Lecture 14- Dementia and delirium Flashcards
Dementia summary
Dementia is a syndrome (usually progressive) characterised by an appreciable deterioration in cognition resulting in behavioural problems and impairment in the activities of daily living. Decline in cognition is extensive, often affecting multiple domains of intellectual functioning
- Alzheimer’s most common (50-70%)
- Women>men
- Vascular dementia (25%)
- Lewy body (15%_
- Frontotemporal dementia
- AIDS-dementia complex
pathophysiology of alzheimers dementia
- Global atrophy of brain lobes
- Mostly frontal, parietal and temporal lobes
- Sulcus widening
- Enlarged 3rd and 4th interventricular space

2 theories for AD
amyloid hypothesis
abnormal aggregation of Tau protein
The amyloid hypothesis – 1st theory

Abnormal aggregation of the Tau protein- 2nd theory
- Tau is a microtubule associated protein that stabilises microtubules in the cell
- Tau accumulates into intraneuronal masses known as neurofibrillary tangles and as dystrophic neurites
- Abundance of tangles roughly proportion to the severity of clinical disease and cognitive decline
AD RF
- Head injury
- High serum cholesterol and fats
- Lifestyle factors: smoking, midlife obesity and diet high in sat fats
AD history: questions to ask
- Ask RF (inc family history of down syndrome)
- Memory loss –> loss of recent first
- Disorientation to time and place (misplacing items/getting lost)
- Nominal dysphasia à proper name sand low-frequency words decline first
- Apathy
- Decline in ADLs
- Personality/ mood change
Management of AD
- Carer support (OT, community services, ID bracelets)
-
Pharmacological
- Cholinesterase inhibitors
- Antidepressants
- Antipsychotics (controversial)

Vascular dementia pathophysiology
- Common endpoint of many vascular pathologies intracranially
- Infarction
- Leukaoraisois –> disease of white matter also called subcortical leukoencephalopathy
- Haemorrhage
- Alzheimer’s disease –> although not classified as a vascular pathology, AD has a strong vascular risk- factor spectrum

vascualt dementia : history questions to ask
- History of stroke
- Difficulty solving problems
- Apathy
- Disinhibition
- Slow processing
- Poor attention
- Retrieval memory deficit
- Risk factors similar to IHD
Management of VD
Basically reducing risk of further sclerotic/embolic effects
- Antiplatelet therapy/Anticoagulation
- Lifestyle modification
- BP control if HTN
- Statin therapy if elevated LDL cholesterol
- Optimisation of glycaemic control if diabetic
- Carotid endarterectomy if carotid stenosis >70%
- Cholinesterase inhibitors or memantine if concomitant AD
Lewy body dementia pathophysiology
*
- Accumulation of lewy bodies in vulnerable sites of the CNS
- substantia nigra
- temorpal lobe
- frontal lobe
- cingulate gyrus
what are lewy bodies
- Lewy bodies are composed of protein alpha-synuclein, a cytoplasmic protein associated with synaptic vesicles. Other proteins include neurofilament and ubiquitin
- The distribution and density of Lewy bodies are thought to be correlated with clinical syndromes
- Co-existing AD pathology is common
Parkinson’s or Lewy body dementia?

lewy body dementia history taking
History
- Risk factor = old age
- Cognitive fluctuations
- Hallucinations, typically visual and complex; up to 80% of patients
- Motor symptoms → Parkinsonian features present in >85% of patients
- Vivid dreams are accompanied by loss of associated atonia of REM sleep; ‘acting out’ dreams
- Depression
- Repeated falls/syncope
- Urinary incontinence
- Constipation
management of lewy body dementia

Frontotemporal dementia
Aetiology
- Focal neurodegeneration of the frontal or temporal lobes of the brain
- Strong family history

frontotemporal dementia pathophysiology
Pathophysiology
Definitive diagnosis depends on the pathological examination of brain tissue, and identification of patterns of neuronal injury and characteristic intra-neuronal and glial cell inclusions. Specific accumulations found:
- FTD-tau
- FTD-U (ubiquitin)
classification of FTD
3 behavioural presentations of FTD
- Apathetic
- Disinhibited
- Stereotypic
Can be overlapping
Distinction between behavioural FTD vs Primary progressive aphasia
History FTD
- Coarsening of personality, social behaviour, and habits
- Progressive loss of language fluency or comprehension
- Development of memory impairment, disorientation, or apraxias
- Progressive self-neglect and abandonment of work, activities, and social contacts
- Age at onset peak in mid-50s
- FHx
- Altered eating habits
Management of FTD
*not standard dementia medication*
Dependent on patient need:
- Acute irritability, restlessness, agitation, or aggression → benzos
- Home-assistance, respite care
- Compulsions → SSRIs
- Sleeping disturbance → Mirtazapine 1st line
- Distractibility → amantadine
- Gluttony → topiramate
AIDs dementia complex pathophysiology
- As patients with HIV infection live longer thanks to modern treatments, their chance of developing AIDS associated dementia is increasing
- HIV-infected macrophages enter the brain, causing indirect damage to neurones
- Insidious onset, but rapid progression once established
Clinical features of AIDs dementia complex
- Related to global damage but also some manifestations of cerebellar involvement:
- Cognitive impairment
- Psychomotor retardation (slow thoughts and movements, also seen in depression)
- Tremor Ataxia Dysarthria Incontinence






