Movement disorders Flashcards
Classic features of Parkinson’s
TRAP
Tremor (resting)
Rigidity
Akinesia
Postural instability
How to diagnose PD?
Clinical diagnosis - history, exam, response to medications
MRI to exclude other causes
Risk factors for PD
Male Age >60 Family history Heavy metal exposure Pesticides
What’s the goal of treatment in PD?
Symptomatic treatment only
Does not improve balance
Does not prevent progression of disease
How does PD usually start?
Unilateral involvement
List 5 main classes of PD therapy
1) Dopamine replacement
- Levodopa is gold standard for motor symptoms but also has the highest risk of motor complications
2) Dopamine agonist
3) MAO B inhibitors
4) Amantadine
5) Anticholinergics
Treatment options for mild PD
1) MAO B inhibitor
- Selegeline, Rasagiline
- Safinamide is a newly approved drug and is used as an adjunct to levodopa
2) Amantadine
- Monotherapy or add on
- When tremor is predominant
- Also used for management of dyskinesia
3) Anticholinergic therapy
- Benztropine, trihexyphenidyl
- Used in tremor control
- Monotherapy or add on
AEs of MAO B inhibitors
Nausea and headache most common
Confusion and hallucinations
Depression
Beware of drug interactions with ADs
AEs of amantadine
Livedo reticularis
Confusion
Nightmares
AEs of anticholinergic therapy
Cognitive impairment Blurred vision Dry mouth Constipation Urinary retention Dry red itchy skin
Caution in age >65
Rx for moderate PD - when symptoms begin to interfere with functioning
DA agonist - younger people. Avoid >70yo.
DA replacement - older people
List 4 DA agonists
Pramipexole
Rotigotine (patch; bypasses oral absorption)
Ropinirole
Cabergoline
AEs of DA agonists
Nausea, vomiting Drowsiness Pathological gambling, compulsive sexual behaviour and spending Hallucinations Confusion Pedal oedema Orthostatic hypotension Rotigotine patch may cause skin irritation
Start low, go slow
How to stop PD medications particularly DA agonists and levodopa?
Don’t discontinue abruptly due to risk of withdrawal syndrome, acute akinesia or neuroleptic malignant syndrome
Withdrawal can resemble other psychostimulant withdrawal syndromes with prominent psychiatric (anxiety, panic attacks, depression, agitation, fatigue) and autonomic (orthostatic hypotension, diaphoresis) manifestations
Rx for advanced stage PD
Levodopa (gold standard) +/- MAO B inhibitor +/- DA agonist
- Always titrate with IR tablets
If ongoing issues with motor fluctuations and dyskinesia, can consider…
Deep brain stimulation
Apomine infusion
Duodopa
AEs of levodopa
Dyskinesia with prolonged use
- Motor fluctuations and dyskinesia will occur after 5-10 years. Adjuncts are available to reduce motor fluctuation.
Nausea Headache Confusion Hallucinations/delusions Dizziness Orthostatic hypotension
What’s dopamine dysregulation syndrome?
When people get addicted and abuse dopaminergic medications especially IR form, impairing function
What’s punding?
When PD patients repeatedly do purposeless, stereotyped behaviours e.g. sorting or disassembling
Can occur after use of short-acting dopaminergic agents
What is dyskinesia?
Happens with prolonged use of levodopa. Doesn’t happen with DA agonists.
The earlier the onset of PD, the higher the risk
Involuntary movements of limbs, torso, neck and head
Usually dystonic movements and sometimes more choreiform in nature
Why does dyskinesia happen?
It is thought that as PD becomes more advanced, you lose dopaminergic neurons that store dopamine in the basal ganglia, so the individual’s response becomes dependent on plasma levels that fluctuate based on systemic absorption which is erratic
What’s diphasic and peak dose dyskinesia?
Diphasic dyskinesia affects limbs and occurs when dopamine levels rise and fall
Peak dose dyskinesia affects head and neck and occurs when dopamine levels peak
Who should be considered for DBS?
Age <70 (not a hard rule) Severe dyskinesia that affects QOL On and off fluctuation Response to dopaminergic therapy Good cognitive function Tremor that can't be controlled with medication At least 5 years of PD
Need neuropsych assessment
Complications of DBS
Surgical complications
Neuropsychiatric/behavioural issues - higher risk of suicide
Mechanical malfunction
CI to DBS
Dementia
Active psychiatric disorders
Dominant levodopa resistant motor symptoms
Structural abnormalities on MRI
What is duodopa?
Continuous levodopa carbidopia intestinal gel infusion
Through a percutaneous gastrojejunostomy tube that connects to a pump
Less “off times” and more “on” times without dyskinesia
Can titrate dose
Who should be considered for duodopa?
Advanced PD Severe dyskinesia Motor on off fluctuations Dysphagia Unpredictable response to oral medications
With what therapy must melanoma be ruled out?
Duodopa
AE of duodopa
Neuropathy
Surgical complications such as peritonitis, abdominal pain, displacement of tube into stomach
What is apomorphine?
Continuous subcut infusion of dopamine agonist
Via portable infusion pump
Decreases dyskinesia and off time
Who would be suitable for apomorphine?
Advanced PD
Can’t tolerate dopamine
Dyskinesia
AE of apomorphine
Nausea hypotension Subcut nodules Pain, bleeding at needle site Autoimmune haemolytic anaemia Sleep attacks/Drowsiness +/- driving restrictions
When is botox used in PD?
Cervical dystonia (inject into the sternocleidomastoid; risk of dysphagia)
Head tremors
Blepharospasm (involuntary movement of eyes)
Eyelid apraxia (difficulty with eyelid elevation; risk of causing ptosis and diplopia)
Sialorrhea (drooling)
Limb dystonia
Hyperhidrosis (excessive sweating)
Only lasts 12 weeks
List non-motor symptoms of PD
Hallucinations Cognitive decline and dementia Disturbed sleep pattern and REM behavioural disorder Vivid dreams Anosmia Restless leg syndrome Fatigue Depression, anxiety, psychosis
Autonomic symptoms
Postural instability/hypotension (as a result of advanced PD or levodopa)
Constipation
Dysphagia
Neurogenic overactive bladder or underactive bladder
Sexual dysfunction
How to differentiate between PD-dementia and DLB?
PD-dementia - dementia typically occurs about a year after the onset of PD symptoms
DLB - dementia occurs concurrently or prior to onset of PD
List motor symptoms of PD
Masked facies
Decreased blink reflex due to motor slowing
Eyelid apraxia (difficulty opening eyes; usually late feature)
Hypophonia (soft speech) due to glottal rigidity
Micrographia due to bradykinesia and limb rigidity
Dysphagia due to pharyngo-oesophageal motor slowing
Excessive salivation due to decreased swallowing
Camptocormia (severe involuntary flexion of the thoraco-lumbar spine; late feature; may respond to dopamine)
Gait issues - freezing, shuffling, festinating (short and progressively more rapid steps)
List 3 Parkinson’s Plus syndromes
- Multisystem atrophy (MSA)
- Progressively supranuclear palsy
- Corticobasal degeneration
Which drugs can cause parkinsonism?
Dopamine antagonists - antipsychotics, metoclopramide, CCB, AEDs
How does drug induced parkinson’s differ from idiopathic PD?
Symptoms usually bilateral
Do symptoms resolve after stopping offending agent in drug induced parkinson’s?
Not always
Symptoms can persist for long periods of time
List predictors of benign course in PD
Younger age of onset
Female
Tremor predominant
List predictors of poor prognosis in PD
Male Late age of onset Gait and balance issues Dementia Bradykinesia as an initial symptom Poor response to levodopa
