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PSY1003 SEMESTER 2 > PSY1003 SEMESTER 2 - WEEK 4 > Flashcards

PSY1003 SEMESTER 2 - WEEK 4 Flashcards

1
Q

explain what neurocognitive disorder is

A

disorders results in loss of cognitive function due to neurocognitive basis, distinct from psychological disorders (instead arise from direct insult to neural sites like disease, trauma degeneration)

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2
Q

what has NCD been previously referred to in the DSM

A

delirium, amnestic, dementia

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3
Q

why is DSM name changed for a NCD

A

introduction of mild NCD onto diagnosis to represent spectrum. allows mild NCD seeling help, relieve stress as may not yet meet a dementia criteria despite clearly exhibiting symptom

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4
Q

what is the impact of new NCD diagnosis categories in dementia

A

leading cause of death in UK and cant screen due to limited early biomarkers and idiopathic causes, so early NCD diagnostic allows early intervention to provide patient supports

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5
Q

name benefits of early diagnosis of NCDs

A

mild NCD often progress to major NCD allowing early interventions and symptom monitoring
neuropathology underlying NCD often emerge before symptom

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6
Q

why are mild NCDs on rise in young and old

A

increased acquired NCD by head injury (medical advances allowing survival), 21st military tactics causing IED higher proportions of closed brain injury, examination and understanding of cumulative repeated minor brain injury (boxers)

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7
Q

what is NCD diagnosis normally first based on?

A

earliest visible behavioural signs, representing cognitive decline (memory, attention, language, EF, perception, visuospatial skill, learning)

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8
Q

what NCD comorbid with in most case

A

depression, anxiety, personality change and aggression

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9
Q

outline amnesia

A

inability to learn new info, failure to recall past events from past or future events. also presents with gradual onset in dementia due to damage to hippocampus or broader temporal lobe injury

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10
Q

specific traumatic head injuries often results in what type of amnesias?

A

anterograde amnesia: memory loss for info acquired post onset of amnesia

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11
Q

outline attention and arousal deficit in NCD

A

earliest indication of onset NCD
lack of attention, increasing distractibility
performance of well-learnt activities slowed
difficulty focusing and keeping up with conversations

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12
Q

what causes attention and arousal deficits of NCD

A

diffuse neural basis - frontal and parietal regions implicated but network extends to subcortical structures (lowers diagnostic value)

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13
Q

name several EF components associated with prefrontal cortex

A

WM, problem solving, goal-directed behaviour, attentional control, inhibitory control, planning and monitor complex behaviour, change to routine)

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14
Q

how are EF deficits presented in NCDs

A

poor judgement, inappropriate behaviour, erratic mood swing

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15
Q

how can EF deficit be presented in higher order intellectual functionings

A

inability to make simple math calculations, reason deductively, draw on general knowledge when undertaking activity

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16
Q

explain Brocas aphasia

A

disruption of ability producing speech, but comprehension often maintained and non-fluent speech

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17
Q

where is Broca aphasia

A

left frontal and temporal lobes

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18
Q

give symptoms for Brocas aphasia

A

difficulty displayed for word ordering, selection and inflection, agrammatism, anomia, slow stunted articulations

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19
Q

define agrammatism

A

flat delivery of words

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20
Q

define anomia

A

poor word retrieval

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21
Q

explain Wernickes aphasia

A

production of incoherent and jumbled speech with deficit of understanding spoken written language

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22
Q

where is Wernicke aphasia

A

posterior temporal lobe

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23
Q

give symptoms of Wernickes aphasia

A

anomia, intonation remain intact (can covey emotions through spech), structurally intact speech rate, unaware of impairements, reading and writing impairements

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24
Q

define conduction aphasia

A

inability to produce back what someone has said to them

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25
Q

give visuo-perceptual functioning deficit in NCD

A

inability to process sensory info, unable to recognise objects or people, independent of memory loss (agnosia)

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26
Q

name 3 type for agnosia

A

prosopagnosia, amusia, akinetopsia

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27
Q

what is prosopagnosia

A

face blindness, high incidence rate from stroke in right hemisphere, pure rare but more common to struggle identifying familiar face, judging expression, but can still show understanding of components of face (naming nose, lips)

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28
Q

what is amusia

A

deficit of perceptual tone, tune, melodies

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29
Q

what is akinetopsia?

A

movement (motion blindness)- loss of fluid motion perception, stroboscopic vision (slow loads gif), acuity for static objects preserved (able to describe, recognise an object), extreme cases show completely lost motion perception (visual perceptions are series of static images)

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30
Q

what is apraxia

A

loss of ability to execute learned movements, sometime perform behaviour as part of routine (unable on command)distinct, often comorbid with aphasia

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31
Q

what cause apraxia?

A

lesions/posterior parietal lobes degeneration, precise brain area damaged correspond to damage to part of body

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32
Q

whats limb apraxia

A

ability to perform gestures, interact with objects

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33
Q

whats speech apraxia

A

deficits in planning and sequency required movements to produce sounds in speech

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34
Q

explain delirium

A

disturbance of attention and awareness that is reflected in reduced ability to direct, focus, sustain and shift attention. develops over short time, cannot understand simple question, shift attention, usually accompanies memory learning deficit, disorientation, perceptual disturbances/hallucination

35
Q

when does a delirium develop

A

rapidly over hours or days, or after a head injury, can resolve in few hours or week+

36
Q

name 8 DSM-5 specific NCDs

A

Alzheimers,
vascular NCD,
Parkinson NCD,
NCD tramatic brain injuries,
HIV infection NCD,
prion disease NCD,
Huntingtons disease NCD,
frontotemporal NCD

37
Q

what are vascular NCD

A

strokes - aphasia, agnosia, apraxia, paralysis, usually from thrombosis in a left cerebral artery (causes disability in right side)

38
Q

explain NCDs due to HIV infection

A

HIV enters CNS, impairs EF, slows processing speed, attentional task problem, difficulty learning info, poor STM, lacking concentration, leg weakness, slow hand movement, depression

39
Q

what are NCD due to prion disease

A

“mad-cow” disease, spongiform encephalography, attacks brain and CNS causing verbal fluency, numeracy, memory, face recognition, EF deficits

40
Q

what are NCD due to Huntingtons disease

A

involuntary limb jerking, psychosis, mood swing, impairement in cognitive functions of memory, attention, decision making

41
Q

why is identifying specific NCDs cause important

A

determing deficit nature and nueral insult location, providing info for type, onsets, severity, symptom progression. discrimination between neurological/psychological symptom, identify focus for rehab programmes

42
Q

what are NCD diagnosis normally based on

A

neuropsychological testing for cognitive or behavioural impairments- supplemented by brain scans (EEG, fMRI, PET), biomarker assessments (CSF, blood tests), behavioural info, history

43
Q

name difficulties of diagnosing an NCD

A

-NCD symptom/deficit could resemble other disorder
-emergence of psychological problem during early stage of cognitive decline
-misdiagnoses
-symptom overlaps between disorders
-closed head traumas producing memory deficits that resemble Alzheimers
single factors causing broader symptom, such as brain tumor

44
Q

explain a difficulty in diagnosing NCD - symptoms/deficit resmebling other disorders

A

amnesia in dissociative disorders, language and EF deficits in sz. depending on age either diagnosed dementia/sz
motor coordination deficit, paralysis, or sensory input impairment can be in somatic disorders such as conversions disorder

45
Q

explain a difficulty in diagnosing NCD - misdiagnoses

A

improved via brain imaging however can be diagnosed as a rae neurological which can impact rehabilitation, care

46
Q

explain a difficulty in diagnosing NCD - closed head injury causing memory issue

A

diagnosed as Alzheimer’s but a common risk factor age (more likely to diagnosed as dementia, but also a closed head injury from an fall)

47
Q

explain a difficulty in diagnosing NCD - single factors (eg: a brain tumor) causing broader symptom

A

emotionality, speech disorder, sensory perception deficits, aggressiveness

48
Q

explain major NCD when classifying disorders

A

reflect substantial cognitive impairment, in at least one domain (complex attention, EF, memory, learning, language, perceptual-motor, social cognition)
past DSM categorised as being dementia

49
Q

explain mild NCD when categorising

A

moderate imapirement

50
Q

name the key deficits that are present in major NCD

A

language becoming empty, vague, can’t name everyday object
apraxia and agnosia
EF function: difficulty managing new tasks, recalling basic knowledge, difficulty counting or reciting alphabet
poor jdugement- risks, inappropriate joke, poor hygeine, socials conduct

51
Q

give 2 example for NCD assessment

A

Wechsler adult intelligence Scale-IV
Montreal Cognitive assessment

52
Q

outline wechsler adult intelligence scale-IV

A

aggregate measure used to provide a broad score, represent ability of:
1. verbal comprehension
2. perceptual organisation
3. WM
4. info processing speed

53
Q

give 2 advantages of wechsler adult intelligence scale-IV

A

give info on deficits source (alcohol abuse, Alzheimers, stroke)
provides info on developmental stage where deficit emerges

54
Q

give 2 weaknesses of wechsler adult intelligence scale-IV

A

difficult applying - attention, sitting still or apraxia

55
Q

what is included in a montreal cognitive assessment

A

high sensitivity tool used to diagnose a mild NCD, simpler tasks:
1. trail making tasks (processing speed, integration of visuomotor functions)
2. clock drawing tasks (visual neglect)
3. simple word lists (comprehension, WM, repeating words over different time spans)

56
Q

what is role of psychologist in NCDs rehab

A

rehab cognitive and behavioural function
help client develop strategy compensating for deficits
therapy for comorbid disorders
supporting client to structure living environment and accomodate cogntive change

57
Q

name disadvantages of biological treatments in NCDs

A

limited long term efficacy - current intervention can only mask symptoms
adverse side effect
surgical treatment invasive, risky
tractable cause often needed

58
Q

provide an overview of cognitive rehab programmes

A

flexible to nature or length of deficit
gain cognitive functioning in range of domains (basic training, extended practicing task, performance feedback)
digital intervention like virtual environments, memory training programmes, apps

59
Q

explain memory deficit intervention - everyday memory prompts

A

focus on compensatory skill
label cupboard/rooms, pager and diary for aiding recall for daily event (more advanced tech difficult with older patient)
usful in prompting recall of known events, but need other strategies for developing new memory

60
Q

explain memeory deficit intervention - visual imagery mnemonics

A

lead to reliable improvements of memory (associates imagery with memorable item, like number)

61
Q

give evaluation of visual imagery memory interventions mnemonics

A

efficacy depends on memory impaired severity, patient motivation
need explicit prompting and support, and can fail generalising use to new situation (limited everyday value)

62
Q

describe errorless learning

A

training procedure, involve patient being prevents from making any errors whilst learning new skills

63
Q

describe intervention in attentional deficit - APT(attention process training)

A

employ different strategy which promote and encourage attentional abilities, like listening to tape containing targets that patient needs to distinguish (require employing shifts of attention based on previous info like pressing buzzer when word is opposite of previous words)

64
Q

provide support for attentional intervention (APT)

A

support improvement for attention abilities and memory functioning,
APT superior to the basic attention/memory therapy,
shown to provide gain for everyday activity, or you can use TPM

65
Q

what is TPM (follow on from APT)

A

time pressure management - providing client with compensatory skills allowing them to effectively manage slow info processing

66
Q

what do EF intervention usually include?

A

problem solving, planning and goal directed behaviours, with interventions often involving training planning and goal management, problem solving skills

67
Q

what is GMT in EF intervention?

A

goal management training - beneficial impact for sustained attention and goal-directed behaviour either via a therapist or app

68
Q

give 6 stages of GMT

A
  1. evaluate current problem “what am i doing”
  2. specify relevant goal as outcome of successfully addressing problem
  3. partitioning of problem solving (steps)
  4. assist patients with learning and retention of subgoal “do i know steps”
  5. self monitoring of results of action “ am i doing what plan”
  6. goal completed and managed effecively, or redo
69
Q

outline SIT (EF intervention)

A

self-instructional training- learns sets of instructions for talking themselves through particular problem
1. raise personal self awareness of deficit
2. increase problem solving strategies
3. improve emotional self regulation, reduce overall frustration
= holistic, developing individuals awareness of disability

70
Q

explain drawbacks of visuoperceptual intervention

A

lacking cases in agnosia recovery

71
Q

what does visuoperceptual deficits intervention tend to focus on

A

relying on compensatory strategy
eg: prosopagnosia focuses on voice, body shape and gait to help recognitions

72
Q

outline evidence of visuoperceptual interventions (CH)

A

39 year old, male, able to distinguish emotion expression, familiar faces after 11 months systematic practice

73
Q

outline evidence for visuoperceptual deficits intervention (AL)

A

child recovered ability to recognise familial faces after slow and deliberate practice for multiple years (possibly due to increased plasticity as done during still a child)

74
Q

explain visual scanning task (interventions for visuo-perceptual deficits)

A

patient asked to read out coloured numbers on wall (scanning full frontal environment),
manually track red ball projected on wall (help coordinate scanning/physical movement),
react to moving images as projected on wall (faciliate detection of stimulus),
move projected image of wheelchair down 3 lane road whilst avoiding obstacle = reduce unilateral visual neglect symptoms, improve performance on a real-life wheelchair obstacle course

75
Q

what can apraxia mean for everyday task

A

planning and actions sequence deficits due to gesture learning impaired, insults on motor memory system, struggling cooking or dressing, meaning relying on caregiver. unable to plan sequence of action, exhibiting inappropriate gestures (pouring water from closed bottle)

76
Q

in apraxia interventions give examples for how gestural training effective for rehab

A

limb apraxia- demonstrate use of common object, mimic observed gesture, distinguish between appropriate and inappropriate use of objects
associated with significant reduction in errors during everyday tasks

77
Q

when could VR be important in interventions of apraxia

A

when mistakes are dangerous (driving)

78
Q

outline interventions for language deficits

A

in generic deficits undergo standard speech therapy- assists with production and comprehension of speech
often with both practicioners and home based computer assisted therapy

79
Q

what does (aphasia interventions) constraint induced movement therapy aim to do

A

often develops compensatory behaviours like pointing which can improve communication but limits speech producing recovery

80
Q

what does constraint induced movement therapy involve?

A

for aphasia = mass practice of verbal responses where unable to gesture (also relevant in stroke recoverys)

81
Q

evaluate using constraint induced movement therapies

A

shown to improve self clinician and observer rating of communication ability, can be efficacious but difficult, frustrating = slow improvement

82
Q

outline interventions in aphasia group communication treatments

A

focuses instead on increasing communications any way
goal-directed, tailored to personal situation
improves communicative abilities when compared with matched patients not in treatment
use speech, art, music etc

83
Q

what are impacts of NCD for caregiver?

A

providing physical, economic, emotional support, restricted socials life, avoidant coping (ignoring problems and aoiding new situ)- correlates with levels of depression in elderly caregivers in dementia

84
Q

what are interventions involved in a caregiver support programme

A

modifying home environment to support sufferer,
training skill to develop self-care behaviours of sufferer, reduce aggression or wandering,
peer support groups

PSY1003 SEMESTER 2 (10 decks)

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