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Biological Psychology > Week 1-Anxiety and Schizophrenia > Flashcards

Week 1-Anxiety and Schizophrenia Flashcards

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1
Q

What happens when the amygdala is damaged (“The case of SM, the fearless woman”)

A

Tried to trigger fear in her but she was fearless. No fear response or avoidancebut still had curious emotions. (The amygdala triggers fear response.)

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2
Q

How many people will suffer anxiety disorders in their lifetime?

A

Anxiety disorders are the most common type of psychological disorder
• Estimated that up to 30% of people will suffer an anxiety disorder at some point in their lives, twice that of mood disorders

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3
Q

Types of anxiety disorders

A

9 different anxiety disorders according to DSM-5
•Specific phobia (persistent, irrational fears of specific
objects, activities or behaviours)
• Social anxiety disorder (overwhelming fear of social
situations)
• Generalised anxiety disorder (excessive worry, restlessness, trouble sleeping)
• Panic disorder (reoccurring unexpected panic attacks)
• Agoraphobia (anxiety in situations where the person
perceives their environment to be unsafe)

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4
Q

Brain circuits that control fear responses and the Sympathetic Autonomic Nervous System
(Fear conditioning in anxiety disorders)

A

Panic attacks can sometimes come out of the blue
Sympathetic Autonomic Nervous System has 2 different divisions-1)Parasympathetic division (Rest and digest) 2) Sympathetic Division (Flight or fight response-activated when we perceive threat)

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5
Q

Treatments for anxiety disorders

A
  • Benzodiazepine and SSRIs (now preferred) are common treatment options
  • Treatments (drugs, exposure therapy) seem to reduce amygdala activity
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6
Q

What is the biological mechanisms of panic attacks?

A

-Panic attacks are similar to the FEAR response

Activation of Sympathetic Autonomic Nervous System

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7
Q

What is the biological mechanisms of panic attacks?

A

-Panic attacks are similar to the FEAR response
ACTIVATION of Sympathetic Autonomic Nervous System
A “fight-or-flight” defence mechanism which
triggers:-
• Increased heart rate
• Increased blood pressure
• Depressed digestive functions
• Mobilized glucose reserves(preparing body for actions to fight a threat or run away)

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8
Q

What is the biological mechanisms of panic attacks?

A

-Panic attacks are similar to the FEAR response
ACTIVATION of Sympathetic Autonomic Nervous System
A “fight-or-flight” defence mechanism which
triggers:-
• Increased heart rate
• Increased blood pressure
• Depressed digestive functions
• Mobilized glucose reserves(preparing body for actions to fight a threat or run away)

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9
Q

How does the Sympathetic Nervous System and HPA Axis work?

A

The Sympathetic Nervous System (Flight or fight response-activated when we perceive threat) is activated by the HPA (Hypothalamic Pituatary Ardenal Cortex)

1)Hypothalamus decides whether a stimulus is stressful or not——>2)Hormone (CRH) released which stimulates pituitary gland(The P in the HPA axis)——–>3)Which in turn.. stimulates adrenal cortex(The A in the HPA axis)———>4)Hormone release: adrenaline/noradrenaline, cortisol———–>5)Increases heart rate, breathing, blood pressure
= the physical symptoms of anxiety/panic

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10
Q

Symptoms of Anxiety

A

Nausea; Dizziness;Hyperventilation; Heart Palpitations;Trembling and shaking; Sweating; Chills or hot flushes; Numbness or tingling

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11
Q

Biological causes of anxiety

A

Excessive fear response (HPA axis
activation) could explain the physical symptoms
ACTIVATION of Sympathetic Autonomic Nervous System

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12
Q

How does the Sympathetic Nervous System and HPA Axis work?

A

The Sympathetic Nervous System (Flight or fight response-activated when we perceive threat) is activated by the HPA (Hypothalamic Pituatary Ardenal Cortex)

1)Hypothalamus decides whether a stimulus is stressful or not——>2)Hormone (CRH) released which stimulates pituitary gland(The P in the HPA axis)——–>3)Which in turn.. stimulates adrenal cortex(The A in the HPA axis)———>4)Hormone release: adrenaline/noradrenaline, cortisol———–>5)Increases heart rate, breathing, blood pressure= the physical symptoms of anxiety/panic

The HPA axis activation could explain the physical symptoms of anxiety and panic attacks.

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13
Q

What controls the HPA axis?

What is the role of the amygdala in the brain?

A

The amygdala controls the HPA axis in the brain.
Amygdala is a small region of the brain next to the hippocampus
• It receives sensory information from the cortex,
thalamus and hippocampus
• It sends projections to the hypothalamus and so can
influence the HPA axis, triggering the fear response

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14
Q

Fear conditioning in Amygdala evidence

A

The involvement of the amygdala in fear
conditioning has been demonstrated in recording
studies in mice

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15
Q

Fear conditioning in Amygdala evidence

A

The involvement of the amygdala in fear
conditioning has been demonstrated in recording
studies in mice.

And functional MRI studies in humans.

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16
Q

What is the biological mechanisms of panic attacks?

A

-Panic attacks are similar to the FEAR response
ACTIVATION of Sympathetic Autonomic Nervous System
A “fight-or-flight” defence mechanism which
triggers:-
• Increased heart rate
• Increased blood pressure
• Depressed digestive functions
• Mobilized glucose reserves(preparing body for actions to fight a threat or run away)

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17
Q

What is the role of the amygdala in anxiety disorders?

A

Amygdala OVERACTIVATION in anxiety disorders

Overactivity of the amygdala to negative stimuli is a common finding in MRI studies of people with anxiety disorders

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18
Q

What is the role of the amygdala in anxiety disorders?

A

Amygdala OVER/HYPERACTIVATION in anxiety disorders

Overactivity of the amygdala to negative stimuli is a common finding in MRI studies of people with anxiety disorders

19
Q

Studying the fear response-Pavlovian fear conditioning

A

Pavlovian fear conditioning
• Repeatedly presenting a neutral stimulus (e.g., a tone)
with an aversive unconditioned stimulus (e.g., a shock)
—–>fear response to the conditioned stimulus (CS)

20
Q

Studying the fear response-Pavlovian fear conditioning

What does this explanation show about amygdala damage and the involvement of the hippocampus?

A

Pavlovian fear conditioning
• Repeatedly presenting a neutral stimulus (e.g., a tone)with an aversive unconditioned stimulus (e.g., a shock)—–>fear response to the conditioned stimulus (CS)

21
Q

Studying the fear response-Pavlovian fear conditioning

What does this explanation show about amygdala damage and the involvement of the hippocampus?

A

Pavlovian fear conditioning
• Repeatedly presenting a neutral stimulus (e.g., a tone)with an aversive unconditioned stimulus (e.g., a shock)—–>fear response to the conditioned stimulus (CS)

A patient with amygdala damage doesn’t show
normal physiological fear response to a conditioned
stimulus, but can remember that the CS predicts a
shock
•A patient with hippocampal damage shows the
opposite: physiological response but no recollection
Amygdala—–>emotional association and response
Hippocampus——> learning the factual
information about fear and its context (fear memories)

22
Q

What does the hippocampus do?

A

Hippocampus is important for fear memories

23
Q

What does the amygdala do?

A

The amygdala is important for processing fear and activating fear response-triggering the HPA axis (causing the physical symptoms of anxiety and panic)
•Amygdala overactivity is seen in anxiety patients.
• Amygdala damage reduces the fear response.

24
Q

Drug treatments for anxiety disorders

A
  • Early treatments of anxiety disorders used benzodiazepines
  • Benzodiazepines work by increasing GABA activity
  • GABA = inhibitory neurotransmitter (makes it less likely that a neuron will fire an action potential or release neurotransmitters)
  • Increased GABA inhibition = sedative/anxiolytic effects(reduced anxiety)
25
Q

What does Benzodiazephine do to the amygdala?

A

Benzodiazepines work by increasing GABA activity
BENZODIAZEPINES REDUCE AMYGDALA ACTIVITY
Benzodiazepines work by increasing GABA activity?

26
Q

Why do we now use SERATONIN to treat anxiety disorders?

How do Seratonin Reuptake Inhibitors(SSRIs) treat anxiety disorders?

A
  • Now, drug treatment has shifted away from benzodiazepines due todependence concerns (addictive)
  • Selective Serotonin Reuptake Inhibitors (SSRIs) increase levels of the neurotransmitter serotonin, and are now the first choice of treatment for most anxiety disorders

SRIs are drugs that increase serotonin levels
Why do SSRIs work in anxiety disorders?
- a single dose of SSRIs DECREASES amygdala activation to fear faces stimulus.
-SSRI treatment reduces amygdala activation in anxious patients
*Also REDUCES hippocampal activityunder stress conditions

27
Q

How does exposure therapy help with phobias?

A

-Over-activation in amygdala disappears after
therapy in phobic patients
-Increased activity in frontal cortex after exposure therapy:cognitive control of fear response

28
Q

What is the prevelance rate of schizophrenia?

A

1%- 1 in 100 people will be diagnosed in their lifetime.

Late adolescence or early 20s esp males

29
Q

History of Schizophrenia

A

•Schizophrenia was first described as ‘dementia praecox’and popularized by Emil Kraepelin in 1893
• Eugen Bleuler was the first to coin the term schizophrenia in 1908
• Some psychiatrists believe Vincent Van Gogh suffered from schizophrenia, with his paintings
inspired by his hallucinations..

30
Q

What is Schizophrenia?

A

Schizophrenia is NOT ‘split/multiple personality’ disorder!
.. It’s actually a very complex and heterogeneous disorder –considerable variability between cases, in terms of symptoms, severity,course, and response to treatment (different symptoms and severity-mild or severe)
.. It has serious consequences: People with schizophrenia are sometimes unable to be part of society and need to be INSTITUTIONALIZED

31
Q

What are the 2 main types of symptoms in Schizophrenia?

A

1) Positive Symptoms: PRESENCE of symptoms
- Delusions (e.g., grandeur-special powers or paranoia)
- Hallucinations (perceptual disturbances, often auditory: “Hearing voices”)
- Disorganised speech → Nonsense sentences or no logical connections

2) Negative Symptoms: ABSENCE of response
- Reduced expression of emotion(lack of emotion in facial expression ;hand gestures; emorion)
- Poverty of speech(hard to intiate and carry on convo)
- Difficulty in initiating goal-directed behaviour(difficulty in daily activities)
- Neglect of personal hygiene

32
Q

How do you diagnose Schizophrenia?

A

DSM-V CRITERIA
Two or more of the following 5 symptoms present for AT LEAST 1 MONTH
At least one of these must be 1, 2, or 3:
1. *Delusions
2. *Hallucinations
3. *Disorganised speech
4. Disorganised or catatonic behaviour
5. Negative symptoms
**Social/occupational dysfunction(impairment of day to day life)
Continuous signs of illness for at least 6 months (with at least 1 month of active symptoms)

33
Q

What are the cycles of symptoms in Schizophrenia?

A

• Positive and negative symptoms seem to worsen and
improve in cycles known as relapses and remissions
• A period of intense positive symptoms = “psychotic
episode”
• Cognitive Symptoms(more stable-present across the illness) also a core feature of Schizophrenia-IMPAIRMENTS OVER COGNITIVE DOMAINS
• Attention: poor ability to maintain attention when doing a task
• Working memory: verbal WM particularly impaired
• Executive function: ‘inflexible’ thinking style
• Unlike other symptoms, these are relatively stable overmthe course of the illness

34
Q

What are the causes of Schizophrenia?

A 
• Schizophrenia is a complex disorder with no single
‘cause’
• Genetics and environment interact to increase risk
• We’ll look at:
• 1. Genetics
• 2. Neurodevelopmental factors
• 3. Brain abnormalities
• 4. Neurotransmitters
35
Q

Explain the genetic causes of Schizophrenia (according to twin studies)

A

• Twin, adoption and family studies
provide consistent evidence that genetic factors are important. (STRONG GENETIC INFLUENCE of Schizophrenia)
• Schizophrenia has a high heritability
• *The child of someone with schizophrenia is 13x more likely than average to develop it
• There is a 48% chance that the identical twin of someone affected also has schizophrenia

36
Q

Which genes cause Schizophrenia? How are the genes affected in Schizophrenia?

A
  • A large number (>100) ‘high-risk’ genes have been identified
  • Some overlap with other disorders (e.g. autism)
  • Includes the dopamine receptor D2 gene (links to treatment)
  • But these explain less than half the genetic variance
  • Gene mutations also have a role
  • Increased paternal (father)age at conception (more mutations) =increased schizophrenia risk
  • Could explain why schizophrenia still present in 1% of the population (quite a large proportion), despite patients not living as long/less likely to reproduce
37
Q

Explain the Gene-Environment interaction causing Schizophrenia?

A

Genetics only explains some of the risk: 85% of individuals with schizophrenia have no first-degree relative with the illness
• Environment also important?
Gene-environment interactions:
Environmental factors can affect gene expression
and/or Genes make a person more vulnerable to develop the disease when exposed to certain environmental factors.

STUDY: Adopted children with a biological schizophrenic mother but no schizophrenia in the
adopting family
Probability for developing schizophrenia is slightly higher,but this effect is greatly magnified if the adopting family is dysfunctional.

38
Q

Other Environmental Factors Causing Schizophrenia

A

NEURODEVELOPMENTAL FACTORS may cause Schizophrenia
-Prenatal factors=> seem to be the most important e.g. infections during pregnancy(influenza, rubella), low birth weight.
These might affect neurodevelopment with the results
only showing later in life.
-Some evidence that cannabis use in adolescence increases risk,particularly in those with genetic
risk.

39
Q

What are the brain abnormalities of a person with Schizophrenia? (Biological Model)

A

• On average, people with schizophrenia have larger
than average ventricles (fluid-filled spaces in the brain),
reduced brain volumes, and less brain connectivity

40
Q

What are the neurotransmitters that are involved in Schizophrenia? Explain the dopamine hypothesis

A

DOPAMINE HYPOTHESIS-Excess dopamine release causes Schizophrenia
• .. Says that schizophrenia results from excess dopamine activity: Neurons release dopamine faster than they should
• Evidence?
• Genetics: 4 of the top 10 gene variants (high risk genes) most strongly associated with schizophrenia are directly involved in dopamine pathways
• Some dopaminergic recreational drugs (e.g., cocaine, amphetamine) can cause hallucinations and delusions

41
Q

Drug Treatments for Schizophrenia

A

—>All ANTIPSYCHOTIC drugs BLOCK dopamine receptors (D2-receptors)
—->D2 receptor Antagonists
—–>leads to improved positive symptoms
—–>Higher dopamine receptor blocking= larger effect on symptoms
There seems to be a threshold amount of D2 binding needed for the treatment to work
Side effects: extrapyramidal symptoms (motor restlessness/rigidity)

42
Q

Explain the use of typical and atypical antipsychotic drugs on schizophrenia

A

• Typical antipsychotics (developed
in 1950s), act on D2 receptors
• Otherwise known as ‘first’generation antipsychotics (or Neuroleptics)
• High incidence of side-effects on motor control (EPS, or extrapyramidal symptoms)

  • Atypical (‘second’ generation) antipsychotics (developed in 1990s)
  • Reduced risk of these side effects on motor system. Act on several dopamine receptors(e.g., D2, D3, D4) and serotonin pathway
  • Have other side effects: e.g. Drowsiness; weight gain
43
Q

Limitations of the dopamine hypothesis on Schizophrenia

A

• Treatment resistance: (1/3 don’t respond to
antipychotics, though might respond to clozapine
which has only weak D2 affinity)
• There may be a ‘non-dopaminergic’ subtype of
schizophrenia?
• Antipsychotics have only LIMITED effects on cognitive impairments and negative symptoms
• Not all patients show higher dopamine levels

44
Q

Explain the alternative GLUTAMATE HYPOTHESIS in explaining Schizophrenia

A

➢ Glutamate hypothesis:- schizophrenia is due to NMDA receptor (asubtype of glutamate receptor) dysfunction
➢ Evidence?-Recreational drugs affecting NMDA receptor
➢ NMDA receptor antagonists, including phencyclidine (PCP) and ketamine have psychological effects which resemble positive, negative
and cognitive symptoms
➢ These drugs make symptoms worse in schizophrenia patients
➢ But - trials of glutamatergic treatments have not been successful
➢ But some researchers think that NMDA dysfunction might contribute to the negative symptoms..
➢ And have knock-on effects on dopamine

Biological Psychology (10 decks)

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