Geriatrics- Dementia Flashcards
What is dementia?
1 an acquired deficit of cognition
2 multiple domains of cognitive impairment (2 or more) affected
3 often includes memory impairment
4 cognitive impairment not due to disturbance of arousal / wakefulness / consciousness
5 deficits sufficient to interfere with social and work activities
6 can be reversible
dementia syndrome
- deterioration from a prior level of intellectual function
- interferes with activities of daily living
- > 1 category of intellectual performance affected
- independent of level of consciousness
-deterioration supported by historical evidence - documented by cognitive tests that are quantifiable, reproducible & for which normative data are available
the dementia syndrome
cognitive decline
behavioural & psychological symptoms
impairment in activities of daily living
What are the primary neurodegenerative diseases that cause dementia?
Alzheimer’s Disease
Vascular Dementia
Lewy Body Disease
Frontotemporal Dementia
What are some secondary systemic and potentially treatable causes of dementia?
Vitamin B-12 Deficiency
Hypothyroidism
What structural brain lesions can lead to dementia?
Tumors
Subdural Hematomas
Large Strokes
Hydrocephalus
What infections of the nervous system can cause dementia?
Neurosyphilis
HIV Infection
Differential diagnosis of dementia
anxiety / depression (“depressive pseudo-dementia”)
delirium
Clinical approach
is there cognitive impairment?
- history from patient & informant
- mental state exam incl. cognitive test such as MMSE
- physical exam: any systemic or other neurological abnormalities to account for symptoms?
- could the symptoms & signs be explained by delirium, anxiety or depression?
-investigations
investigations
- cognitive tests e.g. MMSE
- haematology: FBC, ESR
- biochemical U&E, Cr, liver tests, cholesterol, glucose
- serum B-12, serum & red cell folate
- thyroid function
- syphilis serology
- CT scan brain
HIV test
MRI scan
Cerebral perfusion SPECT scan
EEG
lumbar puncture CSF
What are the types of cortical dementias?
Alzheimer’s Disease
Multi-Infarct Vascular Dementia
Frontotemporal Dementia (Pick’s Disease)
Lobar / Focal Dementias:
- Primary Progressive Aphasia
- Semantic Dementia
- Posterior Cortical Atrophy
What are the types of subcortical dementias?
Small Vessel Subcortical Ischaemic Vascular Disease
HIV Dementia
Lewy Body Disease
Parkinson’s Associated Dementia
Other Parkinsonian Syndromes
Huntington’s Disease
Normal Pressure Hydrocephalus
What types of dementia involve both cortical and subcortical regions?
Prion Diseases (e.g., Creutzfeldt-Jakob Disease)
What are the key differences between cortical and subcortical dementia?
Location of Damage:
Cortical Dementia: Primarily affects the cerebral cortex, leading to impairments in higher cognitive functions.
Subcortical Dementia: Involves damage to the subcortical structures (e.g., basal ganglia, thalamus), affecting motor control and emotional regulation.
Cognitive Symptoms:
Cortical Dementia: Often presents with significant memory loss, language difficulties (aphasia), and perceptual deficits. Common examples include Alzheimer’s disease and frontotemporal dementia.
Subcortical Dementia: Typically features slower cognitive processing, executive dysfunction, and changes in mood or behavior, rather than prominent memory loss. Examples include Lewy Body Disease and Huntington’s disease.
Progression:
Cortical Dementia: Symptoms may progress steadily over time, with clear changes in cognitive function.
Subcortical Dementia: Progression can be more variable, often linked to the underlying disease process (e.g., Parkinson’s).
Physical Symptoms:
Cortical Dementia: Less emphasis on physical symptoms; may see changes in motor function in later stages.
Subcortical Dementia: Often associated with motor symptoms (e.g., tremors, rigidity) early in the disease course.
What are the key features of cortical dementias?
Higher Cortical Functions Affected:
Amnesia: Memory impairment, particularly short-term memory loss.
Dysphasia: Difficulty with language, including speaking or understanding speech.
Dyspraxia: Impaired ability to plan and execute coordinated movements.
Agnosia: Inability to recognize objects, faces, or sounds despite intact sensory function.
Other Cognitive Impairments: Problems with reasoning, judgment, and problem-solving.
What are the key features of Alzheimer-type pathology?
Plaques and Tangles:
- Senile (Neuritic) Plaque:
Thick Arrow: Characterized by the accumulation of beta-amyloid peptides, contributing to neurodegeneration.
- Diffuse Plaque:
Small Arrow: Less dense, more widespread accumulation of beta-amyloid.
Neurofibrillary Tangles:
Star: Composed of hyperphosphorylated tau protein, leading to neuronal dysfunction and cell death.
Beta-Amyloid Angiopathy:
The deposition of beta-amyloid in the walls of blood vessels, increasing the risk of hemorrhage
Brain Atrophy:
Generalized shrinkage of brain tissue, particularly in the hippocampus and cerebral cortex, correlating with cognitive decline.
What is Braak staging, and how does it relate to Alzheimer’s disease?
Definition:
Braak staging is a classification system based on the progression of neurofibrillary tangle pathology in the brain.
Stages:
Stage I: Tangles begin in the entorhinal cortex, which is involved in memory processing.
Stage II: Tangles spread to the limbic system, affecting emotional responses and memory.
Stage III: Tangles extend into the neocortex, impacting higher cognitive functions.
Progression:
The disease typically progresses from the entorhinal area through the limbic system and into the neocortex, correlating with increasing cognitive impairment.
Cognitive symptoms
- amnesia (dysnesia)
amnestic MCI = prodromal clinical phase. Episodic memory loss. Limbic (hippocampal) disease. R vs. L hippocampus. Ribot’s law (“last in, first out”)
2 aphasia (dysphasia)
3 apraxia (dyspraxia)
4 agnosia
5 frontal executive function impairment
6 other – dyslexia, dysgraphia, acalculia, L R disorientation
non-cognitive symptoms
- psychotic – delusions, misidentifications, hallucinations
- mood – depression, anxiety, euphoria.
- behavioural – apathy (70%), agitation (30%), wandering (20%), physical & verbal aggression.
- changes in sleep pattern
- feeding & eating difficulties
- sexual disinhibition
- personality changes
physical symptoms & signs
neurological – primitive reflexes, gait & balance disturbances, stooped posture, myoclonic jerks, seizures, bilateral pyramidal & extrapyramidal signs (late).
incontinence – urinary & faecal
general – weight loss
natural history & progression
episodic & autobiographical memory language deficits visuo-spatial deficits (topographical memory & dressing apraxia) frontal defects.
varies from person to person
difficult to give accurate individual predictions
time to institutionalization:
mild AD: 12% by 1 year; 35% by 2 years
severe AD: 39% at 1 year; 62% by 2 years
time to death: 1 to 16 years. median survival: 5 – 6 years
cause of death? Often systemic infection e.g. pneumonia, UTI
management (I)
- no specific treatment
- explanation to family
- drugs: cholinesterase inhibitors: donepezil, galantamine, rivastigmine; NMDA–R antagonist: memantine
- support for carersgroups e.g. dementia SA
- management of behavioural symptoms: non-pharmacological
- use of anti-psychotics e.g. haloperidol, risperidone, quetiapine
- treatment of intercurrent systemic illnesses
- driving
- testamentary capacity
- placement
What cognitive speed change is commonly seen in subcortical dementias?
Bradyphrenia: This refers to slowness of cognitive processing speed
What emotional state is often observed in patients with subcortical dementia?
Apathy: Patients may show a lack of motivation or interest in activities
