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Neuro > NEURO: Depression > Flashcards

NEURO: Depression Flashcards

1
Q

Discuss the different treatments for mental illness.

A

Examples of treatment for mental illness is cognitive behavioural therapy and pharmacotherapy.

Although these drugs have certainly helped a lot of people and we are in a better place from where we were 30 years ago, there are still major problems. They do not help everyone (resistance), side effects can be severe in some cases, tolerance, dependence, have a narrow therapeutic window and they do not treat all symptoms.
All this made developing drugs for treating mental disorders expensive and difficult and many pharma have got out of this CNS business.

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2
Q

List some characteristics of affective disorders.

A
  • disorders of mood rather than thought / cognition
  • most common is depression
  • major cause of premature death and disability
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3
Q

Describe the two types of depression.

A

1) UNIPOLAR DEPRESSION:
- mood swings in one direction
- most common depressive illness
- 75% cases REACTIVE (induced by environmental factors)
- 25% cases ENDOGENOUS (genetic)

2) BIPOLAR DEPRESSION:
- Oscillation between depression and mania
- Mania: excessive exuberance, enthusiasm, self confidence, impulsive actions, aggression, irritability, delusions of grandiose
- less common
- onset usually in adult life
- strong hereditary tendency (no genes found yet)

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4
Q

What is depression?

A

There are multiple ways to define it:

DEPRESSIVE DISORDER: a low state marked by significant levels of sadness, lack of energy, low self-worth, guilt or related syndromes

MAJOR DEPRESSIVE DISORDER: severe pattern of depression that is disabling and is not caused by factors such as drugs or a general medical condition

DYSTHYMIC DISORDER (DYSTHYMIA): similar to major depressive disorder but less severe/disabling and more long-lasting (chronic)

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5
Q

Why is diagnosing depression hard?

A
  • wide variety of symptoms that patients can report
  • difficult to know when a normal fluctuation in mood becomes depression
  • no single objective test to establish diagnosis
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6
Q

What are some symptoms of depression?

A

EMOTIONAL SYMPTOMS (Q):

  • apathy, pessimism, negativity
  • low self esteem, feeling guilty
  • loss of motivation
  • indecisiveness

BIOLOGICAL SYMPTOMS (Q):

  • reduced activity
  • loss of libido
  • sleep disturbance
  • loss of appetite
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7
Q

What are some screening questions you could ask in a clinical interview?

A
  • During the past month have you often been bothered by feeling down, depressed or hopeless?
  • During the past month have you often been bothered by having little interest or pleasure in doing things?
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8
Q

Who gets depression?

A

GENDER:

  • depression affects around twice as many females as males
  • lifetime prevalence of major depression: 10-25 % for women, 5-12 % for men

AGE:

  • 1st episode of depression usually late adolescence of early adulthood
  • age of onset has been decreasing in recent years
  • is life now more stressful?
  • are we just diagnosing more people with depression?
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9
Q

What are some important factors to consider when dealing with depression?

A

SUICIDE:

  • suicidal thoughts are common among depressed patients
  • 20% depressed individuals will attempt suicide
  • 10% of severe depressives will commit suicide

COMORBIDITY:
- depression is often comorbid with other psychiatric conditions (e.g. withdrawal from drugs of abuse)

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10
Q

With co-morbidity, what are some general medical conditions in which you often find depression?

A
  • terminal illness
  • chronic illness (e.g. chronic pain)
  • thyroid dysfunction
  • neurological disease
  • stroke
  • drug abuse
  • Parkinson’s disease
  • anxiety
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11
Q

What can cause depression?

A

GENETIC PREDISPOSITION?

  • General population: 3.2%
  • First degree relatives of patients: 20%
  • Monozygotic twins: 40-50%

ENVIRONMENTAL FACTORS?

  • Loss
  • Environmental stressors
  • Social isolation
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12
Q

What are the different theories of depression?

A
  • the monoamine theory

- the neuroendocrine theory

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13
Q

What is the major theory of depression?

Describe it.

A

The major theory of depression is the monoamine theory.

  • there is an overall reduced activity of central noradrenergic and / or serotonergic systems
  • reserpine depletes the brain of NA and 5-HT, inducing depression
  • the main antidepressant drugs [amines] act in the brain (Q devise drugs to treat depression)

The lower activity of noradrenergic system leads to an increase in post synaptic receptors. Blocking reuptake to increased amines in synaptic cleft normalises postsynaptic receptor number.
[NA]plasma tends to be higher in depressed patients than in normals – as an increase in anxiety, causes an increase sympathetic activity

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14
Q

What is some evidence against the monoamine theory?

A
  • Difficult to show deficits in brain [NA] & [5-HT] and functioning/ (-) results from CSF, plasma in depressed /individuals respond better to one AD than another
  • Most antidepressant drugs take several weeks for therapeutic effect, but an increase in amines is acute (secondary adaptive changes more important)
  • Some antidepressants are weak/have no effect on amine uptake (e.g trazodone)/no increase in 5HT and NA but they are still antidepressants!
  • Cocaine blocks amine uptake but has no antidepressant effect
  • Decrease in 5HT in dipolar linked to aggression rather than depression
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15
Q

Describe the neuroendocrine theory of depression.

A

THE HPA AXIS:

  • NAergic & 5-HT neurons input to hypothalamus
  • Hypothalamus releases corticotropin-releasing hormone (CRH)
  • CRH acts on pituitary – release of adrenocorticotrophic hormone (ACTH)
  • Cortisol release from adrenal cortex in response to increased ACTH in blood

Amygdala activation stimulates the HPA system but hippocampal activation suppresses the HPA system. Thus, if the system is in disarray, we can get an increase in cortisol which can lead to depression, so we need to consider the amygdala and the hippocampus.

CRH – behavioural effects mimic some depression symptoms

  • decreased hippocampal feedback in depression
  • decreased glucocorticoid receptors (cortisol receptors) in hippocampus
  • Tactile stimulation just after birth activates 5-HT pathways to hippocampus
  • 5-HT triggers long-lasting increase in expression of glucocorticoid receptor gene
  • increase in glucocorticoid receptors in hippocampus

SSRIs increase glucocorticoid receptors in the hippocampus

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16
Q

What are some proofs of neuroplasticity and neurogenesis as a theory of depression?

A
  • Evidence of neuronal loss and decreased neuronal activity in hippocampus and prefrontal cortex (decision making centres)
  • Antidepressants and electroconvulsive therapy (ECT) promote neurogenesis in these regions
  • 5-HT promotes neurogenesis during development (BDNF: brain-derived neurotrophic factor)
  • Increase in Glutamate in the cortex of depressed people (NMDA antagonists potential for depression treatment e.g. ketamine)
17
Q

What are some treatments of affective disorders?

A

ELECTROCONVULSIVE THERAPY (ECT):

  • localised electrical stimulation
  • some evidence of neurogenesis, possible involvement of hippocampus
  • adverse effect: memory loss

PSYCHOTHERAPY:

  • mild to moderate depression
  • overcome negative views

ANTIDEPRESSANTS:

  • tricyclic antidepressants (TCA), block reuptake of NA and 5-HT (imipramine)
  • selective serotonin (5-HT) reuptake inhibitors (SSRI) (fluoxetine)
  • NA-selective reuptake inhibitors (reboxetine)
  • monoamine oxidase inhibitors (MAOI), block degradation of NA and 5-HT (phenelzine)

[All elevate monoamine levels but antidepressant effect takes several weeks]

18
Q

What are some points about using antidepressants to combat affective disorders?

A
  • Increase in monoamines may ‘normalise’ presynaptic and postsynaptic receptors
  • Antidepressants dampen down HPA axis hyperactivity: increased hippocampal glucocorticoid receptor expression
  • SSRIs may promote neurogenesis
19
Q

How can we combat social phobia?

A

After its discovery, the next hypothesis was “if oxytocin has a prosocial effect, then externally administered OXT should be able reverse social deficits”. This was tested in rats.

Brain oxytocin (OXT) reverses defeat-induced social phobia in rodents. 30 min exposure to social defeat (20 min before social preference testing) prevents social preference and results in social avoidance in vehicle-treated rats. Social phobia can be reversed by intracerebroventricular infusion of OXT 20 min before behavioural testing.

20
Q

How can lithium be used to treat affective disorders?

A
  • it stabilises the mood (mania and depression)

- it inhibits enzymes involved in signal transduction

21
Q

What is the evidence of hyperactivity of HPA in depressed patients

A
  • increased [cortisol]plasma in depressed patients
  • increased [CRH] in the cerebrospinal fluid

Genes and environment can contribute to this hyperactivity

Evidence of reduced hippocampal feedback
- decreased hippocampal glucocorticoid receptors
Glucocorticoid receptor expression regulated by early sensory experience

22
Q

How do MAOIs work?

A

MAOI s increase [NA/5-HT]cytoplasm

increase [NA/5-HT]cytoplasm –> increase leakage of amine

increase [NA/5-HT] in synaptic cleft

23
Q

What are the main therapeutic effects of TCAs?

A

Main therapeutic effects:

NA reuptake inhibitor
5-HT reuptake inhibitor
Initially [NA] & [5-HT] in synaptic cleft
Chronic treatment down regulation of 
(β1) & 5-HT2 
⍺2, 5-HT1A/1D (autoR)
Also affect mACh, HR, 5HTR

Good but not ideal

  • long time to produce effect
  • side effects
24
Q

What are the main therapeutic effects of SSRIs?

A

5-HT reuptake inhibitor

Chronic action:
Increase in 5HT in synaptic cleft & somatodendritic area causes 5HT1A autoreceptors to down regulate and therefore to disinhibit the 5HT neuron &  5HT release.  synaptic 5-HT ‘normalises’ 5HT post synaptic receptors which are thought to be upregulated in depression as low 5-HT activity

Neuro (10 decks)

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