Disorders of Attention Flashcards

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1
Q

lesions in the ‘where’ stream lead to…

A

deficits in spatial attention

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2
Q

patient RM had…

A

two strokes which damaged large areas of bilateral-occipito cortex

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3
Q

primary impairment of balint’s syndrome

A

simultanagnosia- inability to focus attention on multiple objects

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4
Q

what does simultanagnosia lead to?

A

considerable conjunction errors when seeing objects for over 10 seconds

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5
Q

what is the parietal lobe important for?

A

feature binding and visual attention

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6
Q

evidence of parietal lobe activity

A
  • greater activity during conjunction search
  • conjunction search disrupted by TMS
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7
Q

hemispatial neglect

A

lack of awareness of stimuli presented to the side of space on the opposite side to the brain damage (contralesional side)

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8
Q

symptoms of hemispatial neglect

A
  1. deficit to attend to information in contralesional space (sensory, representational, and bodily)
  2. unilateral neglect is object based rather than space based (left-hand side of all objects)
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9
Q

what do hemispatial neglect patients also experience?

A

extinction deficits, suggesting different perceptual representations can locally compete for attention

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10
Q

what is neglect an impairment of?

A

the bottom-up stimulus driven system

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11
Q

what are neglect and extinction deficits of?

A

attention

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12
Q

what are ERPs used to observe?

A

when neglect occurs in the visual stream

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13
Q

what do ERPs observe in neglect patients?

A

early processing in neglect patients is similar to controls, but after 150ms there is a large difference

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14
Q

what does experimental psychology show about neglect patients?

A

they fail to accurately identify objects presented to the neglected field- there is no conscious access

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15
Q

priming effect in neglect patients

A

patients can be faster to respond to a semantically related word despite neglecting stimuli, suggesting meaning must be partially processed

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16
Q

where is neglect seen?

A

in damage to right, inferior parietal lobe

17
Q

what does TMS produce?

A

extinction symptoms

18
Q

what do neglect patients benefit from?

A

endogenous cues in both visual fields, as top-down processing is needed to consciously pay attention to the neglected side of space

19
Q

when are neglect patients most impaired?

A

when trying to disengage attention from intact side (struggle with invalid targets failing to activate the exogenous system)

20
Q

attention in neglect patients

A

related to disengaging endogenous attention of attentional spotlight from the ipsilesional side of space, to something happening in the contralesional space

21
Q

most common neurodevelopmental disorder in children

A

ADHD, around 5%

22
Q

three subtypes of ADHD

A
  1. predominantly inattentive
  2. predominantly hyperactive/impulsive
  3. combined inattentive and hyperactive/impulsive
23
Q

predominantly inattentive

A

difficulty in finishing tasks, following instructions, and becoming easily distracted

24
Q

predominantly hyperactive/impulsive

A

difficulty sitting still for long periods, fidgeting, and speaking at inappropriate times

25
Q

combined inattentive and hyperactive/impulsive

A

most common subtype

26
Q

what does the DSMV require for a clinical diagnosis?

A

at least 6 inattention symptoms and 6 hyperactivity/impulsivity symptoms

27
Q

when must symptoms be present?

A

before age of 12 and cause significant impairments in social and academic functioning for a clinical diagnosis

28
Q

structural impairments of ADHD

A
  • 3-4% reduces cortical volume, particularly prefrontal
  • reduced grey matter and cortical connectivity in fronto-parietal attention network
  • reduced cortical connectivity between hemispheres
29
Q

functional impairments of ADHD

A

hypoactivity in prefrontal cortex and endogenous attention network

30
Q

molecular impairments of ADHD

A

imbalance in dopamine and noradrenaline circuits

31
Q

ADHD treatments

A

methylphenidate and dextroamphetamine

32
Q

how do ADHD treatments work?

A

facilitate release of noradrenaline and dopamine to enhance prefrontal cortex and basal ganglia availability