Palliative Care in Parkinson Disease

Last updated 1 Jun 2026 · Palliative care

📋 Key Information Summary

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Palliative care should be introduced early in Parkinson disease (PD) and integrated alongside disease-modifying and symptomatic therapy — not reserved for end of life alone.
Motor fluctuations (wearing-off, on–off phenomena, freezing) worsen in advanced PD and require individualised levodopa dose adjustment, extended-release formulations, and adjunctive agents (MAO-B inhibitors, COMT inhibitors, dopamine agonists).
Non-motor symptoms — pain, autonomic dysfunction, sleep disturbance, hallucinations, depression, and cognitive decline — often cause greater distress than motor symptoms and must be systematically screened.
Dysphagia affects up to 80% of advanced PD patients, raising aspiration pneumonia risk; speech–language pathology assessment and texture-modified diet are essential.
Medication continuity is critical: abrupt withdrawal of dopaminergic agents can precipitate neuroleptic malignant-like syndrome (NMS-LS) or akinetic crisis — a medical emergency.
Antipsychotic use in PD dementia must be restricted to quetiapine or clozapine; haloperidol and risperidone are contraindicated due to worsening parkinsonism.
Subcutaneous (subcut) apomorphine, rotigotine transdermal patches, and levodopa–carbidopa intestinal gel (LCIG / Duodopa®) are key options when oral medication fails.
Advanced care planning, including resuscitation wishes, feeding preferences, and place-of-death preferences, should be documented early and reviewed regularly.
Multidisciplinary team input — neurology, palliative medicine, speech pathology, occupational therapy, physiotherapy, dietetics, social work, and specialist PD nurses — is essential.
Aboriginal and Torres Strait Islander peoples face barriers to palliative care access; culturally safe, community-based models improve outcomes.
Neuroleptic malignant-like syndrome (NMS-LS) from abrupt PD medication cessation presents with rigidity, hyperthermia, autonomic instability, and altered consciousness — treat as a medical emergency with dantrolene or bromocriptine and reinstate dopaminergic therapy.
Depression and anxiety affect 40–50% of advanced PD patients; SSRIs (sertraline, citalopram) and SNRIs (venlafaxine) are first-line, with caution regarding serotonin syndrome with MAO-B inhibitors.

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. While traditionally managed by neurologists focusing on motor symptom control, the palliative care needs of people with advanced PD are increasingly recognised as complex, multidimensional, and deserving of early integrated palliative care.

Palliative care in PD is not synonymous with end-of-life care. International and Australian guidelines recommend that palliative care principles — symptom management, quality of life, psychosocial support, and advance care planning — be introduced from the time of diagnosis and intensified as the disease progresses through Hoehn and Yahr stages IV and V.

Australian Burden of Disease

An estimated 80,000–100,000 Australians live with PD, with approximately 30–40% having advanced disease requiring complex palliative symptom management.
PD prevalence increases sharply after age 65; the median age at diagnosis is 65 years, and median survival from diagnosis is 10–15 years.
The AIHW reports PD as the second most common neurodegenerative condition after dementia, with significant hospital and residential aged-care burden.
Caregiver burden is substantial: up to 60% of primary carers report clinically significant depression and burnout.
Aboriginal and Torres Strait Islander peoples experience barriers to neurology and palliative care services, particularly in remote and very remote areas of Australia.

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Key principle: Palliative care in PD should be introduced early and escalated gradually. Waiting until the terminal phase misses the window for advance care planning, optimal symptom control, and psychosocial support for patients and families.

Motor Fluctuations

Motor fluctuations are among the most disabling features of advanced PD and a major driver of palliative care referral. They result from progressive dopaminergic neuronal loss, narrowing of the therapeutic window for levodopa, and altered pharmacokinetics. Effective management requires a structured approach combining pharmacological adjustment, allied health input, and patient/carer education.

Types of Motor Fluctuations

Type	Description	Timing	Management Strategy
Wearing-off	Return of symptoms before next scheduled dose	Predictable, dose-related	Reduce dose interval, add COMT or MAO-B inhibitor
On–off phenomena	Unpredictable switches between mobile ("on") and immobile ("off") states	Unpredictable	Continuous dopaminergic stimulation (apomorphine, LCIG)
Peak-dose dyskinesia	Involuntary choreiform movements at peak levodopa effect	Related to levodopa peak	Reduce single levodopa dose, add amantadine
Freezing of gait (FOG)	Sudden inability to initiate or continue walking	Often "off"-related; may occur "on"	Cueing strategies, physiotherapy, adjust medication timing
Early morning akinesia	Inability to move on waking before first levodopa dose	Early morning	Extended-release levodopa (e.g., Sinemet CR®) at night; dispersible levodopa on waking

Pharmacological Management of Motor Fluctuations

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Levodopa–Carbidopa (Sinemet®)

Sinemet® · Kinson® · Levocarb® · Dopa decarboxylase inhibitor combination

Adult dose 100/25 mg or 250/25 mg PO TDS–QID; titrate to effect. In advanced PD, smaller more frequent doses (e.g., 100/25 mg 5–6 times daily) reduce peak-dose dyskinesia.

Extended-release Sinemet CR® 100/25 or 200/50 mg PO BD — for overnight and early-morning symptom control

Renal adjustment Use with caution in severe renal impairment (eGFR <15); no specific dose reduction mandated but monitor closely

PBS status ✔ PBS General Benefit

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Entacapone

Comtan® · COMT inhibitor

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

Key notes Extends levodopa half-life by ~30–60%; reduces wearing-off. Diarrhoea is the most common adverse effect. May intensify dyskinesia — reduce levodopa dose by ~20–30% when initiating.

Renal adjustment No adjustment required

PBS status ✔ PBS General Benefit

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Rasagiline

Azilect® · MAO-B inhibitor

Adult dose 1 mg PO daily (0.5 mg if on ciprofloxacin or moderate hepatic impairment)

Key notes Reduces off-time by ~1 hour/day. Avoid tyramine-rich foods at higher doses. Serotonin syndrome risk with SSRIs/SNRIs — use with caution; sertraline and citalopram are safest if antidepressant needed.

Renal adjustment No adjustment required

PBS status ⚕ PBS Authority Required

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Apomorphine (subcutaneous injection)

APO-go Pen® · Dopamine agonist (rescue)

Rescue dose 1–3 mg SC PRN for severe "off" episodes; onset 10–20 minutes

Continuous infusion 1–4 mg/hr via SC pump for refractory fluctuations; pre-medicate with domperidone 20 mg TDS for 3 days prior to initiation to prevent nausea/vomiting

Key notes Requires domperidone pre-treatment. Monitor for QT prolongation. Avoid in patients on QT-prolonging agents. Rotate injection sites to prevent subcutaneous nodules.

PBS status ⛔ Not PBS-listed (Special Access Scheme may apply)

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Amantadine

Symmetrel® · NMDA antagonist

Adult dose 100 mg PO BD (max 400 mg/day); start 100 mg daily

Key notes Only pharmacological agent with evidence for reducing dyskinesia. Livedo reticularis, ankle oedema, confusion, and hallucinations are common adverse effects in elderly patients.

Renal adjustment Reduce dose by 50% if eGFR 30–60 mL/min; reduce by 75% if eGFR 15–30; avoid if eGFR <15

PBS status ✔ PBS General Benefit

Advanced Therapies for Refractory Motor Fluctuations

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When oral pharmacotherapy is insufficient, device-aided therapies may be considered in selected patients. These include subcutaneous apomorphine infusion, levodopa–carbidopa intestinal gel (LCIG / Duodopa® via PEG-J), and deep brain stimulation (DBS). In the palliative setting, LCIG and apomorphine infusion are more commonly used as DBS carries surgical risks and is generally reserved for earlier disease stages.

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Levodopa–Carbidopa Intestinal Gel (LCIG)

Duodopa® · Continuous jejunal infusion

Administration Continuous jejunal infusion via PEG-J tube; morning bolus followed by continuous infusion (typically 60–120 mL/day of 20/5 mg/mL gel), with extra boluses PRN

Key notes Significantly reduces off-time and dyskinesia severity. Requires PEG-J insertion (interventional gastroenterology). Complications include tube dislodgement, stoma infection, and jejunal polyposis. Requires specialist PD nurse training for pump management.

PBS status ⛔ Authority Required (STREAMLINED 8263) — specialist initiation only

Freezing of Gait — Non-Pharmacological Strategies

Auditory cueing: rhythmic auditory stimuli (metronome, music) to initiate stepping.
Visual cueing: laser-line walking sticks, floor markings, or transverse lines on floor.
Attentional strategies: counting, stepping sideways, marching in place.
Physiotherapy: cueing-based gait training, balance exercises, and falls prevention programmes.

Non-Motor Symptoms

Non-motor symptoms (NMS) in PD are ubiquitous and often more distressing to patients and carers than motor features. In advanced disease, NMS dominate the clinical picture and are the primary driver of reduced quality of life, nursing home placement, and carer distress. Systematic screening using validated tools such as the Non-Motor Symptoms Scale (NMSS) or the MDS-NMS is recommended.

Key Non-Motor Symptom Domains in Advanced PD

Autonomic

Orthostatic Hypotension

Supine BP ≥20/10 mmHg drop on standing. Non-pharmacological: increased fluid (2–2.5 L/day), salt loading, compression stockings, slow positional changes. Pharmacological: fludrocortisone 0.1 mg PO daily or midodrine 2.5–10 mg PO TDS.

Assessment: active standing BP, 24-hour ambulatory BP monitoring

Psychiatric

Hallucinations & Psychosis

Visual hallucinations in 20–40% of advanced PD, often medication-related. First step: reduce anticholinergics, amantadine, dopamine agonists, MAO-B inhibitors. Second step: quetiapine 12.5–50 mg nocte or clozapine (requires FBE monitoring — risk of agranulocytosis).

Setting: Outpatient neurology or inpatient if acute behavioural disturbance

Cognitive

PD Dementia (PDD)

Cognitive impairment sufficient to impair daily function, typically developing ≥1 year after motor onset. Rivastigmine 3 mg PO BD (titrate from 1.5 mg BD) is PBS-listed for PDD. Avoid antipsychotics other than quetiapine or clozapine. Cholinesterase inhibitors may modestly improve cognition and behaviour.

Setting: Outpatient with neuropsychological assessment; consider ACAT for residential care if severe

Pain in Advanced PD

Pain affects 40–85% of PD patients and is multifactorial: musculoskeletal (rigidity, dystonia), central/neuropathic, akathitic, and related to "off" periods. Approach:

Optimise dopaminergic therapy

Pain worsening in "off" periods responds to levodopa adjustment. Consider continuous dopaminergic stimulation.

Neuropathic pain agents

Pregabalin 25–150 mg PO BD or gabapentin 100–300 mg PO TDS. Duloxetine 30–60 mg PO daily for comorbid depression and pain. Avoid TCAs in cognitive impairment.

Palliative opioids

Low-dose oxycodone 2.5–5 mg PO BD or morphine 2.5–5 mg SC for refractory pain. Transdermal fentanyl for patients with dysphagia. Use with constipation prophylaxis (macrogol).

Multimodal approach

Physiotherapy, heat/cold therapy, massage, acupuncture. Address nocturnal pain and early morning dystonia with overnight levodopa CR or rotigotine patch.

Depression and Anxiety

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Drug interaction caution: Combining SSRIs/SNRIs with MAO-B inhibitors (rasagiline, selegiline) carries a theoretical risk of serotonin syndrome. In practice, sertraline (≤100 mg/day) and citalopram (≤20 mg/day) are considered safest when used with MAO-B inhibitors at standard doses. Monitor closely for agitation, tremor, clonus, and hyperthermia.

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Sertraline

Zoloft® · SSRI

Adult dose 50 mg PO daily, titrate to 100–200 mg daily. Start low in elderly (25 mg daily).

Renal adjustment No adjustment required

PBS status ✔ PBS General Benefit

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Mirtazapine

Avanza® · NaSSA antidepressant

Adult dose 15 mg PO nocte, titrate to 30 mg nocte. Sedating at lower doses — useful for insomnia and appetite stimulation.

Renal adjustment Use with caution; clearance reduced ~30% in moderate renal impairment

PBS status ✔ PBS General Benefit

Sleep Disturbance

REM sleep behaviour disorder (RBD): Dream enactment, risk of injury to patient and bed-partner. Clonazepam 0.5–2 mg PO nocte (most effective) or melatonin 3–12 mg PO nocte. Safety measures: padding bed edges, removing firearms/sharp objects, bed-partner safety education.
Insomnia: Optimise dopaminergic therapy for nocturnal akinesia. Consider levodopa CR at bedtime or rotigotine patch. Avoid benzodiazepines long-term in cognitively impaired patients.
Excessive daytime somnolence (EDS): Assess for dopaminergic over-stimulation, sleep apnoea, and depression. Modafinil 100–200 mg PO mane may be trialled (limited evidence).

Autonomic Dysfunction Beyond Orthostasis

Symptom	Prevalence	Management
Constipation	60–80%	High-fibre diet, adequate fluids, macrogol 3350 (Movicol®) 1–3 sachets daily. Avoid bulk-forming agents if dysphagia. Prucalopride 2 mg PO daily for refractory constipation.
Urinary urgency/frequency	30–70%	Mirabegron 50 mg PO daily (preferred — less CNS penetration than oxybutynin). If anticholinergic needed: solifenacin 5 mg PO daily (caution in PDD).
Sialorrhoea	30–50%	Glycopyrrolate 1 mg PO BD–TDS, sublingual atropine 1% drops (1–2 drops sublingually PRN), botulinum toxin injections to parotid/submandibular glands, or referral for radiotherapy in refractory cases.
Gastroparesis	70–100%	Domperidone 10 mg PO TDS (before meals) — does not cross BBB. Avoid metoclopramide (dopamine antagonist — worsens parkinsonism). Small frequent meals. Assess impact on levodopa absorption.

Dysphagia

Dysphagia affects up to 80% of people with advanced PD and is a major contributor to aspiration pneumonia, malnutrition, and mortality. Oropharyngeal dysphagia in PD is characterised by delayed swallowing initiation, reduced lingual control, pharyngeal residue, and upper oesophageal sphincter dysfunction. Silent aspiration is common — patients may not exhibit overt choking.

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Aspiration pneumonia is the leading cause of death in advanced PD. Proactive dysphagia screening, speech pathology assessment, and aspiration precautions are critical palliative interventions.

Assessment

Bedside swallow assessment: Speech–language pathology (SLP) evaluation including water swallow test, texture tolerance assessment, and observation of meal.
Instrumental assessment: Videofluoroscopic swallowing study (VFSS) or fibreoptic endoscopic evaluation of swallowing (FEES) to objectively characterise aspiration pattern and guide texture modification.
Nutritional status: Dietitian assessment, body weight monitoring, Mini Nutritional Assessment (MNA), and serum albumin/pre-albumin.
MBS item: Speech pathology services under MBS items 10960, 10962 (Chronic Disease Management plan) or public hospital outpatient SLP.

Management Strategies

Texture modification

International Dysphagia Diet Standardisation Initiative (IDDSI) framework. Levels 0–7 for fluids and foods. Start with soft and mildly thick fluids; adjust based on VFSS/FEES findings.

Swallowing strategies

Chin tuck, supraglottic swallow, effortful swallow technique. Upright positioning (≥60°) during and 30 minutes after meals. Small boluses, slow feeding pace.

Medication formulation adjustments

Switch to dispersible or liquid formulations where available. Levodopa dispersible tablets can be dissolved in small volumes of water. Rivastigmine oral solution available. Avoid crushing modified-release formulations.

Enteral feeding decision

PEG or nasogastric tube (NGT) for nutritional support if inadequate oral intake. In advanced PD with significant cognitive impairment, discuss goals of care: PEG placement may not prevent aspiration and may not improve comfort. Individualised decision with family and multidisciplinary team.

Percutaneous Endoscopic Gastrostomy (PEG) Considerations in Palliative PD

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Important: PEG placement in advanced PD with dementia requires careful goals-of-care discussion. Evidence does not support PEG improving survival or quality of life in advanced dementia. However, in cognitively intact patients with isolated dysphagia, PEG can facilitate medication delivery and hydration. LCIG (Duodopa®) delivery via PEG-J is a separate indication and may be appropriate in selected patients with refractory motor fluctuations.

Medication Continuity

Medication continuity is a critical safety consideration in advanced PD. Abrupt withdrawal or significant dose reduction of dopaminergic agents — including levodopa, dopamine agonists, MAO-B inhibitors, and amantadine — can precipitate a neuroleptic malignant-like syndrome (NMS-LS) or akinetic crisis. This is a life-threatening medical emergency.

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NEVER abruptly cease dopaminergic medications in PD. Even in the terminal phase, levodopa should be continued (via NG/PEG if unable to swallow) or gradually weaned over days to weeks. Abrupt cessation can cause NMS-LS: hyperthermia (>38°C), severe rigidity, autonomic instability, altered consciousness, elevated CK, and multi-organ failure — mortality 10–20%.

Common Scenarios Threatening Medication Continuity

Scenario	Risk	Mitigation Strategy
Hospital admission (nil by mouth)	PD medications omitted or delayed during fasting for procedures, ICU admission, or perioperative periods	Ensure PD medications are continued via NG/PEG when nil by mouth. Liaise with neurology early. Medication charts must include specific timing (e.g., "100/25 mg levodopa every 3 hours 0600–2200"). Never substitute antipsychotics for confusion.
Dysphagia — medication unable to be swallowed	Missed doses if no alternative formulation	Use dispersible levodopa (dissolve in water, give via NG tube). Rotigotine transdermal patch bypasses swallowing. Rivastigmine transdermal patch (Exelon Patch®). SC apomorphine as rescue or continuous infusion.
Antipsychotic prescribed for agitation	Typical antipsychotics (haloperidol, droperidol) and atypical agents (risperidone, olanzapine) worsen parkinsonism	Only quetiapine 12.5–50 mg or clozapine are safe. EDUCATE emergency and inpatient teams. Place medication alerts on patient's file. Consider MedicAlert bracelet.
Anti-emetic prescribing	Metoclopramide and prochlorperazine are dopamine antagonists — worsen parkinsonism	Use domperidone (does not cross BBB), ondansetron, or granisetron for nausea/vomiting. Avoid all centrally-acting anti-emetics.
Residential aged care — medication mismanagement	Medication timing errors, substitution errors, or omission during night shifts	Specialist PD nurse liaison with RACF staff. Simplified medication regimen where possible. Clear medication administration instructions in care plan. Consider rotigotine patch to reduce dosing frequency.

Transdermal and Non-Oral Options for Medication Continuity

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Rotigotine Transdermal Patch

Neupro® · Dopamine agonist (transdermal)

Adult dose Start 2 mg/24hr patch once daily; titrate by 2 mg/24hr weekly to max 8 mg/24hr (adjuvant to levodopa). Apply to clean, dry skin on abdomen, thigh, upper arm, or flank. Rotate sites daily.

Key notes Provides continuous dopaminergic stimulation. Avoids first-pass metabolism. Useful when swallowing is unreliable. Application site reactions common. Store refrigerated before use.

Renal adjustment No adjustment required

PBS status ⚕ PBS Authority Required

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Rivastigmine Transdermal Patch

Exelon Patch® · Cholinesterase inhibitor (transdermal)

Adult dose 4.6 mg/24hr patch once daily for 4 weeks → 9.5 mg/24hr → max 13.3 mg/24hr if tolerated. Apply to upper back, upper arm, or chest. Rotate sites.

Key notes PBS-listed for PDD. Transdermal formulation has fewer GI adverse effects than oral. Avoid if body weight <50 kg (higher plasma levels). Monitor for bradycardia and syncope.

Renal adjustment No adjustment required

PBS status ⚕ PBS Authority Required

End-of-Life Medication Management

In the final days to weeks of life in PD, the goals shift to comfort. However, medication continuity remains paramount even at end of life:

Continue levodopa via NG/PEG if possible — sudden cessation may cause distressing rigidity and dystonic posturing.
If continuing oral/enteral levodopa is no longer possible or desired, convert to a transdermal rotigotine patch (if not already on a dopamine agonist) or gradually reduce levodopa over 1–2 weeks.
Manage secretions with sublingual glycopyrrolate or hyoscine butylbromide SC.
Anticipate and treat terminal agitation with midazolam SC (2.5–5 mg SC PRN or continuous infusion 0.5–2.5 mg/hr) as per palliative care guidelines.
Ensure syringe driver compatibility of PD medications if using continuous subcutaneous infusion for symptom control at end of life.

Pathophysiology of Advanced Parkinson Disease

Understanding the neurobiology of PD progression underpins palliative care decision-making and explains why symptoms become increasingly complex and medication-responsive.

Neuropathological Progression

Stage 1–2 (Braak staging): Alpha-synuclein pathology begins in the olfactory bulb and dorsal motor nucleus of the vagus (causing anosmia, constipation, REM sleep behaviour disorder — prodromal symptoms).
Stage 3–4: Progression to the substantia nigra pars compacta (motor symptoms emerge), locus coeruleus, raphe nuclei, and amygdala (causing depression, anxiety, sleep disturbance).
Stage 5–6: Neocortical involvement — frontal, temporal, and parietal cortices (causing dementia, hallucinations, severe autonomic dysfunction). This correlates with advanced PD and palliative care needs.

Pharmacological Basis of Advanced Disease

As striatal dopaminergic neurons degenerate beyond ~80%, the therapeutic window for exogenous levodopa narrows dramatically. Motor fluctuations arise because:

Reduced presynaptic dopamine storage capacity means response is dependent on continuous exogenous delivery.
Pulsatile dopamine receptor stimulation (from intermittent oral levodopa) causes downstream receptor sensitisation and dyskinesia.
Gastric emptying is delayed in PD, causing erratic drug absorption and unpredictable on–off responses.
Non-dopaminergic systems (serotonergic, noradrenergic, cholinergic) degenerate independently, explaining non-motor symptoms that do not respond to levodopa.

Clinical Presentation & Diagnostic Criteria

Advanced PD — Clinical Features

Advanced PD is characterised by Hoehn and Yahr stage IV–V (bilateral symptoms with postural instability, wheelchair-bound or bed-bound without assistance). The clinical presentation encompasses both motor and non-motor domains:

Domain	Features
Motor	Wearing-off, on–off fluctuations, peak-dose dyskinesia, freezing of gait, festinating gait, postural instability with falls, camptocormia, severe rigidity, dystonia (especially foot dystonia in early morning/off periods)
Cognitive	PD dementia (PDD) — attention, executive dysfunction, visuospatial impairment, fluctuating cognition. Must develop ≥1 year after motor onset (otherwise may be dementia with Lewy bodies — DLB)
Psychiatric	Visual hallucinations (formed, often benign initially), delusions (paranoid — spouse infidelity, people in house), depression (40–50%), anxiety/panic (often in off states), apathy, impulse control disorders (gambling, hypersexuality — dopamine agonist-related)
Autonomic	Orthostatic hypotension, constipation, urinary urgency/incontinence, gastroparesis, erectile dysfunction, sialorrhoea, thermoregulatory failure
Swallowing	Oropharyngeal dysphagia, drooling, pharyngeal residue, aspiration (often silent)
Sleep	RBD, insomnia, excessive daytime somnolence, nocturia, restless legs
Pain	Musculoskeletal, dystonic, central/neuropathic, akathitic — often under-recognised

Diagnosis of PD Dementia (PDD)

MDS Clinical Diagnostic Criteria for PDD (2007, revised): Core features include diagnosis of PD (MDS criteria) with dementia developing ≥1 year after motor onset. Impairment in ≥2 cognitive domains (attention, executive, visuospatial, memory). Functional impact on daily activities. Key distinction from DLB: motor symptoms precede cognitive decline by ≥1 year.

Investigations

Investigations in advanced PD serve three purposes: confirming disease staging, monitoring treatment-related adverse effects, and excluding reversible causes of symptom deterioration (infection, metabolic derangement, medication effects).

Essential Cognitive assessment Montreal Cognitive Assessment (MoCA), Addenbrooke's Cognitive Examination (ACE-III), or comprehensive neuropsychological battery. MoCA <26 suggests cognitive impairment; MoCA <20 warrants PDD workup. Repeat annually or with clinical change.

Essential Non-Motor Symptoms Scale (NMSS) or MDS-NMS Validated screening tool covering cardiovascular, sleep, mood, perceptual, attention, gastrointestinal, urinary, sexual, and miscellaneous domains. Score guides treatment priorities.

Available Blood tests — FBC, UEC, LFTs, TFTs, vitamin B12, folate, CRP/ESR Exclude metabolic causes of confusion (uraemia, hyponatraemia, hypothyroidism). B12 deficiency may mimic or worsen parkinsonian symptoms. Monitor for clozapine-induced agranulocytosis if on clozapine (fortnightly FBE for 18 months, then monthly).

Available Videofluoroscopic Swallowing Study (VFSS) / FEES Instrumental dysphagia assessment. VFSS available in major hospitals; FEES increasingly available in tertiary centres and via mobile services. MBS item for SLP outpatient review under CDM plan.

Available Postural blood pressure (active standing) Measure supine BP, then 1 min and 3 min standing. Drop ≥20 mmHg systolic or ≥10 mmHg diastolic confirms orthostatic hypotension. Essential assessment at every visit in advanced PD.

Available QTc monitoring (ECG) Baseline and periodic ECG if on domperidone, quetiapine, or citalopram. QTc >500 ms or increase >60 ms from baseline — reassess medications.

Specialist DAT-SPECT (DaTscan®) Not usually required in advanced PD (diagnosis is established). May be useful to distinguish PD from drug-induced parkinsonism or essential tremor if diagnostic uncertainty remains.

Specialist MRI Brain Not for PD diagnosis per se but to exclude vascular parkinsonism, normal pressure hydrocephalus, or structural lesions. Important in atypical presentations.

Referral Palliative care assessment Referral to specialist palliative care for symptom burden, advance care planning, and end-of-life care. In Australia, public hospital palliative care services and community palliative care (e.g., Silver Chain in WA) are available. MBS items for specialist palliative care consultation (items 98, 110).

Risk Stratification & Severity Scoring

Palliative care referral and escalation in PD should be guided by clinical staging and symptom burden rather than prognosis alone. The following framework integrates disease stage, symptom burden, and care needs:

Early Integration

Hoehn & Yahr Stage II–III

Motor fluctuations emerging. Early advance care planning. Introduction of palliative care principles. GP-led care with neurology review 6–12 monthly. Screen for depression, anxiety, cognitive change. Address caregiver needs.

Setting: GP, outpatient neurology

Active Palliation

Hoehn & Yahr Stage IV

Postural instability, falls risk, significant dysphagia onset, PD dementia, hallucinations, autonomic failure. Palliative care team involvement. Advance care plan documented. Multidisciplinary team review. Medication rationalisation. Falls prevention. Symptom burden assessment (NMSS).

Setting: Community palliative care, neurology, specialist PD nurse

End of Life

Hoehn & Yahr Stage V

Wheelchair/bed-bound. Severe dysphagia, recurrent aspiration. Cachexia. Severe cognitive impairment. Comfort-focused care. Medication via NG/PEG or transdermal. Management of secretions, pain, agitation. Family support and bereavement care.

Setting: Home (with community palliative care), hospice, or inpatient palliative care unit

Prognostic Indicators in Advanced PD

Falls with fracture (hip fracture mortality in PD: 30–40% at 1 year).
Dysphagia with recurrent aspiration pneumonia.
PD dementia with severe functional dependence.
Cachexia (BMI <18.5 kg/m²) — associated with ~50% 1-year mortality.
Institutional placement — median survival from RACF placement in advanced PD is approximately 2–3 years.
Older age at onset, male sex, and hallucinations independently predict faster progression.

Monitoring

Ongoing monitoring in advanced PD palliative care should be structured to capture motor and non-motor symptom progression, medication adverse effects, and evolving care goals.

Every visit

Active standing BP — assess for orthostatic hypotension (supine → standing 1 and 3 min). Document symptom burden (brief screening questions on pain, hallucinations, mood, sleep, falls). Review medication adherence and timing. Assess swallowing (clinical observation during consultation).

Every 3–6 months

Motor assessment: MDS-UPDRS Part II–IV or Hoehn & Yahr staging. Cognitive screening: MoCA or ACE-III. Nutritional status: weight, BMI, dietary intake assessment. Caregiver wellbeing: Zarit Burden Interview or simple screening questions. Review advance care plan.

Every 6–12 months

Comprehensive bloods: FBC, UEC, LFTs, TFTs, B12, folate, vitamin D, calcium. FBE for clozapine: fortnightly × 18 months, then monthly (if applicable). ECG: if on QT-prolonging medications. Bone health: DEXA scan if risk factors; vitamin D and calcium supplementation (PBS-listed).

As clinically indicated

Dysphagia reassessment after any aspiration event, weight loss >5%, or change in swallow function. Neuropsychological assessment if cognitive decline noted or driving/financial capacity needs evaluation. Palliative care review if symptom burden escalating or goals of care changing.

Special Populations

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Elderly (>80 years)

All dopaminergic agents Start at lowest dose, titrate slowly. Increased sensitivity to hallucinations and orthostatic hypotension. Fall risk assessment mandatory at every visit.

Anticholinergics (trihexyphenidyl, benztropine) Avoid in elderly — confusion, urinary retention, constipation, falls. Strongly associated with cognitive decline.

Quetiapine Start 12.5 mg nocte; monitor for sedation, falls, metabolic effects. Prefer over all other antipsychotics in PD.

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Renal Impairment

Amantadine Contraindicated if eGFR <15. Reduce dose by 50% if eGFR 30–60. Accumulation risk: confusion, hallucinations, livedo reticularis.

Rivastigmine No dose adjustment required but monitor closely for GI adverse effects.

Levodopa No specific adjustment but renal impairment may alter levodopa metabolism. Monitor for dyskinesia and hallucinations with dose adjustments.

Glycopyrrolate Renally excreted; reduce dose in CKD. Monitor for anticholinergic toxicity.

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Hepatic Impairment

Rasagiline Contraindicated in severe hepatic impairment (Child-Pugh C). Reduce to 0.5 mg daily in moderate impairment (Child-Pugh B).

Entacapone Use with caution in hepatic impairment; dose reduction may be needed. Monitor LFTs.

All PD medications Hepatic impairment alters metabolism of many PD drugs. Monitor for increased adverse effects and adjust doses conservatively.

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Young-Onset PD (<50 years)

General considerations Young-onset PD may have a different trajectory with more dystonia and dyskinesia but slower cognitive decline. Palliative care needs evolve over decades. Family planning, employment, and psychological impact require specific support. Genetic counselling may be appropriate (LRRK2, PRKN, PINK1, GBA mutations).

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Cognitively Impaired / PD Dementia

Rivastigmine Only cholinesterase inhibitor with PBS authority for PDD in Australia. Transdermal patch preferred (fewer GI effects). Monitor for bradycardia.

Antipsychotics Quetiapine or clozapine ONLY. Clozapine requires blood monitoring (TGA-mandated). Ensure no other antipsychotics are inadvertently prescribed during hospital admissions.

Advance care planning Document capacity-based advance directives EARLY before cognitive decline progresses. Engage substitute decision-maker under state/territory guardianship legislation.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander peoples face significant barriers to accessing palliative care and neurology services. Culturally safe, community-based models of care are essential to improve outcomes for Indigenous Australians with advanced PD.

Access to specialist care

Neurology and palliative medicine specialists are concentrated in major cities. Remote and very remote communities (particularly in NT, WA, and QLD) have limited or no access. Telehealth (MBS items 99200–99215) and visiting specialist programmes (e.g., RFDS) are critical. Aboriginal Community Controlled Health Organisations (ACCHOs) should be engaged as primary coordinating hubs.

Cultural safety in palliative care

Palliative care models developed for non-Indigenous populations may not align with Indigenous concepts of health, Country, family, and end of life. Yarning-based approaches, family-inclusive decision-making, and understanding of sorry business and sorry camps are essential. The Palliative Care Australia "National Palliative Care Standards" (5th edition) include specific guidance on culturally safe care for First Nations peoples.

Medication access and continuity

Remote communities may have limited pharmacy access and medication supply chains (Remote Area Aboriginal Health Services — Section 100). PD medications requiring refrigeration (rotigotine patches before application, Duodopa gel) may be challenging. Medication continuity during patient transfer between community, clinic, and hospital is a known risk. Close liaison between ACCHO, hospital pharmacy, and remote health worker programmes is essential.

Health literacy and communication

Educational materials should be available in accessible formats — visual aids, plain English, and where possible, local language translations. Aboriginal and Torres Strait Islander health workers and health practitioners play a vital role in explaining complex medication regimens and advance care planning concepts. Recognise that some communities may have different understandings of "dementia" and palliative care.

Hospital and transfer of care risks

Indigenous patients with PD are at high risk of medication errors during hospital transfer — particularly omission of PD medications during fasting, inappropriate antipsychotic use, and delayed recognition of NMS-LS. Implementing a "PD Passport" or medication alert system in hospital electronic records is recommended. Specialist PD nurse liaison during admissions reduces harm.

Data and funding

The AIHW reports that Aboriginal and Torres Strait Islander peoples have higher rates of hospitalisation for PD-related complications (falls, aspiration pneumonia) but lower rates of specialist palliative care access. Closing the Gap Target 1 (life expectancy) and the National Aboriginal and Torres Strait Islander Palliative Care Strategy (2022) provide frameworks for improvement. Funding for Indigenous-specific palliative care programmes through the Department of Health and Aged Care should be actively pursued.

📚 References

1. Titova N, Chaudhuri KR. Palliative care and Parkinson's disease: emerging issues and challenges. J Parkinsons Dis. 2022;12(s1):S47–S56.
2. Bouca-Machado R, Lennaerts J, Bloem BR, Ferreira JJ. Palliative care for patients with Parkinson's disease: study protocol for a mixed-methods study. BMC Palliat Care. 2023;22(1):45.
3. Australian Institute of Health and Welfare (AIHW). Dementia in Australia. Cat. no. DEM 2. Canberra: AIHW; 2024.
4. Movement Disorder Society. MDS Clinical Diagnostic Criteria for Parkinson's Disease. Mov Disord. 2015;30(12):1591–1601.
5. Emre M, Aarsland D, Albanese A, et al. Rivastigmine for dementia associated with Parkinson's disease. N Engl J Med. 2004;351(24):2509–2518.
6. Bhidayasiri R, Saksornchai K, Kaewwilai L, Phanthumchinda K. A study of the Parkinson's Disease Non-Motor Symptoms Scale (PD-NMSS) in a Thai population. J Mov Disord. 2011;4(2):103–107.
7. Palliative Care Australia. National Palliative Care Standards. 5th edn. Canberra: Palliative Care Australia; 2018.
8. Australian Government Department of Health and Aged Care. National Aboriginal and Torres Strait Islander Palliative Care Strategy 2022–2025. Canberra: Commonwealth of Australia; 2022.
9. Antonini A, Moro E, Godeiro C, Reichmann H. Medical and surgical management of advanced Parkinson's disease. Mov Disord. 2018;33(6):900–908.
10. Politis M, Wu K, Molloy S, G Bain P, Chaudhuri KR, Piccini P. Parkinson's disease symptoms: the patient's perspective. Mov Disord. 2010;25(11):1646–1651.
11. Olanow CW, Kieburtz K, Odin P, et al. Continuous intrajejunal infusion of levodopa-carbidopa intestinal gel for patients with advanced Parkinson's disease: a randomised, controlled, double-blind, double-dummy study. Lancet Neurol. 2014;13(2):141–149.
12. Fox SH, Katzenschlager R, Lim SY, et al. International Parkinson and Movement Disorder Society evidence-based medicine review: update on treatments for the motor symptoms of Parkinson's disease. Mov Disord. 2018;33(8):1248–1266.
13. Royal Australian College of General Practitioners (RACGP). Medical Care of Older Persons in Residential Aged Care Facilities. 4th edn. Melbourne: RACGP; 2006 (updated 2023).
14. Boersma I, Jones J, Carter J, et al. Parkinson disease patients' perspectives on palliative care needs: what are they telling us? Neurol Clin Pract. 2016;6(3):209–219.
15. National Stroke Foundation. Clinical Guidelines for Stroke Management 2017: Dysphagia. Melbourne: National Stroke Foundation; 2017. (Referenced for dysphagia assessment framework applicable to PD.)

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).