Lecture 7: Disorders Flashcards

1
Q

Positive symptoms of schizophrenia

A
  • delusions
  • hallucinations
  • though disorders
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2
Q

Negative symptoms of schizophrenia

A
  • apathy
  • lack of emotion
  • anhedonia
  • asociality
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3
Q

Cognitive symptoms of schizophrenia

A
  • attention
  • learning/memory
  • problem solving
  • abstract thinking
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4
Q

Family studies

A

Fisher
-looked at the prevalence rate of schizophrenia in children of MZ twins where one parent had schizophrenia

-prevalence rate is similar and greater then general pop

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5
Q

Adoption studies

A

*eliminates effects of shared environment

Heston

  • followed people born of parent in mental hospital
  • 50 control children

-16.6% of children who’s mother had schizophrenia were also diagnosed with it

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6
Q

Diathesis-stress model

A

=that genetics underpin however needs an environmental trigger

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7
Q

The dopamine hypothesis

A

=believed that positive symptoms of dopamine related to increased levels of dopamine

-Antipsychotic drugs reduce levels of dopamine (antagonists as block receptors)

•Amphetamines results in paranoid schizophrenic symptoms

  • cause dopamine and norepinephrine release and prevents breakdown
  • act as dopamine agonists
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8
Q

Dopamine hypothesis currently

A
  • The levels of the dopamine metabolite, HVA, is not increased in patients with schizophrenia
  • Increased number of dopamine receptors or increased sensitivity of receptors are what is important-increased sensitivity of receptors/number of receptors not increase of dopamine
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9
Q

Negative/cognitive: brain damage

A

• Enlarged ventricles
• Prefrontal cortex
-Goal-directed behaviour, speech, decision making
-Poor performance on studies designed to tap prefrontal cortex performance
-Reduced grey matter
-Low metabolic rate in prefrontal cortex

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10
Q

What causes brain damage (schizophrenia)

A

*use of epidemiological studies

  • Season of birth
  • Viral epidemics
  • Population density
  • Substance abuse
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11
Q

Relationship between positive and negative symptoms

A

Genetic and/or environmental causes results in:

  1. Abnormalities in DA transmission and prefrontal cortex
  2. Abnormalities in DA transmission cause prefrontal abnormalities
  3. Abnormalities in Prefrontal cause abnormal DA transmission
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12
Q

PCP and ketamine

A
  • cause all 3 types of symptoms
  • caused by reduced metabolic activity in the frontal lobes
  • indirect antagonists of NMDA receptors which decrease activity in the prefrontal cortex
  • also decrease the level of DA utilisation
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13
Q

Traditional treatments

Schizophrenia

A
  • decrease DA transmission in mesolithic pathway

- reduce positive but increase negative and cognitive symptoms

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14
Q

New treatments

Schizophrenia

A
  • Decrease activity in the mesolimbic system
  • Increase DA activity in the prefrontal cortex
  • Partial agonist*= compete with dopamine with the brain for the receptor, have high affinity for receptors, act to a lesser extent that dopamine, bind more regularly, activate much less, so in mesolimbic pathway activity is decrease, positive symptoms decreased
  • still get net increases in activity than what you’d get from dopamine itself
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15
Q
  • Major depressive disorder

* Bipolar disorder

A

• Major depressive disorder

  • Depressed mood
  • Loss of interest/pleasure
  • Changes in sleep, appetite, attention, suicidal thoughts

• Bipolar depression

  • Symptoms of depression
  • Episodes of mania – intense elation, flight of ideas
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16
Q

Etiology

A
  • Heritable
  • Sullivan et al., (2000): meta-analysis 37 % heritability for MDD
  • Kelsoe (1997): Bipolar disorder 70 % concordance rate between MZ twins, 25 % for DZ
  • Genetic predisposition to developing but need an environmental trigger
17
Q

Monoamine oxidase (MAO) inhibitors

A
  • destroys excess monoamine transmitter in terminal boutons
  • inhibitors inhibit this breakdown

-increases availability of DA, serotonin and norepinephrine

18
Q

Tricyclic antidepressants

A
  • Inhibit the reuptake of serotonin and norepinephrine into terminal buttons
  • Increase post-synaptic potentials
19
Q

Biological treatments: ECT

A
  • Used to treat seizures and found improved mood
  • Decreases brain activity
  • TMS: stimulate very specific areas of the brain, target regions of the brain involved in depression
20
Q

Monoamine hypotheses

A

• What do we know from the treatments?
-Preventing the reuptake of monoamines = decreases in depression
• Depression results from decreased activity of monoaminergic neurons
-Serotonin and norepinephrine: believed underpinned by decreases in availability of these
• However, too simple
-Drugs take several weeks to have an effect
-lag between metal health improvement and when drug took its initial effect
-No increase in metabolites

21
Q

Neuroimaging

A

• MDD associated with brain regions activated by emotions
-Amygdala
-Prefrontal cortex
-Anterior cingulate cortex
• Treatment : reduce ACC activity and increase PFC activity
-The ACC connects to the amygdala
-The ACC connects to the PFC which connects to the amygdala
-Decreased activity in the amygdala (involved in what emotions people have, fight and flight)
-by decreasing activity in amydala, decrease attention to negative stimuli

22
Q

OCD

A
  • Obsessive: persistent, uncontrollable, irrational thoughts
  • Compulsions: repetitive and excessive acts that reduce anxiety
  • Causes marked distress and impairs functioning
23
Q

OCD ethology

A
  • Genetic: Higher concordance rate in MZ vs. DZ twins
  • Infections: basal ganglia-injury triggers OCD
  • Brain injury: basal ganglia; prefrontal cortex; cingulate gyrus-all regions altered neural functioning which relates to OCD
  • Neural activity: frontal lobes, prefrontal cortex, cingulate cortex, caudate nucleus
  • Involved in emotional reactions
  • Cause vs. Effect?-altered neural causes OCD or other way around?
24
Q

Treatment OCD

A

• Decrease in symptoms associated with decrease neural activity in caudate nucleus and prefrontal cortex
• Destroy fibre bundles:
-Prefrontal and cingulate cortices with the limbic system
-Basal ganglia and prefrontal cortex
• Drugs
-SSRIs
-Serotonin has an inhibitory effect on behaviour
-Prefrontal cortex and basal ganglia are influenced by serotonin