w3: MCI + Alzh Flashcards
Why Differentiate Between Depression and Dementia?
Importance:
Misdiagnosis can delay appropriate treatment.
Depression is often reversible; dementia generally is not.
Accurate diagnosis informs effective interventions and improves quality of life.
Overlap: Both can present with cognitive and emotional symptoms, making differentiation challenging.
Risks:
Depression increases the likelihood of developing dementia.
Older adults with untreated depression may experience accelerated cognitive decline.
Key Differences Between Depression and Dementia
Subjective Complaints:
Depression: Significant cognitive complaints, often out of proportion to objective findings.
Dementia: Less awareness of cognitive problems or minimisation of issues.
Severity of Cognitive Impairments:
Depression: Milder impairments; may stabilise or improve with treatment.
Dementia: Severe and progressively worsening deficits.
Memory Performance:
Depression: Improved recall with cues; difficulties stem from executive dysfunction.
Dementia: Poor recall even with cues; linked to hippocampal and cortical pathology.
Qualitative Patterns:
Depression: Generalised, non-specific deficits; subcortical profile (processing speed, verbal fluency).
Dementia: Domain-specific impairments; cortical profile (memory, visuospatial skills).
Effective Diagnostic Techniques
Clinical Assessment:
Focus on how each disorder contributes to emotional, behavioural, and cognitive functioning.
Educate medical team, patient, and family.
Screening for Depression:
Use psychometric instruments:
Beck Depression Inventory-II (BDI-II)
Hamilton Depression Rating Scale (HDRS)
Geriatric Depression Scale (GDS)
Neuropsychological Evaluation:
Use structured memory tasks (e.g., California Verbal Learning Test).
Repeated assessments to monitor progression:
Improvement or stability = Likely depression.
Continued decline = Suggestive of dementia.
Patterns in Cognitive Profiles
Depression:
Responds to treatment.
Effort-related deficits; struggles with delayed recall but improves with cues.
Subcortical deficits: slower processing, verbal fluency issues.
Dementia:
Structural brain changes and progressive decline.
Poor recall despite cues; recognition impaired.
Domain-specific impairments (e.g., memory in Alzheimer’s).
Considerations for Coexisting Conditions
History of depression increases the risk of persistent cognitive impairments.
Vascular disorders (e.g., stroke, hypertension) moderate the relationship between depression and dementia.
Depression can accelerate cognitive decline and the progression from Mild Cognitive Impairment (MCI) to dementia.
Differential Diagnosis Tips
Medication Review: Check for medications causing depression-like symptoms (e.g., beta-blockers, corticosteroids).
Cued Recall Tasks:
Depression: Better performance with cues.
Dementia: Limited benefit from cues.
Dual-Tasking and Praxis:
Depression: Performs better on dual-tasking.
Dementia: Struggles significantly.
Serial Position Effect:
Depression: U-shaped pattern (better recall of early and late list items).
Dementia: Recency advantage (better recall of late items only).
Key takeaways depression and dementia
Depression reflects effort-related deficits and stabilises with treatment.
Dementia reflects structural brain changes and shows progressive decline.
Late-life depression with cognitive impairment raises concerns for underlying dementia.
Screening, objective assessments, and monitoring are critical for effective differentiation.
Normal Aging: Key Facts
life expectancy, cognitive changes and practical implications
Life Expectancy:
Average: 76 years for men, 81 years for women in the US.
Fastest-growing age group: “Oldest old” (85+ years).
Cognitive Changes:
Preserved Abilities:
Implicit memory (skills/routines).
Vocabulary and general knowledge.
Declined Abilities:
Processing speed, working memory, executive control, memory (e.g., source/contextual recollection), and visuospatial abilities.
Practical Implications:
Regular neuropsychological testing is vital to distinguish normal aging from pathological decline.
Structured environments and compensatory strategies can aid cognitive functioning.
Theories of Normal Aging
dedifferentiation theory, processing-speed theory, scaffolding theory
Dedifferentiation Theory:
Decline in neural specificity; sensory and cognitive functions become more interrelated.
Implications:
Sensory impairments may cascade into broader cognitive challenges.
Neural reorganisation compensates for hippocampal and temporal lobe decline.
Processing-Speed Theory:
Cognitive decline driven by slower information processing.
Impacts:
Tasks requiring quick, complex operations.
Reduced synchronisation between cognitive stages.
Scaffolding Theory:
The brain compensates for structural decline by recruiting additional resources.
Mechanisms:
Strengthening or forming neural connections.
Involves the prefrontal cortex for compensatory processing.
Structural Brain Changes in Aging
Overview:
Volumetric shrinkage, white matter density decline, loss of dopaminergic receptors, and accumulation of neurofibrillary tangles and plaques.
Affected Brain Areas:
Hippocampus: Memory and navigation.
Prefrontal Cortex: Executive functions.
Cerebellum: Motor skills.
White Matter: Myelin degradation slows signal transmission, affecting multitasking and problem-solving.
Functional Changes:
Increased bilateral activation during tasks, compensating for structural decline.
Cognitive Changes in Normal Aging
Processing Speed:
Slower visual-motor tracking, sequencing, and set-shifting.
Earlier processed information may decay before integration.
Working Memory:
Reduced capacity to hold/manipulate temporary information.
Affects multi-step problem-solving and reasoning.
Executive Control:
Difficulty suppressing irrelevant stimuli and slower decision-making.
Memory:
Preserved: Gist retention.
Declined: Source memory and contextual recollection.
Language:
Word-finding difficulties (“tip of the tongue”).
Declined verbal fluency (semantic and lexical).
Visuospatial Abilities:
Challenges in visuoperception, visuoconstruction, and spatial orientation.
Mechanisms of Decline
normal ageing
Slowed Processing Speed:
Impacts task efficiency and accuracy.
Causes fragmented understanding due to information decay.
Reduced Inhibitory Control:
Difficulty filtering distractions, leading to attentional dysregulation.
Effortful vs. Automatic Processing:
Effortful processing declines, but automatic processing remains intact.
Practical Implications- of normal decline
Preservation of Abilities:
Use tasks reliant on gist memory or familiar stimuli.
Compensatory Strategies:
Minimise distractions; provide structured cues for effortful tasks.
Clinical Assessment:
Monitor changes regularly through neuropsychological testing to detect early pathological conditions.
Individual Factors in normal Cognitive Aging
Cognitive Reserve:
Dense neural networks and efficient synaptic connections enhance resilience.
Education and occupational complexity build cognitive reserve.
Physical Health:
Cardiovascular/metabolic health and sensory function impact cognition.
Interplay of Factors:
Education, health, and occupation interact to influence cognitive outcomes.
Dementia Definitions
Dementia is a syndrome due to disease of the brain, usually
chronic, characterized by a progressive, global deterioration in
intellect including memory, learning, orientation, language,
comprehension and judgment
Consequence: loss of independent living skills (both social and workrelated)
Mild Cognitive Impairments (MCI)
subjective and objective cognitive symptoms greater than expected
for an individual’s age and education level which do not interfere with
activities of daily life
MCI can be a transitional stage between “normal” aging and dementia
Current Clinical Diagnostic Criteria (NIA-AA, 2011)
MCI
Concern Regarding Cognitive Change:
Evident decline from prior functioning.
Concerns may come from:
The patient.
An informant (family, friend).
A clinician.
Impairment in One or More Cognitive Domains:
Cognitive performance below age/education expectations:
Memory: Difficulty learning/recalling information.
Attention: Trouble focusing or filtering distractions.
Language: Word-finding difficulties.
Executive Function: Issues with planning, decision-making.
Visuospatial Skills: Navigational challenges.
Preserved Functional Independence:
Independence in daily life maintained, with mild inefficiencies in complex tasks (e.g., paying bills).
Not Demented:
Cognitive changes do not impair social/occupational functioning significantly.
Requires evidence of intraindividual change through clinical history or repeated evaluations.
Subtypes of MCI
-
Amnesic MCI (a-MCI):
o Primary impairment in the memory domain.
o Often considered a precursor to Alzheimer’s Disease.
single domain: : impairments are evident in one memory domain
–> AD
multiple domain: impairments are evident in more than one domain (memory + other)
–> AD/VaD
-
Non-Amnesic MCI (na-MCI):
o Impairment in non-memory domains (e.g., attention, executive function, visuospatial skills).
o May be linked to other conditions such as vascular dementia or Parkinson’s Disease.
single domain: impairments are evident in one cognitive domain
multiple domain: impairmets evidenct in more than one cogntive domain
risk of = FTD, DLB, PDD
Clinical Importance MCI diagnosis
- Early Identification:
o MCI represents a critical window for intervention and monitoring, as it may progress to dementia, particularly Alzheimer’s Disease. - Assessment Challenges:
o Differentiating between normal aging, MCI, and early dementia requires careful clinical evaluation and neuropsychological testing. - Treatment Implications:
o Lifestyle modifications (e.g., diet, exercise), cognitive training, and management of comorbid conditions (e.g., hypertension, diabetes) can slow progression.
o Regular follow-ups to monitor changes in cognition and function are essential
