Parkinson’s Disease Flashcards
What is the underlying pathophysiology for Parkinsons?
Degeneration of dopaminergic neurones in the substansia nigra of the basal ganglia leading to progressive fall in production of dopamine
Basal ganglia is associated with controlling voluntary movement and learning specific movements
What is the classic triad for Parkinsons?
What are important clinical features which patients might present with?
NOTE: tends to be assymetrical presentation
Resting tremor (pill rolling)
Rigidity (cogwheel i.e. due to tremor super-imposed on bradykinesia)
Bradykinesia
Others:
- stooped posture + forward tilt
- shuffling gait
- reduced arm swing
- facial masking
- anosmia
- depression
- sleep disturbances and insomnia (can have REM sleep disorder i.e. calling out or acting out dream)
- postural instability
- cognitive impairment + memory problems
- micrographia
- constipation
- urinary symptoms
- autonomic dysfunction= orthostatic hypotension
- drooling
What are the charactertistics of the tremor seen in Parkinsons? How can it be differentiated from a benign essential tremor?
Assymetrical
4-6 Hz frequency i.e. occurs 4-6 times a second
Pill rolling
Worst at rest + when patient distracted i.e. asked to do another task with the other hand
Better on intentional movement
Re-emergent i.e. will return >2 secs after assuming different position
No change with alcohol
Why is the rigidity seen in Parkinsons termed “cogwheel”?
Tension in arm which gives way in small increments i.e. jerks
Due to tremor being super-imposed on rigidity
How does bradykinesia manifest in clinical presentation?
I.e. everything becomes slower and smaller
Micrographia= Smaller handwriting
Shuffling gait= smaller steps
Difficulty initiating movement= from standing still to walking
Difficulty turning when standing
Hypomimia= reduced facial movements and expressions
What are examples of Parkinson’s-plus syndromes?
What are their features?
What are the red flags for Parkinson’s plus syndromes?
Multiple system atrophy
- degeneration of neurones in multiple systems, which can include the basal ganglia
- present with autonomic dysfunction i.e. postural hypo, constipation, abnormal sweating and sexual dysfunction
- present with cerebellar dysfunction= ataxia
Dementia with lewy bodies
- dementi with features of Parkinsonism
- progressive cognitive decline
Progressive supranuclear palsy
- vertical gaze paresis
- tendency to fall backwards
RED FLAGS
- falls w/i 6 months of Parkinson’s diagnosis
- dystonia
- poor levodopa response
What are differential diagnoses for Parkinsons disease?
Vascular Parkinsons Lewy-body parkinsons Drug-induced Parkinsonism -neuroleptics -antiemetics drugs -sodium valproate Parkinson plus syndromes
How is Parkinson’s diagnosed?
Hx + examination for clinical diagnosis
MRI to exclude stroke or tumours in the basal ganglia
DaTscan= used to differentiate between idiopathic and drug-induced parkinsons
-“comma” shaped basal ganglia becomes “dot” shaped and the changes are asymmetrical
How is Levodopa used to manage Parkinsons?
What drugs can be given in combination with Levodopa and why?
(Tailored to individual)
Levodopa + carbidopa/benserazie
-synthetic dopamine used to boost own dopamine levels
-given in combination with drug to prevent levodopa being converted to dopamine prior to crossing the BBB i.e. helps to maxmise effects of levodopa and minimise side effects
NOTE: Levodopa becomes less effective over time so it is resevered for when other forms of treatment are not managing symptoms
COMT inhibitors (Entacapone) -inhibit COMT-enzyme which metabolised levodopa in body and brain with the aim to slow the breakdown of levodopa to extend the duration of its effects
Apparent from Levodopa, what other drugs can be used to treat Parkinson’s?
Dopamine Agonists i.e. Bromocryptine/Pergolide/Caberogoline
-mimic dopamine
-less effective that levodopa
-used to delay use of levodopa OR in combo to reduce the dose of levodopa required
NOTW: can cause pulmonary fibrosis with prolonged use
Monoamine Oxidase-B inhibitors i.e. Selegiline + Rasagiline
- inhibits enzyme which normally acts to break down dopamine i.e. increases the circulating concentration of dopamine
- used to delay the use and then to decrease the dose of levodopa required
Why side effects can occur in Parkinson’s disease treatment and what are they?
Dose is too high leading to levels of dopamine being too high
Results in dyskinesia= excessive motor activity
- Dystonia i.e. excessive muscle contraction= abnormal postures and exaggerated movements
- Chorea i.e. jerky abnormal involuntary movements
- Athetosis i.e. involuntary twisting or writhing movements= hands, fingers, feet
How can the non-motor problems associated with Parkinson’s be managed?
If dementia
-rivastigmine
Psychiatric complications i.e. hallucinations
-Quetiapine
Depression + anxiety
-SSRIs
Sleep disturbance
- Clonazepam
- melatonin
