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Clinical neuroscience > Lecture 20- Anxiety > Flashcards

Lecture 20- Anxiety Flashcards

1
Q

define anxiety

A

a feeling of worry, nervousness, or unease about something with an uncertain outcome

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2
Q

Symptoms

A
  • Palpitations
  • Sweating
  • Trembling or shaking
  • Dry mouth
  • Difficulty breathing
  • Chest pain or discomfort
  • Nausea or abdominal distress (e.g. butterflies in stomach)
  • Feeling dizzy, unsteady, faint or light-headed
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3
Q

Why do we get anxious?

A
  • Fight or flight e.g. cave man response to danger
  • To stay safe and preserve the gene pool to reproduce
    • Activates motor system e.g. to run away
    • Activates sympathetic nervous system
      • Increased HR and forced contraction
      • Dilated bronchi
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4
Q

the stress reaponse linked to

A
  • Limbic- hypothalamus-pituitary-adrenal axis
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5
Q

the limbic system is made up of

A
  • Hippocampus formation
    • Hippocampus, dentate gyrus, part of the Para hippocampal gyrus
  • Septal area
  • Amygdala
  • +/-
  • Prefrontal cortex
  • Cingulate gyrus
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6
Q

The hippocampus

A
  • Involved in memory and expressions of emotion
  • Curved piece of cortex
  • Folded into medial surface of temporal lobe
  • Occupies floor of temporal horn of lateral ventricle
  • Three parts: subiculum, hippocampus proper, dentate gyrus
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7
Q

The amygdala

A
  • Buried in the roof of lateral ventricle
  • Collection of nuclei
  • Inputs of sensory information, brainstem, thalamus, cortex
  • Outputs to cortex, brainstem and hypothalamus
  • Drive related behaviours and processing of associated emotions
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8
Q

Prefrontal cortex and anterior cingulate gyrus

A

Both have modulatory effect on processes associated with the hypothalamus

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9
Q

Hypothalamus

*

A

Many connections to different areas

Hypothalamic activation increases

  • CRH (cortisol releasing hormone) which causes the AP to secrete ACTH (adrenocorticotropic hornone) which cases the adrenal cortex to release cortisol
  • Cortisol causes
    • increase of energy metabolite levels
    • suppression of the immune system
    • inhibition of allergic and inflammatory processes
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10
Q

When does the stress response become a problem?

A

When the threat is a psychological response and not physical e.g. being chased by a tiger

e.g. not natural when you cant run away

Stress is not always bad… however when there is too much it becomes counter intuitive

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11
Q

outline the fight or flight response that originates from the hypothalamus

A

1) Adrenal medulla activation- adrenaline
2) Adrenal cortex activation- steroids

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12
Q

what allows maintenance of stress

A

cortisol (longer acting than adrenaline)

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13
Q

general adaption syndrome

A
  1. alarm reaction
  2. resistance
  3. exhaustion
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14
Q

anxiety disorders

A
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15
Q

Aetiology of anxiety disorders

A

Cant diagnose people this way

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16
Q

GABA and anxiety disorders

A
  • GABA is the main inhibitory neurotransmitter
  • GABA levels are decreased in cortex in patients with panic disorder
  • Benzodiazepines increase GABA transmission so reduce anxiety
    • Quick fix
17
Q

Serotonin and anxiety disorders

A
  • Increased levels of serotonin (due to SSRIs) may stimulate serotonin receptors in hippocampus
    • SSRI- serotonin selective reuptake inhibitors
      • SSRI block serotonin reuptake so more remains in synaptic cleft
  • Leads to neuroprotection, neurogenesis and reduction of anxiety ​
18
Q

Treatment of anxiety disorders

A
  • Mainstay of treatment is SSRIs
    • Cognitive behavioural therapy
    • Can use pregabalin – a GABA analogue

Don’t use benzodiazepines long term

19
Q

why shouldnt you take benzodiazepines long term

A
  • Benzo withdrawal- makes you feel good quickly, become tolerance- Benzo withdrawal
  • Loads of side effects
20
Q

Cognitive behavioural therapy

A
21
Q

OCD is primarily characterised by

A

obessessions and compulsions

22
Q

obsessions

A

Thoughts that persist and dominate an individual’s thinking despite their awareness that the thoughts are either entirely without purpose, or have persisted and dominated their thinking beyond the point of relevance or usefulness

Unpleasant and repugnant, often causing anxiety

23
Q

Compulsions

A

A motor act (or sometimes a thought) resulting from an obsession

Acting out a compulsion may relieve the anxiety provoked by its associated obsession, but frequently carrying out the compulsion is also unpleasant

24
Q

obsessions are…..

A

always unpleasant

25
Q

to neutralise obssessions people with OCD

A

develop compulsions (aka neutralising rituals)

  • ‘obsessional motor acts. May result from an obsessional impulse that leads directly to the action, or they may be mediated by an obsessional mental image or fear’
  • e.g. ‘I need to turn the light switch on and off ten times or my family will die’
  • Can lead to patients wasting a lot of time!
  • Can also have mental compulsions e.g. repeating phrases
26
Q

Diagnostic criteria for OCD

A
  • Obsessions and/or compulsions must be present on most days for at least 2 weeks
  • Obsessions and compulsions have the following features:
    • Originate in the mind of the patient
    • Repetitive and unpleasant
    • Acknowledged as excessive or unreasonable
    • Patient tries to resist, but at least one obsession/compulsion is unsuccessfully resisted
27
Q

OCD pathophysiology (theories)

A

unclear

28
Q

hypotheses of OCD pathophysiology

A
  • Basal ganglia re-entrant circuits
  • Reduced serotonin levels
    • SSRIs help
  • Altered activity in a range of cortical areas (cause or effect?)
  • Autoimmune aetiologies
29
Q

OCD and basal ganglia re-entrant circuits

A
  • The cortex projects to the basal ganglia, and these then project back up to the cortex via the thalamus
  • This is an example of a ‘re-entrant’ loop, where obsessional thoughts can re-enter the cortex having entered the basal ganglia
  • This may be due to overactivity in the direct pathway
  • Treatments that inhibit thalamic (and hence cortical) activity by reducing the direct pathway or increasing the indirect pathway may hold promise (e.g. subthalamic nucleus stimulation)
30
Q

autoimmne aetiologies of OCD

A
  • There may be cross-reactivity with certain streptococcal antigens and the basal ganglia (PANDA)
31
Q

OCD Treatment

A
  • Biological
    • SSRIs +/- antipsychotics
    • Deep brain stimulation?
  • Psychological
    • CBT and variety of other interventions
  • Social
    • Family support
    • Groups etc.
32
Q

Post traumatic stress disorder

A
  • Within 6 months of a traumatic event of exceptional severity e.g. in a warzone, torture, not relationship breakdown
  • Evidence of trauma
  • Repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams
  • Conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma
33
Q

Pathophysiology of PTSD

A
  • Unclear
    • Evidence of amygdala hyperactivity causing exaggerated behavioural responses
    • However, low levels of cortisol!
34
Q

Treatment of PTSD

A
  • Biological
    • SSRIs
    • Maybe short term benzodiazepines
  • Psychological
    • CBT
    • Eye movement desensitization reprocessing therapy
  • Social
    • Charities are particularly active, such as ‘Help for Heroes’

Clinical neuroscience (30 decks)

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