Neuroscience 18b – Depression and Anxiety

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Neuroscience 18b - Depression and Anxiety
Anil Chopra
1. List some key features of the clinical diagnoses of depression and anxiety
2. Outline how depressive disorder (‘clinical depression’) is different from ‘being
miserable’
3. Give a basic account of the epidemiology and aetiology of depression and anxiety
disorders
4. Have a rudimentary understanding of some of the psychological processes
relevant to depression or anxiety
5. Define the monoamine hypothesis of depression
Locations of the main monoaminergic nuclei within the brainstem
 The monoaminergic system of the CNS originates from small groups on neurones
in the brainstem which then project widely to all areas of the CNS
 NA – locus coeruleus to whole CNS
 5-HT (5-hydroxytryptamine) – Raphe nucleus in brainstem to whole CNS
 Dopamine – Nigrostriatal, mesolimbic and mesocortical pathways. Also found
in the hypothalamic-pituitary projection
Depression
Depression is defined as a clinically recognisable set of symptoms or behaviour
associated with distress and with interference with personal functions.
The depressed mood has to be:
- Persistent – all the time
- Pervasive – affects many tasks
- Diurnal variation – changes throughout the day
Symptoms of Clinical Depression Include:
• Low mood
• Poor concentration
• Lack of energy
• Hopelessness
• Tearfulness
• Suicidal thoughts
• Loss of interest
• Sleep disturbance
• Antiedonia
• Appetite disturbance
•
Weight
disturbance
• Constipation
• Menstrual
disturbance
• Decreased libido
It also has an effect on memory in that it:
- increases the latency of positive memories
- decreases the latency of negative memories
- decreases certain autobiographical memories especially those of positive
events.
o Seen especially in patients with history of childhood abuse.
o Seen in patients who drug overdose.
Associated with deficits in problem solving
The manifestation of depression is
thought to be a cognitive process
with a number of different causes:
 Genetic – family history
 Developmental
o Emotional deprivation
o Maternal separation
o Parental discord and
childhood abuse
 Neuroticism
 Situational factors
o Loss events
o Chronic difficulties e.g.
money/housing
o Lack of social support
70% of suicides have a history of
depression and 15% of depressed
people commit suicide.
Recognition of is incredibly important clinically because it causes great distress and
suffering not only to the patient but all those connected with him/her. It increases the
burden of illness, reduces quality of life, reduces healing and is associated with a
substantially increased suicide rate.
- Rate of depressives = 3%
- Rate of those who self harm = 0.3%
- Rate of those who commit suicide = 0.03%.
Epidemiology
Lifetime risk
5-10%
Risk to 1º relatives
Sex ratio (F:M)
Average age of onset
15%
2:1
27 yrs
Unipolar illness – characterised by mood swings in the same direction with a
relatively late onset. Reactive depression is suffered by 3-4 % of the population
during their lifetime. It occurs due to stressful life events and shows non-familial
suffering. Endogenous depression (1% of the population) is unrelated to external
depression and shows a familial pattern. Drug treatment is via a trial method (different
drugs and drug classes are tried until one is found that works with side effects that do
not outweigh the beneficial effects).
Bipolar illness (manic depression) – characterised by oscillating depression and
mania. It is less common with a relatively early onset and strong familial pattern. The
best drug for treatment is lithium.
The monoamine hypothesis of depression
This was first described by Schildkraut. It states that depression results from a
functional deficit of the central monoaminergic transmission, and that mania results
from a functional excess of monoaminergic transmission. Pharmacological evidence
in some cases supports the theory (e.g. TCAs) and in others does not (e.g. cocaine,
amphetamine), and biochemical evidence is inconsistent. Even though the general
conclusions remain firm, they delayed onset of the clinical effect of drugs indicates
that the adaptive changes may be more important (e.g. down-regulation of - and 2adrenoceptors).
Anxiety
Anxiety is a physiological state characterized by cognitive, somatic, emotional, and
behavioral components. These components combine to create the feelings that we
typically recognize as fear, apprehension, or worry.
Symptoms
 Anxious rumination – negative
thought
 Autonomic arousal
o Palpitations
o Sweating
o Diarrhoea
o Nausea
 Hyper vigilance
o Poor concentration
o Irritability
o Insomnia
Disorders of Anxiety
 PHOBIC ANXIETY DISORDERS – characterised by onset as a result of a
particular stimulus/ circumstance. These circumstances tend to be avoided and
anticipatory anxiety when the circumstance is expected.
o Social phobia
o Agoraphobia
o Specific phobias
 PANIC DISORDER – regular attacks of anxiety without a particular stimulus.
Symptoms often include:
o Palpitations
o Chest pain
o Hyperventilation
o Depersonalisation/derealisation
o Fears e.g. ‘going mad’, losing control
 GENERALIZED ANXIETY DISORDER - characterized by excessive,
uncontrollable and often irrational worry about everyday things, which is
disproportionate to the actual source of worry.
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