Neurology: AD, VD, LBD, FTD, PD, ET Flashcards
AD
- epidemiology
- genetic, environmental risk factors
- pathophysiology
MOST COMMON DEMENTIA Genetic -sporadic, late - APOE4 -inherited - APP, PSEN1,2 -Downs
Environment
- brain/SC injury, CVA
- drugs, alcohol, vitamin deficiency, hypoglycemia
- HIV, HSV, syphilis
Pathophysiology
- cerebral atropy, esp hypothalamus - wide sulci, narrow gyri, large ventricles
- extracellular amyloid plaque, intracellular tau tangles
AD
- presentation
- management specific to AD
- drugs to avoid
Gradual cognitive decline
- poor short term memory
- confusion, increased anxiety
Later
- agnosia, aphasia, apraxia, amnesia
- hallucinations, depression, delusions, disinhibition
NORMAL GAIT, POSTURE
Drug 1st line - cholinesterase inh -donepezil, rivastigmine, galantamine 2nd line - NMDA ant -memantine
Avoid antidepressants
Antipsychotics only to be used if risk to self/others
VD
- epidemiology
- pathophysiology
- risk factors
2nd most common dementia
-CV risk factors damage brain => synergy with AD
Vascular risk factors
- Stroke, TIA, AF, CVD
- HTN, DM, high cholesterol, smoking
VD
- presentation
- investigations, diagnosis
Stepwise progression in cognitive decline
- focal neuro deficits
- attention, concentration
- memory, gait, speech, emotional disturbances
Diagnostic criteria
- presence of cognitive decline that interferes with ADLs - confirmed with clinical neuropsych examination
- CV disease - confirmed with neuro signs/brain imaging
- relationship between decline and CVD - onset of dementia within 3 months of stroke/abrupt or fluctuating stepwise decline
VD
-management specific to VD
If comorbid with AD/LBD - same as AD
Vascular optimisation to slow progression
Supportive management for all
Tailored to individual
- cognitive stimulation programmes, music/arts therapy
- home adaptations
- physio for movement difficulties
- SALT input for speech and swallow
Differentials you want to rule out
-reversible causes
Drugs - medication review (BZ, opioids, anticholinergics, antipsychotics, antidepressants, alcohol)
Endocrine - hypothyroid, Addisons
Mental - depression
Nutritional - B12 (ataxia, memory loss, gait abnormalities), thiamine deficiency (Wernicke’s enceph, Korsakoff psychosis)
Trauma - subdural haemorrhage
Malignancy - brain tumour
Infection - syphillis
LBD
- epidemiology
- pathophysiology
- presentation
- diagnosis, investigation
- presentation
3rd most common dementia
-asynuclein in SNPC
Fluctuating cognitive impairment Followed by Parkinsonian symptoms -visual hallucinations -falls, gait instability -incontinence, constipation, RBD
Clinical diagnosis - confirm with DATSCAN
Management - same as AD
-avoid neuroleptics
FTD
- epidemiology
- pathophysiology
- types and presentation
Most common in U65
-atrophy of FTL, neurofibrillary tangles
50% - Behavioural variant - executive cognitive dysfunction
- early disinhibition, loss of empathy, impulsivity
- hyperorality, dietary change
- other cognitive areas
50% - Language variant
Semantic dementia - problems with matching names to objects
Non fluent aphasia - slow hesitant speech,
-difficulty finding right word
-grammatical errors, difficulty understanding complex sentences
FTD
-management specific to FTD
Do not use cholinesterase inh/memantine
Pharmacological management when conservative measures have failed
-irritability - lorazepam
-compulsions - SSRIs (citalopram)
PD
- epidemiology
- genetic, environmental risk factor
Men, 65+
Most are idiopathic
Genetic - PARK1 gene overexpressed
Environmental - unclear
Degeneration of dopaminergic neurons in SNPC => Lewy body formation
PD presentation
-prediagnosis - non brain signs
Prediagnosis
- constipation
- autonomic dysfunction => OH, urogenital dysfunction
- anosmia, visual changes
- REM behaviour disorder
- depression+anxiety
- face-like mask
- micrographia
PD presentation
- early stage
- late stage
Early stages - classic unilateral triad
- bradykinesia - shuffling, difficulty initating mv, reduced arm swing
- cogwheel rigidity
- pillrolling resting tremor - worse when stressed/tired, improves with voluntary mv
Advanced stages - on off dyskinesias
- flexed posture, dystonias, freezing
- gait instability, falls
- dysarthria, dysphagia
- dementia
- psychosis, hallucinations
Basal ganglia thalamocortical loop
-how does this link to the pathophysiology
D1 => activation promotes mv via direct path
D2 => activation inhibits mv inhibition via indirect path
Low D => inactivity of D1, overactivity of D2
Increased ACh => resting tremor
PD
- diagnosis, investigations
- differentials you want to rule out
Clinical diagnosis but can be confirmed by DATSCAN
Degenerative
-MSA, PSP
Reversible
- drug induced (metaclopramide, haloperidol, prochlomethazine) - acute onset motor, rigitidy and resting tremor not common => improved with procyclidine
- stroke, head trauma, encephalitis, Wilsons
