Affective Disorders Flashcards
Spectrum of disorders
BAD
- type 1 and type 2
Unipolar disorder
- MDD
Others
- cyclothymia
- dysthymia
Kindling hypothesis of affective disorders
Major stressors trigger initial onset
Successive affective episodes become less tied to stressors and occur more spontaneously
More attacks = more destabilised (increase severity and recurrence)
Neuroanatomy and Neuroendocrinology in affective control - areas involved
Interplay among prefrontal cortex, basal ganglia, limbic system
- neocortex - higher functions, behavioural response, perception
- amygdala - fear/aggressive behaviour, emotions
- hippocampus - memory (recent)
- corpus striatum (bg) - automatic movement regulation
Cortico-striato-thalamo-cortical circuits
- implicated in depression and OCD
- theoretical basis of treating depression/OCD by DBS
Difficulty in diagnosis of affective disorders
Change in mood difficult to detect
Lack of insight
Under-reporting
Stigmatisation
Which stage of development is most critical/vulnerable to affective disorders?
Adolescence
– self awareness, early detection and early intervention is important
primary, secondary and tertiary prevention (illness, diagnosis, suicide)
Differential Diagnosis of low mood
Mood disorders
- Major depressive disorder
- BAD
- Cyclothymia
- Dysthymia
- Recurrent depressive disorder
Anxiety disorders
Schizoaffective disorder
Secondary to medical condition e.g. hypothyroid
Secondary to substance abuse
Normal sadness/ grief
Classical symptoms of low mood - somatic, cognitive, psychotic
Somatic
- early morning (2hrs early) wakening with dysphoria, agitation +/- initial insomnia, frequent awakening
- diurnal variation - mood worse in the morning
- LOA and LOW
- Psychomotor agitation (restless, pacing, scratching) or retardation (slow speech, long pauses, limited expressions - mutism in severe cases)
- loss of libido/amenorrhea
(other physical symptoms e.g. aches, constipation)
Cognitive
- poor concentration and memory
- poor self esteem (helpless, worthless)
- guilt 自責
- hopelessness
- suicide or self-harm
Psychotic (in severe cases)
- mood congruent delusions/hallucinations e.g guilt, disease (hypochondriacal), death, nihilism (such as blocked bowels in Cotard’s syndrome), derogatory voices
Other symptoms e.g. depersonalisation, obsessional symptoms, phobia, conversion
Severe depression with psychosis vs Schizophrenia
Psychosis only during mood symptoms *Temporal relationship *Mood congruent psychotic symptoms (vs incongruous affect and bizarre delusions in schizophrenia) Determine predominant symptoms Examine mental state
Assessment of low mood - Hx
Hx
- core symptoms (low mood, anhedonia, fatigue)
- biological symptoms
- cognitive
- r/o BAD (hx of elated mood), psychosis
MUST include
- risk assessment
- functional assessment
- psychotic/manic features
- common psychiatric comorbidities e.g. GAD, OCD, PTSD, SA, pain
- physical comorbidities
Investigations for low mood - social, psychological, physical
Social
- collateral info from GP, family
Psychological
- mood diary
- self-report inventories
Physical - CBC for anaemia, infection, high MCV - TFT for hypothyroid - Ca for hyperCa - LFT and GGT for alcoholism - RFT, Urea and electrolytes for hypoNa (prescribe SSRI) - fasting BG for chronic illness [Others e.g. urine drug screen, VitB12/folate if suspected]
(CT brain only when psychotic or poor cognition since organic disease rarely just presents with mood changes)
Major Depressive Disorder Diagnostic Criteria
- FIVE OR MORE of the following for >TWO WEEKS
- low mood MOST OF THE DAY, NEARLY EVERYDAY (pervasive) 低落
- markedly diminished interest or pleasure in all activities (anhedonia) 提唔起徑
- significant (>5% change in 1 month) LOW/weight gain or loss/gain of appetite
- insomnia/hypersomnia
- psychomotor agitation or retardation (observable and subjective e.g. restlessness)
- loss of energy (anergia)
- negative cognition – worthlessness/excessive guilt, hopelessness, helplessness
- inability to concentrate leading to poor memory (depressive pseudodementia in severe cases of elderly)
- recurrent thoughts of death/suicide/self-harm - Cause significant impairment and distress
- Not attributable to physiological effects of substance or other medical condition
- Not better explained by schizophrenia, delusional disorder, schizoaffective etc
- Never been manic or hypomanic episode
MDD epidemiology - lifetime risk, F:M, peak age
Lifetime risk: 20% - one of the most important causes of disability
F>M 2:1
Peak onset late 20s-40s but higher prevalence in 65+
More common in urban populations/ adverse socio-economic factors e.g homeless
Diversity in clinical presentation - mood, somatic, stupor, atypical, memory
Mood
- Agitated depression: more common in older patients
- apathy, irritable, anger
Somatic
- pain, discomfort (could be main complaint) – may have hypochondriacal preoccupation
Retarded depression
- prominent psychomotor retardation
Depressive stupor
- rare, severe case
- motionless, mute, refuse to eat and drink
- can be manic, depressive or psychotic
Atypical depression
- increased sleep, appetite/weight, severe anxiety and interpersonal sensitivity
(suggestive of BAD, or seasonal affective disorder)
Memory
- pseudo-dementia in elderly
Post-psychotic depression
- depression syndrome after tx of psychotic symptoms of schizophrenia
MDD - aetiology endogenous - genetics and personality
Genetics
- parents, siblings, children of severely depressed patients have higher lifetime risk for mood disorder (10-15%) than general population (1-2%)
- 30-40% heritability
- 7% of first degree relatives, 37% concordance in twin studies
(no genes consistently identified - 5HT transport/receptor, BDNF, tryptophan hydroxylase)
Personality
- no single personality type a/w MDD
- coping style, resilience, neuroticism (easily stressed, moody, anxious, shy)
- borderline, OCD
MDD - aetiology reactive
Environmental factors:
- predisposing:
- –> chronic stress e.g. social support, unemployment, marriage difficulties, raising young children, chronic pain or illness (Parkinson’s, malignancy)
- –> early life experiences e.g. parental separation (<11yrs old), poor upbringing
- precipitating: acute stressors e.g. bereavement, childbirth, (infection)
- –> not causal but a/w increased risk of depression 6x in the 6 months after moderately severe life events
- perpetuating:
- –> abnormal psychological mediation e.g. emotional processing, tendency to rmb unhappy events, unrealistic beliefs, cognitive distortions in overgeneralising
- –> abnormal biochemical processes – reduced 5HT and NA
MDD - neuroanatomy and neuroendocrinology
Brain
- reduced volume of hippocampus (temporal lobe), amygdala, prefrontal cortex, basal ganglia
- white matter hyper intensities on imaging
Hormonal factors
- increase CRH, ACTH, cortisol (50% patients) with loss of diurnal rhythm of cortisol
- subclinical hypothyroid in 30%
- MONOAMINE DEFICIENCY hypothesis (NA, 5HT, DA)
“Organic” causes of depression - suspicious symptoms, possible causes
Suspect when:
- acute, severe, atypical onset
- late-onset
- no apparent stress or precipitating events
Possible causes:
- endocrine - hypothyroid, Cushing’s, Addison’s, hyperPTH
- alcohol and SA
- drugs e.g. sedatives, Parkinson’s drugs, steroids, anti-HT (beta blockers, methyldopa), statins, opiates
- infection e.g. influenza, tertiary neurosyphilis, HIV
- SOL of brain causing structural damage to areas regulating mood e.g. tumour, CVA
- MS, Parkinson’s, Huntington’s
- others: chronic pain, malignancy
Remember medical problems can precipitate depression but depression can aggravate medical problems as well e.g. DM, MI, dementia
MDD - associations with DM + PPS, and diet
DM-MDD (double burden)
- risk doubled of comorbid MDD in DM patients
- depression a/w 60% increased risk of T2DM
(may be due to lifestyle, decreased activity, hyperplagia, decreased QOL, drugs S/E)
High prevalence of painful physical symptoms (PPS) comorbid with MDD
- a/w more severe illness, poorer QOL, lower response and remission rates
Diet
- lower levels of tryptophan (5HT precursor) and VitB12/Folate (synthesis of DNA, 5HT, NA, DA)