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Depression seminar ppt
1. OUTLINE
1. CASE VIGNETTE
2. GENERAL INTRODUCTION
3. NOMENCLATURE
4. WHY IMP.TO TREAT IT?
5. DIAGNOSTIC CRITERIAS
6. CAUSE/EPIDEMIOLOGY/COURSE/OUTCOME
7. TREATMENT OPTIONS
8. OTHER VARIANTS.
2. CASE VIGNETTE*
A divorced 39 year old businesswoman and
mother of a 5-year-old repeatedly presented to her
primary care clinician complaining of headaches
and gastrointestinal distress. Physical examination
and laboratory tests were unrevealing. The patient
reported feeling anxious and “under lots of stress.”
History-taking revealed that she suffered from
insomnia, low energy, chronic depression ,
pessimism, thoughts of inadequacy, and guilt.
Because she had felt this way much of her life, she
had never thought to report it; moreover, she did
not like to bother her doctor…
* (WOMEN’S HEALTH in Primary Care; Vol. 2, No. 11/NOV. 1999)
3. CASE VIGNETTE*
Patient was given a SSRI. Initially experienced
worsening of her GIT symptoms but encouraged
by doctor to continue therapy. In 2 weeks, she
noted not only relief of her physical symptoms
but also the best mood she had ever experienced.
At first she feared that she was getting “manic,”
but her doctor determined that her ability to sleep
was not impaired, her thoughts were not racing,
and she was not acting impulsively. The patient
soon adjusted to her newfound euthymia.
* (WOMEN’S HEALTH in Primary Care; Vol. 2, No. 11/NOV. 1999)
4. DYSTHYMIC DISORDER: INTRODUCTION
● Dysthymic disorder, often labeled “minor” or
“mild”depression, has fewer and less severe acute
symptoms than does major depression.
● However, dysthymic disorder may persist for years
and remain unrecognized—both by the patients
themselves (who may believe they just have
“depressive personalities” and thus never seek
treatment) and by their clinicians.
● Left untreated, it can be as debilitating as major
depression,if not more so.
5. INTRODUCTION( cont..)
● People with dysthymic disorder often believe they
simply have “depressive personalities,” as being
depressed is the only mood state they have ever
known.
● They often report passive suicidal ideation but are
resigned to the misery of their lives.
● These people frequently have family histories of
mood disorders.
6. INTRODUCTION( cont..)
● They may abuse alcohol in an attempt to
self-medicate their mood, and they are at risk for
other comorbid disorders, such as panic disorder
and social phobia.
● Approx. 1/3 of the subjects with minor depression
had a past history of MDD, and nearly half had a
family history of unipolar depressive disorder;
however, neither factor affected the severity of
minor depressive symptoms.
● Individuals with a history of major depressive
disorder freely traverse between major depressive
disorder, minor depression, and subsyndromal
depressive symptoms
7. NOMENCLATURE
● Kahlbaum ( 1863)- first clinical description →
clinical form of melancholia.
● Kraepelin (1921)- depressive temperament.
● DSM-II (1968)- Neurotic depression – emphasis on
personality states.
● ICD-9 (1979)- listed ‘Depressive Neurosis’- heavily
influenced by psychoanalysis.
8. NOMENCLATURE
● DSM-III- (1980) – introduced ‘dysthymia’ - Paradigm shift
from neurotic personality disorder to current concept of
affective or mood disorder. Also led to change in approach
to treatment.
● DSM – IV → More emphasis on cognitive features and
patterns of course.
● ICD10 -dysthymia included depressive neurosis,
depressive PD, neurotic depression (>2 yrs) and persistent
anxiety depression.
● Large areas of overlap inevitably exist between depression
of dysthymia, MDD and personality disorders.
9. DYSTHYMIC DISORDER
Why it is imp. to treat it:
● The Rand Medical Outcomes Study of more than 11,000
patients in medical and mental health settings found that
having just two depressive symptoms (ie, subsyndromal
depression) was more debilitating than having
hypertension, coronary artery disease, diabetes, back
problems, or lung diseases.
● Patients with subsyndromal depression spent too much
time in bed, experienced inordinate pain, and functioned
poorly in social and occupational roles.
● Patients with dysthymic disorder actually fare worse over
time than do patients with major depression.
10. DYSTHYMIC DISORDER
Why it is imp. to treat it:
● Patients with major depression may have a few terrible
weeks or months, but with treatment, they often recover.
In contrast, dysthymic patients may know nothing but
suffering for decades or even their entire lives.
● Constant guilt, self-doubt, and low energy erode or inhibit
interpersonal skills, diminishing the likelihood of social
and occupational success
● Dysthymic patients are at high risk for eventually
developing a superimposed major depression (double
depression), which only requires an additional couple of
symptoms for a few weeks during a frequently lifelong
dysthymic course.
11. DIAGNOSTIC CRITERIA FOR DYSTHYMIC
DISORDER(DSM 5)
A.Depressed mood for most of the day, for more days than
not, as indicated by either subjective account or
observation by others, for at least two years.
(Note: In children and adolescents, the mood can be
irritable and the duration is decreased to at least one
year.)
B.Presence of at least two of the following:
1. Increase or decrease in food consumption.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feelings of hopelessness.
12. DIAGNOSTIC CRITERIA FOR DYSTHYMIC
DISORDER(DSM 5)
C. During the two-year period of the disturbance, symptoms have
not subsided for more than two months at a time.
D. No major depressive episode has occurred during the first two
years of the disturbance.
E. The patient has never experienced a manic episode, mixed
episode, hypomanic episode, or cyclothymic disorder.
F. The disturbance does not occur exclusively during the course of
a chronic psychotic disorder, such as schizophrenia or
delusional disorder.
G. The symptoms are not due to the direct physiologic effects of a
substance (eg, an abused drug, a medication) or a general
medical condition (eg, hypothyroidism).
H. Clinically significant impairment in social, occupational or
other imp. areas of functioning.
13. DYSTHYMIC DISORDER
key points in diagnosis:
1.Age at onset is frequently 35 years of age or older
2.Work-oriented person up until now, serious and
overachiever
3.Physical symptoms typically dominate more than
depression
4.Obsessive personality (mild compulsive personality)
5.Daily mood fluctuations (80%)
6.Hard on oneself
7.Many are reluctant to rest
( Kasahara 1996.)
14. NEUROTIC DEPRESSION vs ENDOGENOUS
DEPRESSION
Evidence against distinction:
● Prospective F/U of neurotic depressive shown progression
to major, endogenous, bipolar and psychotic depression.
(Bromisch et al, 1985)
● Shortened sleep latency in neurotic depression which is a
biological marker of depression.
● Dysthymia is often complicated by MDD (double
depression).
(Akiskal et al, 1997)
● Family studies show heritability of MDD is weak unless
dysthymia/minor depressions are counted as cases in first
degree relatives.
(Kendler et al, 1992)
15. NEUROTIC DEPRESSION vs ENDOGENOUS
DEPRESSION
● All point to new paradigm in which depressive Sx are
expressed in a spectrum of severity → subsyndromal to
syndromal levels in which subthreshold Sx acquired
clinical significance. (Judd et al, 2002)
● In a study of >20000 outpatients, subsyndromal depressive
(SD) symptoms- in those who did not meet criteria for
MDD or dysthymia causes significant psychosocial
dysfunction and disability, even exceeding hypertension,
diabetes, GI and lung diseases; dispelling the myth of
‘benign’ depression.
(Wells et al, 1989)
16. DYSTHYMIC DISORDER
Cause :
● Genetics : Family history could increase likelihood
six-fold.
● Biological Factors:
Neurotransmitters-
Serotonin, Nor-epinephrine, Dopamine
Sleep disorders
Light deprivation
● Reproductive Hormones:
Sudden fluctuations of estrogen & progesterone
● Cluster C personality traits:
17. DYSTHYMIC DISORDER
Epidemiology:
● Life time prevalence in adults of 3.1% (MDD-4.4%).
(NIMH ECA study)
● F:M :: 2:1
● Frequent comorbidity (up to 75%) particularly MDD, anxiety
disorders and substance abuse .
(Weisman et al, 1988)
● India: 32% of patients with depression .
(Chadda et al, 1992)
● ↓ Frequency of psychomotor retardation/ agitation, insomnia,
loss of appetite/ libido, suicidal ideas compared to MDD.
(Singhal et al, 1991)
18. DYSTHYMIC DISORDER
Epidemiology:
● 12-month prevalence in U.S.A. is apprx. 0.5% for
persistent depressive disorder and 1.5% for chronic major
depressive disorder.
( DSM-5 )
● 25% have one prior episode of major depression.
● 17% have 2 or more prior MD episodes.
● 41% have F/H/O depression.
● 35% have F/H/O alcoholism.
(Judd et al., 1997)
19. DYSTHYMIC DISORDER
Course:
● Insidious onset dating back to childhood and run in chronicity
(2 yrs or more).
● Median duration of five years before first superimposition of
MDD .
(Keller et al, 1982)
● 26% of cases had previous underlying chronic depression .
● 50-90% of patients develop MDD during course of disorder.
● Treatment emergent hypomania in 10-30% (F/H/O BPAD).
● Co-morbidity increases chances of MDD-87% in borderline
patients and 93% in ASPD .
(Perry, 1985)
20. DYSTHYMIC DISORDER
Outcome:
In extensive studies by NIMH group (n=10,526)
Subsyndromal symptoms were associated with higher
adverse outcomes like :
● ↑Use of medical/psychiatric services, hospitalization,
disability benefits & ↑Lifetime suicidal attempts .
● 3% of SSD met criteria for major depression 1yr later 5% -
minor depression (with mood Sx).
● Of MDD patients → at 1 yr F/U→ 28% - continued to meet
MDD, 15% minor depression, 20% SSD.
(Judd, et al 1996)
21. DYSTHYMIC DISORDER
Outcome:
● In another study – 12 year F/U ,subsyndromal depressions
(combining minor, dysthymic and subthreshold
depression) were observed 3 times more frequently (43%
weeks) than syndromal MDD (15%).
(Judd, et al 1996)
● Concept supported by a twin study where four or fewer
criterion A symptoms, syndromes composed of symptoms
involving no or minimal impairment, and episodes of less
than 14 days duration all significantly predicted both
future depressive episodes in the index twin and risk of
major depression in the co-twin.
(Kendler KS, Gardner CO Jr.,
1998)
22. DYSTHYMIC DISORDER
SPECIAL GROUPS:
● Children: Data insufficient
● Elderly: n= 224 patients, >60 yrs, SSD defined as >10
on HDRS Subsyndromal depression was common
(estimated point prevalence of 9.9% compared with
6.5% for major depression, 5.2% for minor depression,
and .9% for dysthymic disorder), associated with
functional disability and medical co morbidity to a
degree similar to major or minor depression, and
often treated with antidepressant medications.
(Lyness J et al. 1999)
24. USE T.A.C.C.T.
FOR ENGAGEMENT
T ell – provide basic information about illness
A sk – about concerns/beliefs
(cognitive/emotional)
C are – develop rapport; respond to emotions
C ounsel – provide information relevant to
concerns and explanatory model
T ailor – develop plan collaboratively
25. PSYCHOEDUCATION
● Depressed patients are more likely to comply with
treatment when properly educated about their condition.
● The treating clinician should present major depression and
dysthymic disorder as medical illnesses that are prevalent,
treatable, and not the patient’s fault.
● Depressive disorders bear comparison to hypertension,
asthma, and other potentially recurrent or chronic medical
conditions. It may help to explain the biochemical
rationale for treatment—namely, that medications affect
neurotransmitters, such as serotonin (eg, SSRIs),
norepinephrine (eg, nortriptyline, desipramine,
reboxetine), or both (eg, venlafaxine), and that these
effects will treat depression.
26. PHARMACOTHERAPY
● A basic treatment principle is that what works for
major depression also often works for “minor”
depression.
● An exception is electroconvulsive therapy, which
is usually reserved for psychotic, extremely severe,
or treatment-refractory depression.
● Antidepressant medications and psychotherapies
have demonstrated efficacy in treating depression
of mild-to-moderate intensity and best result
when both combined.
(Stewart JW et al,1992)
27. PHARMACOTHERAPY
Antidepressants
● Not recommended for the routine treatment of persistent
subthreshold depressive symptoms or mild depression
because the risk-benefit ratio is poor.
● Consider them for people with
● Past history of moderate or severe depression.
● Initial presentation of subthreshold depression that has
been present for a long period (typically >2 years).
● Subthreshold depressive symptoms or mild depression that
persists after other interventions.
( Kasahara ;1996.)
28. PHARMACOTHERAPY
● Antidepressants have largely equal efficacy and
choice should be largely dependent on:
● Side-effect profile
● Patient preference
● Previous experience of treatments
● Propensity to cause discontinuation symptoms
● Safety in overdose
● Interaction potential
29. PHARMACOTHERAPY
● Almost all antidepressant medications have
roughly equal efficacy.
● However, medications differ in their effects on
individual patients and in their potential for
producing adverse effects.
● Therapeutic response is generally 60% to 70% in
patients with major depression and around 50%
to 55% for those with dysthymic disorder.
( J. C. MARKOWITZ;
1999)
30. PHARMACOTHERAPY
● SSRIs as first-line treatment for depression, ideally in
generic form.
● Administered each morning, SSRIs can be started at what
are often standard therapeutic dosages.
● For elderly patients, the starting doses can be halved.
● If in doubt, a good rule of thumb is: Begin low and build
up.
( J. C. MARKOWITZ; 1999)
31. PHARMACOTHERAPY
● In general, SSRIs are well tolerated.
● Acute side effects, which tend to be mild, include dry
mouth, jitteriness, gastrointestinal distress ,and
headache.
● Chronic side effects can include weight gain, a
restriction of emotional range (not caring anymore)
and, probably most damningly, sexual dysfunction.
● Various antidotes have been proposed to treat the
sexual side effects of SSRIs.
(Segraves RT; 1998)
32. PHARMACOTHERAPY
Precautions with SSRI’s:
● Associated with increased risk of bleeding
(consider prescribing gastroprotective agent in
older people who are taking NSAIDs)
● Higher risk of drug interactions with fluoxetine,
fluvoxamine and paroxetine.
● Increased risk of suicidal ideation/behaviour in
younger patients taking antidepressants.
33. PHARMACOTHERAPY
● Good response seen with non-SSRI antidepressants
upto therapeutic dose levels-eg, to 200 to 300 mg/d
for most tricyclic antidepressants (nortriptyline, the
only exception, is titrated by serum levels) and to 60
mg/d or higher for monoamine oxidase inhibitors.
● Sleep inducers and anti-anxiety drugs according to
need of patient.
34. PHARMACOTHERAPY
● Fluoxetine is significantly superior to placebo in
reducing minor depressive disorder symptoms within
a 12-week period however improvement in
psychosocial function may take longer than 12 weeks.
(Am J Psychiatry 2004;)
● Escitalopram wasn’t judged to have any clinically
important advantages over other antidepressants
● No advantage found for ‘dual action’ antidepressants
(e.g. duloxetine and venlafaxine) over other drugs .
● Venlafaxine and Tricyclic antidepressants (except
lofepramine) associated with greater risk of death
from overdose.
35. PSYCHOTHERAPY
● Low intensity psychosocial interventions:
● Individual guided self-help based on cognitive behavioural therapy
(CBT) principles
● Computerised cognitive behavioural therapy (CCBT)
● A structured physical activity programme
● High intensity psychological interventions
● CBT (group or mindfulness-based)
● Interpersonal Therapy (IPT)
● Behavioural activation
● Behavioural couples therapy
● Others
● Counselling
● Short-term psychodynamic psychotherapy
● Group-based peer support programmes is a low-intensity option for
those with chronic physical health problems.
(NICE CG 90, Oct 2009)
36. PSYCHOTHERAPY
● CBT and IPT are manual-guided, once weekly, 12- to
20-week therapies that were originally developed to
treat major depression.
● Both have been repeatedly tested in randomized
,controlled clinical trials and shown to be about as
effective as medication for outpatients who have
non-delusional major depression.
● Like medications, CBT and IPT have been less fully
evaluated as treatment for dysthymic disorder, but
they show promise for that as well.
37. PSYCHOTHERAPY
● Psychotherapies may also smooth out interpersonal
difficulties and life frictions that may precipitate
future depressive episodes.
● But all psychotherapies may not be equal. Far less
research has been done on the utility of many other
forms of psychotherapy, such as psychodynamic
psychotherapy, as treatments for depression.
● On the longer term, psychological interventions for
patients with subthreshold depression may have an
effect on the incidence of major depressive disorders.
38. COGNITIVE BEHAVIOURAL THERAPY
● CBT focuses on the irrational, negative thoughts that
“automatically” arise in the minds of depressed
individuals.
● Because these thoughts fit their mood, depressed patients
tend to take them for granted. Yet such thoughts cause
suffering and discourage depressed patients from coping
with life.
● CBT therapists help depressed patients to scrutinize such
thoughts and weigh the evidence for and against believing
them.
● As patients learn to do this, their negative thoughts and
their depressive syndrome fade.
(Beck AT et al;1979)
39. INTERPERSONAL THERAPY
● IPT focuses on depression as a medical illness and helps
patients recognize the connection between depressed
mood and recent life events, such as deaths (complicated
bereavement or pathologic grief) role disputes (struggles
with significant others), and role transitions (major life
upheavals or changes).
● If patients can improve their life situation and, contrary to
their expectations, they usually can, the depressive
syndrome will lift.
● Despite its impressive research record, IPT was, until
recently, less widely practiced than CBT; therapists trained
in IPT may be harder to find.
(Klerman GL et al ;1984)
40. ST. JOHN’S WORT
● Hypericum perforatum (St.John’s wort) is a popular
example of a “natural” remedy for depression.
● Many clinical studies comparing the effectiveness of St
John’s wort with placebos and antidepressant medication.
Most have found the herbal remedy to be superior to
placebo and equivalent to standard antidepressants for the
treatment of mild to moderate depression.
● Patients who have been self-medicating with St. John’s
wort should be told to discontinue the drug before
starting treatment with an SSRI or other antidepressant.
(Black Dog Institute ;Oct. 2012)
41. OMEGA-3 FATTY ACIDS
● Long-chain Omega-3 fatty acids, EPA and DHA, have been
used successfully to both prevent and treat depression.
● EPA is the Omega-3 that actually treats depression
because it specifcally addresses the physiologic
consequences of depression and lowers the stress
response. Both of these are found in fatty fsh.
● DHA helps prevent depression, but studies so far have
found that it does not treat it by itself. It is usually
combined with EPA. Tere is a vegetarian source of DHA,
but no vegetarian source of EPA; fsh oil is still the best
source.
(Puri BK et al;2001)
42. BRIGHT LIGHT THERAPY
● An illumination level of 10,000 lux for 30 to 40
minutes is the most commonly used dosage. But
lower light intensities have also been effective.
● Regular home lighting is not sufficiently bright to
alleviate depression. Light therapy first thing in the
morning is more effective than light therapy later in
the day.
● A 2004 study combining bright light exposure and
physical exercise showed that this treatment may be
an effective way of relieving depressive symptoms.
(Leppämäki S et al;2004)
43. EXERCISE
● Strongest effects are for aerobic exercise, but weight
lifting and stretching are also helpful.
● If exercise at a moderate level, it is safe during
pregnancy or breastfeeding even.
● For mild-to-moderate depression
• Frequency: 2 to 3 times a week
• Intensity: moderate
• Duration: 20 to 30 minutes
(Rethorst CD et al ;2009)
44. ANTHROPOSOPHY
● Is a spiritual science whose practical applications
include biodynamic agriculture, anthroposophical
medicinal products.
● A 4-year study of the efectiveness of anthroposophic
therapies in the treatment of depression evaluated 97
outpatients from 42 medical practices in Germany, with
chronic depression, anthroposophic therapies were
followed by long-term clinical improvement.
(Hamre H et al;2006)
45. AROMATHERAPY
● Is the use of essential oils to treat a variety of
conditions like minor depression, anxiety etc.
● Various aromatherapy oils, diluted in carrier oil like
almond or olive oil, are massaged into the skin, where
they are absorbed into the blood-stream.
● Naturopathic physicians use aromatherapy to treat
depression, anxiety, insomnia, and stress-related disorders
and to manage chronic pain.
(Perry N et al;2006)
46. DIETARY CHANGES/SUPPLEMENTS
● Depressive symptoms are exacerbated by nutritional
imbalances, including frequent consumption of
caffeine; excessive sucrose consumption; deficiencies
in vitamins and minerals (biotin, folic acid, and other
B vitamins, vitamin C, calcium, copper, iron,
magnesium, potassium); imbalances in amino acids;
and food allergies.
● Dietary Recommendations : Omega-3 Fatty Acids,
Dietary Magnesium ,5-Hydroxytryptophan, Ginkgo
Biloba, Siberian ginseng (Eleutherococcus senticosus),
S-adenosylmethionine.
47. OTHERS
● Sleep hygiene
● Relaxation therapy
● Yoga and deep breathing techniques
● Spirituality and religiosity
● Prayer, music and dance therapy
48. ● Cochrane review of 25 RCTs which compared exercise with
either no treatment / established treatment and found
that exercise seems to improve depressive symptoms .
(Mead et al., 2009)
● 5 RCTs utilizing different forms of yoga in mild to severe
depression- potentially beneficial effects of yoga reported but
trials were not methodologically robust.
(Pilkington et al.,2005)
● Higher levels of religious involvement are positively
associated with indicators of psychological well-being and
less depression, suicidal thoughts and behavior.
( Moreira- Almeida et al.,2006)
49. MAINTENANCE TREATMENT
● Pharmacotherapy has demonstrated efficacy in
protecting against relapse and recurrence of major
depression and dysthymic disorder.
● Psychotherapies have begun to show prophylactic
efficacy as well.
● It is recommend that patients continue taking
antidepressants for at least a year, a period of
protection during which they can regain their
confidence.
50. MAINTENANCE TREATMENT
● If they have had multiple episodes of depression, it is
recommended that maintenance medication for at
least several years.
● Research has shown that maintenance medication
should be continued at its acute dosage.
● Treatment with IPT, even at the low “dose” of one
session per month, also has shown maintenance
benefits in treating highly recurrent major depression.
(Frank E et al;1990)
51. BRIEF PSYCHOTHERAPY DURING CHRONIC
STAGE
1.As the condition becomes chronic, the focus
gradually shifts from the “rest” that is emphasized
during the acute phase to “social reintegration.”
2.Take every opportunity to repeatedly convey that
people can recover from mood disorders.
3.With discretion, discuss the patient’s life history
and family relationship.
4.Study the fluctuations in the patient’s conditions
over a 2- or 3-week period without getting hung
up on daily progress.
52. BRIEF PSYCHOTHERAPY DURING CHRONIC
STAGE
5.Occasionally discuss which symptoms have
improved and which remain compared to the
initial consultation.
6.Provide opportunities to reconfirm the
significance of drug therapy.
7.Consider the psychological and physical
exhaustion of the patient’s family and friends and
provide them with as much psychological support
as possible.
(Kasahara 1996)
53. TYPICAL THERAPEUTIC COURSE
● Antidepressant response follows a predictable sequence:
first side effects, next physical improvement, then mood
improvement.
● Depressed patients, who may be discouraged when they
initially experience only side effects, should be forewarned
and encouraged to see the side effects as harbingers that
the medication is getting into their system and starting to
work.
● Next, neurovegetative symptoms and work function may
improve.
● It may take several weeks to see improvement, and the full
benefits of a given dosage may not be apparent for at least
four to six weeks.
54. TYPICAL THERAPEUTIC COURSE
● Patients who do not respond to an adequate
antidepressant trial—a minimum of four weeks at a
therapeutic dosage—are likely to feel still more
demoralized and depressed. They need reassurance
that depression is treatable and that many other
treatment options remain.
● Such patients may benefit from additional medication
trials (non-response to one antidepressant does not
preclude response to another), the addition of
antidepressant psychotherapy (such as CBT or IPT),
or other complementary treatments.
55. DYSTHYMIC DISORDER
Treatment outcome:
● Most classes of antidepressants (SSRI’s, TCA’s, MAOI)
shown to be effective.
● 75% of dysthymic patients have sustained remission for
five or more years.
● 15% experience ‘over correction’→ hypomania (F/H/O
BPAD, social phobic traits).
● Predictors of good response : Female, late onset, +ve DST,
+ve sleep EEG, F/H/O depression.
● Interpersonal therapy, marital therapy and CBT shown
promise but little credible evidence for effective
monotherapy in dysthymia.
● Combination of drugs and psychotherapy gives best
results.
56. DYSTHYMIC DISORDER
Treatment Outcome:
● Inpatients of SSD eight-week treatment with fluvoxamine
was associated with a substantial decrease in depressive
symptomatology and a normalization of psychosocial
functioning. Placebo-controlled double-blind
confirmation warranted.
(Rapaport MH, Judd LL 1998)
● In a trial of psychotherapy (CBT, SBFT, NST) n= 99 youth,
at the end of acute treatment 26 were well, 18 were
subsyndromal, and 55 were still depressed. (38%) of the
subsyndromally depressed were functionally impaired,
and showed a protracted time to recovery.
(Brent et al., 2001)
57. DYSTHYMIC DISORDER
Recovery & Relapse
● Spontaneous recovery in 13% subjects over one year.
● Rate of recovery from double depression at 2 years
exceeds that of MDD (97% vs 79% ).
● However only 39% out of 97% recovered from chronic
phase of dysthymia.
● Thus dysthymic subjects are more likely than those
with MDD and no dysthymia to have depressive sx on
2 years F/U.
(WPA Working Group,1995)
58. DYSTHYMIC DISORDER
Recovery & Relapse
● After 5 yr F/U, 52% met criteria for Dysthymia at the end.
● Co morbid anxiety disorder, cluster C and depressive
personality features, and chronic stress were associated
with lower rate of recovery.
● Predictors of MDD at F/U include, F/H/O dysthymia,
poor parenting, childhood abuse, neuroticism /cluster C .
(Klein et al, 2000)
59. DEPRESSIVE PERSONALITY DISORDER
● Characterized by low self esteem, self-derogation,
brooding, pessimism and submissiveness.
● Included in nosological systems before DSM-III (DSM-II,
ICD-9).
● Subsumed under Dysthymia in DSM-III/III-R and ICD-10.
Returned in DSM-IV as part of Personality Disorders-NOS.
Distinction from Dysthymia:
● Depressed mood is not a core feature.
● More emphasis on personality states.
60. DEPRESSIVE PERSONALITY DISORDER
Course:
● ↑ freq of current mood disorder (33%) , lifetime mood
disorder (MDD 22% ; BPAD 22% ; Dysthymia 19%).
● ↑ family H/O MDD (23.1% vs 11.7% in controls) .
● Treatment rates similar to controls but more
impairment.
● Overlap with Dysthymia is 44-78%.
● Theoretically responds better to psychotherapy, but
should be treated aggressively as it may represent
prodrome / sequelae of MDD.
(Klein & Miller, 1993)
61. CYCLOTHYMIA
● Biphasic mood swings- abrupt shifts with each
phase lasting for few days with infrequent
interphase euthymia.
● At least 4 of following
1.Lethargy alternating with hyperactivity.
2.Shaking self esteem alternating between low
self-confidence and overconfidence.
3.↓ verbal output alternating with talkativeness.
62. CYCLOTHYMIA
4.Mental confusion alternating with sharpened and
creative thinking .
5.Unexpected fearfulness alternating with excessive
punning and jocularity .
6.Interested self-absorption alternating with uninhibited
people seeking.
( Akiskal et al ;1998)
63. CYCLOTHYMIA
Treatment outcome
● Lithium (600-900) was effective in 25 out of 46 pts in
an open label study over 1 yr period.
● Valproate (500-750) has also been used with success.
● Clinical Imp: In addition to IPR problems, ↑ drug
abuse, as hypomanic episodes are difficult to ascertain
from history, assessing cyclothymia in clinically
depressed pts is a more sensitive and specific
approach to the diagnosis of bipolar II.
64. BPAD AND SUBSYNDROMAL SYMPTOMS
● BPAD patients with subsyndromal symptoms had
high rates of comorbidity (anxiety, eating disorders),
lower GAF scores than euthymics and similar
treatment rates as patients with full episodes.
(MacQueen et al, 2003)
● Patients given lithium carbonate to achieve low-range
levels had 2.6 times the risk of major affective relapse
as those given lithium for standard-range levels and
nearly twice the risk of developing subsyndromal
symptoms.
( Keller M et al 1992)
65. SUBSYNDROMAL SEASONAL AFFECTIVE
DISORDERS (SSAD)
Criteria for diagnosis
1) Difficulty for two consecutive winters lasting at least 4
weeks – decreased AE, efficiency, socialization, change in
rating habits, weight or sleep pattern.
2) Subjectively normal – no illness or disorder.
3) Not sought medical help.
4) Not recognizable from outside (flu / overwork)
5) Socio-occupational dysfunction not severe.
6) No H/O major affective disorder in winter .
7) No serious medical illness.
(Kasper et. al., 1989)
66. SUBSYNDROMAL SEASONAL AFFECTIVE
DISORDERS (SSAD)
Course and outcome
● Mainly atypical symptoms
● Onset in October – accentuation in Jan/Feb, offset in
March.
● Outcome ---Out of 20 patients – 2 individuals MDD, 2
dysthymia.
● Significantly higher cluster C personally disorder (OC,
avoidant, dependent, passive aggressive).
● Individuals with high degree of vulnerability may reach
threshold of SAD symptoms if they are exposed to lack of
light.
● 31% categorized as RBD over a 1 yr period.
(Kasper et al, 1992)
67. SUBSYNDROMAL SEASONAL AFFECTIVE
DISORDERS (SSAD)
● Neither met criteria for major affective disorder nor had
sought treatment for winter difficulties, but who
nevertheless experience mild dysfunction and vegetative
changes as in SAD.
● Bright light beneficial only in subjects who report a history
of symptomatic seasonal changes Favorable response also
found in F/U studies.
(Kasper et al, 1989)
68. MIXED ANXIETY AND DEPRESSIVE DISORDER
(MADD)
● Characterized by dysphoria for at least 1 month combined
with other depressive and anxiety symptoms that are sub
threshold for both primary affective and anxiety disorder.
● ICD-10-defines MADD where neither affective nor anxiety
sx are more prominent than other; autonomic symptoms
be present and significant life change should not be
associated with onset of Sx. Finally, researchers may
develop their own criteria in ICD-10.
● Prevalence- 0.8- 2.5% in epidemiological studies and from
5-15% in primary care settings.
● As many as 50% may receive lifetime diagnosis of GAD /
MDD.
69. MIXED ANXIETY AND DEPRESSIVE DISORDER
(MADD)
Treatment Recommendations
● SSRI’s
● Buspirone : Antidepressant at higher doses
● BDZ- insufficient if depressive symptoms are severe, less
effective for mild anxiety.
● Non-Pharma- CBT, anxiety management, relaxation,
cognitive restructuring.
● Treatment continued after remission with monitoring for
development of full syndrome disorders.
(Cameron RP & Schatzberg AF,2002)
70. ADJUSTMENT DISORDERS
● Transient situational PD(DSM-I) → Transient
situational disturbance (DSM-II) → Adjustment
disorders (DSM –III)
● F/M = 2:1
● Definition : Emotional or behavioral response when
exposed to an identifiable stressor – within a specified
period of exposure; marked distress /socio
occupational dysfunction ; not meeting criteria for
more severe disorders, remits after disappearance of
stressor.
71. ADJUSTMENT DISORDERS
Course
● Benign course in adults compared to adolescent (recovery
rate 71% Vs 44%) at 5yrs F/U.
● Adults – 71% remitted, 8% - intervening problem – 21% -
MDD/ Alcohol.
● Adolescents – 44% remitted, 13% intervening illness, 43% -
major psychiatric morbidity.
(Andreason & Hoenk, 1982)
● Major predictors for depression were the chronicity of
illness and presence of behavioral symptoms .
● In another study (n=52) – F/U – 3yrs Psychiatric co
morbidity 31% .
(Despland, 1997)
72. ADJUSTMENT DISORDERS
Treatment outcome
● Psychotherapy – crisis intervention, counseling, group
therapy.
● BDZ e.g. Alprazolam
● TCA/ Buspirone in alcohol users due to risk of
dependence.
Data on outcome not available. Difficult to obtain
stable study cohort.
73. PREMENSTRUAL DYSPHORIC DISORDER (PMDD)
● Late luteal phase dysphoric disorder / PMS.
● Occur in last week of luteal phase in most cycles during
the past year-remit absent in week premenses.
● Essential symptoms include marked depressed mood,
appreciable anxiety, pronounced affective lability, anger
and decreased interest in activities.
● Other Sx include ↓concentration, lethargy, change in
appetite, sleep pattern, somatic symptoms.
● DSM-IV placed under Depressive disorder NOS-
replacing LLPDD – (DSM III-R) in Unspecified Mental
Disorder.
74. PREMENSTRUAL DYSPHORIC DISORDER (PMDD)
Epidemiology 3-8% prevalence
Etiology
● Biological– High E/P ratio ; Fluid/ electrolyte balance.
● Psychosocial – Socio cultural beliefs ; mother- daughter
communication .
● Psychoanalytic – Ambivalent pregnancy desire & conflicts
of sexual preference.
Course – Data is inadequate. PMDD is neither a variant of
depression nor anxiety disorder as it has irritability and
affect lability rather than depression or anxiety as main
features.
76. MATERNITY BLUES
● Transitional depressive state or lability of mood
(insomnia, fatigue, tearfulness) in first ten days after
delivery.
● Prevalence 4-50%
● 44% of pts (7/16) → Post partum depression; 25%
persisted > 3 months.
● Postpartum depression often undiagnosed and
untreated.
(Cox et al, 1982; Nagata et al,
2000)
77. CONCLUSION
● Dysthymic disorder is a chronic form of depression
that is often wrongly dismissed as “mild.” Over time it
can be even more devastating than major depression.
● Furthermore, dysthymic disorder often goes
undiagnosed. Patients may suffer from it for years
before realizing something is wrong.
● Guilt, self-doubt, and low energy erode interpersonal
skills, diminishing the likelihood of social and
occupational success.
78. CONCLUSION
● A basic treatment principle is that what works for
major depression also works for “mild” depression.
● Pharmacotherapy options include selective serotonin
reuptake inhibitors (often used as first-line
treatment), tricyclics, and monoamine oxidase
inhibitors.
● Psychotherapies such as cognitive behavioral therapy
and interpersonal therapy also can be effective.
● SSRI’s in combination with Cognitive Behavioral
Therapy has best evidence of success.