSTHYMIA
 BIPOLAR DISORDERS
 CYCLOTHYMIA
 MOOD DISORDERS DUE TO A GENERAL
MEDICAL CONDITION

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)

6. MAJOR DEPRESSIVE DISORDER

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

8. DIFFERENTIAL DIAGNOSIS
 CLINICAL INTERVIEW
 PSYCHOMETRIC SCALES (PHQ-9 or QIDS-SR;
MDQ;)
 BASELINE BLOOD TESTS: METABOLIC PANEL,
CBC WITH DIFF, TFT’S, TESTOSTERONE
LEVEL,VITAMINS LEVELS, LIPID PROFILE
 RULE OUT BIPOLAR DISORDER

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. 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. 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. 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. ONE MANIC OR HYPOMANIC EPISODE
 Changes the diagnosis to a Bipolar
Disorder
 Changes the treatment
 Changes the outcome

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)

15. BIO-PSYCHO-SOCIAL
 ASSESSMENT
 FORMULATION
 TREATMENT

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. 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. 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. 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. BRAIN IMAGING
 Decreased left prefrontal cortex (PFC) blood
flow and metabolism
 Basal ganglia abnormalities
 Increased amygdala activity
 Abnormalities in hippocampus

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. QUESTIONS?

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. BIOLOGICAL TREATMENTS
TMS – the new kid on the
block
Light therapy

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. TMS
Requires a Neurostar
Device
Chair
Computer system

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. 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. 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. 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. 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. 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. 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. 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

51. NUTRITION
• SPECIAL DIETS?
• FOOD PREFERANCES
(CARBOHYDRATES CRAVINGS)?
• EMOTIONAL EATING?
• NUMBER OF MEALS PER DAY?
• SNACKS?

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. GOALS of MEDITATION
• Used in psychiatric and medical practices for
stress management
• Depression relapse prevention programs
• Pain treatment
• Eating disorders
• etc

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. 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. 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. 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. 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. 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. HYPNOSIS APPLICATIONS
 Ego strengthening
 Anxiety
 Depression
 Stress reduction
 Public speaking fear
 etc

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. 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. QUESTIONS?

74. MOOD DISORDERS by DSM-IV TR
 MAJOR DEPRESSIVE DISORDER
 DYSTHYMIA
 BIPOLAR DISORDERS
 CYCLOTHYMIA
 MOOD DISORDERS DUE TO A GENERAL
MEDICAL CONDITION

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. 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. 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. 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. 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. 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. 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. PHARMACOTHERAPY of BIPOLAR
DISORDER
 Treatment of acute mania
 Treatment of acute bipolar depression
 Maintenance treatment of bipolar disorder

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. 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. 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. 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. 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. 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. OTHER TREATMENTS
TMS, Light therapy, ECT
All the other treatments discussed in the MDD
treatment
Therapy including the education about the
disorder

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. QUESTIONS?