236 - Dementia Flashcards
what is the diagnostic criteria for dementia?
acquired memory impairment for at least 6m plus impairment in one or more cognitive domains:
- executive functioning - abstract thinking, judge, reason
- language - expressive and receptive
- praxis - learned motor tasks
- gnosis - ability to recognise objects, faces, sensory info
what is the prevalence of dementia?
5% of >65s but 22% of 85-90 - 20 million worldwide
name some differentials for dementia?
- depression - low mood, worthlessness, guilt, suicide, anhedonia, appetite change, sleep disturb, fatigue, conc - also pseudodementia (aware of memory loss)
- delirium - acute confusion sudden onset and fluctuating. associated with physical illness (infection, drugs, alcohol)
- vitamin deficiency. vit B1 (thiamine) >wernickes, B12, folate
- hypothyroidism - depression
- hepatic/renal impairment
- normal pressure hydrocephalus -abnormal CSF resorption - enlargement of ventricles and compression
what is the difference between dementia and mild cognitive impairment?
does not interfere with activities of daily living
who does alzheimers affect?
- > 50% of dementias
- > 70s and more females 2:1
- family hx - apolipoproteins E-4 allele and Presenilin
- down’s syndrome
- head injuries
what is thought to cause alzeimers?
- neurofibrillary tangles - changes to Tau proteins that act as glue to hold neuron microfobrils together
- senile plaques - extracellular deposits of amyloid in grey matter between neurons or cerebral blood vessel walls. Especially in hippocampus (memory area)
- cerebral cortex atrophy - association regions and medial temporal lobe
- overactivation of NMDA receptors by glutamate. deficiencies in reuptake by astroglial cells in synaptic cleft
- leads to cholinergic dysfunction and cholinergic input to hippocampus and amigdala from basal forebrain
what is the difference between alzheimers and vascular dementia?
- AD - dementia with insidious onset and progressive gradual decline.
- VD - Abrupt onset, stepwise deterioration, fluctuating cognitive performance, gait and incontinence, neuro signs (focal deficits/stroke), evidence of vascular disease on brain imaging
who does vascular dementia affect and what causes it?
- 20-25% of dementias
- > 60s, more male than female, hypertensives and those with cardiovascular risk factors
- either focal (2ndry to thrombtic or embolic vascular occlusion - affects white matter or cerebrum and deep grey nuclei of thalamus and striatum) r difuse (2ndry to HTN or stenosis of vessels)
what is dementia with Lewy bodies?
- 10-15% of dementias
- Lewy bodies are intracellular aggregates of alpha-synuclein protein causing disruption to dopaminergic and cholinergic systems of brain
- criteria - dementia plus one of: visual hallucinations, parkinsonism, reduced alertness plus one of: REM behaviour disorder or non specific neuro signs. If symptoms soon after parkonism then DLB
what is fronto-temporal dementia?
- picks disease
- fronto-temporal atrophy
- early onset, more males, behavioural changes (personality and inappropriate behaviour), loss of speech with memory and skills intact, FH
how could a patient with dementia be assesed?
*mini mental exams
- Addenbrookes Cognitive Exam (ACE III)
- Montreal Cognitive Assessment (MoCA)
6 item CIT (Kingshill)
*Clock drawing test
*CT to exclude other path
*MRI - regional atrophy and cerebrovascular disease
how would you manage mild to mod alzheimers and DLB?
- Aceytlcholinesterase Inhibitors eg donepezil, rivastigimine, galantamine
- inhibit ACh breakdown and incr conc in synaptic cleft
- gastric irritation and ulceration, bradycardia, epilespy, asthma, prostatism
how would you manage advanced alzeimers or mild AD when unresponsive to ACh-esterase?
- NMDA receptor antagonists eg memantine
* inhibits glutamate by blocking NMDA receptors - reduces glutamate’s excitotoxic effects
how would you treat vascular dementia?
aspirin, statin, BP management and glucose management, lifestyle change
what is neurodegeneration and what causes it?
- chronic, progressive neuronal loss
- genes and toxins by:
- apoptosis
- autophagia
- necrosis by:
- infarction, neuroinflammation
- misfolded proteins > plaques and hyperphosphrylated Tau (tangles)
- oxidative stress
- glutamate release after cell death> cycle
what types of memory are there?
- short term memory
- long term memory - short term made perm
- working memory - held for mins to complete task
- declarative (explicit) - semantic memories (concepts) and episodic (autobiographical) - stored in medial temp lobe, thalamus and hypothalamus
- non-declarative (implicit) - procedural memory/skills/habits in striatum, motor learning in cerebellum and emotional conditioning in the amygdala
what types of amnesia are there?
- retrograde
- anterograde
- transient global amnesia - both retro and antero
how is memory created?
sensory input > cortical association areas (identify stimulus, make sense and plan) > parahippocampal /rhinal cortices (storage of long term memory > hippocampus (consolidation of short term/working memory into long term) > mamilary bodies (hypothalamus) and thalamus (recognition, smell, emotion)
what do the hippocampus and amygdala do?
- hippocampus - learning of newinfo, consolidation to long term memory with cortex communication, place memory
- amygdala - emotional info learning and its consolidation
what is affected in korsakoffs syndrome
- irreversible damage to medial thalamus and maillary bodies - caused by thiamine (vit B1) deficiency - may also cauuse Wernickes encephalopathy
- causes antero/retrograde amnesia and cofabulation (cannot distinuish between imagination and memory)
what does each lobe of the brain do?
- occipital - visual cortex
- parietal - attending to stimuli (where is it)
- temporal - identify nature of stimuli (what is it)
- frontal - planning appropriate response (what should I do about it)
what is the parietal cortex responisible for?
- integration of visual, auditory and somatosensory information
- damage causes sensory neglect, conceptual neglect, motor neglect and hemiasomatognosia (denial that part of body is theirs) on contralateral side of body
what is apraxia/
inability to carry out a motor task in response to a spoken command
what is the temporal cortex responsible for?
- identifying nature of stimuli
- damage causes agnosia (loss of knowledge)
- inf temp cortex - visual agnosia (cant identify objects)
- fusiform gyrus (med temp occipital) - prosopagnosis (cant identify faces)
- middle temp cortex - movement agnosia (cant tell between stationary and moving)
what is the frontal cortex responsible for?
- mediates behaviour - restraint, intiative and order
- damage causes inability to plan sequence of events, loss of thought flexibilty, perservation, loss of focus, passivity, apathy, expressive aphasia
what are wernickes and brocas areas responsible for/
- wernickes- understanding speech
* brocas - makes speech
what are wernickes and brocas aphasia?
- wernickes - inability to understand language - fluent speech but makes no sense (little repetition but good syntax and grammar)
- brocas - ability to understand language but inability to produce own halting speech - repetitive, disordered syntax and grammar
