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Neurological Diseases > Depression and Bipolar > Flashcards

Depression and Bipolar Flashcards

1
Q

Mood Disorders

A
  • Known as affective disorders
  • Primarly disorders of mood rather than thought
  • Two key emotions on the continuum: depression and mania
  • Unipolar depression: only depression
  • Bipolar disorder: mania that alternate with periods of depression
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2
Q

Depression Prevalence

A
  • 17% of adults experience depression (women more than men)

- Approx 50% of ppl will recover in 6 weeks and 90% within a year

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3
Q

Suicide

A
  • Between 6 and 15% of those with severe depression commit suicide
  • Over 1 million people commit suicide each year
  • Senior citizens have the highest rate of suicide of all age groups
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4
Q

Depression: 5 main areas of functioning

A
  • Emotional symptoms: feeling miserable, empty, lack of pleasure
  • Motivational symptoms: lacking drive, initiative, spontaneity
  • Behavioural symptoms: less active, productive, loss/gain appetite, sleep disturbances
  • Cognitive symptoms: hold negative view of themselves, pessimism
  • Physical symptoms: headaches, general ache and pain
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5
Q

Diagnosing Unipolar Depression

A
  • DSM-IV Criteria for Major Depressive Disorder
    Criteria 1: Major depressive episode
  • Marked by 5 or more symptoms eg depresison mood or irritable, change in sleep/activity
  • Present nearly everyday lasting two or more weeks
    Criteria 2: NO history of mania
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6
Q

Cause of Depression: Biopsychosocial Model

A
  1. Psychological
  2. Biological
  3. Social
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7
Q

Causes of Depression: genetic factors

A
  • Studies suggest some people have inherit a biological predisposition
  • AS many as 20% of relatives of those with depression also have depression themselves, compared to less than 10% of the general population
  • Twin studies demostrate a strong genetic component (concordance rates for identical twins = 46%)
  • May be tied to specific genes eg. 5-HT transporter gene
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8
Q

Causes of Depression: brain anatomy

A

Brain anatomy and circuits

  • Researchers have determined that emotional reactions of various kinds are tied to brain circuits
  • circuit responsible for unipolar depression has begun to emerge
  • likely areas involved include: perfrontal cortex, hippocampus, amydala, subgenual cingulate, brain steam
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9
Q

Causes of Depression: Biochemical factors

A
  • clinical depression is associated with neurochemical alterations in the brain
  • main biological theory of depression is the monoamine hypothesis first proposed in 1965
  • Endocrine system/hormone release: people with depression have been found to have abnormal levels of cortisol
  • People with depression have been found to have abnormal melatonin secretion (difficult sleeping)
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10
Q

Monoamine Hypothesis

A
  • Monoamines: include 5-HT, dopamine, NA and A
  • Depression is associated with a deficiency in the neurotransmitters NA and 5HT
  • Seratonin is more assoicated with mood
  • NA is more associated with motor activity
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11
Q

Evidence for Monoamine Hypothesis

A
  • many drugs that enhance the activity of NA and seratonin will elevated mood (and conversely, drugs that decrease the activity of NA or 5HT will depress mood)
  • Genetic studies linking 5HT transporter gene
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12
Q

Evidence against Monoamine Hypothesis

A
  • Studies aiming to show changes in monoamine pathway activity are largely negative
  • Amphetamines and cocaine do not have an antidepressant effect
  • Antidepressant medications boost monoamine levels immediately but therapeutic effect is delayed by weeks
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13
Q

Antidepressant Drugs

A
  • Main types:
  • MAO Inhibitors: increases cytosolic stores of NA or 5HT
  • Monoamine (NA and 5HT) reuptake inhibitors: tricyclic antidepressants (first generation) and SSRIs (second generation)
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14
Q

Monoamine Oxidase (MAO) Inhibitors

A
  • Slows down the body’s production of MAO
  • MAO breaks down monoamines
  • MAO inhibi stop this breakdown from occuring
  • This leads to a rise in NA activity
  • About half of patients who take these drugs are helped by them
  • SE: blood pressure may rise to a potentially fatal level is one eats food with tyramine (cheese, banana and wine) while take MAOIs
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15
Q

Tricyclics

A
  • Tricyclics block the reuptake process, thus increasing NT activity in the synapse
    Strong evidence:
  • 60-65% of patients find symptom improvement
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16
Q

Second-generation Antidepressants

A
  • SSRIs: structurally diff from MAOI and tricyclics
  • Only act on 5HT
  • as effective as tricyclics but clinicians prefer because it is harder to overdose and there are no dietary restrictions and fewer side effects
17
Q

Schizophrenia

A
  • ‘Split mind’ - actually refers to a split from reality
  • Schizophrenia spectrum disorders
  • Characterised by disorganised thinking, emotions and behaviours that are disparate with their situations
  • Disturbed perceptions, including delusions and hallucinations
18
Q

Pschyosis

A
  • A state defined by a loss of contact with reality
  • the ability to perceive and respond to the environment is significantly disturbed; functioning is impaired
  • Symptoms may include hallucinations and/or delusions
  • Psychosis may be substance-induced or caused by brain injury, but most appear in the form of schizophrenia
19
Q

Schizophrenia: Symptoms

A

Three categories:

  1. Positive symptoms
    - pathological additions to a person’s behaviour e.g. delusions, hallucinations, disordered thinking
  2. Negative symptoms
    - pathological deficits to a person’s behaviour e.g. blunted/flat affect, loss of volition, social withdrawal
  3. Psychomotor/disorganised symptoms:
    - awkward movements, repeated grimaces, add gestures ( can be extreme = catatonia)
    - Disorganised speech
20
Q

Course of Schizophrenia

A

Three phases:

  1. Prodromal: beginning of deterioration, mild symptoms
  2. Active: symptoms become increasingly apparent
  3. Residual: a return to prodromal levels, 1/4 recover, 3/4 continue to have residual symptoms
21
Q

Diagnosis: Schizophrenia

A
  • DSM-IV
  • Symptoms persist for 6+ months
  • Type I: dominated by positive symptoms (may be more closely linked to biochemical abnormalities in the brain)
  • Type II: dominated by negative symptoms (may be tied to structural abnormalities in the brain)
22
Q

What causes Schizophrenia

A

Biological View:

  1. Diathesis-Stress Model:
    - Combination of biological and genetic vulnerabilities (diathesis) and environmental stress (stress) that both contribute to the onset of Schizophrenia
  2. Biological Vulnerabilities
    - Genetic factors
    - Brain abnormailities
    - Biochemical abnormalities
23
Q

Schizophrenia: genetic factors

A
  • Family pedigree studies: Schizophrenia is more common among relatives of people with the disorder
  • first degree relatives = 10%
24
Q

Schizophrenia: Brain structure

A

Abnormal brain structure

  • radiological evidence- enlarged ventricles
  • Smaller temporal lobes and abnormal BF to certain areas of brain
  • Overactivity of thalamus and amygdala
25
Q

Schizophrenia: Biochemical abnormalities

A

Dopamine Hypothesis

  • theory attricutes symptoms of Schizophrenia to disturbed and hyperactive dopaminergic signal transduction
  • certain dopamine neurons fire too often
  • particularly common in type I
26
Q

Dopamine Hypothesis evidence

A

FOR:
- antipsychotic medications which acts as antagonists of DA D2 receptors
- Extra DA receptors have been noted in the brains of Schizophrenia patients
- PD patients can develop Schizophrenia symptoms if they take too much L-Dopa
AGAINST:
- atypical antipsychotics also bind to D1 and 5HT receptors
- only seems to explain type I Schizophrenia

27
Q

Schizophrenia: Treatments

A
  • Primarily antagonists of DA D2 receptor
  • reduces symptoms in 65% of patients
  • produce the maximal level of improvement in the first 6 months of treatment
28
Q

Antipsychotic Drugs: SEs

A
  • disturbing movement problems: most common is similar to PD eg. tremour and muscle rigidity
  • Tardive dyskinesia
29
Q

Bipolar: Diagnosis

A
  • Criteria 1: manic episode (3 or more symptoms of mania lasting one week or more)
  • criteria 2: history of mania - if currently experiencing hypomania or depression
    Types:
    1. Bipolar I disorder: full manic and major depressive episodes
    2. Bipolar II disorder: hypomanic episodes and major depressive episodes
30
Q

Causes of Bipolar

A
  1. genetic factors
  2. brain structure abnormalities
  3. ion transport abnormalities
  4. biochemical abnormalities
31
Q

Bipolar: genetic

A
  • children of a bipolar parents face 8-25% chance

- a number of SNPs and genes have been associated with increased risk of bipolar eg. CACNA1C

32
Q

Bipolar: brain structure

A
  • Basal ganglia and cerebellum
33
Q

Bipolar: ion transport

A
  • may cause neurons to fire too easily (mania) or too stubbornly (depression)
34
Q

Bipolar: NTs

A

Permissive theory:

  • Low 5HT may ‘open the door’ to a mood disorder and permit NA to define the particular form the disorder will take
  • low 5HT + low NA = depression
  • low 5HT + high NA = mania
35
Q

Bipolar: treatments

A
  • lithium and other mood stabilisers

Neurological Diseases (24 decks)

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