Parkinson's disease Flashcards
Parkinson’s disease - what is it a triad of?
A movement disorder characterised by
1 - resting tremor
2 - rigidity
3 - bradykinesia
Pathology of Parkinson’s disease
reduction of dopamine secretion in the substantia nigra - lewy bodies appear in substantia nigra
sometimes genetic mutations
Epidemiology - affected age group?
is it rare?
typically starts aged 55-65
second most common neurodegenerative disease after alzheimers
Presentation of Parkinson’s disease
Slowly Progressive
- motor function
i) slow movements (problems initiating movements, reduced arm swing, reduced amplitude of a repetitive movement with time)
ii) resting tremor (‘Pill rolling’, can be ^ by having them concentrate)
iii) gait/balance disturbances - small shuffling gait
iv) cogwheel rigidity
NO WEAKNESS tho
-non motor autonomic dysfunction (orthostatic hypotension, constipation, urinary problems, sleep disturbance, psychiatric symptoms (visual hallucinations))
other features for diagnosis (NICE - step 3)
unilateral onset with persistent asymmetry
70-100% response to L-dopa
hyposmia - cant smell
l-dopa - after 5-10 years.. common things to happen
motor fluctuations - on/off stiff/bradykinetic phases - tend to be more off's as dose wears off axial problems (balance, speech, gait disturbance)
parkinson’s disease dementia - 3 features
occurs 1 year + after Parkinson’s diagnosis
1 - presence of parkinson’s in limbs
2 - frequent visual hallucinations
3 - frequent fluctuations in lucidity
how is diagnosis made
it is clinical - tests can exclude other things
CT/MRI brain - if L-dopa doesnt do anything
if patient is young - ceruloplasmin levels (wilsons disease) and syphilis
management - non medical
parkinson specialist nurses physiotherapy/exercise occupational therapy SALT nutritional support
management - medical treatments
levodopa
dopamine agonists (pramipexole, ropinirole, rotigotine)
entacapone, tolcapone (catecholamine-O-methyltransferase inhibitors - degrade dopamine)
benztropine - ACh inhibitors
Deep brain stimulation
risk factors for parkinsons
pesticide gene variants (LRRK2)
substantia nigra - anatomy
part of of basal ganglia - one each side of mid brain - controls moment- connects to motor cortex
Made of two parts:
1) pars reticulata - receives signals from striatum (=caudate+putamen), then relays message to thalamus via GABA
2) pars compacta - sends message to striatum via dopamine (nigrostriatal pathway) this part is affected in parkinsons
dopamine - overview
cant cross blood brain barrier - levodopa (precursor) can. Dopa decarboxylase converts it to dopamine
the drug is given with carbidopa which inhibits dopa decarboxylase which is outside the brain. carbidopa cant cross the blood brain barrier so levodopa can be converted into dopamine in the brain still
Parkinson’s and strength
Do they even lift?
Is there a reduction in strength
There is no weakness/loss of strength in Parkinson’s. This is important for differentiating it between things.
That and they cant smell