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2nd Year: Brain and Behaviour > Mental disorders > Flashcards

Mental disorders Flashcards

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1
Q

Define PTSD.

A

Post-traumatic stress disorder: an anxiety disorder caused by frightening, stressful or distressing events.

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2
Q

List symptoms of PTSD.

A

Recurrent dreams, flashback episodes and intense psychological distress.

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3
Q

The symptoms of PTSD often cause the sufferer to avoid confronting the bad memories. What social consequences does this have? List 4.

A
  1. Diminished interest in social activities
  2. Feelings of detachment
  3. Suppressed emotions
  4. A sense of bleakness, hopelessness
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4
Q

‘Psychological distress’ is listed as a symptom of PTSD. What does this include? Give 4 examples.

A
  1. Difficulty sleeping
  2. Irritability and anger
  3. Difficulty concentrating
  4. Heightened reactions to noise/movements
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5
Q

People with PTSD tend to have poor mental and physical health. True or false?

A

True.

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6
Q

Who is more likely to be affected by PTSD, men or women?

A

Women.

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7
Q

Twin studies have shown a genetic susceptibility in developing PTSD. True or false?

A

True.

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8
Q

List 6 factors that makes someone MORE likely to suffer from PTSD after a stressful event.

A
  1. Trauma occurs at a young age
  2. Exposure to numerous traumatic events
  3. A father with a depressive disorder
  4. Poor education history
  5. Poor social support
  6. Pre-existing disorder e.g. panic, anxiety or depression
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9
Q

Give support for the theory that developing PTSD is more likely if you have experienced more traumatic events.

A

Kolassa et al. in 2010: studied survivors of the Rwandan genocide and found a correlation.

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10
Q

Genes have been implicated in the predisposition to developing PTSD. What genes are affected? List 3.

A
  1. Dopamine D2 receptors
  2. Dopamine transporters
  3. Serotonin transporters
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11
Q

Damage to which brain area has been implicated in PTSD? Why?

A

The hippocampus: the hippocampus is one of the brain areas associated with the HPA axis involved in the stress response.

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12
Q

Give evidence showing that the hippocampus is involved in PTSD. List 2 studies.

A
  1. Gurvits et al. in 1996: hippocampal volume was reduced in veterans with combat-related PTSD. The loss was proportional to the amount of combat the veterans had experienced.
  2. Lindauer et al. in 2005: police officers with PTSD had a smaller hippocampus than other police officers without PTSD.
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13
Q

A study by Gilbertson et al. in 2002 suggested that a smaller hippocampus in PTSD sufferers actually predated exposure to stress. True or false?

A

True.

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14
Q

A study by Gilbertson et al. in 2002 suggested that a smaller hippocampus in PTSD sufferers actually predated exposure to stress. True or false?

A

True: the study suggested a smaller hippocampus was a predisposition not a consequence.

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15
Q

How did Gilbertson’s study prove that a smaller hippocampus is a predisposition to PTSD not a cause?

A

They studied 40 pairs of identical twins where one brother fought in the Vietnam war. All the men that returned with PTSD has smaller hippocampal volumes, as did their non-suffering twin brothers at home.

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16
Q

The PFC (prefrontal cortex) is responsible for regulating the responses of the amygdala. True or false?

A

True.

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17
Q

It was found by Shin et al. in 2005 that people with PTSD shower an increased activation of the amygdala when shown fearful expressions. What about the activity of the PFC?

A

PFC activity was reduced, showing less emotional control in PTSD sufferers.

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18
Q

What are a) VAMs and b) SAMs?

A

a) Verbal accessed memories

b) Sensory accessed memories

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19
Q

What are a) VAMs and b) SAMs?

A

a) Verbal accessed memories

b) Sensory accessed memories

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20
Q

VAMs can be replaced with C-reps. What is a C-rep?

A

A ‘contextual representation’

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21
Q

What is the current view about the encoding of traumatic events?

A

They are not encoded contextually, i.e. the subject does not remember exactly what happened and instead the memories are associated with representations from the sensory cortex and the responses of the amygdala.

Basically during trauma they were so stressed they didn’t have a clue and all the remember is the sensations and how the felt.

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22
Q

Thus what is the current view of retrieval of traumatic memories?

A

Retrieval in the form of flashbacks is caused by a bottom-up response from the sensory cortex and amygdala, as opposed to a top-down response from the cortex as normal memories are retrieved.

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23
Q

Define schizophrenia.

A

A serious mental disorder characterised by disordered thoughts, delusions and hallucinations.

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24
Q

Schizophrenia can be positive, negative or cognitive. True or false?

A

True.

25
Q

How is a positive symptom of schizophrenia characterised?

A

By its manifestation, e.g. delusions, hallucinations or thought disorders.

26
Q

‘Thought disorder’ simply means irrationality. True or false?

A

True.

27
Q

Schizophrenics have difficulty organising their thoughts. How is this manifest?

A

They cannot distinguish between rational and absurd ideas. They jump between conversational topics very quickly as they make associations. They often use meaningless words or favour rhyme over meaning.

28
Q

Define a delusion.

A

A false belief.

29
Q

List 3 classic delusions involved in schizophrenia.

A
  1. Persecution: they fear they are being plotted against
  2. Grandeur: they feel like have god-like power or possess secret knowledge
  3. Control: they fear someone is monitoring or controlling them
30
Q

Define a hallucination.

A

A perception of a stimulus that is not actually present.

31
Q

What is the most common hallucination of a schizophrenic?

A

Auditory: they believe someone is talking to them

32
Q

How is a positive symptom of schizophrenia characterised?

A

By increased manifestation, e.g. delusions, hallucinations or thought disorders.

33
Q

What are the negative symptoms of schizophrenia characterised by?

A

A diminution of normal behaviour: reduced emotional or social responses, lack of speech, anhedonia, withdrawal

34
Q

What are the negative symptoms of schizophrenia characterised by?

A

A diminution of normal behaviour: reduced emotional or social responses, lack of speech, anhedonia, withdrawal etc.

35
Q

What are the cognitive symptoms of schizophrenia?

A

Lack of attention, learning and memory deficits, poor thinking and problem solving. These are closely coupled to the negative effects of the disease.

36
Q

Describe the typical onset of schizophrenia.

A

It begins gradually, over a period of 3-5 years. The negative symptoms emerge first, followed by cognitive symptoms. The positive symptoms are the last to appear.

37
Q

Describe the dopamine hypothesis of schizophrenia.

A

Over-activity at dopaminergic synapses causes the positive symptoms of schizophrenia.

38
Q

What is chlorpromazine?

A

A first generation antipsychotic drug: it blocks dopamine receptors and thus reduces the positive symptoms of schizophrenia only.

39
Q

After chlorpromazine, numerous antipsychotic drugs have been developed. What do they all have in common?

A

They block D2 and D3 receptors.

40
Q

Define a neuroleptic.

A

A drug that supresses neuronal function by working as D2 receptor antagonists.

41
Q

Which part of the brain is concerned with hallucinations?

A

The mesocorticolimbic brain, the part involved with emotion.

42
Q

Give 4 negative effects of neuroleptic drugs in the treatment of schizophrenia.

A
  1. Movement disorders
  2. Hyperprolactinemia (increased blood prolactin)
  3. Tardive dyskinesia of the facial/oral muscles
  4. Sialorrhoea (dribbling)

This discourages sufferers from taking their meds.

43
Q

Give one of the most severe side effects of chlorpromazine.

A

Aplastic anaemia: the WBCs do not mature

44
Q

Give a drug that apparently reduces the symptoms of both positive and negative schizophrenia.

A

Clozapine.

45
Q

The more selective the D2 antagonist, the better the drug. True or false?

A

False: the more selective the drug, the worse the side effects.

46
Q

List drugs that act as dopamine agonists and thus induce symptoms characteristic of positive schizophrenia. How do they work?

A

Amphetamine and cocaine block dopamine reuptake.

L-DOPA causes dopamine synthesis.

47
Q

Who found that intravenous injection of amphetamine caused elevated dopamine levels in the striatum, and thus an increase in the positive symptoms of schizophrenia?

A

Laurelle et al. 1996

48
Q

It was previously thought that schizophrenics had an elevated level of dopamine receptors in the brain. Is this belief still held?

A

Not really: after post-mortem analyses and PET scans with radioactive ligands it was found schizophrenics may have an elevated level of D2 receptors but this is unlikely to be the primary cause of the disorder.

49
Q

It was previously thought that schizophrenics had an elevated level of dopamine receptors in the brain. Is this belief still held?

A

Not really: after post-mortem analyses and PET scans with radioactive ligands it was found schizophrenics ‘may’ have an elevated level of D2 receptors but this is unlikely to be the primary cause of the disorder.

50
Q

Some structural abnormalities have been found in the brains of schizophrenics. Where do these seem to occur?

A

In the frontal lobes, hippocampus and temporal lobes.

51
Q

Some reduction in brain volume has been observed. True or false?

A

True.

52
Q

In schizophrenia neural circuits are drastically altered. Thus is can be thought of as a developmental disease. True or false?

A

True: schizophrenia was first discovered in young people between 16-24 years old by Franz Kraepelin, who described it as ‘dementia pricox’ or dementia of the young.

53
Q

Newer antipsychotic medicines are atypical (less specific D2 antagonists). What other NT do they modulate?

A

They often affect serotonin function as well. This has leads scientists to believe the dopamine theory of schizophrenia is simplistic.

54
Q

What other NT has been implicated in schizophrenia?

A

Glutamate: abnormally low NMDA glutamate receptors have been found in the brains of schizophrenics.

55
Q

Why might glutamate affect schizophrenia?

A

Glutamate is involved in the functioning of the frontal lobes and the hippocampus. Glutamate regulates dopamine release.

56
Q

Which drugs further implicate glutamate in schizophrenia?

A

Phencyclidine and ketamine block glutamate action. Ketamine binds NMDA receptors. This can causes cognitive impairments like memory loss characteristic of schizophrenia.

57
Q

Glutamatergic medication treats the positive symptoms of schizophrenia. True or false?

A

False: it has no effect.

58
Q

There is a genetic factor in developing schizophrenia. Are these genes directly causal?

A

No: there are many genes involved that all increase vulnerability.

59
Q

DZ twins have a 17% risk of developing schizophrenia. What is the risk in MZ twins?

A

48%.

If the disease was fully genetic the risk would be 100%.

2nd Year: Brain and Behaviour (20 decks)

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