Parkinson Disease & Movement Disorders

📋 Key Information Summary

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Parkinson disease (PD) affects approximately 80,000 Australians and is the second most common neurodegenerative condition after Alzheimer disease; prevalence increases sharply after age 60.
Diagnosis is clinical — the MDS Clinical Diagnostic Criteria (2015) require bradykinesia plus resting tremor and/or rigidity, with supportive features (clear levodopa response, rest tremor, olfactory loss) strengthening confidence.
Red flags for atypical parkinsonism include early falls, symmetric onset, rapid progression, supranuclear gaze palsy, cerebellar signs, and early autonomic failure — these should prompt specialist reassessment.
Levodopa/carbidopa (e.g. Sinemet®) remains the most effective symptomatic therapy across all ages; starting with levodopa is recommended for most patients aged ≥65 or those with significant functional impairment.
Dopamine agonists (pramipexole, ropinirole, rotigotine) and MAO-B inhibitors (selegiline, rasagiline, safinamide) are alternatives for younger patients to delay levodopa-related motor complications.
Motor complications — wearing-off, peak-dose dyskinesia, and on–off phenomena — affect up to 50% of patients within 5–10 years of levodopa initiation and require stepwise pharmacologic adjustment.
Non-motor symptoms (constipation, orthostatic hypotension, REM sleep behaviour disorder, depression, cognitive impairment, pain) are common, often more disabling than motor features, and must be actively screened.
A levodopa challenge test (single-dose 250 mg levodopa with objective UPDRS-III scoring) is recommended when diagnostic uncertainty exists — a ≥30% improvement supports PD diagnosis.
Advanced therapies — deep brain stimulation (DBS), levopa–carbidopa intestinal gel (Duodopa®), and subcutaneous apomorphine infusion — should be considered when motor complications are inadequately controlled by oral medications.
Aboriginal and Torres Strait Islander Australians may face delayed diagnosis due to limited specialist access in remote areas; culturally appropriate education and telehealth neurology services are essential.
All patients require a multidisciplinary team approach including physiotherapy, speech pathology, occupational therapy, dietetics, and psychology, coordinated through the GP.

Introduction & Australian Epidemiology

Parkinson disease (PD) is a progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of alpha-synuclein-containing Lewy bodies. It is the second most common neurodegenerative condition in Australia after Alzheimer disease and is the fastest-growing neurological disorder globally in terms of prevalence, disability, and deaths.

Australian Burden of Disease

An estimated 80,000–100,000 Australians are living with PD (AIHW 2023), with approximately 30–40 new diagnoses per 100,000 population per year.
Prevalence increases with age: approximately 1–2% of Australians aged ≥65 and up to 4% of those aged ≥85 are affected.
Men are 1.5 times more likely to be diagnosed than women.
The total economic cost of PD in Australia exceeds $10.7 billion annually (including direct health costs, informal carer costs, and lost productivity).
PD is the 14th leading cause of death in Australia, with a median survival of 12–15 years from diagnosis when optimally managed.

Risk Factors

Factor	Detail
Age	Strongest risk factor; incidence rises sharply after age 60
Male sex	Male-to-female ratio approximately 1.5:1
Genetic	LRRK2, GBA, SNCA, PINK1, PARK7 mutations; family history increases risk 2–5×
Environmental	Pesticide exposure (rotenone, paraquat), rural living, heavy metals, well-water drinking
Protective	Caffeine consumption, smoking (epidemiological association only — not a therapeutic recommendation), physical activity
Head injury	Moderate-to-severe traumatic brain injury increases risk approximately 1.5–2×

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Growing prevalence: The number of Australians with PD is projected to double by 2040 due to population ageing, placing increasing demand on neurology services, allied health, and aged-care supports. Early diagnosis and proactive management are essential to optimise quality of life.

Diagnosis of Parkinson Disease

The diagnosis of PD remains fundamentally clinical. There is no single confirmatory laboratory test or imaging modality. The Movement Disorder Society (MDS) Clinical Diagnostic Criteria (2015) provide a structured framework with ascending levels of diagnostic certainty.

MDS Clinical Diagnostic Criteria (2015)

Core motor feature (mandatory): Bradykinesia, defined as slowness of movement and progressive decrement in amplitude or speed with repeated actions, must be present.

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Bradykinesia is the cardinal feature. PD cannot be diagnosed in the absence of bradykinesia. The combination of bradykinesia with at least one of resting tremor (4–6 Hz, predominantly distal, decreases with voluntary movement) and/or lead-pipe rigidity (with or without cogwheeling) constitutes the core motor parkinsonism triad.

Supportive Criteria (increase diagnostic confidence)

Clear and dramatic beneficial response to dopaminergic therapy (levodopa or dopamine agonist challenge)
Presence of levodopa-induced dyskinesias
Rest tremor of a limb (documented on examination)
Positive olfactory loss or cardiac sympathetic denervation on MIBG scintigraphy

Absolute Exclusion Criteria

Cerebellar abnormalities (gait ataxia, limb ataxia, cerebellar oculomotor dysfunction)
Supranuclear gaze palsy (vertical down-gaze limitation characteristic of PSP)
Primary progressive aphasia or semantic/alogic variant frontotemporal dementia within 5 years of motor onset
Parkinsonism restricted to lower limbs for >3 years (consider vascular parkinsonism)
Treatment with a dopamine-blocking agent consistent with drug-induced parkinsonism

Red Flags for Atypical Parkinsonism

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Consider atypical parkinsonism (MSA, PSP, CBD, DLB) if any of the following are present: rapid progression requiring wheelchair within 5 years, early severe dysphagia or dysarthria, early recurrent falls (<3 years from onset), symmetrical parkinsonism, lack of levodopa response at adequate doses (>600 mg/day for ≥2 months), early severe autonomic failure, early hallucinations unrelated to medication, myoclonus, pyramidal tract signs, or alien limb phenomenon.

Atypical Condition	Key Distinguishing Features
Multiple System Atrophy (MSA)	Early autonomic failure (urinary incontinence, orthostatic hypotension), cerebellar ataxia (MSA-C) or parkinsonism (MSA-P), stridor, poor levodopa response
Progressive Supranuclear Palsy (PSP)	Vertical supranuclear gaze palsy, early falls (within 1 year), axial rigidity, retrocollis, pseudobulbar palsy
Corticobasal Degeneration (CBD)	Asymmetric limb rigidity, alien limb phenomenon, cortical sensory loss, apraxia, myoclonus
Dementia with Lewy Bodies (DLB)	Dementia preceding or within 1 year of parkinsonism, visual hallucinations, fluctuating cognition, REM sleep behaviour disorder

Investigations

No routine blood test confirms PD. Investigations serve to exclude secondary causes and support diagnosis where clinical uncertainty exists.

Essential Full blood count, renal function, liver function, thyroid function, vitamin B12, calcium Exclude metabolic and endocrine mimics; MBS item 66833 (broad panel)

Essential Medication review Exclude drug-induced parkinsonism (metoclopramide, prochlorperazine, haloperidol, certain antipsychotics)

Available DaTscan (¹²³I-ioflupane SPECT) MBS item 61337 — confirms presynaptic dopaminergic deficit; distinguishes PD/DLB from essential tremor, drug-induced parkinsonism, psychogenic tremor; funded when diagnostic uncertainty exists after specialist review

Available Olfactory testing (Sniffin' Sticks or UPSIT) Hyposmia is an early non-motor feature; useful supportive investigation — available in specialist centres

Referral DAT/PET imaging (¹⁸F-DOPA PET) Available at major PET centres (e.g. Royal Melbourne, RPA, Austin); not PBS-funded; used in research and complex diagnostic cases

Referral Transcranial sonography (TCS) Substantia nigra hyperechogenicity — supportive marker; available in select movement disorder centres

Specialist Genetic testing (LRRK2, GBA, PRKN, PINK1, SNCA) Consider in young-onset PD (<50), strong family history, or for clinical trial eligibility; Medicare-funded through genetics services

Levodopa Challenge Test

When diagnostic uncertainty remains, a supervised levodopa challenge is the gold-standard supportive test:

Withhold all dopaminergic medications for ≥12 hours (≥24 hours for extended-release formulations)
Administer a single dose of levodopa/carbidopa 250/25 mg (Sinemet®) or dispersible levodopa/benserazide 100/25 mg (Madopar®)
Score UPDRS-III (motor) before and 60–90 minutes after dosing
A ≥30% improvement in UPDRS-III motor score is considered a positive response and strongly supports idiopathic PD
False negatives may occur in early disease or with inadequate dosing

Initial Pharmacologic Therapy

The choice of initial dopaminergic therapy in PD is one of the most important treatment decisions and must be individualised based on patient age, symptom severity, functional impact, comorbidities, and patient preference. There is no single "correct" first-line agent — the key decision is between levodopa and dopamine agonists, with MAO-B inhibitors as a third option for mild symptoms.

Treatment Algorithm by Age and Severity

1

Mild symptoms, younger patients (<65 years)

Consider dopamine agonist or MAO-B inhibitor as initial monotherapy to delay levodopa-related motor complications. Add levodopa when functional needs increase.

2

Moderate symptoms, any age

Levodopa/carbidopa is the most effective initial therapy. Start low (e.g. 50/12.5 mg TDS) and titrate gradually. Appropriate for patients aged ≥65 or those with significant functional impairment.

3

Tremor-predominant

Levodopa is effective for tremor. If tremor remains refractory, consider addition of anticholinergics (benztropine, trihexyphenidyl) — use cautiously in elderly due to cognitive side effects. Beta-blockers (propranolol) may help coexistent essential tremor.

First-Line Agents

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Levodopa / Carbidopa

Sinemet® / Kinson® · Combination · Gold-standard symptomatic therapy

Adult dose Start 50/12.5 mg PO TDS with food; titrate every 5–7 days to effect; maintenance range 100/25 mg TDS to 200/50 mg five times daily

Max dose Levodopa component ≤1000–1500 mg/day (higher doses under specialist supervision)

Paediatric dose Not indicated in children; juvenile parkinsonism managed by paediatric neurologist

Renal adjustment No specific dose adjustment; use with caution in severe CKD

Key ADRs Nausea, orthostatic hypotension, drowsiness, hallucinations; motor complications with long-term use

PBS status ✔ PBS General Benefit

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Levodopa / Benserazide

Madopar® · Combination · Equivalent efficacy to carbidopa combination

Adult dose Start 50/12.5 mg PO TDS; titrate to 100/25 mg TDS–QID as needed; dispersible formulation available (Madopar® dispersible) for morning akinesia

Key notes Dispersible tablet useful for patients with dysphagia and for rescue dosing during "off" episodes

PBS status ✔ PBS General Benefit

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Pramipexole

Sifrol® / Mirapexin® · Non-ergot dopamine agonist

Adult dose Start 0.125 mg PO TDS (immediate-release) or 0.375 mg once daily (extended-release, Sifrol® ER); titrate weekly by 0.375 mg/day; target 1.5–4.5 mg/day in divided doses

Renal adjustment CrCl 35–59 mL/min: max 1.5 mg/day; CrCl 15–34 mL/min: max 0.75 mg/day; avoid if CrCl <15 mL/min

Key ADRs Nausea, oedema, somnolence, impulse control disorders (gambling, hypersexuality, compulsive shopping — must counsel), hallucinations

PBS status ✔ PBS General Benefit

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Ropinirole

Requip® · Non-ergot dopamine agonist

Adult dose Start 0.25 mg PO TDS; titrate by 0.75 mg/week; target 3–9 mg/day in divided doses (IR) or 2–24 mg once daily (XL)

Key ADRs Similar to pramipexole — nausea, oedema, somnolence, impulse control disorders

PBS status ✔ PBS General Benefit

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Rotigotine

Neupro® · Non-ergot dopamine agonist (transdermal patch)

Adult dose Start 2 mg/24 hours patch once daily; titrate weekly by 2 mg/24 hours; maintenance 4–8 mg/24 hours

Key advantages Continuous dopaminergic stimulation; useful in patients with dysphagia, gastroparesis, or adherence difficulties; apply to clean, dry, intact skin on abdomen, thigh, upper arm, or flank; rotate sites

Key ADRs Application site reactions (very common), nausea, somnolence, impulse control disorders

PBS status ⚠ PBS Restricted Benefit

MAO-B Inhibitors

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Rasagiline

Azilect® · Irreversible MAO-B inhibitor

Adult dose 1 mg PO once daily (monotherapy or adjunct to levodopa)

Renal adjustment No adjustment required

Key ADRs Headache, nausea, arthralgia, dyspepsia; avoid with SSRIs/SNRIs (serotonin syndrome risk) — discuss with psychiatrist if co-prescribing needed

PBS status ⚠ PBS Authority Required

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Selegiline

Eldepryl® · Irreversible MAO-B inhibitor

Adult dose 5 mg PO mane, 5 mg PO at lunchtime (avoid evening dosing — may cause insomnia); max 10 mg/day

Key ADRs Insomnia, nausea, orthostatic hypotension; amphetamine metabolites may cause confusion in elderly

PBS status ✔ PBS General Benefit

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Safinamide

Xadago® · MAO-B inhibitor with glutamatergic modulation

Adult dose 50 mg PO once daily for 2 weeks, then 100 mg once daily as adjunct to levodopa

Key advantage May help with both motor fluctuations and dyskinesia; dual mechanism

PBS status ✖ Not PBS-listed (as of 2025; may change — check current PBS)

Levodopa vs Dopamine Agonists — Key Trade-offs

Factor	Levodopa	Dopamine Agonists
Motor efficacy	Superior; most effective agent for motor symptoms	Good but generally inferior to levodopa for bradykinesia and rigidity
Motor complications	Higher risk of wearing-off and dyskinesia with long-term use	Delayed onset of motor complications (by 2–3 years on average)
Impulse control disorders	Lower risk	Hallucinations/psychosis	Risk increases with dose and disease duration	Higher risk, particularly in elderly and those with cognitive impairment
Peripheral ADRs	Nausea, orthostatic hypotension (reduced by carbidopa/benserazide)	Nausea, oedema (peripheral), somnolence, sleep attacks
Best for	Patients ≥65, significant functional impairment, cognitive concerns	Younger patients (<65), mild symptoms, desire to delay motor complications

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Impulse control disorders (ICDs): Dopamine agonists carry a significant risk of ICDs including pathological gambling, compulsive sexual behaviour, compulsive spending, and binge eating. Risk is higher in males, younger patients, those with a personal or family history of gambling or substance use, and at higher doses. All patients and caregivers must be counselled about ICDs before initiation, and screened at every visit using a structured questionnaire (e.g. QUIP-RS).

Adjunctive Therapies for Early Disease

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Amantadine

Symmetrel® · NMDA antagonist / dopamine release enhancer

Adult dose 100 mg PO BD (morning and early afternoon)

Renal adjustment CrCl 30–50: 100 mg daily; CrCl 15–29: 100 mg on alternate days; CrCl <15: avoid

Key uses Mild levodopa-induced dyskinesia; antiviral prophylaxis for influenza A is a secondary indication

PBS status ✔ PBS General Benefit

Motor Complications

Motor complications are the hallmark of advancing PD and are directly related to chronic levodopa use, progressive dopaminergic denervation, and the short half-life of standard levodopa formulations (approximately 90 minutes). Up to 50% of patients develop motor fluctuations within 5 years of levodopa initiation, rising to 70–80% at 10 years.

Types of Motor Complications

Early / Mild

Wearing-Off

Predictable end-of-dose deterioration; symptoms return before the next scheduled dose. The earliest and most common motor fluctuation. Recognised by shortened duration of benefit (<4 hours per dose) and consistent timing relative to dosing.

Management: Adjust oral therapy — see below

Moderate

Peak-Dose Dyskinesia

Involuntary choreiform or dystonic movements occurring at the time of peak levodopa plasma concentration. Usually axial (head, trunk) or limb. Associated with high levodopa exposure and younger age of onset. May be functional (improving mobility) or troublesome (impairing function).

Management: Reduce peak levodopa dose or switch to continuous delivery

Severe / Advanced

On–Off Phenomena

Unpredictable, rapid fluctuations between "on" (mobile) and "off" (immobile) states, independent of dosing intervals. Represents advanced disease with loss of buffering capacity. "Off" periods may be prolonged (hours) and associated with painful dystonia.

Management: Advanced therapies — DBS, apomorphine, Duodopa®

Diphasic Dyskinesia

A less common pattern where dyskinesia occurs at both the onset and end of a levodopa dose, with a relatively immobile period in between. Often painful (dystonic) and more difficult to manage than peak-dose dyskinesia.

Stepwise Management of Motor Complications

Step 1: Optimise Levodopa Delivery

Fractionate doses — smaller, more frequent doses of levodopa (e.g. 100/25 mg four to five times daily instead of 200/50 mg three times daily)
Use dispersible levodopa (Madopar® dispersible) for faster onset during "off" periods
Take levodopa on an empty stomach (30 minutes before meals) — protein competes with levodopa for intestinal absorption; advise consistent protein distribution across the day
Consider controlled-release formulations (e.g. Sinemet CR, Madopar HBS) for nighttime symptoms — note: may worsen daytime dyskinesia due to unpredictable absorption

Step 2: Add Adjunct Therapies

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Entacapone

Comtan® · COMT inhibitor

Adult dose 200 mg PO with each levodopa dose (up to 8 times/day, max 1600 mg/day)

Mechanism Inhibits catechol-O-methyltransferase, prolonging levodopa half-life by approximately 30–50%; reduces wearing-off

Key ADRs Diarrhoea (most common, may require discontinuation), urine discolouration (orange-brown), dyskinesia (dose reduction of levodopa often needed when adding entacapone)

PBS status ⚠ PBS Authority Required

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Levodopa / Carbidopa / Entacapone

Stalevo® · Triple combination tablet

Adult dose Available in five strengths (50/12.5/200, 75/18.75/200, 100/25/200, 125/31.25/200, 150/37.5/200 mg); replace equivalent levodopa dose; taken with each dose

Key advantage Reduces pill burden; improved adherence versus separate tablets

PBS status ⚠ PBS Authority Required

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Opicapone

Ongentys® · Third-generation COMT inhibitor

Adult dose 50 mg PO once daily at bedtime (taken with levodopa doses during the day)

Key advantage Once-daily dosing; lower risk of diarrhoea compared to entacapone; no hepatotoxicity concern (unlike tolcapone)

PBS status ⚠ PBS Authority Required

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Apomorphine (subcutaneous injection)

Apomine® · D1/D2 dopamine agonist — rescue therapy

Adult dose 1–3 mg SC PRN for "off" episodes; onset 10–20 minutes; duration 60–90 minutes; pre-treat with domperidone 10–20 mg TDS (start 3 days before first dose) to prevent nausea/vomiting

Key advantage Rapid rescue for unpredictable "off" episodes; can be self-administered by patient or carer

PBS status ⚠ PBS Authority Required

Step 3: Consider Advanced Therapies

Referral to a movement disorder specialist should be considered when motor fluctuations are not adequately controlled with oral medication adjustments (Step 1 and 2). Advanced therapies include:

Therapy	Mechanism	Indications	Availability
Deep Brain Stimulation (DBS)	Bilateral STN or GPi electrode implantation delivering continuous high-frequency stimulation	Motor fluctuations and/or dyskinesia inadequately controlled medically; good cognitive function; no active psychiatric illness; good levodopa response (≥30% improvement)	Available at major centres: Royal Melbourne, Westmead, Flinders, Royal Brisbane, Sir Charles Gairdner
Levodopa–Carbidopa Intestinal Gel (Duodopa®)	Continuous jejunal infusion via PEG-J stoma providing stable levodopa levels	Severe motor fluctuations and dyskinesia refractory to optimised oral therapy; unsuitable for DBS	PBS Authority Required — specialist-initiated only
Subcutaneous Apomorphine Infusion	Continuous SC apomorphine via pump, providing 12–16 hours of continuous dopaminergic stimulation	Motor fluctuations in patients not suitable for DBS or Duodopa; can be trialled before more invasive options	Specialist-initiated; requires domperidone cover

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DBS contraindications: Significant cognitive impairment (dementia), active major psychiatric disorder (untreated depression, psychosis), inability to cooperate with programming, age >75 (relative), severe brain atrophy, and uncontrolled anticoagulation. All candidates require formal neuropsychological assessment pre-operatively.

Non-Motor Symptoms

Non-motor symptoms (NMS) are ubiquitous in PD and are often more disabling than the motor features. They may precede motor onset by years (prodromal PD), contribute significantly to reduced quality of life, predict nursing home placement, and are frequently under-recognised. Up to 95% of patients with PD report at least one NMS, and the mean number per patient is 7–10.

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Screening tool: The Non-Motor Symptoms Questionnaire (NMSQuest) is a validated 30-item patient-completed screening tool recommended for use at every annual review. Alternatively, the MDS-NMS (84 items) provides a comprehensive assessment for specialist settings.

Autonomic Dysfunction

Symptom	Prevalence	First-Line Treatment
Constipation	60–80%	Dietary fibre, adequate fluids, regular exercise; macrogol 3350 (Movicol®); osmotic laxatives; if refractory: prucalopride (Resotran®) 2 mg daily — PBS Authority Required
Orthostatic hypotension	30–50%	Review and reduce antihypertensives; increase salt and fluid intake; compression stockings; fludrocortisone 50–200 mcg/day PO (PBS General Benefit); midodrine 2.5–10 mg PO TDS (PBS Authority Required for orthostatic hypotension)
Urinary dysfunction	30–70%	Exclude UTI; bladder training; avoid evening fluids; for overactive bladder: solifenacin (Vesicare®) 5–10 mg/day or mirabegron (Betmiga®) 25–50 mg/day — specialist advice for refractory cases
Sialorrhoea (drooling)	30–50%	Glycopyrrolate (glycopyrronium) 1 mg PO BD–TDS; botulinum toxin injections to salivary glands (specialist); speech therapy for swallow strategies
Gastroparesis	20–50%	Small frequent meals; avoid high-fat meals; may impair levodopa absorption — consider liquid levodopa or jejunal delivery; domperidone 10 mg PO TDS (PBS General Benefit) — preferred prokinetic in PD (does not cross BBB)

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Metoclopramide is CONTRAINDICATED in Parkinson disease. Metoclopramide is a D2 receptor antagonist that crosses the blood–brain barrier and will worsen parkinsonian symptoms. Use domperidone (which does not cross the BBB) as the prokinetic of choice in PD.

Sleep Disorders

Sleep Disorder	Features & Treatment
REM Sleep Behaviour Disorder (RBD)	Dream enactment behaviour (punching, kicking, shouting during sleep); very common in PD (30–50%); may precede motor symptoms by decades. First-line: clonazepam 0.5–2 mg PO nocte or melatonin 3–12 mg PO nocte. Safety measures: remove sharp objects from bedside, place mattress on floor, consider bed rails.
Excessive Daytime Somnolence	Affects 20–40%. Review dopaminergic medications (DA agonists and levodopa are common causes); address sleep hygiene; exclude sleep apnoea (polysomnography referral). Modafinil 100–200 mg mane may be considered — not PBS-listed for PD.
Insomnia	Common; often multifactorial (nocturia, off-periods, pain, RBD, mood disorder). Optimise dopaminergic therapy for nocturnal off-periods (controlled-release levodopa at bedtime). Avoid benzodiazepines long-term in elderly — prefer melatonin or trazodone.
Restless Legs Syndrome	Overlap with PD is common. Dopamine agonists (pramipexole, ropinirole) or gabapentin enacarbil (Horizant®) are first-line. Check ferritin level — supplement if <75 mcg/L.

Mood and Cognitive Changes

Depression

Prevalence: 40–50% of PD patients; may be reactive or neurobiological (related to serotonin and dopamine depletion)
Screening: PHQ-9 or Montgomery–Åsberg Depression Rating Scale (MADRS) at diagnosis and annually
First-line pharmacotherapy: SSRIs (citalopram 10–20 mg/day or sertraline 50–100 mg/day) — generally well-tolerated in PD
SNRIs (venlafaxine 75–150 mg/day, desvenlafaxine 50–100 mg/day) are an alternative — may also help with pain and fatigue
Tricyclic antidepressants (nortriptyline 25–75 mg nocte) may be useful when insomnia and pain are comorbid — caution with anticholinergic burden and cardiac effects
Non-pharmacological: cognitive behavioural therapy (CBT) has level-1 evidence in PD depression; exercise therapy is beneficial

Anxiety

Prevalence: 25–40%; frequently co-exists with depression and often fluctuates with motor "off" periods
SSRIs/SNRIs as above; benzodiazepines to be avoided long-term due to fall risk and cognitive effects
Psychological therapies (CBT, mindfulness-based stress reduction) are effective

Cognitive Impairment and Dementia

Mild cognitive impairment (PD-MCI) affects 20–30% at diagnosis; PD dementia (PDD) develops in up to 80% over 15–20 years
Screening: Montreal Cognitive Assessment (MoCA) — validated in PD; repeat annually
PDD treatment: rivastigmine (Exelon®) 1.5 mg PO BD, titrate to 6 mg BD over 4–8 weeks — PBS Authority Required for PDD; transdermal patch (4.6 mg/24 hours, titrate to 9.5 mg/24 hours) available for patients with swallowing difficulties
Avoid anticholinergics (benztropine, trihexyphenidyl) in patients with cognitive impairment — will worsen cognition
Review and reduce polypharmacy; avoid anticholinergic medications and benzodiazepines

Psychosis and Hallucinations

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Management of PD psychosis: First step is to reduce or discontinue (in order) anticholinergics, MAO-B inhibitors, dopamine agonists, amantadine, and COMT inhibitors — NOT levodopa, which should be reduced last. If symptoms persist, initiate an atypical antipsychotic: pimavanserin (Nuplazid®) — not currently PBS-listed in Australia; quetiapine 12.5–50 mg nocte (off-label but widely used); clozapine 12.5–50 mg (effective but requires blood monitoring). Olanzapine and risperidone are CONTRAINDICATED in PD — will worsen parkinsonism.

Pain in Parkinson Disease

Pain affects 40–80% of PD patients and is classified into five types (PD Pain Classification Scale):

Type	Description	Management
Musculoskeletal	Joint stiffness, frozen shoulder, postural deformities	Physiotherapy, optimise dopaminergic therapy, simple analgesics
Dystonic	Early morning foot dystonia, "off"-period dystonia	Optimise levodopa; botox for focal dystonia
Central / Neuropathic	Burning, tingling, diffuse pain not explained by musculoskeletal cause	Duloxetine 60 mg/day; gabapentin/pregabalin; amitriptyline (caution in elderly)
Akathitic	Restlessness and inner unease, often during "off" periods	Optimise dopaminergic therapy; clonazepam
Primary (central)	Unexplained, unresponsive to levodopa	May require opioid-based analgesia under specialist guidance

Other Non-Motor Symptoms

Fatigue: Affects 30–50%. Assess for depression, sleep disorders, anaemia. Exercise, energy conservation strategies. Modafinil (off-label) may be considered.
Anosmia / Hyposmia: Present in >90% of PD patients, often earliest prodromal feature. No effective treatment; advise on food safety (inability to detect spoiled food or gas leaks).
Dysphagia: Progressive; speech pathology assessment essential; modified diet textures (IDDSI framework); swallowing exercises (Lee Silverman Voice Treatment — LSVT LOUD).
Sexual dysfunction: Common and under-discussed. May be dopaminergic medication-related (hypersexuality) or disease-related (erectile dysfunction, vaginal dryness). PDE5 inhibitors for erectile dysfunction; dose adjustment of dopamine agonists for ICD-related hypersexuality.

Special Populations

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Pregnancy

General PD is rare in women of childbearing age (juvenile-onset/young-onset). Most dopaminergic medications have limited safety data in pregnancy. Teratogenicity data for levodopa, dopamine agonists, and MAO-B inhibitors is limited but reassuring in small case series.

Levodopa Considered relatively safe; generally continued at lowest effective dose if symptomatic PD requires treatment. Teratogenic risk appears low but data is limited.

Dopamine agonists Bromocriptine and cabergoline (for prolactinoma) have the most pregnancy safety data. Pramipexole, ropinirole, and rotigotine lack adequate data — discontinue if possible.

MAO-B inhibitors / Amantadine Contraindicated in pregnancy — discontinue. Amantadine is associated with cardiovascular malformations.

Breastfeeding Levodopa and dopamine agonists may suppress prolactin and reduce lactation. Risk-benefit discussion essential with patient and obstetrician/neonatologist.

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Elderly (≥75 years)

Levodopa First-line agent in the elderly — dopamine agonists carry higher risk of hallucinations, impulse control disorders, and somnolence in this age group. Start at lower doses (50/12.5 mg BD–TDS) and titrate slowly.

Avoid anticholinergics Benztropine and trihexyphenidyl are associated with confusion, urinary retention, constipation, and falls — contraindicated in elderly PD patients.

Fall prevention Falls are the leading cause of morbidity. Physiotherapy, home safety assessments, and medication review (reduce sedatives) are essential.

Polypharmacy review Regular medication review with GP; avoid medications that worsen PD (metoclopramide, antipsychotics, centrally-acting anticholinergics).

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Renal Impairment

Levodopa No specific dose adjustment required, but use with caution in severe CKD — monitor for increased ADRs (nausea, orthostatic hypotension).

Pramipexole Requires dose reduction — CrCl 35–59 mL/min: max 1.5 mg/day; CrCl 15–34: max 0.75 mg/day; CrCl <15: avoid.

Amantadine Significant renal clearance — dose reduction mandatory in CKD; avoid if CrCl <15 mL/min. Risk of toxicity (confusion, livedo reticularis).

Entacapone / Opicapone No specific adjustment, but use with caution. Tolcapone (not available in Australia) requires hepatic monitoring.

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Hepatic Impairment

Levodopa Use with caution; dose reduction may be needed in severe hepatic impairment. Monitor LFTs at baseline.

Entacapone Avoid in severe hepatic impairment — hepatic metabolism. Tolcapone (not available in Australia) is contraindicated in liver disease.

Rasagiline / Selegiline Metabolised hepatically — use with caution in moderate impairment; avoid in severe hepatic failure.

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Cognitive Impairment / Dementia

Prioritise levodopa Dopamine agonists, anticholinergics, and amantadine should be weaned as they significantly worsen cognition and hallucinations.

Rivastigmine Only cholinesterase inhibitor with PBS authority for PD dementia — 1.5 mg BD titrated to 6 mg BD; transdermal patch for dysphagia.

Delirium prevention PD medications must NEVER be abruptly stopped — risk of neuroleptic malignant-like syndrome. Continue levodopa through hospital admissions; ensure adequate hydration and infection management.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians have a lower overall prevalence of diagnosed PD compared with non-Indigenous Australians, but this may reflect under-diagnosis rather than a true lower incidence. Barriers to early diagnosis and optimal management are significant, particularly in remote and very remote communities.

Access to specialist care

There is a severe shortage of neurologists and movement disorder specialists in remote and regional Australia. Telehealth neurology services (MBS items 99200, 99203, 99212) are essential to bridge this gap and should be actively offered. The Australian and New Zealand Association of Neurologists (ANZAN) supports virtual movement disorder assessments.

Diagnostic delays

Indigenous Australians in remote communities may present later with more advanced disease. Early symptoms (tremor, stiffness, slowness) may be attributed to ageing or arthritis. DaTscan availability is limited to capital cities — travel requirements are a significant barrier. Culturally appropriate health education about PD symptoms in community-controlled health services is needed.

Medication access and adherence

Access to PBS medications through Remote Area Aboriginal Health Services (RAAHS) and Section 100 (S100) programs is critical. Extended-release formulations and patches (rotigotine, rivastigmine patch) may be preferable where medication adherence is difficult. Medicine management programs through Aboriginal Community Controlled Health Organisations (ACCHOs) should be utilised.

Multidisciplinary care

Access to physiotherapy, speech pathology, occupational therapy, and dietetics is severely limited in remote communities. Use of telehealth allied health consultations, Fly-In Fly-Out (FIFO) specialist services, and Royal Flying Doctor Service (RFDS) referrals are essential. Carer support programs should be culturally safe and involve family and community Elders.

Cultural considerations

Dementia and cognitive decline carry particular cultural sensitivities in some Aboriginal and Torres Strait Islander communities. Health literacy resources should be co-designed with local communities. The term "dementia" may need to be contextualised in culturally appropriate language. Advance care planning should respect cultural obligations and family decision-making processes.

Comorbidities

Higher rates of cardiovascular disease, diabetes, chronic kidney disease, and rheumatic heart disease in Indigenous Australians may complicate PD management and increase drug interaction risks. Regular medication review and a holistic, whole-person approach within ACCHOs is essential.

ℹ️

Recommended resources: Australian Institute of Health and Welfare (AIHW) — Aboriginal and Torres Strait Islander Health Performance Framework; Parkinson's Australia Indigenous health resources; RHDAustralia clinical guidelines for culturally safe neurological care; HealthInfoNet (www.healthinfonet.ecu.edu.au) for Indigenous-specific health data.

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