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neuro 2 > neurocognitive disorders > Flashcards

neurocognitive disorders Flashcards

1
Q

what are NCDs?

A

insult to neural sites from disease, physical trauma, genetic predisposition that give rise to loss of cognition/funtion

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2
Q

what are some of the common causes of NCDs?

A

Alzheimer’s, Parkinson’s, stroke, closed brain injury

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3
Q

NCDs include disorders in which the primary deficit is in _________

A

cognitive function

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4
Q

are NCDs acquired or developed?

A

acquired

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5
Q

NCDs represent a _____ from previous level of function

A

decline

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6
Q

why has the name in the DSM-5 changed for NCDs?

A

to allow the intro of mild neurocognitive disorders into diagnostic criteria, moving towards NCDs being on a spectrum

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7
Q

what are the changes of the DSM for major NCDs?

A

memory impairment no longer essential for diagnosis, impairment in only 1 cognitive domain is sufficient for diagnosis

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8
Q

why is it important that cognitive impairments that don’t reach the threshold for dementia are now classified as mild NCDs?

A

patients still have symptoms that interfere with everyday life and experience a problem they need help with. new criteria allows them to receive appropriate support to function > relieves stress

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9
Q

why with an increasing pop is it important the DSM criteria has changed?

A

increasing ageing population means increased demand for expertise in dementia, clear need for early diagnosis, mild NCDs provides earlier treatment

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10
Q

_______ is the leading cause of death in the UK

A

dementia

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11
Q

what are the benefits of an early diagnosis of NCDs?

A

people with mild NCDs often progress to display major NCDs, early intervention and close symptom monitoring, neuropathology emerges before onset of symptoms

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12
Q

why are NCDs on the rise in young and old people?

A

increasing brain injuries from more extreme sports/wars, more sophisticated medical treatments so more people surviving brain trauma resulting in developing NCDs later on, increasing cumulative effects from repeated brain injuries

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13
Q

what are NCDs typically a result of?

A

neural insult or CNS dysfunction

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14
Q

inability to learn new info and recall past and recent events =

A

amnesia

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15
Q

specific traumatic head injuries often result in _________ amnesia

A

anterograde

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16
Q

what parts of the brain result in anterograde amnesia?

A

hippocampus or temporal lobe injury

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17
Q

what type of deficits provide the earliest indication of onset of degenerative NCDs?

A

attention and arousal deficits

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18
Q

what are the symptoms of attention and arousal deficits?

A

lack of attention, increased distractibility, performance of well learnt activity slowed, difficulty focusing on conversation

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19
Q

what brain regions are implicated with attention and arousal deficits?

A

frontal and parietal

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20
Q

aphasia =

A

language deficits (difficult producing/comprehending speech)

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21
Q

difficulty initiating speech or producing complex words, not coherent, poor word retrieval, non-fluent speech = what type of aphasia?

A

Broca’s

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22
Q

production of incoherent jumbled speech, rate and fluency maintained but meaningless speech, unaware of impairment = what type of aphasia?

A

Wernicke’s

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23
Q

difficulty repeating speech = what type of aphasia?

A

conduction

24
Q

anomia =

A

poor word retrieval

25
Q

inability to process sensory info due to neural insult e.g. may be unable to recognise objects/people =

A

visa-pereptual functioning > agnosia

26
Q

prosopagnosia =

A

face agnosia

27
Q

amusia =

A

music agnosia

28
Q

akinetopsia =

A

movement agnosia

29
Q

loss of familiarity of known faces, struggle to identify family/friends, face processing problems = what type of agnosia?

A

prospopagnosia

30
Q

what will patients with prosopagnosia still show an understanding of?

A

face components (can name facial features)

31
Q

is pure prosopagnosia rare or common?

A

rare

32
Q

loss of fluid motion perception, stroboscopic vision, very debilitating, static objects visual acquity is preserved = what type of agnosia?

A

akinetopsia

33
Q

what is an example of a motor deficit?

A

apraxia

34
Q

loss of ability to carry out learnt movements despite the desire and physical ability to do so =

A

apraxia

35
Q

what is apraxia typically caused by?

A

lesion or degeneration of posterior or parietal lobe

36
Q

inability to perform gestures or interact with objects using limbs = what type of apraxia?

A

limb apraxia

37
Q

deficit in planning and sequencing the required movements to produce sounds in speech =

A

speech apraxia

38
Q

executive function deficits include…

A

WM, problem solving, goal directed behaviour, attentional control, inhibitory control, planning and monitor complex behaviour

39
Q

how are executive function deficits often expressed?

A

poor judgement, inappropriate behaviour, erratic mood swings

40
Q

why is it necessary to identify specific causes of NCDs?

A

determine nature and location of neural insult, provide details about symptoms and progression, discriminate between neurological and psychiatric symptoms, identify focus for rehab programmes

41
Q

what are the different methods of diagnosis

A

brain scans (EEG, PET, fMRI), biomarker assessments (CSF, blood), behavioural info, historical context

42
Q

what does the WAIS-IV assessment provide info on?

A

source deficits, info on developmental stage that deficits emerge

43
Q

describe the Trail Making task used to assess NCDs

A

quicker and more specific than WAIS-IV, patients have to connect circles by alternating between letters and number (A>1>B>2>C>3 etc)

44
Q

how long does the trail making task take?

A

5-10 mins

45
Q

what does the trail making task allow the evaluation of?

A

processing speed, visual scanning, integration of vasomotor functions, letter-number sequencing

46
Q

what are the difficulties associated with diagnosing NCDs?

A

overlap in symptoms of different neurological disorders, emergence of psychological problems when decline affects everyday life

47
Q

what is a common risk factor for NCDs?

A

age

48
Q

reflect substantial cognitive impairment, correspond to disorders previously categorised as dementias = major or mild?

A

major

49
Q

reflect more moderate impairments = major or mild?

A

mild

50
Q

distinction between mild and major NCD =

A

extent of deterioration, interference with everyday activities

51
Q

what is the role of a psychologist in rehabilitation?

A

restoring previously affective cognitive and behavioural functions, develop new skills, provide therapy for comorbid disorders, skills to help structure living environment

52
Q

what are some of the problems with cognitive interventions?

A

limited long term efficacy, adverse side effects, surgical = risky and invasive, tractable causes often needed

53
Q

with visuo-perceptual deficit interventions, they often rely on compensatory strategies as recovery is rare. what would these include?

A

if can’t focus on face recognition then focus on voice, body shape, gait to assist recognition

54
Q

what do patients with aphasia often develop for their lack of coherent speech?

A

compensatory behaviours e.g. increased gesturing/pointing

55
Q

what does CIMT intervention aim to do?

A

improve speech by mass practice of verbal responses only > unable to gesture or point
(effective but difficult and frustrating for some patients)

56
Q

why is group communication treatment different from CIMT?

A

allows communication and info exchange through any possible route e.g. miming, pointing, gestures, noise > not limited to speech

neuro 2 (13 decks)

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