Parkinson's DIsease Flashcards
Pathological changes seen in Parkinson’s Disease
Loss of dopaminergic neurons in the substantia nigra
- nigral cells projecting into the striatum are mostly affected (nigrostriatal pathway), causing a loss of dopamine in the striatum
- also associated with Lewy bodies (eosinophilic inclusions) in the basal ganglia, brainstem and cortex
Clinical features of Parkinson’s Disease
Non-motor symptoms - autonomic dysfunction (postural hypotension, constipation, urinary frequency and dribbling saliva) Sleep disturbance Reduced sense of smell Depression, dementia and psychosis
What is the classical Parkinsonism triad?
- extrapyramidal signs
1) Hypertonia
- rigidity and tremor gives ‘cogwheel rigidity’
2) Bradykinesia
- slow to initiate movement
- actions are slow and decrease in amplitude with repetition e.g. blinking
- festinant gait (shuffling, pitched forward)
- decreased arm swing
- freezing at obstacles or doors (poor simultaneous motor and cognitive function)
- expressionless face
3) Tremor
- worse at rest, ‘pill-rolling’
Differential diagnosis for Parkinson’s Disease
Anything that displays features of Parkinsonism (parkinson plus syndromes)
Progressive supranuclear palsy
Multi-system atrophy
Cortico-basal degeneration
Lewy body dementia
Seconday causes
- vascular parkinsonism
- drugs (anti-psychotics and metaclopramide )
- toxins (e.g. Wilson’s disease displays wide neurological problems)
- trauma
- encephalitis
- neurosyphilis
Cerebrovascular disease
- lacunar infarcts of the basal ganglia
- small vessel disease of the cerebral white matter
Toxins - MPTP (prodrug to the neurotoxin MPP+)
When should medications be started in Parkinson’s Disease
Focus is on symptom control as progression can’t be slowed down
- start management only when symptoms have a significant impact on life, as efficacy of treatment decreases over time, as side effects increase
Medications involved in management of Parkinson’s Disease
Levodopa
- dopamine precursor (converted to dopamine within nigroatriatal neurons by DOPA decarboylase)
- can cross BBB while dopamine can’t
Domperidone/Carbidopa
- prevents peripheral conversion of L-DOPA into dopamine and causing n/v
Dopamine agonists
- e.g. ropinirole or pramipexole (transdermal)
- used to delay starting L-dopa treatment, or to decrease L-dopa requirements
MAOB inhibitors e.g. selegilene
- MAOB metabolises dopamine, so inhibition of it prolongs the action of dopamine in the brain
- used as dopamine agonists are
Apomorphine
- potent dopamine agonist
- sc continuous infusion to even end-of-dose effects
- rescue pen for sudden freezing
Anticholinergics
- limit motor symptoms
- used in young patients or those on antipsychotics
MDT in the management of Parkinson’s disease
Physiotherapists Speech and Language therapist Occupational therapists Neurologist Community nurse GP
Aetiology of Parkinson’s Disease
Sporadic - normally
Multiple genetic loci
Average age of onset around 60 years old
Prevalence increases with age
How is Parkinson’s Disease diagnosed?
Clinical - based on core features
- frontotemporal and cerebellar dementia excluded
Signs worse on one side than the other in early disease
If differential suspected - MRI
DaTscan
- functional neuroimaging
- can visualise dopamine degeneration
Role of physiotherapist is Parkinson’s
Aim to keep people moving and independent with daily activities
Improving/maintaining good posture, balance and fitness through exercise, helping with movement and walking, helping to prevent and manage falls, maintaining or improving effective breathing and helping with pain relief
Role of speech and language therapist in Parkinson’s
Help with difficulties in swallowing or communication affecting QoL or causing social isolation
Role of occupational therapist in Parkinson’s
Finding ways to continue working, keeping up hobbies and leisure interests
Recommending changes to make living environments safer and more comfortable
Equipment to maintain independence
