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Clinical neuroscience > Lecture 21– Mood disorders > Flashcards

Lecture 21– Mood disorders Flashcards

1
Q

mood disorders

A

depression

bipolar (Type 1 and 2)

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2
Q

core symptoms of depression

A
  • Patient usually have the symptoms continually for 2 weeks and consist of
  • CORE SYMPTOMS
    • Low mood
    • Lack of energy
    • Lack of enjoyment & interest
  • Depressive thoughts
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3
Q
  • Somatic symptoms/Biological symptoms of depressive disorders
A
  • Lack of appetite
  • Weight loss
  • Stopping drinking – electrolyte imbalance
  • Slow speech
  • In severe cases may have psychotic symptoms
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4
Q

Difference between a normal adjustment reaction and clinical depression

A
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5
Q

Physical health differentials: depression

A
  • Hormone disturbance such thyroid dysfunction
  • Vitamin deficiencies such as vitamin B12
  • Chronic disease e.g. renal, CVS & liver failure
  • Anaemias
  • Substance misuse e.g. alcohol, cannabis & stimulants
  • Hypoactive delirium
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6
Q

a presentation of depression

A
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7
Q

mania is the

A

opp to depression

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8
Q

Features of Mania (opposite of depression)

A
  • Elated Mood
  • Increased energy
  • Pressure of speech
  • Decreased need for sleep
  • Flight of ideas
  • Normal social inhibitions are lost
  • Attention cannot be sustained
  • Self esteem is inflated, often grandiose
  • May have psychotic symptoms
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9
Q

a presentation of mania

A
  • Elated Mood
  • Increased energy
  • Pressure of speech
  • Decreased need for sleep
  • Flight of ideas
  • Normal social inhibitions are lost
  • Attention cannot be sustained
  • Self esteem is inflated, often grandiose
  • May have psychotic symptoms
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10
Q

Physical health differentials: Mania

A
  • Iatrogenic e.g. steroid induced
  • Hyperthyroidism
  • Delirium
  • Infection e.g. encephalitis, HIV, syphyllis
  • Head injury
  • (intoxication with stimulants)
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11
Q

diagnosing bipolar affective disorder

A
  • Diagnosis is made following 2 episodes of a mood disorder at least one of which is mania or hypomania.
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12
Q
  • Hypomania
A

(literally “under mania” or “less than mania”) is a mood state characterized by persistent disinhibition and mood elevation (euphoria), with behavior that is noticeably different from the person’s typical behavior when in a non-depressed state.

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13
Q

Therefore you don’t ever have to have a diagnosis of …….. to be given the diagnosis bipolar disorder.

A

depression

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14
Q

Bipolar 1

A

discrete episodes of mania only or mania and depression

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15
Q

Bipolar 2

A

discrete episodes of hypomania only or hypomania and depression.

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16
Q

time course of bipolar disorder

A

Euthymia= normal mood

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17
Q

Brain structures involved in mood disorders

A

• Limbic system

  • Frontal lobe
  • Basal ganglia
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18
Q

Circuits involved in mood disorders

A

The main hypothesis is that mood is determined by functional circuits between these brain areas. E.g. the frontal lobe projects to parts of the limbic system which in turn connects to the basal ganglia and the brainstem. This affects:

  • Cognitive processed (thoughts)
  • Sympathetic output
  • Parasympathetic output
  • Motor systems
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19
Q

the limbic system function

A
  • Emotion
  • Motivation
  • Memory
20
Q

Possible limbic system changes in mood disorders

A

limbic system include the amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus.

21
Q

Frontal lobe functions

A

The frontal lobe form 2/3 of the total cortex

  • Motor function
  • Language (Broca’s area)
  • Executive functions (purposeful goal directed behaviours)
  • Attention
  • Memory
  • Mood
  • Social and moral reasoning
22
Q

The prefrontal cortex

A
  • The ventromedial prefrontal cortex – is thought to be involved in the generation of emotions.
  • While the orbital prefrontal cortex is thought to be involved in emotional responses – possibly via connection with the amygdala.
23
Q

Possible frontal lobe changes in mood disorders

A
24
Q

Basal ganglia functions

A

motor and psychological

  • Motor function; malfunction of the basal ganglia are implicated in neurological illnesses such as
    • Parkinson’s disease
    • Wilson’s disease
    • Huntington’s disease
  • Psychological function:
    • Emotion
    • Cognition
    • Behaviour
25
Q

Possible basal ganglia changes in mood disorders

A
26
Q

Overall – involvement several circuits could account for symptoms

  • For depression:
A
  • Prefrontal cortex: Slowing of thought, executive dysfunction. Altered emotional processing.
  • Amgydala: Abnormal emotional processing
  • Basal ganglia: Impaired incentive behaviour. Psychomotor changes.
27
Q

The two main neurotransmitters for depressive disorders are:

A
  • Serotonin
  • Noradrenaline (aka norepinephrine)
28
Q

Serotonin and Noradrenaline (aka norepinephrine) are both

A

monoamines

29
Q
  • Monoamine hypothesis
A
  • Suggests that depressive disorder is due to abnormality in the availability of these neurotransmitters.
  • Less evidence re. role of neurotransmitters in mania
30
Q

where is seratonin produced

A

in the raphe nuclei (rostral and caudal) of the brainstem and transproted to cortical areas and limbic system

31
Q

Seratonin thought to have roles in:

A
  • Sleep
  • Impulse control (link with suicide)
  • Appetite
  • Mood
32
Q

Serotonin is thought to be ….. in depression.

A
  • Serotonin is thought to be low in depression.
33
Q

evidence to support that seratonin is low in depression

A
  • SSRI’s (Selective serotonin reuptake inhibitors), SNRI (Serotonin and norepinephrine reuptake inhibitors), TCA’s (Tricyclic antidepressants) & MAOi’s (Monoamine oxidase inhibitors) all successfully treat depression by increasing levels of serotonin in synaptic cleft
  • 5HIAA (metabolite of serotonin) is low in the CSF of patients with depression (particularly those who have attempted suicide).
  • Tryptophan (precursor for serotonin) depletion causes depression and is high in depressed people
34
Q

where is noradrenaline produced

A
  • Produced in the locus coeruleus (pons) and projects to limbic system and the cortex
35
Q

​NA Functions in the brain:

A
36
Q

Role of noradrenaline in mood disorders

A

NA thought to be decreased in depression:

  • Antidepressants (e.g. SNRI’s, NARI’s and some TCA’s) that increase NA successfully treat depression.
  • Patients who have recovered from depression who show decreased NA levels, have significantly higher rates of relapse.
  • Postmortem studies of depressed patients vs controls
37
Q

biological treatment of depression

A
  • First line = Selective Serotonin Reuptake inhibitors. (SSRIs)
  • Other options: SNRI’s, TCA’s etc
  • Life threatening/treatment resistant: ECT (Electroconvulsive therapy)
38
Q

Psychological treatment of depression

A

First line treatment for depression: CBT

39
Q

Social treatment of depression

A

Help with e.g. isolation, social stressors (including housing, finances)

40
Q

Biological treatment of mania

A
  • First line: antipsychotics
  • Alternatively: mood stabiliser
41
Q

Psychological treatment of mania

A

Acutely unlikely to be helpful, longer term – psychoeducation re. BPAD, triggers and signs of relapse.

42
Q

Social treatment of mania

A

Treat in a place of safety – where risk to self and others is minimal. Consideration of implications of mania e.g. debts (excessive spending).

43
Q

Biological treatment of bipolar depression

*

A
  • Biological – Can use antidepressant – but ONLY with mood stabiliser cover.
    • ECT
    • Lithium
44
Q

Psychological treatment of bipolar depression

A

– CBT

45
Q

social treatment of bipolar depression

A
  • Help with e.g. isolation, social stressors (including housing, finances)
46
Q

Maintaining stability in bipolar disorder

A
  • Biological
    • Mood stabilisers e.g. lithium, sodium valproate- shouldn’t be used on women of a child bearing age (anticonvulsant)
    • Antipsychotic (used as a mood stabiliser e.g. Quetiapine)
  • Psychological
    • Psychoeducation re. bipolar affective disorder.
    • CBT – to help prevent relapses
  • Social
    • Consideration of BPAD on employment e.g. shift work.
    • Involvement of family, education of family etc.

Clinical neuroscience (30 decks)

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