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Week 3 Articles Flashcards

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1
Q

Livingston (dementia prevention, intervention and care)

Introduction

Introduction

A
  • Dementia affects nearly 50 million people globally.
  • AD is most common
  • Dementia results from complex interplay between genetic, environmental and lifestle factors
  • Dementia usually occurs after 65 years old, when comorbidity is common
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2
Q

Livingston (dementia prevention, intervention and care)

Dementia vs mild cognitive impairment

A

Dementia = the decline affects activities of daily living and social functioning

Mild cognitive impairment = patients can still engage in complex activities, but greater effort or new strategies might be required.
* Usually happens before dementia

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3
Q

Livingston (dementia prevention, intervention and care)

Aim

Introduction

A

Update findings by reviewing new evidence in risk reduction, early diagnosis, interventions and care.

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4
Q

Livingston (dementia prevention, intervention and care)

Key conceptual shift

Introduction

12 modifiable risk factors identified

A

Dementia is a lifelong condition, with modifiable risk factors throughout life that account for 40% of dementia cases globally:
1. Less education
2. Hypertension
3. Hearing impairment
4. Smoking
5. Obesity
6. Depression
7. Physical inactivity
8. Diabetes
9. Low social contact
10. Traumatic brain injury: strongly linked to dementia; risk increases with severity and frequency.
11. Excessive alcohol consumption: 21 units per week is associated with increased risk.
12. Air pollution

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5
Q

Livingston (dementia prevention, intervention and care)

Demographics and dementia

Prevention of dementia

A

Number of people with dementia is rapidly increasing due to ageing populations.

Some countries have a decline due to better education, health and lifestyle factors

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6
Q

Livingston (dementia prevention, intervention and care)

Complexity of dementia neuropathology complicates prevention

Prevention of dementia

A
  • Some risk factors are modifiable
  • Dementia is heterogeneous and risk factors may vary or coexist for different
  • The effect of lifestyle changes on cognitive decline has mixed findings.
  • Age is the greatest risk factor but is non-modifiable.
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7
Q

Livingston (dementia prevention, intervention and care)

Focus on resilience

Prevention of dementia

Cognitive reserve (definition, how it works, how to build it, implications for risk and diagnosis)

A

Refers to the brain’s resilience to neuropathological damage.

It helps explain why some individuals with significant brain pathology do not show clinical symptoms of dementia.

How it works:
* Individuals with higher cognitive reserve can tolerate more AD pathology before showing cognitive impairment.
* This does not prevent the disease pathology but it delays clinical expression.

How to build cognitive reserve:
* developed and maintained through life experiences, especially with education, occupation complexity, social engagement, learning, bilingualism, and cognitively stimulating activities.

Implications for risk and diagnosis:
* May mask early symptoms
* Once symptoms appear, they may decline much faster as the underlying disease is often more advanced.
* Thus, eucation and cognitive activities are key prevention targets.

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8
Q
A
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9
Q

Livingston (dementia prevention, intervention and care)

Key takeaways

Prevention of dementia

A

Prevention strategies should be life-course based, targeting different age groups.
* Early life = improve education
* Midlife = address hearing loss, hypertension, TBI, alcohol misuse, and obesity
* Later life = manage smoking, depression, physical inactivity, social isolation, diabetes and air pollution

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10
Q

Livingston (dementia prevention, intervention and care)

Emphasised interventions

Prevention of dementia

A
  • Education access early in life builds cognitive reserve
  • Hearing aids may protect against cognitive decline - encouraged in midlife.
  • Smoking cessation reduces risk across all age groups.
  • Physical activity is broadly protective, and should be encouraged at all stages.
  • Managing depression may delay or prevent dementia, especially when symptoms arise in midlife or later life.
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11
Q

Livingston (dementia prevention, intervention and care)

Preclinical AD

Early detection of preclinical AD

A
  • AD pathology can begin 20 years before symptoms.
  • Early AD has pathogenic changes but no memory impairment (includes extracellular deposition of amyloid protein and intracellular accumulation of tau protein).
  • Early detection focuses on biomarkers, not symptoms (CSF (low amyloid and high tau), PET imaging (amyloid/tau), Blood-based (emerging, cheaper and more scalable).
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12
Q

Livingston (dementia prevention, intervention and care)

Rational for early detection

Early detection of preclinical AD

What they targert, aim and challenge

A
  • Clinical trails now target pre-symptomatic stages
  • Aim = slow or stop disease before neurodegeneration is advanced
  • Challenge = most biomarker-positive people never develop dementia, especially older adults
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13
Q

Livingston (dementia prevention, intervention and care)

Ethical and practical issues

Early detection of preclinical AD

A
  • Concenrs about psychological impact of preclinical diagnosis
  • Risk of over-diagnosis and lack of treatment options
  • May exacerbate inequalities (only accessible to high-resource settings)
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14
Q

Livingston (dementia prevention, intervention and care)

Definition

Mild cognitive impairments

What is it, prevalence, divisions

A
  • Considered as an intermediate state between healthy ageing and early dementia, which sometimes reverts to healthy cognition
  • It is best to conceptualise it as a probability state, which can be used to delineate a population at higher risk of dementia, with cognitive decline not meeting diagnostic criteria for dementia
  • Affects more people than dementia = 4-19% of people 60+

Can be divided into:
* Amnesic mild cognitive impairment = individuals with a particular impairment of episodic memory often thought to likely develop AD
* Non-amnesic mild cognitive impairment

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15
Q

Livingston (dementia prevention, intervention and care)

Prodromal AD

Mild cognitive impairments

A

Those with amnesic mild cognitive impairment and a positive cerebrospinal fluid AB and tau biomarker test, or positive AB scan.
* These people are more likely to develop AD

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16
Q

Livingston (dementia prevention, intervention and care)

Risk factors for progression from mild cognitive impairment to AD

Mild cognitive impairment

A
  • Diabetes, pre-diabetes, metabolic syndromes, lower serum folate concentrations, presence of neuropsychiatric symptoms = all increase the risk
  • Less education = does not increase the risk of progression
  • Meditarranean diet = decreases the risk of progression
  • Gender differences: men (prevention of strokes) and women (prevention of depression andanticholinergic medications)
  • Mild behavioural impairment = increases risk of progression due to presence of late-life neuropsychiatric symptoms
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17
Q

Livingston (dementia prevention, intervention and care)

Interventions

Mild cognitive impairments

Cognitive interventions, exercise, multimodal, and medication

A

Cognitive interventions: improvements on objective memory outcomes immediately after training but global cognition did not improve with cognitive training.

Exercise interventions: mixed evidence that it can improve cognitive outcomes.

Multimodal and multi-component interventions targeting heterogeneous: might reduce risk of cognitive decline but not trial in mild cognitive impairment specifically.

Medication: no evidence of delay conversion but some reduce amyloid protein in the brain (cholinesterase inhibitors should not be used).

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18
Q

Livingston (dementia prevention, intervention and care)

Cognitive testing

Making the diagnosis

Which one is common and how to interpret results

A
  • Many short validated cognitive tests
  • MMSE commonly used (lacks sensitivity in those with high premorbid education and early impairment)
  • Results should be interpreted in the light of premorbid education, language, and literacy skills and any current motor, hearing and visual impairment.
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19
Q

Livingston (dementia prevention, intervention and care)

Neuroimaging

Making the diagnosis

A

Structural neuroimaging: regional and progressive brain atrophy helps distinguish the common causes of dementia.
* Disproportionate hippocampal atrophy = AD
* Medial temporal lobe atrophy = differentiates between AD and healthy ageing.
* MRI = high specificity and sensitivity

Vascular abnormalities: prerequisite for diagnosis of vascular dementia
* Clinically significant vascular burden = either many lacunae, strategiec infarcts, or white matter lesions
* Degree has to credibly account for clinical cognitive impairments

Recommended is MRI (if not tolerated, then CT)

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20
Q

Livingston (dementia prevention, intervention and care)

Functional and molecular imaging

Making the diagnosis

A
  • FDG-PET = in-vivo assessment of brain metabolism and supports assessment of frontotemporal dementia
  • Functional imaging = helps distinguish between dementia with lewy bodies and those due to dopamine depletion.
  • Molecular imaging of amyloid or tau = promising method for AD (most helpful for young onset or unexplained progressive dementias, amyloid PET (good), tau imaging (only research tool), MRI incorporating diffusion imaging (good for prion disease)
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21
Q

Livingston (dementia prevention, intervention and care)

Cerebrospinal fluid and blood biomarkers

Making the diagnosis

A
  • Routine testing is currently not recommended
  • It has the potential to elucidate the dementia subtype at an early stage (can identified up to 15 years before clinical presentation)
  • Should be reserved for when rare reversible causes of cognitive decline are suspected.
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22
Q

Martinez (hidden sister of motor fluctuations in PD)

Introduction

Introduction

Background, definition (NMF, MF), key issues

A

Background:
* motor fluctuations from L-dopa treatment have been long known; non-motor fluctuations (NMF) received less attention

Definition:
* NMF are fluctuations in non-motor symptoms (neuropsychiatric, autonomic, and sensory) often paralleling or independent from motor fluctuations (MF)

Key issues:
* Difficulty to detect due to subjective nature and lack of patient insight.
* Often more disabling than MF
* Under-assessed due to lack of standardised tools.

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23
Q

Martinez (hidden sister of motor fluctuations in PD)

Epidemiology of NMF

Clinical presentation and epidemiology of NMF

MF and NMF presentation, prevalence, fluctuation timing, progression

A
  • NMF often co-occur with MF, but can occur independently
  • Prevalence: highly-variable (17% to 100% in PD patients with MF)
  • Fluctuation timing = non-motor symptoms (NMS/NMF) are frequent in the OFF motor state.
  • Progression: NMS/NMF responding to dopamine may improve early but worsen later as therapy becomes less effective.
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24
Q

Martinez (hidden sister of motor fluctuations in PD)

Types of NMF

Clinical presentation and epidemiology of NMF

A
  1. Neuropsychiatric = most common (mood swings, apathy)
  2. Autonomic = GI (constipation, nausea, abdominal pain/bloating)
  3. Sensory = pain, akathisia, dysesthesia
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25
# Martinez (hidden sister of motor fluctuations in PD) Mechanisms and risk factors | Pathophysiology of NMF ## Footnote MF mechanism, NMF mechanisms, Risk factors
MF mechanism: pulsatile dopamine stimulation + disease progression = erratic postsynaptic signaling. NMF mechanism: * Shares dopaminergic involvement but involves different brain circuits (limbic, associative). * Electrophysiology = dysregulation in cortical synchronisation may affect both motor and cognitive/emotional functions. * Neurotransmitters = involvement of dopamine, serotonin, norepinephrine, and acetylcholine. Risk factors: * Early-onset PD * Long disease duration * High L-dopa doses * Female sex
26
# Martinez (hidden sister of motor fluctuations in PD) Symptoms/fluctuations | Neuropsychiatric fluctuations ## Footnote ON/OFF, impulsivity related NMF, cognitive fluctuations
Symptoms during OFF: apathy, anxiety, depression, fatigue, bradyphrenia Symptoms during ON: euphorica, impulsivity, hyperactivity, hallucinations Impulsivity related NMF = shares features with addiction (cravings and withdrawals) Cognitive fluctuations: OFF state bradyphrenia improves with dopamine, but executive functions may worsen in ON.
27
# Martinez (hidden sister of motor fluctuations in PD) Underlying cause | Neuropsychiatric fluctuations
Degeneration of mesocorticolimbic dopaminergic circuits, especially ventral tegmental area (TVA)
28
# Martinez (hidden sister of motor fluctuations in PD) Key receptors | Neuropsychiatric fluctuations
D3 (limbic areas) and D1/D2 (motor areas)
29
# Martinez (hidden sister of motor fluctuations in PD) Imaging | Neuropsychiatric fluctuations ## Footnote Stuctural and functional
Structural imaging: correlates between NMF and limbic area abnormalities (ex: caudate, OFC, ventral striatum) Functional imaging: dopaminergic modulation affects mood/cognition
30
# Martinez (hidden sister of motor fluctuations in PD) Autonomic fluctuations ## Footnote Symptoms, pathogenesis, evidence
Symptoms (mostly in OFF): sweating, light headedness, urinary urgency, constipation, nausea. Pathogenesis: * Likely involves both central and peripheral autonomic systems. * May involve noradrenergic dysfunction in addition to dopamine. Evidence: mixed; some symptoms improve with L-dopa, others do not consistently fluctuate.
31
# Martinez (hidden sister of motor fluctuations in PD) Sensory disturbances and pain
Pain types: * Diffuse or localised (limbs, trunk, chest) * OFF-period pain = most common Mechanisms: * Peripheral = rigidity/dystonia-related * Central = dysfunction in striatal processing of sensory input Evidnece: pain often improves with dopaminergic treatment Other sensory symptoms: RLS, burning sensations, akathisia (also OFF related).
32
# Martinez (hidden sister of motor fluctuations in PD) Sleep disorders
* Common in PD, but not clearly fluctuating * Some nocturnal symptoms (RLS, nocturia) improve with dopamine * ON state effects: psychotropic stimulation may cause insomnia * Conclusion = sleep problems not considered classic NMF
33
# Martinez (hidden sister of motor fluctuations in PD) Evaluation tools | Management of NMF
* No validated specfic tools for NMF
34
# Martinez (hidden sister of motor fluctuations in PD) Treatment of NMF | Management of NMF ## Footnote First line treatment, advanced therapies
First line treatment: 1. Optimise dopaminergic therapy to reduce OFF states (dose splitting, long-acting L-dopa, agnosists) 2. Experimental drugs (safinamide (motor and mood NMF), rotigotine (pain, mood and sleep)). 3. Behavioural therapies (CBT for impulsivity and mood). Advanced therapies: 1. Apomorphine infusion (improves NMS, less evidence for neuropsychiatric effects, risks = compulsive use). 2. Levodopa (provides continuous stimulation (reduces NMF), improves mood, sleep, GI, QOL) 3. Deep brain stimulation (reduces severity, may increase apathy, reduction of meds after DBS may worsen mesolimbic symptoms)
35
# Martinez (hidden sister of motor fluctuations in PD) Conclusion
* NMF are frequent, disabling, and underrecognised. * Strongly impacts QOL and independence. * Should be considered a core target in PD management.
36
# Snowden (neuropsychology of HD) Huntington's disease (HD) | Introduction ## Footnote Definition, prevalence, age of onset, progression
HD: a progressive, inherited neurodegenerative disorder marked by motor, cognitive, and psychiatric disturbances. * Dominated by cognitive and behavioural changes, which often precede motor symptoms, Prevalence: highest in EU Age of onset: * Mean = 40 years * Juvenile = 5% of cases * Late onset = 70s-80s Progression = gradual * Diagnosis may follow 10+ years of underlying changes.
37
# Snowden (neuropsychology of HD) Cause and inheritance of HD | Introduction
CAG trinucleotide repeat expansion in the huntingtin gene on chromosome 4 Inheritance: autosomal dominant, fully penetrant = 50% risk of offspring of an affected parent.
38
# Snowden (neuropsychology of HD) Site of degeneration, pathophysiology and progression | Neuropathology
Site: neostriatum (caudate + putamen) Pathophysiology: mutant huntingtin protein -> neurotoxicity and neuronal death Progression: spreads beyond striatu due to disrupted connectivity.
39
# Snowden (neuropsychology of HD) Triad | Clinical characteristics
Motor, cognitive and neuropsychiatric symptoms Motor symptoms: * Chorea = rapid, involuntary movements (face, trunk, limbs) * Dystonia, bradykinesia, rigidity = parkinsonism-like (more prominent in juvenile) * Insight = affected individuals often underreport motor symptoms Cognitive and neuropsychiatric symptoms: * Less evident but recognition is crucial * Contributes greately to affected person's loss of functional independence * Greatest impact on families
40
# Snowden (neuropsychology of HD) Neuropsychological features: psychomotor slowing | Clinical characteristics
Psychomotor slowing: * Earliest and most predictive symptom * Detected via timed tasks * Significance = appears pre-manifest and predicts functional decline.
41
# Snowden (neuropsychology of HD) Neuropsychological features: Executive dysfunction | Clinical characteristics
* Impairments in planning, organising, sequencing, set shifting, and divided attention. * Automaticity issues (even simple dual tasks are effortful)
42
# Snowden (neuropsychology of HD) Neuropsychological features: memory impairment | Clinical characteristics
* Profile: poorer free recall than recognition/cued recall and executive-related strategies impairement. * Tasks affected: serial reaction time, motor sequence learning. * Underlying cause: frontal strial pathway disruption
43
# Snowden (neuropsychology of HD) Neuropsychological features: emotion processing and social cognition | Clinical characteristics
Emotion recognition deficits: * initially thought specific to disgust * Later shown to affect anger, fear, and cross-modal (vocal) emotions Early symptom, even preclinal. Social cognitive impairments: * theory of mind deficits * Reduced empathy and interpersonal sensitivity * Difficulty recognising sarcasm, social cues, and trustworthiness. * Leads to social breakdown.
44
# Snowden (neuropsychology of HD) Neuropsychological features: other cognitive domains | Clinical characteristics
No aphasia/agnosia/apraxia, but: * Reduced speech, intelligibility due to motor issues. * Complex syntax processing can be hard. Visuospatial impairments: high-level discrimination, integration, mental rotation and visual search. Functional impact: less than psychomotor/executive domains.
45
# Snowden (neuropsychology of HD) Neuropsychiatric features | Clinical characteristics ## Footnote Trajectories and clinical relevance
Apathy, irritability, and depression are most prominent. Trajectories: * Apathy: early onset, progressive * Irritability: peaks mid desease, declines later. * Depression: can occur anytime, may worsen apathy and cognition. Clinical relevance: * Apathy correlates with disease progression. * Irritability may pre-date motor symptoms. * Suicide risk elevated, peaks in prodromes and early functional decline.
46
# Snowden (neuropsychology of HD) Neuropsychological assessment strategy ## Footnote Primary role, core domains to assess, tools, adjust by stage
Primary role: * Early detection * Monitoring progression * Measuring treatment outcomes Core domains to assess: * Psychomotor speed * Executive function * Memory * Emotion recognition * Control for motor and psychiatric effects on test performance. Preferred tools: timed tasks, symbol digit, verbal fluency. Adjust by stage: 1. Early = detect subtle changes (pre-manifest) 2. Late = short, tolerable assessments.
47
# Snowden (neuropsychology of HD) Lab and radiographic investigations ## Footnote Genetic testing, imaging findings
Genetic testing: * CAG repeat testing * Predicts if a person will develop HD, but not when. * Used for diagnosis and research eligibility Imaging findings: * Striatal atrophy even in pre-manifest phase. * Correlates with psychomotor speed and executive dysfunction * Increased cortical activation = neural compensation.
48
# Snowden (neuropsychology of HD) Treatment ## Footnote Pharmacological, non-pharmacological, behavioural
No cure. Pharmacological: * tetrabenazine = for chorea but risk of depression * SSRIs = for irritability and depression Non-pharmacological: * Assistive technology: informal (calandars) and formal (ACT) (use increases with progression, limite evidence for QOL impact). * Cognitive and physical training (evidence of improved executive function, white matter structure and gray matter volume, encouraging but more RCTs needed). Behavioural interventions: * Structure, routine, stimulation help reduce apathy. * Family education is critical * Awareness is often impaired = affects engagement and insight.
49
# Snowden (neuropsychology of HD) Recommendations: diagnosing manifest HD | Conclusion
Include test battery - timed psychomotor tasks, executive function tests, memory tests, emotion recognition etc.
50
# Snowden (neuropsychology of HD) Recommendations: detecting pre-manifest HD | Conclusion
Focus on psychomotor speed, the earliest detectable cognitive deficit Recommended tools: * symbol digit modalities test and stroop test.
51
# Snowden (neuropsychology of HD) Recommendations: for longitudinal assessment | Conclusion
Use timed psychomotor tasks because they are the most sensitive change. Useful in: * Clinical trials * Monitoring progression * Evaluating intervention effectiveness
52
# Snowden (neuropsychology of HD) Recommendations: functional assessment and intervention | Conclusion
For predicting functional ability: * Psychomotor is key predictor of functional decline, reduced independence, lower QOL, and caregiver burden * Executive dysfunction strongly correlates with real-life impairments and need for external support.
53
# Snowden (neuropsychology of HD) Recommendations: cognitive and behavioural interventions | Conclusion
Managing cognitive symptoms: * Encourage single-tasking over multitasking. * Break complex tasks into simple, manageable steps * Use external structure and memory aids to compensate for deficits. Boosting engagement and motivation * People with HD may not initiate activities on their own but they respond well to stimulation and encouragements/guidance. * Use external prompts and structured routiens to reduce apathy and increase paritcipations
54
# Snowden (neuropsychology of HD) Recommendations: multidisciplinary interventions | Conclusion
Combining physical and cognitive training can: * improve executive functions * Enhance brain structures * Support neural compensation
55
# Snowden (neuropsychology of HD) Recommendations: behavioural symptom assessment | Conclusion
Use standardised behavioural scales specific to HD. Include informant reports to supplement patient-reported outcomes, due to common lack of insight.
56
# Ascherio (initiation and prevention of multiple sclerosis) MS and modifiable risk factors | Introduction
MS is multifactorial and caused by interactions between genetic and environmental factors. * Genes play a role but environmental contribution is emphasised. Key modifiable risk factors that influence MS initiation and progression: * Epstein-Barr virus (EBV) infection * Vitamin D deficiency * Cigarette smoking
57
# Ascherio (initiation and prevention of multiple sclerosis) Gene and environment ## Footnote Peak, risk, genetics
MS peaks in young adulthood and declines after age 50 Lifetime risk = 1 in 400 for white non-hispanics Genetics: * Concordance = 25% in monozygotic twins and 5% in dizygotic twins * HLA are the strongest genetic risks. * Rare variant of vitamin D metabolism gene increases MS risk * High heritability but 80-90% of MS patients do not have family history
58
# Ascherio (initiation and prevention of multiple sclerosis) Geography and migration
MS incidence increases with latitude, especially in northern hemisphere * Exceptions: Low MS in artic (genetic protection) and High MS in Sardinia (genetic vulnerability) * This is disapearing in US and EU due to lifestyle or environmental changes Migration: * Young age at migration = MS risk resembles destination * Late migration = retain origin risk * Supports early-life environmental exposure as critical
59
# Ascherio (initiation and prevention of multiple sclerosis) Epstein-Barr Virus (EBV) | Specific risk factors ## Footnote Evidence, mechanisms, prevention
Epidemiological evidence: * Ubiquitous virus; often asymptomatic in adulthood. * Infectious mononucleosis in adolescence (2-3x increased MS risk, but less in kids) * Hygiene hypothesis = increasing hygiene and thus reducing exposures to infections might increase susceptibility to MS (under-exposure so bad immune system). * EBV itself leads to MS but resilience to EBV early in can prevent it due to immune build up. Implications/prevention: * No effective vaccine yet * Potential stategies = early life exposure to EBV and use of EBV biomarkers
60
# Ascherio (initiation and prevention of multiple sclerosis) Vitamin D | Specific risk factors ## Footnote Evidence, mechanisms, prevention
Epidemiological evidence: * Vitamin D status reflects sunlight exposure; deficiency linked to higher MS risk. * High MS incidence in areas with low UV exposure unless diet compensates. * Vitamin D effects also supported by genetic studies Mechanisms: * Vitamin D has immunomodulatory effects (promotes regulatory T cells and lowers pro-inflammatory cytokines, also enhances microbial clearance) Prevention: * Supplementation * May reduce MS incidence and improve outcomes in high-risk groups.
61
# Ascherio (initiation and prevention of multiple sclerosis) Cigarette Smoking ## Footnote Risk, gender differences, mechanism
* Smoking increases risk by 50% with dose-dependent effect. * Stronger effect in men, may explain rising female:male MS ratio Mechanisms: * Promotes inflammation, blood-brain barrier disruption, demyelination, and autoimmunity Snuff is not associated with MS = points to inhalation-specific harm.
62
# Ascherio (initiation and prevention of multiple sclerosis) Integration of risk factors | Specific risk factors
* EBV, low vitamin D, and smoking contribute independently. * Combined risk = 8x * EBV antibody titre is the strongest non-genetic predictor. * Combined with genetics, risk may increase, though the absolute risk remains low.
63
# Ascherio (initiation and prevention of multiple sclerosis) Conclusion ## Footnote Best prevention strategies and future potentials
Best current prevention strategies: * Vitamin D supplementation * Smoking cessation Future potential: * EBV-targeted treatments or vaccines.
64
# Kington (executive function deficits in FASD and ADHD) Fetal Alcohol Spectrum disorder (FASD) | Introduction ## Footnote Definition, symptoms (3 areas), Partial FAS
Extreme conseqeunce of alcohol exposure during pregnancy with executive functions being the key to their functional impairments (esp academic and adaptive domains). Characterised by symptoms in 3 areas: * Prenatal/postnatal growth retardation * Craniofacial abnormalities * CNS dysfunction (cognitive and behavioural abnormalities) Partial FAS = those who do not have all characteristics but evidence of some dysmorphic characteristics.
65
# Kington (executive function deficits in FASD and ADHD) FASD vs ADHD cognitive profiles differences | Introduction
FASD = unresponsive to stimulant medication and better academic and cognitive outcomes if idetified/treated early. ADHD = more behavioural and neuropsychological impairments.
66
# Kington (executive function deficits in FASD and ADHD) Executive functions | Executive functions ## Footnote Definition
Includes higher-order cognitive skills for goal-directed behaviour such as WMM, planning, inhibition, cognitive flexibility etc. It is multidimensional and involves prefrontal cortex and its connections
67
# Kington (executive function deficits in FASD and ADHD) EF and FASD | Executive functions ## Footnote Cause, deficits in.., long-term impact on..
Caused by prenatal acohol exposure Leads to pervasive neurodevelopmental disruption EF deficits in: WM, Planning, Inhibition, Cognitive flexibility Long-term impact on academics, social behaviour and adaptive functioning
68
# Kington (executive function deficits in FASD and ADHD) EF and ADHD | Executive functions ## Footnote Disorder (genetics and onset), deficits in..
Highly heritable disorder with onset in childhood Deficits in EF are central to ADHD pathology, especially in inhibition, WM, and self-regulation. However, impairments are typically less global than in FASD.
69
# Kington (executive function deficits in FASD and ADHD) Behavioural ratings of EF | Executive functions
* Performance-based EF tests = controlled conditions * Behavioural ratings (ex: BRIEF) = real-world functioning
70
# Kington (executive function deficits in FASD and ADHD) Aims and Hypotheses | Methods ## Footnote 3
Which domains of EF are most consistently impaired in children with FASD, compared to controls (TD)? * Expected to result in significant differences, reflecting deficits in a wide range of EF * No predictors about the magnitudes of differences Is the pattern and magnitude of defcits in children with dysmorphy greater than children without dysmorphy (partial FAS) compared to TD? * Both groups expected to significantly differ from TD Is the neurocognitive profile more globally impaired in FASD compared to ADHD? * EF expected to significantly differ between them on all measures expect attentional vigilance, WM and response inhibition.
71
# Kington (executive function deficits in FASD and ADHD) FASD vs Controls (TD) | Results
* Moderate EF impairments for FASD vs TD * FASD more consistently large deficits in planning, fluency, set-shifting, and WM compared to TD * FASD has moderate deficits in vigilance and inhibition compared to TD
72
# Kington (executive function deficits in FASD and ADHD) Partial FAS vs TD | Results
Moderate EF * Large deficits in planning, fluency, set shifting * Moderate deficits in WM
73
# Kington (executive function deficits in FASD and ADHD) Performance-based EF | Results ## Footnote FASD, ADHD, TD
* FASD showed significantly lower scores across all EF tasks * ADHD showed impairmed on WM takss, but not as broad. * TD outperformed both clinical groups.
74
# Kington (executive function deficits in FASD and ADHD) BRIEF Ratings | Results ## Footnote FASD and ADHD
* Both FASD and ADHD rated significantly more impaired than TD * FASD showed more metacognitive difficulties than ADHD * ADHD showed more behavioural regulation problems than FASD
75
# Kington (executive function deficits in FASD and ADHD) EF and Academic performance | Results
* EF, especially WM, significantly predicted reading and math performance * Strongest associations seen in FASD group
76
# Kington (executive function deficits in FASD and ADHD) Summary of key findings | Discussion
Both FASD and ADHD have EF impairments, but FASD is more severe and global. Bheavioural ratings show that real-life EF problems differ by disorder: * FASD = poor planning, orgnaisation (MI) * ADHD = impulse control, emotional regulation (BRI). Working memory is a critical cognitive marker and predictor of academic success.
77
# Kington (executive function deficits in FASD and ADHD) Overlap vs distinction | Discussion ## Footnote Shared features vs distinct features between FASD and ADHD
Shared features: * EF deficits * Poor WM * Academic struggles Distinct features: * FASD = broader, ADHD = more behavioural. * FASD = worse on planning and shifting * ADHD = more impuslivity-driven
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# Kington (executive function deficits in FASD and ADHD) Conclusion
* FASD and ADHD may appear behaviourally similar but differ cognitively * Performance tests + behavioural ratings together offer the best insight. * EF testing should be routinely integrated into assessments for both groups.

NeuroPsychology (4 decks)

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