Movement Disorders — Written Clinical Reasoning

SAQ 1 — Advanced Parkinson's Disease with Motor Complications, Psychosis and Cognitive Decline (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, addressing the wearing off, the peak-dose dyskinesia, the visual hallucinations, the freezing of gait and falls, and the cognitive decline. Justify each decision with reference to evidence and guideline recommendations. ^[1]

Model Answer

Problem list (4 marks): ^[1]

1. Wearing off (end-of-dose deterioration) — each levodopa dose now lasts only 2 hours; off-time is causing functional impairment.
2. Peak-dose dyskinesia — choreiform movements 1 hour after each dose, reported as more disabling than the off periods.
3. Visual hallucinations — formed, detailed, with retained insight; early feature of PD psychosis, may herald cognitive decline.
4. Freezing of gait with falls — a levodopa-resistant axial symptom and major falls risk; three falls in a month is a red flag.
5. Cognitive decline — MoCA 24/30 is at the threshold for mild cognitive impairment; the hallucinations and gait freezing suggest non-dopaminergic (Braak stage 4 to 6) disease progression.
6. Polypharmacy — he is on four dopaminergic agents from three drug classes, increasing the risk of hallucinations and orthostatic hypotension. ^[1]

Management of wearing off and dyskinesia (5 marks): ^[1]

The central principle here is that dyskinesia is the dominant complaint and must drive the strategy — chasing the off-time with more levodopa would worsen the dyskinesia. My approach: ^[1]

• Reduce the size of each levodopa/carbidopa dose and increase the frequency — for example, switch from 100/25 six times daily to 75/18.75 (three-quarter tablet) every 2 hours while awake, smoothing the plasma levodopa profile. This lowers the peaks (reducing dyskinesia) while maintaining total daily dopaminergic stimulation (reducing off-time).
• Add amantadine 100 mg once or twice daily — the only oral agent with good evidence for reducing levodopa-induced dyskinesia (Snow et al, PMID 10803797). Extended-release amantadine 274 mg once nightly is specifically approved for dyskinesia and off-time reduction. I would monitor for confusion and hallucinations, which may limit use in this patient who already has cognitive change.
• Consider reducing or weaning the dopamine agonist (ropinirole) — agonists contribute to dyskinesia and are the highest-risk class for hallucinations in this cognitively changing patient. I would wean ropinirole slowly (over weeks) to avoid dopamine agonist withdrawal syndrome, transferring the dopaminergic load to levodopa. The rasagiline may be continued or also weaned if hallucinations persist.
• If oral optimisation fails to control both the dyskinesia and the off-time, I would escalate to device-aided therapy: levodopa-carbidopa intestinal gel (LCIG) via PEG-J, continuous subcutaneous apomorphine infusion, or deep brain stimulation. Given his cognitive decline (MoCA 24) and hallucinations, GPi-DBS would be preferred over STN-DBS (better neuropsychiatric profile, Follett PMID 20519680), and a formal neuropsychological assessment would be mandatory before any surgical referral. Cognitive decline and active psychosis are relative contraindications to DBS and would need careful multidisciplinary discussion. ^[1]

Management of visual hallucinations (4 marks): ^[1]

Visual hallucinations in PD reflect a combination of dopaminergic therapy (especially agonists), disease progression (Braak limbic and cortical stages), visual pathway dysfunction, and emerging cognitive impairment. My approach, in order: ^[1]

1. Exclude delirium and treat reversible contributors — check for infection (urine, chest), check electrolytes, review all medications for anticholinergic load, and assess sleep. Many 'PD hallucinations' in clinic are unmasked delirium.
2. Reduce and simplify dopaminergic therapy — wean and stop the dopamine agonist (ropinirole) first, as it carries the highest neuropsychiatric risk; reduce anticholinergics and amantadine if present; minimise levodopa to the lowest effective dose (accepting some worsening of motor function — a difficult but necessary trade-off). The rule is: reduce agonists before reducing levodopa, because levodopa has the lowest neuropsychiatric burden.
3. Add a cholinesterase inhibitor — rivastigmine (licensed for PD dementia) or donepezil, which improve both cognitive function and psychotic features, particularly in patients with co-existing cognitive impairment as this man has.
4. If an antipsychotic is unavoidable — the only evidence-based options are pimavanserin (a selective 5-HT2A inverse agonist, FDA-approved for PD psychosis; not available in ANZ/UK) ^[3] or low-dose quetiapine (12.5 to 25 mg at night, off-label, with caution). I must explicitly avoid haloperidol, chlorpromazine, risperidone and olanzapine, which can cause catastrophic worsening of parkinsonism and, in patients with underlying DLB, fatal neuroleptic sensitivity. ^[4] I would counsel the patient and family about the residual risk of quetiapine and document the discussion. ^[1]

Management of freezing of gait and falls (4 marks): ^[1]

Freezing of gait (FOG) is largely levodopa-resistant and reflects non-dopaminergic disease progression; escalating dopaminergic therapy will not help and may worsen cognition and orthostatic hypotension. My approach: ^[1]

• Optimise the on-state first — ensure the patient is not under-treated for off-period freezing (which DOES respond to levodopa). A structured motor diary and adjustment of dosing intervals is the first step.
• Cueing strategies — visual cues (lines on the floor, a laser-cane projecting a line to step over), auditory cues (marching to a metronome set at the patient's preferred cadence, counting 'one-two-three-go'), and attentional strategies (consciously shifting weight, rocking before stepping). These are taught by a PD-specialist physiotherapist and are the most effective intervention for FOG.
• Physiotherapy — PD-specific exercise programmes (LSVT BIG, PDSAFE) improve balance and reduce falls.
• Falls risk assessment — review orthostatic hypotension (check lying and standing blood pressure; reduce causative medications; consider compression stockings, fludrocortisone or midodrine), review vision, review the home environment (occupational therapy for grab rails, removal of rugs), and consider a walker or rollator (though freezing can paradoxically worsen with a frame — a laser-walker is preferred).
• Address the cognitive contribution — FOG has a strong fronto-executive component; cognitive impairment worsens FOG, so the cholinesterase inhibitor may help both problems. ^[1]

Management of cognitive decline and overall integration (3 marks): ^[1]

A MoCA of 24/30 in the setting of PD of 11 years' duration, with hallucinations and gait freezing, is consistent with PD mild cognitive impairment progressing toward PD dementia. I would: ^[1]

• Establish a baseline with serial MoCA (6 to 12 monthly).
• Refer for formal neuropsychological assessment to characterise the cognitive profile (frontal-executive vs posterior-cortical).
• Add a cholinesterase inhibitor (rivastigmine) for both the cognitive and psychotic features.
• Screen for and treat depression, which is common and worsens cognitive performance.
• Initiate advance care planning — discuss goals of care, appoint a substitute decision-maker, document preferences around hospitalisation, feeding (PEG placement in advanced PD dysphagia does not improve outcomes and increases aspiration risk), and palliative care input for end-stage disease.
• Multidisciplinary review: neurology, PD nurse specialist, physiotherapy, occupational therapy, speech pathology (for voice and swallow assessment), dietetics, and social work. ^[1]