Somatic symptoms/Biological symptoms of depressive disorders

Lack of appetite Weight loss Stopping drinking – electrolyte imbalance Slow speech In severe cases may have psychotic symptoms

Lecture 21– Mood disorders Flashcards by Saskia Chapman

mood disorders

depression

bipolar (Type 1 and 2)

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core symptoms of depression

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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Somatic symptoms/Biological symptoms of depressive disorders

Lack of appetite
Weight loss
Stopping drinking – electrolyte imbalance
Slow speech
In severe cases may have psychotic symptoms

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Difference between a normal adjustment reaction and clinical depression

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Physical health differentials: depression

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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a presentation of depression

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mania is the

opp to depression

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Features of Mania (opposite of depression)

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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a presentation of mania

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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Physical health differentials: Mania

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

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diagnosing bipolar affective disorder

Diagnosis is made following 2 episodes of a mood disorder at least one of which is mania or hypomania.

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Hypomania

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

depression

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Bipolar 1

discrete episodes of mania only or mania and depression

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Bipolar 2

discrete episodes of hypomania only or hypomania and depression.

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time course of bipolar disorder

Euthymia= normal mood

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Brain structures involved in mood disorders

• Limbic system

Frontal lobe
Basal ganglia

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Circuits involved in mood disorders

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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the limbic system function

Emotion
Motivation
Memory

Possible limbic system changes in mood disorders

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

Frontal lobe functions

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

The prefrontal cortex

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.

Possible frontal lobe changes in mood disorders

Basal ganglia functions

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

**Possible basal ganglia changes in mood disorders**

**Overall – involvement several circuits could account for symptoms** * For depression:

* **Prefrontal cortex:** Slowing of thought, executive dysfunction. Altered emotional processing. * **Amgydala**: Abnormal emotional processing * **Basal ganglia**: Impaired incentive behaviour. Psychomotor changes.

The two main neurotransmitters for depressive disorders are:

* Serotonin * Noradrenaline (aka norepinephrine)

Serotonin and Noradrenaline (aka norepinephrine) are both

monoamines

* Monoamine hypothesis

* Suggests that depressive disorder is due to abnormality in the availability of these neurotransmitters. * Less evidence re. role of neurotransmitters in mania

where is seratonin produced

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

Seratonin thought to have roles in:

* Sleep * Impulse control (link with suicide) * Appetite * Mood

Serotonin is thought to be ..... in depression.

* Serotonin is thought to be low in depression.

evidence to support that seratonin is low in depression

* **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 i**ncreasing 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

where is noradrenaline produced

* Produced in the locus coeruleus (pons) and projects to limbic system and the cortex

NA Functions in the brain:

Role of noradrenaline in mood disorders

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

biological treatment of depression

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

Psychological treatment of depression

First line treatment for depression: CBT

Social treatment of depression

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

Biological treatment of mania

* First line: antipsychotics * Alternatively: mood stabiliser

Psychological treatment of mania

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

Social treatment of mania

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

**Biological treatment of bipolar depression** *

* Biological – Can use antidepressant – but ONLY with mood stabiliser cover. * ECT * Lithium

Psychological treatment of bipolar depression

– CBT

social treatment of bipolar depression

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

Maintaining stability in bipolar disorder

* **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.