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Neurobiology of Mental Illness > Lecture 2 - OCD > Flashcards

Lecture 2 - OCD Flashcards

1
Q

What percentage of the population does OCD affect?

A

1-2%

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2
Q

What type of disorder is OCD classed as?

A

Anxiety disorder

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3
Q

What does OCD stand for?

A

Obsessive-compulsive disorder

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4
Q

What are obsessions?

A

Intrusive thoughts that you cannot get rid of.

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5
Q

What are compulsions?

A

Actions you feel driven to perform as a result of your obsessions.

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6
Q

Why do compulsions end up acting as a positive reinforcer for behaviour?

A

Compulsions relieve the negative affect caused by the obsessions.

(negative reinforcement)

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7
Q

There is a high co-morbidity between OCD and which other mental illness?

A

Depression

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8
Q

OCD is often treated with what?

A

Anti-depressants

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9
Q

How could Freud explain anxiety?

A

Insufficient control of the Id by the Ego.

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10
Q

What are Y-Bocs?

A

A measure used to quantify OCD symptoms. Stands for the Yale-Brown Obsessive-Compulsive Scale.

It establishes the time occupied by obsessive thoughts, time-intervals that thoughts are free from obsessions, interference that obsessions cause and their associated distress.

The higher the score, the more compulsive you are deemed to be/the worse your symptoms are.

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11
Q

Why does the compulsion eventually become impulsive?

A

The compulsion occurs so frequently that it becomes habit - sufferers end up performing the action without thought.

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12
Q

What is the difference between compulsive and impulsive actions?

A

Impulsive actions are rewarding, and performed without consideration for consequences (very ID), whereas compulsive actions are performed to relieve negative feelings - acts as a negative reinforcer.

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13
Q

What is the most common treatment for OCD?

A

SSRIs - selective serotonin reuptake inhibitors.

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14
Q

What is the recommended OCD treatment?

A

CBT

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15
Q

What do the basal ganglia co-ordinate?

A
  • sequential processing
  • control initiation
  • switching
  • modulation
  • termination of serial processes

Involved in building up sequences of behaviour into meaningful, goal-directed repertoires. Also functions a bit like an evaluator.

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16
Q

What did Atmaca et al., (2007) find about structural differences in OCD patients?

A

Found significant differences in:

  • overall white matter volume
  • volume of the left and right thalamus

between OCD patients and controls.

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17
Q

What is the neurobiological mechanism of OCD?

A

Dysfunction in the cortico-striatal-thalamo-cortical circuit mechanism.

Input from stimuli is registered in the visual and then frontal cortex.

If salient enough, basal ganglia evaluation will occur (according to communication from the thalamus back to the cortex)

Amplitude/salience of signal will determine the pathway taken.

If direct pathway, positive feedback occurs, strengthening the signal each time it is evaluated.

If indirect pathway (activated by the less extreme stimuli), salience/strength of signal weakens each time.

In OCD, output from OFC takes direct pathway more frequently than normal, due to a lower threshold of activation. Therefore, the signal for regular stimuli becomes progressively bigger (amplitude) each time it is processed in the positive feedback loop that the CSTC has become. which may lead to over-exaggerated saliency and therefore increased anxiety/perceived threat.

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18
Q

What is the limitation of the neurobiological model of OCD?

A
  • Explains the signal in terms of saliency, but not for it’s appraisal/reward.
  • Doesn’t explain why one OCD group may have more direct pathway activation/why the threshold is lower.
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19
Q

What did Pujol et al., (2004) find about structural differences between OCD patients and controls?

A

Used voxel based morphology and found significant reduced gray matter volume in the orbitofrontal cortex, medial frontal gyrus and other regions of OCD patients, compared to healthy matched controls.

20
Q

Damage to thalamic and pallidal regions leads to what?

A

Onset of compulsive symptoms.

Figee et al., 2013

21
Q

A small stroke or damage to the frontal cortex leads to what?

A

Disappearance of/improvement in OCD symptoms.

Figee et al., 2013

22
Q

What functional connectivity findings are established in OCD patients, according to results from Harrison et al., (2013)?

A
  • greater connectivity between striatum and frontal cortex (OFC and ACC) in OCD patients compared to healthy controls.
  • Y-Boc scores correlated with striatal-fronto connectivity (more severe the symptoms, the greater the over-connectivity)

Suggests overactivity in the CSTC loop.

23
Q

What are the disadvantages of using questionnaires such as Y-Bocs to assess symptoms?

A
  • Self administered

- May be anxiety-inducing for some patients (OCD)

24
Q

Why is OCD classed as a compulsive, rather than impulsive disorder?

A

OCD patients do not engage in compulsive behaviours to feel good, they do it because it makes them feel less negative.

25
Q

What is the earliest evidence of OCD?

A

Extremely severe cases of influenza which caused brain swelling, leading to brain damage. One of the first areas to be damaged are, and were, the basal ganglia.

Surviving influenza patients had reductions in swelling, but also had Parkinson’s and experienced OCD symptoms (among other symptoms).

26
Q

What is the main function of the basal ganglia in relation to OCD?

A

Appraisal/Evaluation.

27
Q

What is a limitation of using brain structure to compare patients and controls?

A

Brain regions are not standardised between people. One individual’s orbitofrontal cortex is another’s prefrontal cortex. This means that differences in structure may not necessarily mean different volumes of the relevant areas assumed.

28
Q

What percentage of patients respond to DBS of the striatum in treatment-resistant OCD?

A

60%

29
Q

What is the rate of symptom reduction when striatal DBS is used in treatment-resistant OCD?

A

80% decrease in obsessive-compulsive symptoms

30
Q

Your ventral striatum is very important for what? And which component of the V striatum is responsible for this?

A

Reward.

Nucleus accumbens

31
Q

What did Figee et al., (2013) find about reward, DBS and OCD? What does this suggest?

A

When striatal DBS was applied to OCD patients, activity in the nucleus accumbens increased in response to reward cues. When this DBS was not applied, the OCD patients’ nucleus accumbens decreased in activation.

Implies that DBS’ reduction of ventral striatum connectivity normalises its responses to rewarding cues in OCD patients. Strongly suggests a maladaptive interaction between the striatum and frontal cortex in OCD.

32
Q

What does ERN stand for and what does It reflect?

A

Error related negativity.

It is a negative EEG potential originating from the frontal cortex (ACC to be specific), which occurs 50-150ms after an error is perceived.

33
Q

What are the differences in ERN between OCD patients and controls, found by Gehring et al., (2000)? What does this suggest?

A

OCD patients have greater ERNs in response to mistakes over the frontal cortex compared to matched controls.

Suggests hyperactivation of the frontal cortex.

34
Q

What have some studies found regarding ERNs and Y-BOC scores in OCD patients?

A

The larger the ERNs OCD patients have, the greater their Y-BOC score, and so the more severe their symptoms.

(Result is not replicated consistently)

35
Q

What did Riesel (2011) find about genetics and ERNs in OCD and what does this suggest?

A

Relatives of OCD patients that, themselves, did not have OCD, had aberrant (increased) ERNs too, suggesting a genetic element to OCD.

36
Q

What did Figee et al., (2013) find about DBS, frontal activity and symptomatic events?

A

DBS normalises (decreases) the frontal cortex (ERN) response to symptomatic stimuli/events.

37
Q

Describe normal functioning of the direct pathway in the cortico-striatal-thalamic-cortical circuit.

A

Direct pathway:

  • frontal cortex excites the striatum after perception of a visual stimulus.
  • striatum inhibits the internal globus palliadus (GPi) and substantia nigra (SNr), which typically inhibits the thalamus.
  • therefore the thalamus is more active than before, due to less striatal inhibition, leading to arousal for the visual stimulus.
38
Q

Describe normal functioning of the indirect pathway in the cortico-striatal-thalamic-cortical circuit.

A

Information for the visual stimulus leads to frontal excitation of the striatum.

  • striatum inhibits the globus palliadus external (GPe), which typically inhibits the subthalamic nucleus (STN).
  • STN has mmore excitatory output towards the globus palliadus internal (GPi )and substantia nigra (SNr), which typically inhibits the thalamus.
  • thalamus is therefore inhibited, leading to the signal for the isual stimulus dying down once the thalamic signal reaches back to the frontal cortex.
39
Q

What did Atmaca et al., (2007) find about structural differences between the OCD brain and controls?

A

OCD patients, compared to healthy had:

  • increased white matter volume
  • significantly smaller left and right OFC volumes.
  • significantly greater left and right thalamus volumes
  • almost-significant difference in left anterior cingulate cortex (part of frontal area in the CSTC)
  • correlation between their Y-BOCS score and their left and right OFC, and between their Y-BOCS and their left thalamus.
40
Q

What did Atmaca et al., (2007) find about structural differences between the OCD brain and controls?

A

OCD patients, compared to healthy had:

  • increased white matter volume
  • significantly smaller left and right OFC volumes.
  • significantly greater left and right thalamus volumes
  • almost-significant difference in left anterior cingulate cortex (part of frontal area in the CSTC)
  • correlation between their Y-BOCS score and their left and right OFC, and between their Y-BOCS and their left thalamus.
41
Q

Which evidence did Atmaca et al.’s (2007) study about structural differences between OCD and control brains reference, relating to their finding of volumetric OFC differences and the pathophysiology of OCD? What does this suggest?

A

Rubin et al., (1992) and Kwon et al., (2003): functional neuroimaging studies showing that OFC activity is increased in OCD patients compared to healthy controls.

Saxena et al., (1999): heightened OFC activity in OCD patients is decreased after treatment.

Suggests that OFC activity may be involved in the expression of OCD symptoms.

42
Q

What is the disadvantage of the method used in Atmaca et al’s (2007) study on structural differences between OCD patients and controls?

A

Used volumetric MRI which essentially measures the size of each brain area.

  • correlational not causational
  • requires definition of a brain area. One man’s OFC is another’s PFC.
43
Q

What are the two main approaches with structural/volumetric MRI methodologies?

A
  • region of interest (ROI) approach, which identifies a specific brain region in participants, and then measures & compares the volume/some aspect of structure.
  • whole brain, where the entire brain is compared and researchers let the data tell them where the differences are. This is voxel-based morphology.
44
Q

What did Denys et al., (2010) find about the efficacy of DBS to treat OCD?

A

Bilateral DBS in the ventral striatum led to a maximum 80% reduction n OCD symptoms.

45
Q

What did Figee et al., (2013) find about the restoration of fronto-striatal networks in OCD?

A
  • DBS disrupting the striatum leads to improvement in OCD symptoms.
  • Potentially due to the breaking/weakening of striatal-fronto connectivity.
  • The greater the drop in fronto-striatal connectivity, the greater the reduction in symptoms.

Suggests a causative mechanism in OCD.

46
Q

What has been found regarding the application of DBS during a reward task in OCD patients?

A

Before DBS, OCD patients had a decrease in their BOLD activity in response to a reward task. Control patients intuitively increased in the BOLD signal of their nucleus accumbens, which is the centre for reward processing.

Once DBS was applied to the nucleus accumbens, the BOLD signal increased in OCD patients in response to the task.

Suggests that striatal DBS reduces the striatum’s connectivity with frontal regions, normalising its response to rewarding cues.

(Figee et al., 2013)

Neurobiology of Mental Illness (10 decks)

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