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PSY1003 > PSY1003 W4 Neurocognitive disorders > Flashcards

PSY1003 W4 Neurocognitive disorders Flashcards

1
Q

what are neurocogntivie disorders?

A

insult to neural sites gives rise to symptoms (disease, trauma, degeneration)

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2
Q

Psychological disorders

A

experiences/environment/genes can give rise to problematic thoughts and behaviours.

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3
Q

Common causes of NCDs

A

dementias, stroke, traumatic brain injury.

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4
Q

Key features of NCDs

A

primary clinical deficits is in cognitive function. Acquired rather than developmental: decline from a previous level of function.
Started to see NCDs as a spectrum to allow the introduction of mild NCDs.

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5
Q

Why is the introduction of mild NCDs important?

A

patients with mild NCD expeiernce a very real problem and deserve support, they used to have to try again in a few years “not sick enough”

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6
Q

Why would we benefit of an early diganosis for NCDs?

A

Mild NCDs often progress to major NCDs. Diagnosis allows for early intervention & monitoring of symptom. Neuropathology underlying NCDs often emerges well before symptoms.
Limitations: early diagnosis are not easy, early interventions are limited in terms of long-term efficacy.

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7
Q

Why mild NCDs rise in both young and old?

A

increases in acquired NCDs following injuries, more brain trauma (medical advance, military tactics, repeated minor brain injuries (sports)

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8
Q

Common NCDs impairments and their neural bases

A

1- Cognitive impairments.
2- Learning and memory deficits.
3-Attention and arousal deficits.
4- Deficits in Executive functions
5-Language deficits

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9
Q

1- Cognitive impairments

A

diagnosis typically made on earliest visible behvaioural signs. represent cognitve decline, traceable neural basis. Vital role in assessing these abilities.

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10
Q

2-Learning and Memory deficits: Amnesia:

A

inability to learn new information, failure to recall past events, failure to recall recent events.

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11
Q

2- Learning and Memory deficits: anterograde amnesia

A

Specific traumatic head injury often result in anterograde amnesia: memory loss for acquired information after onset of amnesia, gradual onset in dementia, damage to hippocampus (temporal lobe).

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12
Q

3-Attention adn arousal deficits

A

earliest indication of onset of degenerative NCDs, lack of attention or increased distractibility, diffuse neural basis (frontal and parietal regions implicated but netxworks extend to subcortical structures)

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13
Q

4- Defects in Executive functions

A

May include: Working memory, Problem solving, Goal directed behavior, Attentional control, Inhibitory control, Planning and monitor complex behavior, Change in routine.
Often expressed in NCDs as poor judgement, inappropriate behavior, or erratic mood swings

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14
Q

5- Language deficits

A

Aphasia: broca, werniches, conduction

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15
Q

Aphasia

A

Difficulty producing +/or comprehending speech: Very common feature of NCDs, Several flavors

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16
Q

Broca’s aphasia

A

Difficulty initiating speech or producing complex words. comprehension often maintained. difficulties with word ordering, seleciton, inflection, poor word retrieval, articulation.

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17
Q

Wernicke’s aphasia

A

Production of incoherent jumbled speech. Poor word retrieval, structually intact speech rate, reading and writtign impairements. Speech rate and fluency maintained.

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18
Q

Conduction aphasia

A

Difficulty repeating speech.

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19
Q

Visuo-perceptual functioning

A

Inability to process sensory information due to neural insult. = Patients may be unable to recognise objects or people, Independent of memory loss.

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20
Q

Visuo-perceptual functining: agnosia

A

comes in many forms = Faces (prosopagnosia), Music (amusia), Movement (Very rare, but hugely debilitating) (akinetopsia)

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21
Q

Visuo-perceptual functining: prosopagnosia

A

face blindness, face processing problem (high incidence rate in right hemisphere stroke), pure prosopagnosia is rare, loss of familiarity of known faces (struggle to identify friends/family), unable to judge expressions, typically show an understanding of the components of the face.

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22
Q

Visuo-perceptual functioning Akinetopsia

A

Loss of fluid motion perception (vision becomes stroboscopic. Acuity for static objects preserved = Recognition is normal. Analogous to watching a poorly loaded video or gif.
Some extreme cases: motion perception is eliminated completely, and visual perception becomes a series of static images.

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23
Q

Motor deficts: Apraxia

A

The loss of ability to execute learned movements.
May be able to perform a behavior as part of a routine, but unable to on command.
Typically cause by lesion or degeneration of posterior parietal lobe

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24
Q

Limbi apraxia

A

ability to perform gestures, interact objects. Apraxia of speech (= deficit in planning and sequencing the required movements to produce sounds in speech. Distinct from aphasia (but often comorbid).)

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25
Q

DSM-5 causes of NCDs

A
  • Alzheimer’s disease
  • Vascular NCDs
  • NCD due to Parkinson’s disease
  • NCD due to traumatic brain injury
  • NCD due to HIV infection
  • NCD due to prion disease
  • NCD due to Huntington’s disease
  • Frontotemporal NCD
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26
Q

Difficulties diagnosing NCDs

A

Symptoms/ deficits resemble other disorders, with early stages of cognitive decline, partially alleviated by brain imaging in but not fully.
Closed head trauma may produce memory deficits that resemble, single factors may cause broad symptoms.
Age is a risk factor.

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27
Q

Major NCDs

A

Reflect substantial cognitive impairment. Correspond to disorders previously categorized as dementias.

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28
Q

Mild NCDs

A

Reflect more moderate impairments.

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29
Q

NCDs a spectrum

A

Cog deficits may be similar.
 Mild: manageable but may require more time or cognitive resources/strategies.
 Major: will typically require assistance with such tasks.
 Specific NCDs can present as mild or major.

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30
Q

Deficits in major NCDs

A

Language may become vague and empty, may present with apraxia and agnosia, EF functions are common, poor judgment and insight.

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31
Q

Wechsler adult intelligence scalle-4

A

combined measures to provide scores on abilities (verbal comprehension, perceptual organization, WM, information processing speed), also provides info on source of deficits and developmental stage at which deficits emerged.

32
Q

Montreal cognitve assessment

A

high sensitivity tool used to diagnose mild NCDs, simpler, early deficits.

33
Q

Bioloigical treatments

A

aim to stabilize or slow degenerative disorders (pharmacological interventions, deep brain stimulation. Can provide significant quality of life improvement but limited long-term efficacy (current interventions can only masks symptoms, side effects

34
Q

terventions for memory deficits: everyday memory prompts and

A

Full recovery of lost memory abilities often difficult, compensatory strategies (lubing cupboards)

35
Q

Interventions for memory deficits: vidual imagery nmemonics.

A

lead to reliable memory improvement, efficacy depends on severity of memory impairment, patients’ motivation.
Patients may also need explicit prompting and support.

36
Q

interventions for memory deficits

A

attention process training, employs different strategies to promote and encourage attentional abilities. (e.g., listening to tape that contains targets that must be distinguished) Supports improvements in attentional abilities and memory functioning.

37
Q

Interventions for EF

A

some overlap with interventions for memory and attention (specific interventions for prob solving, planning, goal directed behaviors).
Goal management training: beneficial effects on sustained attention and goal-directed behavior, may be therapist or app driven.

38
Q

Interventions for apraxia

A

Deficits in planning and sequence of actions (gesture learning)
Gestural training effective in rehabilitation for e.g. limb apraxia (Demonstrate use of a common object)
Contemporary research using virtual reality promising, but not currently in wide use.

39
Q

Interventions for aphasia 1-Constraint induced movement therapy

A

often develop compensatory behavior (gesturing, can improve communication but limit recovery of speech production). CIMT for aphasia: mass practice of verbal responses, when are unable to gesture, stroke recovery, improve communication abilities.

40
Q

interventions for aphasia

A

CIMT efficacious but can be difficult and frustrating for some patients: slow improvement in symptoms, group communication treatment (increase communication and information exchange through possible route), goal directed patient should have specific communication goals tailored to personally relevant situation. Not limited to speech : art music ect.

41
Q

Wisconsin card sorting task

A

a widely used test of executive functioning where individuals must sort cards for a number of trials using one rule and then sort cards using a different rule.

42
Q

Mini Mental state examinatin (MMSE)

A

a structured test that takes 10 minutes to administer and can provide reliable information on a clients overall levels of cognitive and mental functioning.

43
Q

Delirium

A

a disturbance of consciousness that develops over a short period of time.
The main feature is a disturbance of attention and awareness, and the disturbance is reflected in a reduce ability to direct, focus, sustain and shift attention. Develops over a short period of time.

44
Q

NCD due prion disease

A

(‘mad cow disease’ (fatal infectious disease known as spongiform encephalopathy) attacks the brain and central nervous system.

45
Q

HIV infections

A

human immunodeficiency virus type 1, tends to enter the central nervous system early in the illness and neurological difficulties can develop in up to 60% of those infected. HIV infections appears to cause these cognitive impairments in a variety of ways. MRI scans indicate that it is associated with progressive cortical atrophy in the grey and white matter in the brain, particularly in the later stages of the disease.

46
Q

Prion Disease

A

represents a group of conditions that affect the nervous system in humans and animals

47
Q

NCD due to traumatic brain injury

A

main common causes of neurological impairment, result from blunt or penetrating trauma to the head as a result of direct injury.

48
Q

Degenerative disorders

A

neurocognitive disorders that are characterized by a slow, general deterioration in cognitive, physical and emotional functioning as a result of progressive physical changes in the brain

49
Q

Cardiovascular accident

A

otherwise known as a troke, stroke result from either a blockage or breaking of the blood vessel in the brain.

50
Q

Stroke

A

sudden loss of consciousness resulting when the rupture or occlusion of a blood vessel leads to oxygen lack in the brain.

51
Q

Infraction

A

the injury caused when the blood flow to the brain is impeded in some way, resulting in damage to the brain tissue fed by that blood flow.

52
Q

Haemorrhage

A

when a blood vessel in the brain ruptures and affects local brain tissue

53
Q

Cerebral embolism

A

a blood clot that forms somewhere in the body before travelling through the blood vessels and lodging in the brain, causing the brain cells to become damaged as a result of oxygen starvation.

54
Q

Cerebral thrombosis

A

an injury caused when a blood clot forms in an artery supplying blood to the brain and interrupts the blood supply and brain cells are starved of oxygen.

55
Q

Aneurysm

A

a localized bulging in a blood vessel caused by disease or weakening of the vessel wall.

56
Q

Agnosia

A

the loss of the ability to recognize objects, persons sounds, shapes or smells while the specific sense is not defective and there is no significant memory loss

57
Q

Prefrontal cortex

A

an area of the brain which Is important in maintaining representations of goals and the means to achieve them.

58
Q

Neurogibrillary tangles

A

abnormal collections of twisted nerve cell threads which result in errors in impulses between nerve cells and eventual cell death.

59
Q

Acetylcholine

A

a neurotransmitter that appears to be involved in learning and memory.

60
Q

Beta amyloid plaques

A

abnormal cell development, possibly caused by abnormal protein synthesis in the brain, which clump together with the consequence of killing healthy neurons.

61
Q

Frontotemporal NCDs

A

associated with a loss of neurons from the frontal and temporal regions of the brain that leads to progressive development of behavioral and personality changes and language impairment.

62
Q

Pros of genetic testing in assessing risk of dementia

A

help genetic researchers understand the disease better and so improve treatment.
Encourage someone to adopt a healthier lifestyle.
Allow people who are at risk to benefit from new treatments that may become available in future.
Help people plan for the future.

63
Q

Cons of genetic testing assesing risk of dementia

A

Genetic defect cannot be repaired, experience could be very hard emotionally and not provide conclusive results. Could result in discrimination.

64
Q

Mutant Huntingtin (mHtt)

A

A protein which causes cell death in the basal ganglia and contributes to Huntington’s disease.

65
Q

NCD due to Hungtington’s disease

A

an inherited, degenerative disorder of the central nervous system caused by dominant gene.

66
Q

Allostatic state

A

a biological state of stress.

67
Q

Lewy bodies:

A

abnormal protein deposits that disrupt the brains normal functioning.

68
Q

Assessing NCDs

A

Assessment in clinical neuropsychology is based on a range of cognitive tests and can be supplemented by blood tests, chemical analyses of cerebrospinal fluids, and brain scans such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI).

69
Q

treatment for memory deficits

A

use of assistive technology (such as smartphones) or specific memory training procedures (visual imagery mnemonics or errorless learning procedures.)

70
Q

treatment for deficits in executive functioning

A

problem‐solving training such as goal management training (GMT) or self‐instructional training (SIT).Holistic rehabilitation methods collectively attempt to address cognitive, emotional, and functional impairments, as well as physical disability

71
Q

treatment for deficits in language

A

depend on the nature of the problem, but (common e.g. constraint‐induced movement therapy (CIMT) and group communication treatment.)

72
Q

Cogntiive rehabilitatin programme

A

directed at improving function within specific cognitive deficits (e.g., memory, language).

73
Q

Rehailitation programmes for attention deficts.

A

Attention process training (APT) and time pressure management (TPM).

74
Q

Treatment of apraxia

A

Gestural training and the use of virtual reality environments can be utilised to treat apraxia and deficits in coordinated self‐help behaviours.

75
Q

NCDs drug treatments

A

use of cholinesterase inhibitors (Alzheimer’s disease), levodopa (Parkinson’s disease), thrombolytic therapy (CVAs and strokes), and antiretroviral drugs (HIV dementia).

76
Q

Deep brain stimulation (DBS)

A

alleviates symptoms of Parkinson’s disease by delivering electrical stimulation to the thalamus and basal ganglia.

PSY1003 (10 decks)

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