Mood Disorders

Introduction
■ MOOD persistent or sustained emotion or feeling tone
that influence person’s behavior & colors her or his
perception of being in the world
■ Mood Disorders
❑ Bipolar Disorders I ❑ Others
❑ Bipolar Disorders II ■ Postnatal depression
❑ Unipolar Depression ■ Premenstrual dysphoric
disorder
❑ Dysthymia
■ Seasonal affective
❑ Cyclothymia disorder (SAD): also
❑ Minor Depressive Disorder called "winter
❑ Recurrent Brief Depressive Disorder depression"
❑ Mixed Anxiety & Depressive Disorders
DEPRESSION
Clinical Features
■ CENTRAL FEATURES
❑ Depressed Mood
❑ Lack of Enjoyment
❑ Reduced Energy
❑ Negative Thinking
❑ Slowness
❑ Decreased Social & Occupational Functioning
Clinical Features
■ Appearance
❑ Dress & Grooming NEGLECTED
❑ Facial Features
■ turning downward of the corners of the mouth
■ Vertical Furrowing of the eyebrow
■ Reduced rate of Blinking
❑ Shoulders bent
❑ Head Inclined forward
❑ Gaze Directed downward
❑ Reduced gestural movements
Clinical Features

■ Mood
❑ MISERY
❑ Does not substantially react with happy
circumstances
❑ Differ from ordinary sadness
❑ Black cloud prevailing mental activities
❑ Diurnal variation: worse in the morning
Clinical Features
■ Depressive Cognitions
❑ Worthlessness
❑ Pessimism
■ Hopelessness
■ Suicide & Death Wishes
❑ Guilt
■ Past trivial acts of dishonesty
■ Letting someone down
■ Attributes his situation to moral weakness &
personal failing
Clinical Features
■ Behavior
❑ Lack of interest & enjoyment anhedonia
■ No enthusiasm for previously enjoyable
activities
■ No pleasure in everyday living
❑ Social withdrawal
❑ Reduced energy
■ Lethargic
■ Leaves tasks unfinished
■ Sometimes associated with restlessness
Clinical Features
■ Psychomotor Changes
❑ Psychomotor Retardation
■ Slow movement
■ Slow speech (Latency)
❑ Agitation
■ Inability to relax
■ Mild degree: plucking the fingers or making
restless movements of the legs
■ Severe : pacing up & down
❑ Anxiety & irritability
Clinical Features
■ Biological Symptoms
❑ Include
■ Sleep disturbance (early morning awakening)
■ Diurnal variation of mood
■ Loss of appetite
■ Loss of weight
■ Constipation
■ Loss of libido
■ Amenorrhea
❑ In severe degrees of depression
Clinical Features
■ Other features
❑ Obsessional symptoms
❑ Panic attacks
❑ Dissociative symptoms
❑ Poor memory (pseudodemetia)
Severe depression & Psychotic depression

❑ More severe form of symptoms

❑ Complete loss of function
❑ Delusion (mood congruent, themes of
nondelusional thinking)
■ Guilt
■ Impoverishment

■ Persecutory

■ Nihilistic Delusions (Cotard’s syndrome)

❑ Their bowels have been destroyed, so they will never be able to pass faeces again.
❑ They are penniless and have no prospect of ever having any money again.
❑ Their whole family has ceased to exist and that they themselves are dead.

❑ Hallucinations
 Other Variants
■ Agitated Depression
■ Retarded Depression
■ Postnatal depression
■ Premenstrual dysphoric disorder
■ Seasonal affective disorder (SAD): also called "winter depression"
■ Depressive Stupor (motionlessness & muteness)
■ Atypical Depression
❑ Mood reactivity
❑ Overeating & oversleeping
❑ Leaden paralysis (extreme fatigue & heaviness in the limbs
❑ Pronounced anxiety
❑ Sensitivity to rejection
 DSM-5 Diagnostic of Major Depressive Disorder (MDD)
▪ Five (or more) of the following symptoms have been
present during the same 2-week period and represent a
change from previous functioning: at least one of the
symptoms is either (1) depressed mood or (2) loss of
interest or pleasure.
1. Depressed mood most of the day, nearly every day.

2. Markedly diminished interest or pleasure in all, or almost

all, activities most of the day, nearly every day.
 DSM-5 Diagnostic of Major Depressive Disorder (MDD)
3. Significant weight loss when not dieting or weight gain (e.g., a
change of more than 5% of body weight in a month), or decrease
or increase in appetite nearly every day.
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt
nearly every day.
8. Diminished ability to think or concentrate, or indecisiveness,
nearly every day.
9. Recurrent thoughts of death (not just fear of dying), recurrent
suicidal ideation.
Mild Depression
■ Mild depression is not mild!!!
■ Additional symptoms (anxiety, phobias,
obsessions)
■ Difficulty falling asleep
■ No biological symptoms
■ Worsening of symptoms in the evening
■ When chronic called dysthymia
 Lifetime Prevalence Rates of Depressive
Disorders
■ Life time prevalence= 5-10% (some studies found it
as low as 1% and others as high as 30%).
■ The Iraqi Mental Health Survey (IMHS) found
lifetime prevalence of depression in males around
5% and in females around 10%.
■ The prevalence rate of depression is not fixed
between studies.
■ SEX: MDD two fold greater prevalence in
women
■ Age
❑ Mean age of onset 40
❑ Increasing incidence below 20
■ Marital Status (single, separated, divorced)
 Etiology: Biological Factors
■ Biogenic Amines
❑ Norepinephrine, serotonin, dopamine
❑ Depletion causes depression
❑ Drugs that increase them treats depression
■ Alterations of Hormonal Regulation
❑ Elevated HPA activity is a hallmark of mammalian stress responses
and one of the clearest links between depression and the biology of
chronic stress.
❑ Hypercortisolemia
❑ Dexamethasone nonsuppression A disturbance of feedback inhibition is tested by
administration of dexamethasone (Decadron) (0.5 to 2.0 mg), a potent synthetic glucocorticoid, which
normally suppresses HPA axis activity for 24 hours. Nonsuppression of cortisol secretion at 8:00 AM the
following morning or subsequent escape from suppression at 4:00 PM or 11:00 PM is indicative of
impaired feedback inhibition.
Etiology: Biological Factors
■ Thyroid axis dysfunction
❑ Approximately 5 to 10 percent of people

evaluated for depression have previously

undetected thyroid dysfunction
■ Alterations of Sleep Neurophysiology: Depression is
associated with a premature loss of deep sleep and an
increase in nocturnal arousal.
Etiology: Structural and Functional Brain Imaging

■ The most consistent abnormality in depressive disorders:

increased frequency of abnormal hyperintensities in
subcortical regions, such as periventricular regions, the
basal ganglia, and the thalamus.
■ Ventricular enlargement, cortical atrophy, and sulcal
widening
■ Some depressed patients also may have reduced
hippocampal or caudate nucleus volumes
Genetic Factors
■ Heritability estimates range from 40-70%
■ families also have high rates of anxiety disorders and
neuroticism.
■ Prevalence in first degree is higher than general
population,
■ Twin Studies
❑ Considering unipolar and bipolar disorders together, these
studies find a concordance rate for mood disorder in the
monozygotic (MZ) twins of 70 to 90 percent compared with
the same-sex dizygotic (DZ) twins of 16 to 35 percent.
Psychosocial Factors
■ Life Events and Environmental Stress
❑ stressful life events more often precede first, rather than
subsequent, episodes of mood disorders
❑ the stress accompanying the first episode results in long-
lasting changes in the brain's biology
❑ losing a parent before age 11
❑ the loss of a spouse.
❑ unemployment
 Psychodynamic Factors in Depression
■ Sigmund Freud and expanded by Karl Abraham is known
as the classic view of depression.
❑ Disturbances in the infant-mother relationship during the
oral phase (the first 10 to 18 months of life) predispose to
subsequent vulnerability to depression;
❑ Depression can be linked to real or imagined object loss;
❑ Introjection of the departed objects
❑ Because the lost object is regarded with a mixture of love and
hate, feelings of anger are directed inward at the self.
Cognitive Behavioral Theory
■ Aaron Beck
❑ Specific cognitive distortions present in persons
susceptible to depression “depressogenic schemata”
❑ Cognitive triad of depression
■ Negative view of the self: a negative self-precept;
■ Negative view of the environment: a tendency to experience the
world as hostile and demanding,
■ Negative view of future: the expectation of suffering and failure
❑ CBT: consists of modifying these distortions
 Cognitive Behavioral Theory
■ Learned Helplessness
❑ The learned helplessness theory of depression connects depressive phenomena to the
experience of uncontrollable events.
❑ When dogs in a laboratory were exposed to electrical shocks from which they could not
escape, they showed behaviors that differentiated them from dogs that had not been
exposed to such uncontrollable events. The dogs exposed to the shocks would not cross a
barrier to stop the flow of electric shock when put in a new learning situation. They
remained passive and did not move.
❑ According to the learned helplessness theory, the shocked dogs learned that outcomes
were independent of responses, so they had both cognitive motivational deficit (i.e.,
they would not attempt to escape the shock) and emotional deficit (indicating decreased
reactivity to the shock).
❑ In the reformulated view of learned helplessness as applied to human depression, internal
causal explanations are thought to produce a loss of self-esteem after adverse external
events. Behaviorists who subscribe to the theory stress that improvement of depression is
contingent on the patient’s learning a sense of control and mastery of the environment.
Differential Diagnosis
■ Medical Disorders
❑ Mononucleosis
❑ Adrenal dysfunction
❑ Thyroid dysfunction
❑ AIDS
❑ Drugs: Cardiac drugs, antihypertensives, sedatives,
hypnotics, antipsychotics, antiepileptics,
antiparkinsonian drugs, analgesics, antibacterials,
and antineoplastics
Differential Diagnosis
■ Neurological Disorders
❑ Parkinson's disease,
❑ Dementing illnesses (including dementia of the
Alzheimer's type)
❑ Epilepsy
❑ Cerebrovascular diseases
❑ Brain Tumors
■ Pseudodemetia
Differential Diagnosis
■ Bipolar versus Depression
■ Substance induced mood disorders
■ Other depressive disorders
■ Other mental health disorders
■ Schizophrenia
■ Uncomplicated bereavment
❑ Mummification
❑ Severe anniversary reaction, which sometimes includes a suicide attempt
Differential Diagnosis
 Investigations
There are no specific tests for depression. Investigations focus on the
exclusion of treatable causes (see above), or other secondary
problems (e.g. loss of appetite, alcohol misuse).
■ Standard tests FBC, ESR, B12/folate, U&Es, LFTs, TFTs, glucose, Ca2+
■ Focused investigations (if indicated by history or physical signs):
❑ CT/MRI, EEG, LP (VDRL, Lyme antibody, cell count, chemistry, protein
electrophoresis)
❑ Dexamethasone suppression test (Cushing's disease)

❑ ACTH stimulation test (Addison's disease)

❑ Urine toxicology (to diagnose drug abuse like Cannabis or Opiates)

❑ Antinuclear antibody

❑ Syphilis serology

❑ HIV testing
 Course and prognosis
■ Duration of one episode is usually: 6 mths – one
year
■ The majority will have recurrence.

■ Suicide attempts are common but completed

suicide is seen in about 4%.
■ Death rate is higher than the general population is
due to the neglect of health and due to suicide.
TREATMENT
■ Hospitalization
❑ Risk of suicide or homicide,
❑ patient's grossly reduced ability to get food and shelter,
❑ the need for diagnostic procedures.
❑ History of rapidly progressing symptoms and the rupture of a
patient's usual support systems
❑ Psychotic symptoms
❑ Initiation of ECT
■ Pharmacotherapy
❑ SSRIs (Selective Serotonin Reuptake Inhibitors)
❑ Tricyclic & Tetracyclic
❑ MAOIs (Mono-amine Oxidase Inhibitors)
❑ Dopamine Reuptake Inhibitors
■ Pharmacotherapy
❑ 4-5 week at optimum dose to have response
❑ maintained for at least 6 months or the length of a previous episode,
whichever is greater
❑ The available antidepressants do not differ in overall efficacy, speed of
response, or long-term effectiveness.
❑ Selection of the initial treatment depends on
■ family history of illness and treatment response
■ symptom severity, concurrent general medical or other psychiatric conditions
■ prior treatment responses to other acute phase treatments
■ potential drug-drug interactions
■ patient preference.
■ Symptomatology: Sedative agent for insomaniac patients, lack of energy/
hypersomnia (more adrenergic/stimulatory agent), OCD symptoms
(clomipramine/SSRI), risk of suicide (avoid TCAs).
❑ Maintenance therapy: continue the effective treatment for 6 mths to 1 yr after
remission in first episode and for at least 5 yrs in recurrent episodes.
■ 5-HT Reuptake Inhibitors (SSRIs )
❑ Citalopram (Celexa) 20-60 mg
❑ Escitalopram (Lexapro) 10-20 mg
❑ Fluoxetine (Prozac) 10-40 mg
❑ Fluvoxamine (Luvox) 100-300 mg
❑ Paroxetine (Paxil) 20-50 mg
❑ Sertraline (Zoloft) 50-150 mg
❑ All SSRIs may cause insomnia, agitation, sedation, GI distress,
and sexual dysfunction. Many SSRIs inhibit various
cytochrome P450 isoenzymes. They are better tolerated than
tricyclics and have high safety in overdose. Shorter half-life
SSRIs may be associated with discontinuation symptoms
when abruptly stopped.
■ Other drugs
❑ Amitriptyline (Elavil, Endep) 75-300
❑ Imipramine (Tofranil) 75-300
❑ Clomipramine (Anafranil) 75-300
❑ Venlafaxine (Effexor) 150-375
■ ECT (Electroconvulsive Therapy)
❑ Retarded depression & Depressive Stupor (after failure of
injectable Lorazepam )
■ Psychological Threapies
❑ Supportive therapy
❑ CBT (Cognitive Behavioral Therapy)
❑ Interpersonal Therapy
Thank you