Parkinsonism Flashcards
What is this a presentation of?
Tremor (worst at rest, pill-rolling), hypertonia (cogwheel rigidity), bradykinesia (actions slow with repetition), shuffling gait, expressionless face.
Parkinsonism
What is the difference in tremor between cerebellar disease and Parkinsonism?
- Cerebellar disease - intention (on action)
2. Parkinsonism - resting
What are the causes of Parkinsonism?
- Primary Parkinson’s disease
- Parkinson’s plus syndromes - PSP, MSA, Lewy body dementia
- Vascular Parkinsonism
- Secondary to drugs
- Wilson’s
What is the pathophysiology of Parkinson’s disease and what is the mean age of onset?
- Loss of dopaminergic neurones in the substantia nigra (par compacta)
- 60 years
What are the clinical motor features of Parkinson’s disease?
Tremor, hypertonia, bradykinesia.
What are the clinical non-motor features of Parkinson’s disease?
Postural hypotension, constipation, depression, daytime sleepiness, anosmia, cognitive dysfunction later on.
How is Parkinson’s disease diagnosed?
- Clinical based on core symptoms
- Symptoms should be unilateral or worse on one side
- Clinical response to dopaminergic therapy is supportive
- If unsure - MRI to rule out structural pathology and consider DaT scan
What is this a presentation of?
Early postural instability (many falls), broad bear-like gait, vertical gaze palsy, rigidity of trunk > limbs, symmetrical in onset, little tremor.
Progressive supranuclear palsy (Parkinson’s plus)
What is this a presentation of?
Early autonomic features (impotence, incontinence, postural hypotension), rigidity > tremor.
Multiple system atrophy (Parkinson’s plus)
Which drugs are responsible for secondary parkinsonism and how is it treated?
- 1st generation antipsychotics, metoclopramide (especially in the young)
- Treat with anti-cholinergic (procyclidine)
How is the cause of parkinsonism investigated?
- Wilson’s should be excluded in those under 40 years old
- If atypical features - acute onset, asymmetrical, early cognitive features, rapidly progressive disease - MRI
- Definitive diagnosis made post-mortem
When should you start L-DOPA in parkinsonism and why should it not be stopped suddenly?
- Only if patient is limited by symptoms (because it needs larger and larger doses with large fluctuations between on/off time)
- Risk of acute akinesia and neuroleptic malignant syndrome
What is the first line treatment for parkinsonism and what are the side effects?
- L-DOPA TDS
2. Dyskinesia (involuntary movements), visual hallucinations, nausea and vomiting.
What is added to a treatment regime for parkinsonism if a patient is already on optimal L-DOPA?
- Dopamine agonists (ropinirole)
- MAO-Bi (rasagiline, selegiline)
- CMOTi (entacapone, tolcapone)
- Amantadine - for drug-induced dyskinesia
- SC apomorphine - for ‘frozen’ patients
- Deep brain stimulation
What is this describing?
An oscillatory, typically rhythmic and regular movement affecting one or more body parts.
Tremor
