PSY1003 W4 Neurocognitive disorders

Question 1

what are neurocogntivie disorders?

Answer 1

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

Question 2

Psychological disorders

Answer 2

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

Question 3

Common causes of NCDs

Answer 3

dementias, stroke, traumatic brain injury.

Question 4

Key features of NCDs

Answer 4

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.

Question 5

Why is the introduction of mild NCDs important?

Answer 5

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”

Question 6

Why would we benefit of an early diganosis for NCDs?

Answer 6

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.

Question 7

Why mild NCDs rise in both young and old?

Answer 7

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

Question 8

Common NCDs impairments and their neural bases

Answer 8

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

Question 9

1- Cognitive impairments

Answer 9

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

Question 10

2-Learning and Memory deficits: Amnesia:

Answer 10

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

Question 11

2- Learning and Memory deficits: anterograde amnesia

Answer 11

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).

Question 12

3-Attention adn arousal deficits

Answer 12

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)

Question 13

4- Defects in Executive functions

Answer 13

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

Question 14

5- Language deficits

Answer 14

Aphasia: broca, werniches, conduction

Question 15

Aphasia

Answer 15

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

Question 16

Broca’s aphasia

Answer 16

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

Question 17

Wernicke’s aphasia

Answer 17

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

Question 18

Conduction aphasia

Answer 18

Difficulty repeating speech.

Question 19

Visuo-perceptual functioning

Answer 19

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

Question 20

Visuo-perceptual functining: agnosia

Answer 20

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

Question 21

Visuo-perceptual functining: prosopagnosia

Answer 21

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.

Question 22

Visuo-perceptual functioning Akinetopsia

Answer 22

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.

Question 23

Motor deficts: Apraxia

Answer 23

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

Question 24

Limbi apraxia

Answer 24

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).)

Question 25

DSM-5 causes of NCDs

Answer 25

- 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

Question 26

Difficulties diagnosing NCDs

Answer 26

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.

Question 27

Major NCDs

Answer 27

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

Question 28

Mild NCDs

Answer 28

Reflect more moderate impairments.

Question 29

NCDs a spectrum

Answer 29

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.

Question 30

Deficits in major NCDs

Answer 30

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

Question 31

Wechsler adult intelligence scalle-4

Answer 31

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.

Question 32

Montreal cognitve assessment

Answer 32

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

Question 33

Bioloigical treatments

Answer 33

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

Question 34

terventions for memory deficits: everyday memory prompts and

Answer 34

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

Question 35

Interventions for memory deficits: vidual imagery nmemonics.

Answer 35

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

Question 36

interventions for memory deficits

Answer 36

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.

Question 37

Interventions for EF

Answer 37

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.

Question 38

Interventions for apraxia

Answer 38

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.

Question 39

Interventions for aphasia 1-Constraint induced movement therapy

Answer 39

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.

Question 40

interventions for aphasia

Answer 40

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.

Question 41

Wisconsin card sorting task

Answer 41

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.

Question 42

Mini Mental state examinatin (MMSE)

Answer 42

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

Question 43

Delirium

Answer 43

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.

Question 44

NCD due prion disease

Answer 44

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

Question 45

HIV infections

Answer 45

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.

Question 46

Prion Disease

Answer 46

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

Question 47

NCD due to traumatic brain injury

Answer 47

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

Question 48

Degenerative disorders

Answer 48

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

Question 49

Cardiovascular accident

Answer 49

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

Question 50

Stroke

Answer 50

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

Question 51

Infraction

Answer 51

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.

Question 52

Haemorrhage

Answer 52

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

Question 53

Cerebral embolism

Answer 53

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.

Question 54

Cerebral thrombosis

Answer 54

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.

Question 55

Aneurysm

Answer 55

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

Question 56

Agnosia

Answer 56

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

Question 57

Prefrontal cortex

Answer 57

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

Question 58

Neurogibrillary tangles

Answer 58

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

Question 59

Acetylcholine

Answer 59

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

Question 60

Beta amyloid plaques

Answer 60

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

Question 61

Frontotemporal NCDs

Answer 61

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.

Question 62

Pros of genetic testing in assessing risk of dementia

Answer 62

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.

Question 63

Cons of genetic testing assesing risk of dementia

Answer 63

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

Question 64

Mutant Huntingtin (mHtt)

Answer 64

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

Question 65

NCD due to Hungtington's disease

Answer 65

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

Question 66

Allostatic state

Answer 66

a biological state of stress.

Question 67

Lewy bodies:

Answer 67

abnormal protein deposits that disrupt the brains normal functioning.

Question 68

Assessing NCDs

Answer 68

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).

Question 69

treatment for memory deficits

Answer 69

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

Question 70

treatment for deficits in executive functioning

Answer 70

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

Question 71

treatment for deficits in language

Answer 71

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

Question 72

Cogntiive rehabilitatin programme

Answer 72

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

Question 73

Rehailitation programmes for attention deficts.

Answer 73

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

Question 74

Treatment of apraxia

Answer 74

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

Question 75

NCDs drug treatments

Answer 75

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

Question 76

Deep brain stimulation (DBS)

Answer 76

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