Overview

• Progressive neurodegenerative disorder.
• Mainly due to degeneration of dopaminergic neurons in the substantia nigra pars compacta.
• Leads to dopamine deficiency in the basal ganglia motor pathways.
• Pathology often includes Lewy bodies, which contain alpha-synuclein.
• Usually idiopathic.
• Around 10–15% of cases may have a genetic/familial component.
• Ask about:
  • Family history of Parkinson’s disease
  • Young-onset disease
  • Similar movement disorders in relatives

Epidemiology

• Prevalence in Australia: approximately 1–2 per 1000 people.
• Prevalence increases with age.
• About 10–15% of patients develop symptoms before age 50.
• Diagnosis can be missed because:
  • Rest tremor may be absent at onset
  • Slowness may be mistaken for ageing
  • Early symptoms may be non-specific
  • Non-motor symptoms may precede motor features

Core clinical features

Classic motor features

• Tremor
• Rigidity
• Bradykinesia
• Postural instability

The key diagnostic feature is bradykinesia, usually with rigidity and/or rest tremor.

Tremor

• Classically a resting tremor.
• Frequency approximately 4–6 Hz.
• Improves with voluntary movement.
• Disappears during sleep.
• Often starts unilaterally.
• Usually asymmetric.
• Commonly affects:
  • Thumb
  • Index finger
  • Hand
• Typical description:
  • “Pill-rolling tremor”

Examination of tremor

• Observe hands at rest.
• Ask patient to rest hands in lap.
• Tremor may be brought out by distraction:
  • Serial 7s
  • Months backwards
  • Moving contralateral limb

Rigidity

• Increased resistance to passive movement.
• Not velocity-dependent.
• Can be present at:
  • Wrist
  • Elbow
  • Neck
  • Lower limbs

Types of rigidity

• Lead-pipe rigidity
  • Uniform resistance throughout passive movement.
• Cogwheel rigidity
  • Ratchety resistance.
  • Often due to rigidity plus superimposed tremor.

Examination of rigidity

• Test passive movement at:
  • Wrist
  • Elbow
  • Shoulder
  • Neck
• Can be enhanced by asking the patient to move the opposite limb.

Bradykinesia

• Means slowness of movement.
• May also include:
  • Hypokinesia — reduced movement
  • Akinesia — absence of movement

Clinical examples

• Difficulty with dextrous tasks:
  • Buttons
  • Handwriting
  • Using cutlery
  • Typing
• Reduced arm swing when walking.
• Slow initiation of movement.
• Reduced facial expression.
• Soft voice.
• Drooling due to reduced swallowing frequency.
• Micrographia.

Examination of bradykinesia

Ask patient to perform repetitive movements for 10–20 seconds:

• Finger tapping
• Hand opening and closing
• Pronation–supination
• Toe tapping
• Foot stomping

Look for:

• Progressive slowing
• Reduction in amplitude
• Hesitation
• Freezing
• Fatiguing of movement

Postural instability

• Usually occurs later in Parkinson’s disease.
• Due to impaired postural reflexes.
• Causes:
  • Falls
  • Retropulsion
  • Festination
  • Reduced balance recovery

Important clinical point

• Early falls are not typical of idiopathic Parkinson’s disease.
• If falls occur early, consider Parkinson-plus syndrome or another diagnosis.

Retropulsion test

• Stand behind the patient.
• Give a brief backward pull at the shoulders.
• Normal response:
  • One or two corrective steps.
• Parkinsonian response:
  • Multiple small backward steps.
  • May fall if unsupported.

Freezing

• Brief, transient inability to initiate or continue movement.
• Commonly occurs:
  • When starting to walk
  • When turning
  • When approaching doorways
  • In crowded or stressful environments

Other freezing-type phenomena

• Freezing of gait.
• Speech freezing or palilalia.
• Difficulty opening eyelids, sometimes described as apraxia of eyelid opening.

Other motor manifestations

• Reduced arm swing.
• Slow shuffling gait.
• Stooped posture.
• Flexed neck, trunk, hips and knees.
• Mask-like facies:
  • Hypomimia
  • Reduced blinking
  • Reduced spontaneous facial expression
• Soft, monotonous voice.
• Dysprosody.
• Drooling.
• Micrographia.
• Festinating gait.
• Difficulty turning.
• Dystonia.
• Dyskinesia, often medication-related in later disease.

Non-motor features

Non-motor symptoms are common and may have a greater impact on quality of life than motor symptoms.

Neuropsychiatric

• Depression.
• Anxiety.
• Apathy.
• Fatigue.
• Sleep disturbance.
• Daytime somnolence.
• Hallucinations.
• Psychosis.
• Impulse control disorders, particularly medication-related.

Autonomic

• Constipation.
• Urinary urgency.
• Bladder dysfunction.
• Erectile dysfunction.
• Orthostatic hypotension.
• Sweating abnormalities.
• Seborrhoea.

Sensory and sleep-related

• Anosmia or hyposmia.
• Abnormal colour perception.
• REM sleep behaviour disorder.
• Restless legs syndrome.
• Pain.

Cognitive

• Attention impairment.
• Executive dysfunction.
• Language difficulties.
• Visuospatial dysfunction.
• Dementia in later disease.

Parkinson’s disease dementia vs dementia with Lewy bodies

• Consider dementia with Lewy bodies if dementia occurs before or around the same time as motor symptoms.
• Suggestive features:
  • Early visual hallucinations
  • Fluctuating cognition
  • Nocturnal confusion
  • Visuospatial impairment
  • Parkinsonism

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Differential diagnoses / aetiological classification of parkinsonism

Differential diagnoses

Essential tremor

• Most common cause of tremor in older adults.
• Typically:
  • Bilateral
  • Action or postural tremor
  • Worse with movement or sustained posture
  • May affect hands, head, jaw or voice
• Handwriting is usually large and shaky rather than small.
• Bradykinesia and rigidity are absent.
• May improve with:
  • Alcohol
  • Propranolol
• Family history is common.
• Can coexist with Parkinson’s disease.

Drug-induced parkinsonism

Common causative drugs:

• Antipsychotics:
  • Haloperidol
  • Risperidone
  • Olanzapine
  • Other dopamine-blocking agents
• Metoclopramide
• Prochlorperazine

Features:

• Often bilateral and symmetrical.
• May develop after starting or increasing causative medication.
• May improve after withdrawal, though recovery can be slow.

Vascular parkinsonism

• Due to cerebrovascular disease affecting basal ganglia or frontal motor circuits.
• Features:
  • Lower-body predominant parkinsonism
  • Gait disturbance
  • Small stuttering steps
  • Pseudobulbar features
  • History of strokes or vascular risk factors
• Often poor response to levodopa.

Dementia with Lewy bodies

• Early cognitive impairment.
• Fluctuating cognition.
• Well-formed visual hallucinations.
• Parkinsonism.
• Rigidity may be more prominent than bradykinesia.
• Antipsychotic sensitivity is common.
• Older antipsychotics should generally be avoided due to risk of severe extrapyramidal effects or neuroleptic malignant syndrome.
• Levodopa may help motor symptoms but can worsen hallucinations or confusion.

Progressive supranuclear palsy

Suggestive features:

• Early falls, especially backwards.
• Early postural instability.
• Frontal cognitive or personality changes.
• Axial rigidity more than limb rigidity.
• Bulbar dysarthria.
• Vertical gaze palsy:
  • Early impaired downgaze
  • Later impaired upgaze and horizontal gaze
• Poor or absent levodopa response.

Multiple system atrophy

Features:

• Parkinsonism plus prominent autonomic dysfunction.
• Orthostatic hypotension.
• Erectile dysfunction.
• Bladder dysfunction.
• Cerebellar signs may occur:
  • Ataxia
  • Broad-based gait
  • Limb incoordination
• Levodopa response is usually poor, although some patients respond initially.
• Levodopa may worsen postural hypotension or neuropsychiatric symptoms.

Advanced Alzheimer’s disease

• Mild parkinsonism can occur in advanced disease.
• Dementia is usually early and dominant.
• If dementia develops after established Parkinson’s disease, consider Parkinson’s disease dementia, though coexisting Alzheimer’s pathology may occur.

Features not typical of idiopathic Parkinson’s disease

Consider alternative diagnosis if any of the following are present:

• Poor or absent levodopa response.
• Marked sensitivity to levodopa.
• Early dementia.
• Early hallucinations.
• Early postural instability.
• Early recurrent falls.
• Early severe orthostatic hypotension.
• Early urinary incontinence.
• Rapid progression.
• Objective limb weakness.
• Cerebellar signs.
• Pyramidal signs.
• Early prominent bulbar symptoms.

Category	Condition	Key distinguishing features / clues
Primary idiopathic Parkinson’s disease	Idiopathic Parkinson’s disease	Usually asymmetric onset; bradykinesia with rest tremor and/or rigidity; typically levodopa responsive; postural instability usually occurs later.
Tremor disorder	Essential tremor	Most common tremor disorder in older adults; bilateral action/postural tremor; worse with movement or sustained posture; may affect hands, head, jaw or voice; handwriting large and shaky rather than micrographic; no bradykinesia or rigidity; may improve with alcohol or propranolol; family history common; can coexist with Parkinson’s disease.
Medication-induced	Drug-induced parkinsonism	Caused by dopamine-blocking or dopamine-depleting drugs; often bilateral and symmetrical; temporal relationship with medication start or dose increase; may improve after withdrawal but recovery can be slow.
	Common causative medications	Antipsychotics including = haloperidol = risperidone = olanzapine and other dopamine-blocking agents; = metoclopramide = prochlorperazine = reserpine = tetrabenazine = alpha-methyldopa = lithium.
Vascular	Vascular parkinsonism	Due to basal ganglia lacunes or diffuse small-vessel disease; lower-body predominant parkinsonism; gait disturbance; small stuttering steps or “marche à petits pas”; pseudobulbar features; vascular risk factors or stroke history; usually poor levodopa response.
Atypical degenerative / Parkinson-plus	Progressive supranuclear palsy	Early falls, especially backwards; early postural instability; vertical gaze palsy, especially impaired downgaze; axial rigidity more than limb rigidity; frontal cognitive or personality change; bulbar dysarthria; poor or absent levodopa response.
	Multiple system atrophy	Parkinsonism with prominent autonomic dysfunction; orthostatic hypotension; erectile dysfunction; urinary incontinence or retention; bladder dysfunction; cerebellar signs such as ataxia, broad-based gait or limb incoordination; levodopa response usually poor or partial; levodopa may worsen postural hypotension or neuropsychiatric symptoms.
	Corticobasal degeneration	Markedly asymmetric parkinsonism; limb rigidity or dystonia; limb apraxia; cortical sensory loss; alien limb phenomenon; myoclonus; poor levodopa response.
	Dementia with Lewy bodies	Dementia before or within 1 year of motor parkinsonism; early cognitive impairment; fluctuating cognition; well-formed visual hallucinations; REM sleep behaviour disorder; antipsychotic sensitivity; levodopa may help motor symptoms but can worsen hallucinations or confusion.
	Parkinson’s disease dementia	Dementia develops after established Parkinson’s disease; consider if cognitive decline occurs later in disease course.
	Frontotemporal dementia syndromes	Behavioural change; executive dysfunction; personality change; may have associated parkinsonism.
	Other degenerative parkinsonian syndromes	Parkinsonism–ALS–dementia complex; progressive pallidal atrophy; hemiparkinsonism–hemiatrophy syndrome.
Heredo-degenerative / genetic-metabolic	Monogenic/familial parkinsonism	Consider with young-onset parkinsonism, strong family history, atypical features or early dystonia; may be autosomal dominant or recessive.
	Huntington’s disease	Chorea is more typical, but parkinsonism can occur; consider with family history, psychiatric symptoms, cognitive decline or caudate atrophy.
	Wilson disease	Important not to miss in younger patients; parkinsonism, dystonia, tremor, psychiatric symptoms, liver disease and Kayser–Fleischer rings.
	Neurodegeneration with brain iron accumulation	Includes pantothenate kinase-associated neurodegeneration; dystonia, parkinsonism, cognitive decline and characteristic MRI changes.
	Neuroferritinopathy	Ferritin light-chain mutation; can cause chorea, dystonia, parkinsonism and cognitive or behavioural symptoms.
	Spinocerebellar ataxias	Some autosomal-dominant spinocerebellar degenerations can present with parkinsonism; look for ataxia, eye movement abnormalities and family history.
	X-linked dystonia-parkinsonism	Rare; usually presents with dystonia and parkinsonism; consider with relevant ancestry or family history.
	Mitochondrial cytopathy	Parkinsonism with multisystem features such as myopathy, neuropathy, hearing loss, ophthalmoplegia, seizures or diabetes.
	Familial basal ganglia calcification / Fahr disease	Parkinsonism, dystonia, chorea, cognitive impairment and psychiatric symptoms; CT brain may show basal ganglia calcification.
Infectious / prion	Post-encephalitic parkinsonism	History of encephalitis; may have atypical neurological features.
	HIV/AIDS-related parkinsonism	Consider with HIV risk, systemic features or immunosuppression.
	Subacute sclerosing panencephalitis	Rare; progressive neurological decline after measles infection.
	Creutzfeldt–Jakob disease	Rapid progression, cognitive decline, myoclonus and atypical neurological signs.
Toxin-induced	Toxin-induced parkinsonism	Exposure history; acute or subacute onset; often symmetrical parkinsonism; may have cognitive or systemic toxicity features.
	Potential toxins	MPTP, carbon monoxide, manganese, mercury, carbon disulphide, cyanide, methanol, ethanol.
Trauma-related	Post-traumatic parkinsonism	May follow significant head trauma; consider with repetitive head injury, boxing/contact sport exposure or post-traumatic neurological decline.
Structural / medical causes	Normal pressure hydrocephalus	Classic triad: gait disturbance, cognitive impairment and urinary incontinence; broad-based magnetic gait; ventriculomegaly on CT/MRI; parkinsonism may be lower-body predominant.
	Brain tumour	Consider with focal neurological signs, headache, seizures, rapid progression or atypical/unilateral parkinsonism.
	Paraneoplastic disease	Rare; consider with subacute onset, weight loss, systemic symptoms or other neurological syndromes.
	Hypothyroidism	Can mimic or worsen parkinsonian features; fatigue, weight gain, cold intolerance, bradycardia, slow movements and cognitive slowing.
	Parathyroid disease	Hyperparathyroidism or hypoparathyroidism may be associated with basal ganglia calcification or movement disorders; consider with abnormal calcium/phosphate, neuropsychiatric symptoms or seizures.
	Non-Wilsonian hepatocerebral degeneration	Occurs in chronic liver disease or portosystemic shunting; can cause parkinsonism, tremor, ataxia and cognitive changes; check liver disease history and LFTs.
Advanced dementia	Advanced Alzheimer’s disease	Mild parkinsonism can occur in advanced disease; dementia is early and dominant; if dementia develops after established Parkinson’s disease, consider Parkinson’s disease dementia, though coexisting Alzheimer’s pathology may occur.

Red flags suggesting an alternative diagnosis

Red flag	Consider
Poor or absent levodopa response	Parkinson-plus syndrome vascular parkinsonism drug-induced parkinsonism
Marked sensitivity to levodopa	Atypical parkinsonism frailty cognitive impairment
Early dementia	Dementia with Lewy bodies Alzheimer’s disease atypical parkinsonism
Early hallucinations	Dementia with Lewy bodies medication effect delirium
Early postural instability or recurrent falls	Progressive supranuclear palsy multiple system atrophy vascular parkinsonism
Early severe orthostatic hypotension	Multiple system atrophy autonomic failure medication effect
Early urinary incontinence	Multiple system atrophy normal pressure hydrocephalus
Rapid progression	Atypical parkinsonism prion disease structural lesion inflammatory/infective cause
Objective limb weakness	Stroke, tumour motor neuron disease structural neurological lesion
Cerebellar signs	Multiple system atrophy spinocerebellar ataxia structural lesion
Pyramidal signs	Vascular disease tumour atypical parkinsonism motor neuron disease
Early prominent bulbar symptoms	Progressive supranuclear palsy motor neuron disease atypical parkinsonism

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Parkinson’s disease examination

General inspection

Look for:

• Mask-like facies.
• Reduced blinking.
• Drooling.
• Reduced spontaneous movement.
• Stooped posture.
• Flexed trunk and neck.
• Tremor at rest.
• Soft, monotonous voice.
• Poverty of movement.
• Seborrhoea or greasy facial skin.

Gait

Assess:

• Difficulty initiating gait.
• Small steps.
• Shuffling gait.
• Festination.
• Reduced arm swing.
• Asymmetrical arm swing.
• Stooped posture.
• En bloc turning.
• Freezing.
• Propulsion.
• Retropulsion.
• Ability to step over obstacles.

Hands and upper limbs

Assess:

• Rest tremor.
• Postural tremor.
• Intention tremor.
• Finger–nose testing.
• Finger tapping.
• Hand opening and closing.
• Pronation–supination.
• Tone at wrists and elbows.
• Cogwheel or lead-pipe rigidity.
• Micrographia.

Face and speech

Look for:

• Hypomimia.
• Reduced blink rate.
• Drooling.
• Monotonous speech.
• Hypophonia.
• Dysarthria.
• Glabellar tap response.

Eye movements

Assess:

• Saccades.
• Upgaze.
• Downgaze.
• Horizontal gaze.

Important point:

• Early downgaze impairment suggests progressive supranuclear palsy rather than idiopathic Parkinson’s disease.

Autonomic features

Check for:

• Orthostatic hypotension.
• Urinary symptoms.
• Erectile dysfunction.
• Constipation.
• Sweating abnormalities.
• Seborrhoea.

Function

Assess impact on:

• Walking.
• Falls.
• Dressing.
• Feeding.
• Writing.
• Driving.
• Work.
• Activities of daily living.
• Medication adherence.
• Cognition.
• Mood and behaviour.

Medication adverse effects

Ask about:

• Dyskinesias.
• Dystonia.
• Visual hallucinations.
• Confusion.
• Postural hypotension.
• Daytime somnolence.
• Impulse control behaviours:
  • Gambling
  • Shopping
  • Hypersexuality
  • Binge eating
  • Compulsive medication use

Neurological examination

Usually normal in idiopathic Parkinson’s disease:

• Power.
• Reflexes.
• Sensation.
• Coordination, except where bradykinesia interferes.

Abnormal findings suggesting alternative diagnosis:

• Pyramidal weakness.
• Hyperreflexia.
• Sensory level.
• Cerebellar signs.
• Marked eye movement abnormality.
• Early severe cognitive impairment.

Mental state

Screen for:

• Depression.
• Anxiety.
• Apathy.
• Psychosis.
• Hallucinations.
• Cognitive impairment.
• Sleep disturbance.

Functional impairment in Parkinson’s disease

Motor disability

• Tremor.
• Bradykinesia.
• Rigidity.
• Shuffling gait.
• Gait freezing.
• Festination.
• Postural instability.
• Falls.
• Dysphagia.
• Dysarthria.
• Micrographia.
• Difficulty with ADLs.

Non-motor disability

• Depression.
• Anxiety.
• Fatigue.
• Sleep disturbance.
• Dementia.
• Psychosis.
• Hallucinations.
• Constipation.
• Bladder dysfunction.
• Sexual dysfunction.
• Orthostatic hypotension.
• Pain.
• Reduced quality of life.

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Investigations:

Key principle

• Parkinson’s disease is primarily a clinical diagnosis.

Investigations may be used to:

• Exclude mimics.
• Assess comorbidities.
• Support diagnosis in unclear cases.
• Establish baseline before treatment.

Possible investigations

• Blood tests if clinically indicated:
  • FBC
  • UEC
  • LFT
  • TFT
  • B12/folate
  • Glucose/HbA1c
• MRI brain if atypical features:
  • Early falls
  • Rapid progression
  • Cognitive decline
  • Focal neurological signs
  • Poor levodopa response
  • Suspected vascular parkinsonism, NPH, tumour or structural lesion
• Olfaction testing:
  • Hyposmia supports idiopathic Parkinson’s disease.
• Levodopa or apomorphine challenge:
  • Improvement supports dopamine-responsive parkinsonism.
• DaTSCAN:
  • May help differentiate degenerative parkinsonism from essential tremor in selected cases.
  • Does not reliably distinguish idiopathic Parkinson’s disease from Parkinson-plus syndromes.

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MANAGEMENT

Management goals

• Improve symptom control.
• Optimise function and independence.
• Maintain quality of life.
• Reduce falls and complications.
• Manage non-motor symptoms.
• Support patient, family and carers.
• Monitor medication benefit, adverse effects and disease progression.

Initial management principles — Parkinson’s disease

1. Confirm the working diagnosis and assess severity

• Parkinson’s disease is primarily a clinical diagnosis.
• Diagnosis is suggested by:
  • Bradykinesia, plus
  • Rest tremor and/or rigidity
  • Usually asymmetric onset
  • Supportive non-motor features such as constipation, anosmia, REM sleep behaviour disorder, depression or autonomic symptoms
• At the initial assessment, document:
  • Main presenting symptom
  • Side of onset
  • Rate of progression
  • Functional impairment
  • Falls history
  • Cognitive symptoms
  • Hallucinations or psychosis
  • Autonomic symptoms
  • Current medication list
  • Exposure to dopamine-blocking drugs
• Explain to the patient that Parkinson’s disease is a chronic, progressive but treatable condition.
• Emphasise that treatment aims to:
  • Improve quality of life
  • Maintain independence
  • Reduce symptoms
  • Preserve mobility and function
  • Support work, driving, relationships and daily activities
• Avoid giving an overly pessimistic explanation at diagnosis.
• Reassure that many people remain functional for years, and that progression is variable.

2. Communicate the diagnosis clearly and safely

Delivering the diagnosis of Parkinson’s disease

GP role

• GP communication is central to the patient’s experience of Parkinson’s disease.
• The first explanation can have a lasting impact on:
  • Patient understanding
  • Acceptance of diagnosis
  • Anxiety
  • Engagement with treatment
  • Health-related quality of life
• Patient dissatisfaction is more likely when:
  • Diagnosis is delayed
  • Several clinicians are involved before diagnosis
  • The explanation is rushed or unclear
  • The patient is not given time to ask questions
  • Anxiety and uncertainty are not acknowledged
• Patient satisfaction improves when the diagnosis is delivered:
  • Sensitively
  • Clearly
  • With practical information
  • With time for questions

https://www1.racgp.org.au/ajgp/2021/november/diagnosis-and-management-of-parkinsons

Before giving the diagnosis

• Ideally offer the option of having a spouse, family member or support person present.
• Ask permission to discuss the suspected diagnosis.
• Explore the patient’s current understanding and concerns.

Useful questions:

• “What do you understand about Parkinson’s disease?”
• “Have you known anyone with Parkinson’s disease?”
• “What worries you most about this possibility?”
• “Have you looked up your symptoms online?”
• “What activities are you most worried about losing?”

Patient preconceptions

• Many patients already have an image of Parkinson’s disease from:
  • Family members
  • Friends
  • Media
  • Internet searching
  • Caring for someone with advanced disease
• Patients may silently fear:
  • Loss of independence
  • Falls
  • Dementia
  • Loss of work capacity
  • Loss of driving
  • Becoming a burden
  • Rapid deterioration
• These fears should be actively explored because patients may not volunteer them.

Explaining the diagnosis

• Use clear, balanced language.
• Avoid excessive detail in the first consultation.
• Explain that Parkinson’s disease is:
  • A clinical diagnosis
  • Based mainly on history and examination
  • Supported by tests when needed
  • Chronic and progressive
  • Usually slowly progressive
  • Treatable symptomatically

Suggested explanation:

“Your symptoms and examination findings suggest Parkinson’s disease. This is a condition where there is reduced dopamine activity in parts of the brain that help control movement. It can cause slowness, stiffness, tremor and walking changes. It can also affect sleep, mood, bowels, bladder and blood pressure. It usually progresses slowly, and there are effective treatments that can improve symptoms and help maintain function.”

Explaining the diagnostic process

• Parkinson’s disease is diagnosed clinically.
• There is no single blood test that confirms it.
• Imaging or other tests may be used to:
  • Exclude other causes
  • Support the diagnosis
  • Assess atypical features
  • Guide specialist review
• Neurology referral is usually recommended for:
  • Diagnostic confirmation
  • Treatment planning
  • Medication advice
  • Assessment for Parkinson-plus syndromes if atypical features are present

Explain motor and non-motor symptoms

Motor symptoms

• Slowness of movement
• Stiffness
• Rest tremor
• Reduced arm swing
• Shuffling gait
• Small handwriting
• Soft voice
• Balance problems, usually later

Non-motor symptoms

• Constipation
• Reduced sense of smell
• Sleep disturbance
• REM sleep behaviour disorder
• Depression
• Anxiety
• Fatigue
• Bladder symptoms
• Sexual dysfunction
• Orthostatic dizziness
• Cognitive changes
• Hallucinations, usually later or medication-related

Important point:

• Non-motor symptoms can be more disabling than motor symptoms.
• They should be explained and actively managed.

Communication approach

• Be honest but hopeful.
• Allow silence and emotional response.
• Avoid minimising the diagnosis.
• Avoid excessive focus on late-stage complications.
• Check understanding regularly.
• Encourage questions.
• Provide written information.
• Arrange early follow-up.

Useful phrases:

• “This is a lot to take in today.”
• “You do not need to remember everything from this appointment.”
• “We will go through this step by step.”
• “There are effective treatments that can help symptoms.”
• “You will not be managing this alone.”
• “Many people continue working, driving and doing normal activities for a long time.”
• “Our focus is to keep you functioning as well as possible.”

Avoid information overload

• Do not overwhelm the patient with:
  • Advanced disease complications
  • Complex medication details
  • Advanced therapies
  • Worst-case scenarios
• Warn that internet information can be anxiety-provoking and may focus on severe disease.
• Recommend reliable patient resources, such as:
  • Parkinson’s Australia
  • Neurologist-provided information
  • Parkinson’s nurse resources, if available

Address impact on daily life

Ask specifically about:

• Work
• Driving
• Exercise
• Family responsibilities
• Hobbies
• Social life
• Independence
• Activities of daily living
• Future planning

Useful framing:

“The aim is not just to treat tremor or stiffness. The aim is to keep you doing the things that matter to you.”

Shared decision-making

• Management should be patient-centred.
• Discuss the patient’s priorities and preferences.
• Consider:
  • Symptom burden
  • Functional impact
  • Occupation
  • Driving
  • Age
  • Comorbidities
  • Medication concerns
  • Support network
  • Patient goals
• Involve the patient in decisions about:
  • Timing of medication
  • Allied health referral
  • Work adjustments
  • Driving review
  • Disclosure to family or workplace
  • Follow-up planning

Follow-up after diagnosis

• Arrange early follow-up after the initial discussion.
• Purpose of follow-up:
  • Recheck understanding
  • Answer new questions
  • Review emotional response
  • Screen for depression and anxiety
  • Review function
  • Discuss treatment options
  • Confirm neurology referral
  • Start allied health referrals
  • Provide further education
• Encourage the patient to bring:
  • Partner or support person
  • Written questions
  • Medication list
  • Symptom diary, if useful

Key messages for the patient

• Parkinson’s disease is chronic and progressive, but usually slowly progressive.
• It is treatable.
• Symptoms vary significantly between individuals.
• They should not judge their prognosis by someone else’s experience.
• Motor and non-motor symptoms can both be managed.
• Exercise and allied health are important early.
• Medication can improve quality of life when symptoms affect function.
• The GP and specialist team will support them over time.
• Early follow-up is important.

3. Refer to neurology

Routine referral

• Refer to a neurologist for:
  • Diagnostic confirmation
  • Baseline assessment
  • Treatment planning
  • Medication titration advice
  • Assessment for Parkinson-plus syndromes if atypical features exist
• A movement disorder neurologist is preferred if available.

What to include in referral

• Symptom onset and progression.
• Side of onset.
• Motor features:
  • Bradykinesia
  • Tremor
  • Rigidity
  • Gait change
  • Freezing
  • Falls
• Non-motor features:
  • Constipation
  • Anosmia
  • REM sleep behaviour disorder
  • Depression/anxiety
  • Orthostatic symptoms
  • Urinary symptoms
  • Cognitive symptoms
  • Hallucinations
• Functional impact:
  • Work
  • Driving
  • ADLs
  • Falls
  • Swallowing
• Medication list, especially:
  • Metoclopramide
  • Prochlorperazine
  • Antipsychotics
  • Lithium
  • Dopamine-depleting drugs
• Examination findings.
• Red flags.
• Relevant investigations already arranged.

4. Do not delay treatment if functionally disabling

• Treatment should be considered when symptoms cause:
  • Physical disability
  • Social disability
  • Reduced quality of life
  • Difficulty with work
  • Difficulty driving
  • Difficulty dressing, eating, writing, typing or walking
  • Distressing tremor
  • Painful rigidity
  • Falls or near-falls
  • Significant bradykinesia
• Neurology referral does not automatically mean medication must wait.
• If symptoms are functionally impairing and the diagnosis is probable, GP initiation of first-line treatment may be appropriate depending on local access, clinician confidence and patient preference.
• AJGP 2025 notes that early levodopa initiation in probable Parkinson’s disease can improve quality of life and may reduce the risks of delayed treatment when specialist access is limited.

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Multidisciplinary team

Involve early where appropriate:

• GP
• Neurologist, preferably movement disorder specialist if available
• Parkinson’s disease nurse, if available
• Physiotherapist
• Occupational therapist
• Exercise physiologist
• Speech pathologist
• Dietitian
• Psychologist or psychiatrist
• Social worker
• Continence nurse
• Urologist if complex bladder/sexual dysfunction
• Geriatrician if frailty, cognitive impairment, falls or polypharmacy

Non-pharmacological management

Exercise and physical therapy

Exercise should be considered a core part of early management.

Useful strategies:

• Aerobic exercise
• Resistance training
• Balance training
• Gait training
• Treadmill walking
• Cued exercise training
• Falls prevention program
• Dance, tai chi or agility-based exercise where suitable
• Stretching and posture work
• Transfer training
• Upper limb function training

Physiotherapy can help with:

• Gait impairment
• Freezing
• Balance
• Transfers
• Falls risk
• Mobility confidence
• Deconditioning prevention

Occupational therapy

Assess and support:

• ADLs
• Home safety
• Falls prevention
• Showering and toileting safety
• Meal preparation
• Dressing aids
• Hand function
• Work-related modifications
• Driving and community access
• Equipment needs

Speech pathology

Consider for:

• Hypophonia
• Dysarthria
• Dysphagia
• Drooling
• Aspiration risk
• Communication strategies
• Swallowing assessment and diet texture advice

Dietitian

Useful for:

• Weight loss or weight gain
• Constipation
• Dysphagia-related dietary modification
• Protein timing if levodopa response affected
• Malnutrition risk
• Bone health and falls risk

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Symptom-specific management

https://www1.racgp.org.au/ajgp/2021/november/diagnosis-and-management-of-parkinsons

Commonly prescribed interventions for non-motor symptoms
Symptom	Intervention	Typical dose ranges	Common side effects
Rapid eye movement sleep behaviour disorder	Clonazepam	0.5–1 mg at night	Somnolence
Insomnia	Sleep hygiene
	Amitriptyline	5–25 mg approximately 2 hours pre-bedtime	Dry eyes Dry mouth Constipation Morning sedation Urinary retention (first exclude bladder outlet obstruction in men)
	Note: Ensure good nocturnal motor control – ‘off’ symptoms (stiffness, cramping) may prevent/disturb sleep
Constipation	Fibre supplement	1–2 teaspoons three times per day	Flatulence Bloating Abdominal discomfort
	Macrogol	1–2 sachets twice per day	Nausea Abdominal discomfort Diarrhoea
	Note: Avoid using anthranoid laxatives (eg senna) for >2 weeks, as there is a risk of bowel dependency and potentiation of constipation
Psychosis	Quetiapine	12.5–75 mg in divided doses	Somnolence
Depression	Paroxetine	20 mg	Gastrointestinal upset Sedation Sexual dysfunction Anorexia
	Venlafaxine XR	75–150 mg	Gastrointestinal upset Insomnia Sedation Hyperhidrosis
Restless legs syndrome	Pramipexole	125–750 μg at night	Nausea Orthostatic dizziness Hallucinations Impulse control disorders Peripheral oedema Withdrawal syndrome if rapidly tapered/ceased Sleep attacks/somnolence
Orthostatic hypotension	Increase fluid (at least 1.5 L/day) and salt intake		Monitor for supine/nocturnal hypertension
	Fludrocortisone	100–300 μg in divided doses (morning, midday)	Oedema Hypertension Hypokalaemia

Orthostatic hypotension

General measures:

• Review medications contributing to hypotension.
• Avoid dehydration.
• Encourage adequate fluids.
• Rise slowly from sitting or lying.
• Avoid prolonged standing.
• Avoid overheating.
• Consider compression stockings or abdominal binder.
• Increase salt intake if appropriate and not contraindicated.
• Elevate head of bed if nocturnal hypertension is an issue.

Medication options, usually with specialist input:

• Fludrocortisone
• Midodrine

Fludrocortisone

• May be used for troublesome postural hypotension.
• Example dose:
  • 0.1 mg mane
  • Increase gradually if needed
  • Maximum often around 0.3–0.5 mg daily depending on specialist advice and tolerability

Monitor for:

• Supine hypertension
• Fluid retention
• Heart failure worsening
• Hypokalaemia
• Peripheral oedema

Dementia, hallucinations and psychosis

General approach

• Clarify whether symptoms are distressing or dangerous.
• Look for reversible contributors:
  • Infection
  • Delirium
  • Pain
  • Constipation
  • Urinary retention
  • Sleep deprivation
  • Medication adverse effects

Medication review

Consider reducing or stopping drugs that worsen hallucinations or confusion, with specialist guidance:

• Anticholinergics
• Amantadine
• Dopamine agonists
• MAO-B inhibitors
• COMT inhibitors
• High levodopa dose, if clinically appropriate

Non-drug strategies

• Regular routine.
• Orientation cues.
• Adequate lighting.
• Sleep optimisation.
• Reduce overstimulation.
• Carer education.
• Music therapy or structured activities may help agitation.

Antipsychotics

Use caution. Parkinson’s disease patients are sensitive to dopamine blockade.

Preferred options when medication is necessary:

• Quetiapine
• Clozapine, usually specialist-supervised due to blood monitoring requirements

Avoid or use extreme caution:

• Haloperidol
• Risperidone
• Olanzapine
• Metoclopramide
• Prochlorperazine

These can worsen parkinsonism.

Depression and anxiety

Management options:

• Psychoeducation.
• Exercise.
• CBT.
• Psychotherapy.
• Sleep optimisation.
• Social support.
• Antidepressants where clinically indicated.

Medication choices need to consider:

• Age
• Falls risk
• Cognition
• Sleep
• Drug interactions
• Autonomic side effects
• Existing Parkinson’s medications

Constipation

Common in Parkinson’s disease and may precede motor symptoms.

Management:

• Adequate fluid intake.
• Dietary fibre if tolerated.
• Regular exercise.
• Toilet routine.
• Review constipating medications.
• Osmotic laxatives, e.g. macrogol.
• Stimulant laxatives if needed.
• Treat severe constipation early to reduce delirium, pain and medication absorption issues.

Bladder and sexual dysfunction

Bladder symptoms

May include urgency, frequency, nocturia or incontinence.

Management:

• Exclude UTI, glycosuria, retention and prostate pathology where relevant.
• Bladder diary.
• Bladder training.
• Pelvic floor physiotherapy.
• Continence nurse referral.
• Review diuretics and fluid timing.
• Urology referral if complex.

Medication caution:

• Anticholinergic bladder medications may worsen cognition and constipation.
• Consider cognitive burden, especially in older patients.

Erectile dysfunction

Management:

• Screen for cardiovascular risk.
• Review medications.
• Consider PDE-5 inhibitor if appropriate.
• Address mood, relationship and autonomic contributors.
• Urology referral if complex.

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Pharmacological treatment principles

https://www1.racgp.org.au/ajgp/2021/november/diagnosis-and-management-of-parkinsons

Commonly prescribed medications for Parkinson’s disease and their side effects
Class	Common formulations	Typical dose ranges	Main side effects	Additional considerations
Levodopa + dopa decarboxylase inhibitor	Levodopa/carbidopa	300–1000 mg levodopa per day, administered 3–5 times/day	Nausea Orthostatic dizziness Somnolence	First-line therapy in most patients
	Levodopa/ benserazide	300–1000 mg levodopa per day, administered 3–5 times/day	Nausea Orthostatic dizziness Somnolence	First-line therapy in most patients
Levodopa + dopa decarboxylase inhibitor + COMT inhibitor	Levodopa/ carbidopa/ entacapone*	300–1000 mg levodopa per day, administered 3–5 times/day	Nausea Orthostatic dizziness Somnolence	Initiation by specialist (neurologist or other Parkinson’s disease specialist) advised
MAO-B inhibitor	Rasagiline	1 mg daily	Usually well tolerated Nausea Orthostatic dizziness Potential serotonin toxicity when combined with other serotonergic medications	Can be first-line treatment for milder symptoms
	Selegiline	2.5–10 mg daily (in two divided doses, morning and midday)	Confusion Nausea Orthostatic dizziness Potential serotonin toxicity when combined with other serotonergic medications
	Safinamide	50–100 mg daily	Usually well tolerated Nausea Orthostatic dizziness Potential serotonin toxicity when combined with other serotonergic medications
Dopamine agonist	Pramipexole	Controlled release: 0.375–3 mg daily   Immediate release: 0.125–1 mg three times daily	Nausea Orthostatic dizziness Hallucinations Impulse control disorders Peripheral oedema Withdrawal syndrome if rapidly tapered/ceased	Use with caution in elderly and those at risk of impulse control disorders (gambling, alcohol use disorder, hypersexual behaviour)
	Rotigotine patch	2–8 mg patch daily	Application site reactions Nausea Orthostatic dizziness Hallucinations Impulse control disorders Peripheral oedema Withdrawal syndrome if rapidly tapered/ceased	Use with caution in elderly and those at risk of impulse control disorders (gambling, alcohol use disorder, hypersexual behaviour)
Anticholinergic	Benztropine	0.5–5 mg daily (in up to 3 or 4 divided doses)	Confusion Urinary retention Constipation Dry mouth Dry eyes	Useful occasionally for prominent rest tremor Use with caution in elderly and those with cognitive frailty
	Trihexyphenidyl	0.5–5 mg daily (in up to 3 or 4 divided doses)	Confusion Urinary retention Constipation Dry mouth Dry eyes	Useful occasionally for prominent rest tremor Use with caution in elderly and those with cognitive frailty
NMDA receptor antagonist	Amantadine	100 mg 1–3 times daily	Hallucinations Peripheral oedema Insomnia Livedo reticularis	Useful for management of dyskinesia Avoid late afternoon or evening administration to reduce risk of insomnia Use with caution in patients with cardiac failure Initiation by specialist (neurologist or other Parkinson’s disease specialist) advised
*Entacapone is a COMT inhibitor and works to prolong the action of levodopa. This can be particularly useful for patients whose Parkinson’s disease symptoms reappear before their next medication dose is due. COMT, catechol-O-methyltransferase; MAO-B, monoamine oxidase-B; NMDA, N-methyl-D-aspartate

• Start medication when symptoms cause functional impairment or reduced quality of life.
• Treatment should be individualised according to:
  • Age
  • Occupation
  • Functional needs
  • Symptom pattern
  • Cognitive status
  • Falls risk
  • Comorbidities
  • Patient preference
• Start low and titrate gradually.
• Use the minimum effective dose.
• Monitor both benefit and adverse effects.
• Avoid dopamine-blocking antiemetics and antipsychotics where possible.

Nausea management

• Nausea is common when starting dopaminergic therapy.
• Avoid:
  • Metoclopramide
  • Prochlorperazine

These can worsen parkinsonism.

• Domperidone may be used for dopaminergic nausea, but consider:
  • QT prolongation risk
  • Cardiac history
  • Drug interactions
  • ECG where clinically appropriate

Levodopa

Mechanism

• Dopamine itself does not cross the blood–brain barrier.
• Levodopa crosses the blood–brain barrier.
• It is converted to dopamine in the CNS by dopa decarboxylase.
• This improves dopamine deficiency in the striatum.

Carbidopa / benserazide combination

Levodopa is combined with a peripheral dopa decarboxylase inhibitor:

• Carbidopa, or
• Benserazide

Benefits:

• Reduces peripheral breakdown of levodopa.
• Allows more levodopa to reach the brain.
• Reduces peripheral adverse effects such as nausea and vomiting.
• Improves motor symptom control.

Clinical role

• Most effective medication for motor symptoms.
• Improves:
  • Bradykinesia
  • Rigidity
  • Tremor
• Particularly appropriate where symptoms are causing meaningful disability.
• There is no benefit in delaying levodopa when symptoms are functionally impairing.

Starting and titrating levodopa

Common practical approach:

• Start low, especially in older or frail patients.
• Example:
  • 50 mg daily for 3–7 days
  • Increase gradually by 50 mg increments every few days
  • Aim initially for around 100 mg three times daily if tolerated
• Many patients with moderate symptoms respond to total daily doses around 300–600 mg/day.
• Dose can be titrated based on:
  • Motor response
  • Nausea
  • Dizziness
  • Orthostatic hypotension
  • Confusion or hallucinations
  • Dyskinesia

If poor or absent response to adequate levodopa trial:

• Reconsider diagnosis.
• Refer early to neurologist.

Levodopa adverse effects

• Nausea and vomiting.
• Orthostatic hypotension.
• Dizziness.
• Confusion.
• Hallucinations.
• Dyskinesias.
• Motor fluctuations.
• Wearing-off phenomenon.
• On–off fluctuations in advanced disease.

Motor fluctuations and advanced disease

As Parkinson’s disease progresses, patients may develop:

• Wearing-off before next dose.
• Shorter duration of medication benefit.
• On–off phenomenon.
• Peak-dose dyskinesia.
• Dose failures.
• Freezing despite medication.
• Anxiety or non-motor symptoms during “off” periods.
• Hallucinations or psychosis.

Management options require specialist input and may include:

• Smaller, more frequent levodopa doses.
• Modified-release preparations in selected situations.
• Addition of adjunct therapy.
• Dopamine agonist.
• MAO-B inhibitor.
• COMT inhibitor.
• Amantadine for dyskinesia in selected patients.
• Device-assisted therapy in advanced disease:
  • Apomorphine infusion
  • Levodopa intestinal gel
  • Deep brain stimulation in selected patients

Dopamine agonists

Examples:

• Pramipexole
• Rotigotine patch
• Ropinirole
• Cabergoline, less commonly used due to ergot-related adverse effects

Mechanism

• Directly stimulate dopamine receptors.
• Longer half-life than levodopa.
• Provide more continuous dopaminergic stimulation.

Clinical role

• Can be used in mild Parkinson’s disease.
• May be useful in younger patients where appropriate.
• Usually less effective than levodopa for motor symptom control.

Adverse effects

• Nausea.
• Dizziness.
• Orthostatic hypotension.
• Daytime somnolence.
• Sudden sleep attacks.
• Hallucinations.
• Leg oedema.
• Impulse control disorders:
  • Gambling
  • Hypersexuality
  • Compulsive shopping
  • Binge eating
  • Punding

Ask about impulse-control symptoms at every review.

MAO-B inhibitors

Examples:

• Selegiline
• Rasagiline, depending on availability/formulary

Clinical role

• Option for mild symptoms.
• May be used as adjunct therapy.
• Generally modest symptomatic benefit.
• Often well tolerated.

Cautions

• Drug interactions.
• Insomnia, particularly with selegiline if taken later in the day.
• Serotonergic medication interactions should be considered.

Anticholinergics

Role

• May help tremor-predominant disease.
• Generally avoided in older patients.

Major limitations

Can worsen:

• Confusion
• Memory impairment
• Constipation
• Urinary retention
• Dry mouth
• Blurred vision
• Glaucoma risk

Best reserved for selected younger patients with troublesome tremor and no cognitive impairment.

Amantadine

Role

• May help tremor in some patients.
• May reduce levodopa-induced dyskinesia in selected patients.

Adverse effects

• Confusion.
• Hallucinations.
• Leg oedema.
• Livedo reticularis.
• Insomnia.
• Renal dose adjustment may be required.

Practical medication safety points

• Avoid dopamine-blocking medications:
  • Metoclopramide
  • Prochlorperazine
  • Haloperidol
  • Many antipsychotics
• Review medication list regularly for:
  • Anticholinergic burden
  • Sedatives
  • Falls-risk medicines
  • Hypotensive drugs
  • Constipating drugs
• Ask specifically about:
  • Falls
  • Wearing-off
  • Dyskinesia
  • Hallucinations
  • Sleep attacks
  • Impulse control behaviours
  • Constipation
  • Orthostatic symptoms
  • Swallowing issues

Follow-up and monitoring

At review, assess:

• Motor symptoms:
  • Tremor
  • Rigidity
  • Bradykinesia
  • Gait
  • Freezing
  • Falls
• Non-motor symptoms:
  • Mood
  • Cognition
  • Sleep
  • Constipation
  • Urinary symptoms
  • Sexual function
  • Pain
  • Fatigue
• Medication response:
  • Onset of benefit
  • Duration of benefit
  • Wearing-off
  • Dose failures
  • Dyskinesia
• Adverse effects:
  • Nausea
  • Dizziness
  • Orthostatic hypotension
  • Hallucinations
  • Somnolence
  • Impulse control disorders
• Function:
  • ADLs
  • Work
  • Driving
  • Exercise
  • Carer burden
  • Home safety

Patient Advice

• Stay Active: Engage in regular, tailored exercise to maintain mobility and balance.
• Healthy Diet: Follow a high-fiber diet, stay hydrated, and manage constipation.
• Cognitive Engagement: Participate in cognitive activities and social interactions to maintain mental function.
• Safety Measures: Make home safety modifications to prevent falls and use assistive devices if needed.
• Seek Support: Join support groups and seek counseling for emotional and psychological support.
• Regular Check-ups: Maintain regular follow-ups with the healthcare team to monitor and adjust the management plan as needed.