University of Oxford

Mood disorders

MOOD (AFFECTIVE) DISORDERS

  

1. Depressive Illness (Unipolar Depression)

 Introduction:

 Very common, rank 4th as a cause of disability worldwide, projected to rank 2nd by 2020. Although effective treatments are available, depression often goes undiagnosed and untreated, often regarded by both patients and physicians as understandable.

Mild depression has a significant morbidity and mortality. Suicide is the leading cause of death in person 20-35 yrs; high percentage (up to 50%) is depression.

Depression disorder also contributes to higher morbidity and mortality when associated with other physical disorders (e.g. MI) and its successful diagnosis and treatment has been shown to improve both medical and surgical outcomes.

There remains an innate reluctance to consider pharmacological interventions for emotional problems, despite overwhelming evidence of efficacy. Also widespread concern that drugs which improve mood must be addictive, despite evidence to the contrary.

Non compliance remains the major reason for treatment failure and often underestimated (up to 40% of treatment failure due to non-compliance).

Diagnosis:

Slight difference between the ICD-10 and the DSM-IV, however the core symptoms are almost identical:

  • Present for at least 2 weeks
  • Depressed mood present most of the day, nearly every day, with little variation and often lack of responsiveness to change in circumstances. There may be diurnal variation in mood with mood worse in the morning.
  • Anhedonia Marked diminished interest or pleasure in all, or almost all activities most of the day.
  • Weight change loss of weight or gain (5% in one month), associated with decreased or increased appetite.
  • Disturbed sleep insomnia (with early morning wakening 2-3 hours sooner than usual) or hypersomia (atypical depression).
  • Psychomotor retardation or agitation both subjectively and objectively
  • Fatigue or loss of energy.
  • Reduced libido
  • Felling of worthlessness or excessive or inappropriate guilt (may be delusional).
  • Diminished ability to think or concentrate or indecisiveness.
  • Recurrent thoughts of suicide or death which may or may not have been acted upon.

 Somatic symptoms, also called ‘biological’, ‘melancholic’ or ‘vital’

  • Loss of emotional reactivity
  • Diurnal mood variation.
  • Anhedonia
  • Early morning wakening
  • Psychomotor agitation or retardation
  • Loss of appetite and weight
  • Loss of libido

Psychotic Symptoms:

  • Delusions e.g. poverty, personal inadequacy, guilt, other nihilistic delusions.
  • Hallucinations e.g. deformity or accusatory voices, cries for help or screaming; bad smell, demons, devil, dead bodies.
  • Catatonic e.g. depressive stupor.

Severity:

Mild, moderate or severe

Subtypes:

? Melancholic or with somatic symptoms

? With psychotic symptoms

? Under ‘other depressive episodes’:

  • Atypical depression (mood depressed but reactive, hypersomnia, hyperplasia, leaden paralysis, oversensitivity to perceived rejection, initial insomnia, reversed diurnal variation, lack of feeling of guilt. In early twenties.
  • Postnatal depression
  • Seasonal affective disorder
  • Premenstrual dysphoric disorder

Indirect presentation

  • Insomnia, or other somatic complaints (e.g. Headache, GI upset)
  • Person from a different cultural background presenting with ‘cultural-specific’ symptoms.
  • Physical disorder masking the depressive features.

Epidemiology:

Prevalence 2-5%

Lifetime rate 10-20%

Sex Ratio M:F 1:2

It is increasing.

Aetiology:

(Bio-Psycho-Social approach / 3Ps Predisposing, Precipitating and Perpetuating)

 1. Biological and genetic factors:

Lack of Monoamines (Serotonin, Noradrenalin, and possibly Dopamine)

Antidepressant work by increasing the above. SSRI (serotonin reuptake inhibitors e.g. Prozac, Cipralex. TCA (old antidepressant which has severe side effects including cardiac) prevent reuptake of both serotonin and noradrenalin. Other new medications such as Effexor work on all three (low dose ?serotonin, moderate dose? noradrenalin then high dose? dopamine).

Above is oversimplification and other transmitters such as GABA and peptide (e.g vasopressin) are involved. There is also link with abnormalities in regulation of many hormones (stress hormones) such as Cortisol and the Hypothalamic-pituitary-adrenal (HPA) axis. New generation antidepressants (in the making) are to target all of the above.

Twin and family studies have shown that there is a genetic basis to many cases of depression; hence a family history is a significant risk for depression

2. Psychological and social factors:

There is strong evidence that psychological factors (e.g. maternal deprivation or other childhood loss) may predispose to depression. Type of personality is also a risk (obsessive compulsive Personality).Life events such as marital separation, job loss and other stresses also play a role.

Other social risk factors include being at home with young children, unemployment, and lack of close confidants

Differential Diagnosis: 

  • Other psychiatric disorders
  • Neurological disorders
  • Endocrine disorders
  • Metabolic disorders
  • Haematological disorders
  • Inflammatory conditions
  • Infections
  • Sleep disorders
  • Medication-related

  

THEREFORE ALWAYS EXCLUDE ORGANICITY AS A PRIMARY CAUSE FOR DEPRESSION.

Course & Prognosis:

Depressive episodes vary from 4-30 wks for mild-moderate cases, to an average of about 6 months for severe cases (25% will last up to 1 yr)

The majority of patients experiencing a depressive episode will have further episodes later in life (risk of recurrence is 30% at 10 yrs, 60% at 20 yrs).Recurrence is greater when there are residual symptoms after remission.

There are good evidence that modern antidepressant treatment impact significantly upon the above, reducing the length of depressive episodes; and if treatment is given long term, the incidence of residual symptoms is less, there are fewer recurrent episodes, and chronicity may be as low as 4%

Mortality suicide 15% (severe) especially requiring hospital admission, overall rate of death is higher than general population with other causes usually due to substance misuse, accidents, cardiovascular disease, respiratory infection and thyroid disorders.

Good prognostic factors: Acute onset, ‘somatic symptoms’. Earlier age of onset

Poor Prognostic Factors: Insidious onset, elderly, residual symptoms, neuroticism, low self confidence, comorbidity (physical or psychiatric. personality disorder), lack of social support

Management & Treatment:  

? History

? MSE (Mental State Examination)

? Physical Examination

? Investigations: Standard test: FBC, ESR, B12/Folate, U&E, LFT, TFT, Glucose, And MSU. Others: EEG, CT/MRI, HIV testing etc (all depends on the history and physical examination. 

?Treatment:

1. Antidepressent: effective in 65-75% of patients. All currently available antidepressant work by increasing the availability of the monoamines (5HT, NA & DA). Many classes are available:

  • SSRIs (Selective serotonin reuptake inhibitors)
  • TCAs (Tricyclic antidepressants)
  • MAOI (Monoamine oxidise inhibitors) and reversible monoamine oxidise inhibitors (RIMAs) inhibitors-tyramine and cheese reaction hypertensive crises requires dietary restriction, good for atypical depression.
  • Seratonin/noradrnaline reuptake inhibitors (SNRIs)
  • Noradrenalin reuptake inhibitors (NARIs)
  • Noradrenalin and specific serotonergic antidepressant (NaSSA)
  • Others: L-Tryptophan, st.John’s wort.

2. Psychotherapy:

CBT (Cognitive-Behavioural Therapy)

IPT (Interpersonal Therapy)

Psychodynamic (Psychoanalysis): lacks evidence based support.

3. Combinationof the above may act synergistically

4. Augmentation (Evidence for lithium and mood stabilisers).

5. ECT: May be considered as first-line therapy when there are severe biological features (significant weight loss) or marked aggression, retardation or suicide risk, psychotic features are prominent.. Consent needed, main risk due to anaesthesia, safe, no aboslolue contraindication.

6. Psychosurgery only in exceptional circumstances when all other fails. Employ stereo tactic method using MRI.

7. Others: Light Therapy, rTMS (repetitive transcranial magnetic stimulation, Magneto-Convulsion Therapy (MCT), Vagus Nerve Stimulation(VNS)

2. Bipolar Illness (Manic-depression):

Diagnosis:

Mania (Bipolar I): A distinct period of abnormally and persistently elevated, expansive, or irritable mood, with 3 (or more) symptoms. lasting 1 week or less if admission is required.

Clinical Features:

  • Elevated mood
  • Increased energy which manifest as over activity, pressed speech, racing thought or reduced need to sleep
  • Increased self esteem, evident as overoptimistic ideation, grandiosity, reduced social inhibition.
  • Reduced attention/ increased distractibility
  • Tendency to engage in behaviour that could have serious consequences such as, preoccupation with extravagant, impracticable schemes, spending recklessly, inappropriate sexual encounter
  • Other behavioural manifestations such as, excitement, irritability, aggressiveness, suspiciousness
  • Marked disruption of work, usual social activities and family life.

Psychotic symptoms: 

  • In severe forms grandiose ideas may be delusional e.g. special power.
  • Persecutory delusions
  • Catatonic behaviour
  • Total loss of insight.  

Hypomania (BPII): 4 days and symptoms less severe and does not interfere with social or occupational function

Epidemiology:

Life time prevalence 3-1.5%

M=F (except Rapid Cycling i.e. more than 4 episodes a year)

Age mean 21yrs, males earlier than females.

Aetiology:

(Bio-Psycho-Social-/ 3Ps Predisposing, Precipitating and Perpetuating)

(Patient must have the genetic predisposability)

Genetic 1st degree relatives are more likely to develop the condition (10-15%). Children of a parent with bipolar disorder have 50% chance of developing a psychiatric disorder (genetic liability appears shared for schizophrenia, schizoaffective, and Bipolarity).

MZ twins 33-90%, DZ twins 25%

Neurotransmitters NA, DA, 5HT and glutamine

HPA axis stress hormones.

Differential Diagnosis:

As in depression exclude organicity (secondary mania)

Medication that may induce mania:

Antidepressant

Other psychotropic medications

Anti Parkinson medications

Cardiovascular medications

Respiratory drugs

Anti infection

Analgesic

Gastrointestinal drugs

Steroids

Others: interferons, cyclosporine, baclofen

Course & Prognosis:

Extremely variable.1st episodes may be hypomanic, manic, mixed or depressive. This may be followed by many years without further episodes, but the length of time between subsequent episodes may begin to narrow. There is often a 5-10 years interval between age of onset and treatment. Depression is much more common to be first, mania can present even at later life (>50).

Mortality and morbidity rates are high, in term of lost work, productivity, effect on marriage (much higher divorce rate). Attempted suicide up to 40% and completed up to 10%

Within the first 2 years of 1st episode, 50% will experience another episode.

Poor prognostic factors: Poor compliance, Unemployment, substance misuse, psychotic features, male, mixed state, rapid cycling.

Good prognostic factors: Mania episode of short duration, later age of onset, good response treatment, and few comorbidity physical problems.

Management & Treatment:

(Bio-psycho-social approach again!!)

Same as depression in term of assessment

  ?First line treatment:

  

Lithium, Antipsychotic, ECT, BDZ (for acute episode).

  ?Second line:

Anticonvulsant: Valproate and Carbamazepine

  ?Psychotherapeutic interventions:

 Most patients will struggle with some of the following issues:

  • Emotional consequences of significant periods of illness and receiving the diagnosis
  • Problems related to stigmatisation and self-esteem
  •  Interpersonal, marriage, family, occupational or academic problems
  • Coming to term with the illness, past event and future concerns

Some selected intervention:

Cognitive Behavioural Therapy (CBT)time limited, with specific aims: educate the patient about bipolar disorder and its treatment, teach cognitive behavioural skills for coping with psychosocial stressors and associated problems, facilitate compliance with treatment and monitor the occurrence of symptoms (relapse signature)

Family Therapy

Support Groups

References

.1.    Stevens L, Rodin I. Psychiatry: An illustrated colour text, Churchill Livingstone 2001

•2.    Steple D. Oxford Handbook of Psychiatry, Oxford University Press, 2006

•3.    Guthrie E & Creed F. Seminars in Liaison Psychiatry. Royal college of Psychiatrist 2007

•4.    World Health Organization (WHO). ICD-10 Classification of mental and behavioural disorders. Churchill Livingstone

•5.    American Psychiatric Association (APA). DSM-IV-TR. Fourth Edition Text Revision. APA Publication

•6.    King D. Seminars in clinical psychopharmacology. Second Edition 2004. Royal College of Psychiatrists

  

  

  

  

  

  

  

  

  

  

  

  

  

  

  

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