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3.6 Neuropsychology > Week 3: Articles > Flashcards

Week 3: Articles Flashcards

1
Q

Why is dementia considered a major global health challenge in the 21st century?

A

Due to its rising prevalence, high disability and dependence burden, and lack of curative treatments.

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2
Q

What is currently the main approach to addressing dementia given the lack of a cure?

A

Focus on prevention, risk reduction, and early detection.

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3
Q

What are some modifiable risk factors for dementia?

A

Lower education, hypertension, obesity, hearing loss, depression, diabetes, inactivity, smoking, social isolation.

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4
Q

How does education in early life impact dementia risk?

A

It builds cognitive reserve, reducing vulnerability to dementia.

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5
Q

Which risk factors are critical to manage in midlife for dementia prevention?

A

Hypertension, obesity, and hearing loss.

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6
Q

Which behaviors should be addressed in later life to reduce dementia risk?

A

Depression, diabetes, sedentary lifestyle, smoking, and social disengagement.

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7
Q

What public health approach is recommended for dementia prevention?

A

Multisectoral policies and lifespan interventions integrated with non-communicable disease efforts.

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8
Q

Why is there interest in detecting Alzheimer’s disease in its preclinical phase?

A

To enable prevention trials, risk stratification, and targeted interventions.

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9
Q

What are common biomarkers used in detecting preclinical Alzheimer’s?

A

Amyloid PET imaging and cerebrospinal fluid analysis.

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10
Q

What are some challenges with using biomarkers for preclinical AD diagnosis?

A

Imperfect prediction, not all progress to dementia, ethical issues with disclosure.

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11
Q

What is mild cognitive impairment (MCI)?

A

Cognitive decline greater than expected for age, not yet interfering with daily activities.

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12
Q

What is the relationship between MCI and Alzheimer’s disease?

A

MCI is often a transitional state, especially amnestic MCI, which more likely progresses to AD.

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13
Q

What is the clinical trajectory of MCI?

A

Variable: may remain stable, revert to normal, or progress to dementia.

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14
Q

How is MCI classified?

A

Amnestic and non-amnestic, based on the primary cognitive domain affected.

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15
Q

What makes diagnosing MCI challenging?

A

Similar presentations to normal aging, psychiatric conditions, and early dementia.

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16
Q

How is dementia diagnosed?

A

Through clinical history, informant input, cognitive testing, and functional evaluation.

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17
Q

Why is physical and neurological examination important in diagnosing dementia?

A

To identify reversible causes and coexisting medical conditions.

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18
Q

What role does neuroimaging play in dementia diagnosis?

A

Excludes structural abnormalities and identifies patterns of different dementia syndromes.

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19
Q

Which imaging techniques are typically used in dementia diagnosis?

A

MRI and CT scans.

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20
Q

Why are laboratory tests used in dementia diagnosis?

A

To screen for metabolic, infectious, or inflammatory contributors.

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21
Q

How does Alzheimer’s disease typically present?

A

With episodic memory impairment.

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22
Q

What is the symptom pattern of vascular dementia?

A

Stepwise progression and focal neurological signs.

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23
Q

What are early symptoms of frontotemporal dementia?

A

Behavioral changes or language impairment.

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24
Q

What characterizes dementia with Lewy bodies?

A

Visual hallucinations, parkinsonism, and cognitive fluctuations.

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25
Why must dementia diagnosis be done with care?
It has significant implications for the patient and family.
26
What should follow a dementia diagnosis?
Clear communication, supportive counselling, and future care planning.
27
What are nonmotor fluctuations (NMF) in Parkinson’s disease?
Fluctuating nonmotor symptoms such as mood, autonomic, and sensory changes in sync with dopaminergic therapy.
28
Why are NMF often under-recognized?
Due to their subjective nature, patient unawareness, and lack of specific assessment tools.
29
How are NMF typically related to dopaminergic therapy?
They often fluctuate with ON/OFF periods of dopaminergic medication.
30
What is the range of NMF prevalence in Parkinson’s patients?
Prevalence varies widely, from 17% to 100%.
31
Which nonmotor symptoms are most common during the OFF state?
Apathy, anxiety, fatigue, and bradyphrenia.
32
Do NMF always correlate with motor fluctuations (MF)?
No, some patients may experience NMF in isolation.
33
What neural circuits are implicated in NMF?
Mesocorticolimbic and autonomic circuits.
34
What role does dopamine play in NMF?
Both dopamine depletion and overstimulation can cause NMF.
35
What is gamma synchrony associated with in PD?
Psychosis or euphoria symptoms.
36
What symptoms are seen during the ON state of neuropsychiatric NMF?
Euphoria, impulsivity, and hyperactivity.
37
What are impulse control disorders (ICDs) linked to?
Overstimulation of dopamine D3 receptors in limbic areas.
38
What evidence supports mesolimbic denervation's role in NMF?
Neuroimaging and pathological studies highlight mesolimbic involvement.
39
What are common autonomic NMF symptoms?
Sweating, urinary urgency, constipation, and orthostatic hypotension.
40
Which state (ON or OFF) are autonomic NMF symptoms more likely to occur?
During the OFF state.
41
What mechanisms may cause autonomic NMF?
Disruption in the central autonomic network and peripheral dysfunction.
42
How common are pain and sensory symptoms in PD patients?
Up to 65% of PD patients.
43
Which mechanisms may explain sensory NMF?
Peripheral rigidity/dystonia and central dopamine-related sensory processing issues.
44
What is the NOMOFA scale used for?
To assess nonmotor fluctuations in PD.
45
How does NOMOFA compare to other NMF assessment tools?
It is the only scale specifically designed for NMF but remains unvalidated.
46
What is the first-line treatment strategy for NMF?
Optimizing dopaminergic therapy (e.g., dose fractionation, long-acting formulations).
47
What role does CBT play in managing NMF?
It is effective in managing ICDs and depression in PD.
48
What are examples of second-line treatments for NMF?
Apomorphine infusion, LCIG, and STN-DBS.
49
What are the risks of apomorphine infusion?
Compulsive use or addiction-like behaviors.
50
What does LCIG therapy offer to PD patients with NMF?
More stable L-dopa levels and symptom improvement.
51
How can STN-DBS affect NMF symptoms?
Improves motor/sensory symptoms but may increase apathy.
52
Why is increased awareness of NMF important for PD care?
They significantly affect quality of life and are currently under-assessed and under-treated.
53
What genetic mutation causes Huntington’s disease (HD)?
A CAG repeat expansion in the huntingtin gene on chromosome 4.
54
What is the inheritance pattern of Huntington’s disease?
Autosomal dominant with full penetrance.
55
When do Huntington’s disease symptoms typically appear?
Around age 40, but onset can range from juvenile to late onset.
56
What are the three primary symptom domains of Huntington’s disease?
Motor, cognitive, and neuropsychiatric.
57
What brain regions are primarily affected in HD?
The neostriatum, including the caudate nucleus and putamen.
58
What is the hallmark motor symptom of HD?
Chorea—dance-like, irregular involuntary movements.
59
What cognitive feature often appears first in HD?
Psychomotor slowing, evident on timed tasks like Stroop and Digit Symbol.
60
What executive dysfunctions are common in HD?
Impaired planning, organization, set-shifting, and verbal fluency.
61
How does memory impairment manifest in HD?
Impaired recall, preserved recognition, and deficits in procedural memory.
62
What emotional recognition deficits occur early in HD?
Difficulty recognizing disgust, anger, and fear.
63
Which cognitive domains remain relatively spared in early HD?
Language, gnosis, and praxis in classical terms.
64
What are the most common neuropsychiatric symptoms in HD?
Apathy, irritability, and depression.
65
What is the role of neuropsychological assessment in HD?
To detect early cognitive changes, track progression, and assess interventions.
66
Which neuropsychological tests are most sensitive in HD?
Symbol-Digit Modalities and Stroop test.
67
What does imaging reveal in pre-manifest HD?
Striatal atrophy and compensatory cortical activity.
68
How is HD diagnosed definitively?
Through genetic testing for CAG repeat expansion.
69
What are effective pharmacological treatments for HD symptoms?
Tetrabenazine for chorea and SSRIs for irritability.
70
What non-pharmacological treatments show promise in HD?
Cognitive interventions, assistive technologies, and behavioral strategies.
71
Why are informant reports important in HD assessment?
They provide context on symptoms that patients may underreport, such as apathy.
72
What areas of the brain show compensatory activity in early HD?
Cortical areas, as shown by functional imaging studies.
73
What are the three leading environmental risk factors for MS?
Epstein–Barr virus (EBV) infection, vitamin D deficiency, and cigarette smoking.
74
What genetic allele is significantly associated with increased MS risk?
HLA-DRB1*1501 allele.
75
Why is MS considered to have a strong environmental component?
Because 80–90% of MS cases have no family history.
76
What does the high concordance in monozygotic vs dizygotic twins indicate about MS?
It shows a genetic component, but not sufficient alone to cause MS.
77
How does migration affect MS risk?
Moving from high- to low-risk areas before adolescence reduces MS risk.
78
What virus is nearly universally found in MS patients?
Epstein–Barr virus (EBV).
79
How does EBV infection influence MS risk?
People who develop infectious mononucleosis have a 2–3 times higher risk of MS.
80
What EBV antibody is strongly associated with later MS development?
Anti-EBNA1 antibodies.
81
What is the proposed mechanism linking EBV to MS?
By activating autoreactive B and T cells, possibly through molecular mimicry.
82
How does vitamin D status relate to MS risk?
Higher vitamin D levels are associated with reduced MS risk.
83
What blood level of 25(OH)D is associated with the lowest MS risk?
Above 99 nmol/L.
84
What are the immunological effects of vitamin D relevant to MS?
It promotes regulatory T cells and suppresses proinflammatory cytokines.
85
How does smoking affect MS risk?
It increases risk by ~50%, especially in men.
86
Why is inhalation critical in smoking-related MS risk?
Because smokeless tobacco does not increase MS risk.
87
How does smoking contribute to MS pathogenesis?
By causing immune dysregulation, oxidative stress, and damaging the blood–brain barrier.
88
What effect has smoking had on the female:male MS ratio?
Rising smoking prevalence may partly explain the increase in female MS cases.
89
What happens to MS risk when high anti-EBNA, low vitamin D, and smoking are combined?
The individual's MS risk can increase more than 200-fold.
90
What are realistic public health strategies for MS prevention?
Vitamin D supplementation and smoking cessation.
91
Is an EBV vaccine currently available for MS prevention?
No, but it is a focus of ongoing research.
92
Why are longitudinal studies important in MS research?
They help identify risk factors and evaluate interventions over time.
93
What is FASD and what causes it?
Fetal alcohol spectrum disorders (FASD) are neurodevelopmental conditions caused by prenatal alcohol exposure.
94
What are executive functions (EF)?
Executive functions include inhibition, working memory, cognitive flexibility, planning, and goal-directed behavior.
95
What EF impairments are common in children with FASD?
Children with FASD often show deficits in inhibitory control, mental flexibility, planning, and working memory.
96
How do EF profiles in FASD differ from ADHD?
FASD shows greater impairments in planning and working memory; ADHD shows more pronounced inhibition deficits.
97
What tasks reveal inhibition deficits in FASD?
Go/no-go paradigms and the Stroop test.
98
How is working memory affected in FASD?
Both verbal and visuospatial working memory are impaired, impacting learning and problem-solving.
99
What EF task shows cognitive flexibility issues in FASD?
Wisconsin Card Sorting Test.
100
What challenges arise from planning deficits in FASD?
Difficulties in task initiation, time management, and completing multi-step activities.
101
What brain regions show abnormalities in FASD?
Prefrontal cortex, cerebellum, basal ganglia, and frontostriatal white matter pathways.
102
What does fMRI reveal about EF in FASD?
Hypoactivation in prefrontal networks during EF tasks.
103
How can EF patterns assist in differential diagnosis?
Broad and severe EF impairments in FASD can help distinguish it from ADHD, especially without physical dysmorphology.
104
Why is early EF screening important?
It helps in identifying at-risk individuals and informing timely interventions.
105
What should clinical assessment of FASD include?
Comprehensive neuropsychological evaluation focusing on EF.
106
What interventions are recommended for FASD?
EF training, behavioral support, and individualized education plans.
107
What awareness is needed for effective FASD support?
Clinicians, educators, and caregivers must understand EF vulnerabilities in FASD.
108
What is the conclusion regarding EF deficits in FASD?
They are broad, enduring, and significantly impact daily functioning, making targeted assessments and interventions essential.

3.6 Neuropsychology (20 decks)

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