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Parkinson’s Disease

A guide for patients, families, and referring GPs

Tap or hover any dotted-underlined term for a plain-English definition.

Most people with Parkinson’s respond well to treatment and live many active years after diagnosis. The right plan is built slowly, person by person — and most of it is medication you take at home, not procedures.

Book a neurology consultation →Read the full guide
At a glance
  • Parkinson’s becomes more common with age — roughly 1 in 100 people over 60 are affected.
  • Levodopa, introduced in the 1960s, remains the most effective symptomatic treatment available.
  • Most people respond well to medication and live many active years after diagnosis — especially when non-motor symptoms (sleep, mood, autonomic) are treated alongside the motor ones.
  • Non-motor symptoms — sleep, mood, constipation, low blood pressure on standing — often matter more day-to-day than tremor.
  • Diagnosis is clinical, supported by examination and selective use of imaging or scoring tools when needed.
  • This page is information. The right first step is your GP — they can refer you to a neurologist.
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What you can do this week

Today

  • Write down what you’ve noticed — tremor at rest, slower movement, stiffness, smaller handwriting, sleep changes, low mood, constipation. Date the timeline if you can.
  • Show the list to someone close to you for a sanity check.

This week

  • Book a GP appointment. Ask whether a neurology referral is appropriate.
  • Bring the timeline and a list of all your current medications, including supplements.

This month

  • If diagnosed: contact Parkinson’s NSW (1800 644 189) for free nurse support, education sessions, and local groups.
  • Start a regular aerobic exercise habit — this is one of the most evidence-supported things you can do.
  • Talk to your GP about referral to a Parkinson’s-experienced physiotherapist.

This is general guidance — tailor it with your GP and neurologist.

I.

Parkinson’s, parkinsonism, and what the difference means

These two words get used as if they mean the same thing. They don’t.

is the umbrella term. It describes a pattern of physical signs — slow movement, stiffness, and tremor — that several different conditions can cause.

Parkinson’s disease is the most common cause of parkinsonism, but not the only one. Other causes include certain medications (drug-induced parkinsonism), small-vessel disease in the brain (vascular parkinsonism), and a group of less common neurodegenerative conditions called the atypical parkinsonisms — covered in section IV.

Getting the right diagnosis matters. The treatments and outlook differ. Drug-induced parkinsonism may resolve when the medication is stopped. Vascular parkinsonism is approached differently from Parkinson’s. Atypical parkinsonisms progress along their own paths and respond less well to standard Parkinson’s medications.

II.

Symptoms

Parkinson’s has both motor (movement) and non-motor features. The non-motor ones often start earliest — sometimes years before the diagnosis — and frequently affect daily life more than the visible motor changes.

Motor symptoms

  • — slowness of movement. Smaller handwriting (micrographia), slower walking, reduced arm swing, less facial expression, softer voice.
  • Rest tremor — classically a slow tremor of a hand or foot when relaxed, settling when the limb is in use. Often starts on one side.
  • Rigidity — stiffness in the limbs and trunk. Often felt as muscle aches rather than “stiffness”.
  • Postural changes — a stoop, a shuffling gait, occasional freezing in doorways or turns, instability with balance — these tend to come later.

Non-motor symptoms

  • — vivid dreams that get acted out (kicking, shouting). Can appear years before motor symptoms.
  • Loss of smell — common, often early.
  • Constipation — very common, often longstanding.
  • Mood changes — depression, anxiety, apathy. Treatable; often under-recognised.
  • Sleep disturbance — insomnia, fragmented sleep, daytime sleepiness.
  • — dizziness on standing.
  • Urinary urgency, sexual changes, sweating changes.
  • Cognitive changes — mild thinking changes in early disease; a higher risk of dementia later.

If two or more of these are present and progressing — particularly slow movement plus a rest tremor or stiffness on one side — talk to your GP about a neurology referral.

III.

What causes Parkinson’s?

Parkinson’s is driven by the gradual loss of cells in a small part of the brain called the that make dopamine, a chemical the brain uses to coordinate movement. Inside the affected cells, an abnormal protein called builds up over years.

Risk factors

  • Age — the strongest single factor. Most cases start after 60.
  • Family history — modestly increases risk. Most Parkinson’s is not inherited; a small fraction of cases are linked to specific gene changes (such as LRRK2 and GBA1) that may be more common in younger-onset disease.
  • Pesticide and herbicide exposure — associated with higher risk in occupational studies.
  • Head injury — particularly with loss of consciousness.
  • Male sex — men are affected somewhat more often than women.

Coffee, tea, and physical activity are associated with lower risk in observational studies. Whether they actively protect, or whether the relationship runs the other way, isn’t fully settled — but the everyday advice (stay active, look after your heart and head) is the same either way.

IV.

Atypical parkinsonism — what looks like Parkinson’s but isn’t

Several conditions produce a Parkinson’s-like picture early on but follow a different path. These are sometimes grouped as the atypical parkinsonisms. They’re less common than Parkinson’s disease itself, but recognising the difference matters because the treatments and outlook differ.

  • — early falls (often backwards), difficulty looking up and especially down, axial stiffness, fixed staring expression.
  • — severe autonomic failure (blood pressure drops, urinary problems, sexual dysfunction), sometimes cerebellar incoordination.
  • — striking asymmetry, difficulty performing learned movements (apraxia), occasionally a hand or arm that feels “not your own” (alien limb).
  • — early dementia, vivid visual hallucinations, fluctuating alertness, REM sleep behaviour disorder. Important: antipsychotic medicines can be dangerous in DLB.
  • Drug-induced parkinsonism — from antipsychotics, some anti-nausea drugs (metoclopramide, prochlorperazine), and others. Often improves when the medication is stopped.
  • Vascular parkinsonism — caused by small-vessel disease in the brain. Usually a more lower-body and gait-led picture; less tremor.

Red flags that argue against straightforward Parkinson’s disease and prompt a closer look include: falls within the first year, very poor or absent response to levodopa, early severe autonomic failure, early cognitive decline, and symmetric symptoms from the start.

V.

How Parkinson’s is diagnosed

There is no single test for Parkinson’s. The diagnosis is clinical — built from a careful history and a movement examination.

The history. Your neurologist will ask about the early features — rest tremor, slowness, stiffness, smaller handwriting, softer voice, reduced arm swing — and about non-motor features that often pre-date them: REM sleep behaviour disorder, loss of smell, constipation, mood changes. A family member who has watched the changes is often the most useful additional voice in the room.

The examination. The neurologist looks for the combination of bradykinesia (the cardinal feature) with rest tremor and/or rigidity, and watches for asymmetry. Where appropriate, motor signs are scored using the — the international structured scoring tool — so changes can be tracked over time.

A brief cognitive screen. Where appropriate, a (Montreal Cognitive Assessment) is used to look for early thinking changes. Formal neuropsychology is reserved for cases where the picture is subtle or atypical.

Imaging is selective, not routine.

  • MRI is sometimes ordered to look for vascular changes, normal-pressure hydrocephalus, or structural lesions.
  • (a dopamine-system scan, sometimes called DaTscan) is used only when the diagnosis is genuinely unclear — for example, to distinguish Parkinson’s from essential tremor or drug-induced parkinsonism. It is not part of the routine work-up.

Imaging happens via a separate referral, not on the day of your consultation. The neurologist will explain what is being arranged and why before you leave.

VI.

Medication treatment

There is no single right starting medication for Parkinson’s. The choice depends on age, what’s bothering you most, other health conditions, and your priorities.

The three main first-line classes:

Levodopa (with carbidopa or benserazide)

is the most effective Parkinson’s medication available. It replaces the dopamine the brain is no longer making enough of. Standard combinations include levodopa/carbidopa (Sinemet, Kinson) and levodopa/benserazide (Madopar). A combination including entacapone (Stalevo) is sometimes used to extend each dose’s effect.

For decades, neurologists held back on levodopa, worried about long-term complications. Current evidence is more reassuring: starting levodopa when symptoms begin to interfere with daily life is the right call for most people. Side effects can include nausea (improves with carbidopa or with food), low blood pressure on standing, and — later in the course — movement fluctuations and .

Dopamine agonists

Pramipexole, ropinirole, and the rotigotine patch work by mimicking dopamine directly. They’re often used in younger patients to delay starting levodopa, or alongside levodopa later. They tend to cause less dyskinesia than levodopa, but more of certain side effects: drowsiness (including sudden onset of sleep — relevant to driving), leg swelling, hallucinations, and (compulsive gambling, shopping, hypersexuality, binge eating). The last one is important to know about — it’s reversible when the medication is reduced or stopped, but easy to miss.

MAO-B inhibitors

Rasagiline, selegiline, and safinamide work by slowing the breakdown of dopamine in the brain. They provide modest symptom benefit and are sometimes used as a first medication in mild disease, or as add-ons later.

Other options as the disease evolves

As Parkinson’s progresses, doses are adjusted and additional medications are added or layered. Amantadine is sometimes used for dyskinesia. COMT inhibitors (entacapone, opicapone) extend the effect of each levodopa dose. Anticholinergic medications (for example, benzhexol) are rarely used now because of cognitive side effects.

What we do. CURA neurologists initiate and titrate standard Parkinson’s medications — levodopa, dopamine agonists, MAO-B inhibitors, and the usual add-ons. We review medication regularly, watch for side effects, and adjust as the condition evolves. Most adjustments happen over telehealth follow-ups once you’re established with us.

What we don’t do in-house. Apomorphine pumps, Duodopa intestinal-gel pumps, and deep-brain stimulation are managed at tertiary movement-disorders centres. If those options become relevant, your neurologist will refer you and continue to share care where appropriate — see advanced therapies.

VII.

Living well with Parkinson’s

Medication is half the picture. The other half is everything else — exercise, sleep, mood, falls prevention, and managing non-motor symptoms.

Exercise — the most evidence-supported thing you can do

Regular aerobic exercise — sustained, enough to raise your heart rate — has the best evidence of any non-medication intervention in Parkinson’s. Add resistance training (strength work) and balance training. Tai chi has good evidence specifically for falls prevention. The right routine is one you can sustain. Start where you are.

Sleep

Sleep problems are common — insomnia, fragmented sleep, daytime sleepiness, and REM sleep behaviour disorder (acting out dreams). Each is treatable. Tell your neurologist about it; it often doesn’t come up unless asked.

Mood and apathy

Depression and anxiety are common in Parkinson’s and are often more disabling than the motor symptoms. Apathy (loss of motivation) is different from depression and easy to mistake for laziness. All three respond to treatment. Talking therapy, antidepressants, and dose adjustments to your Parkinson’s medications can all help.

Falls prevention

Falls become a bigger issue as the disease progresses. Practical steps make a real difference:

  • Address orthostatic hypotension — get up slowly, hydrate well, raise the head of the bed slightly. Sometimes medication adjustment is needed.
  • Remove trip hazards at home (loose rugs, low-light hallways).
  • Wear shoes with grip; avoid backless slippers.
  • Have a balance assessment with a Parkinson’s-experienced physiotherapist.

Constipation

Very common, often longstanding, and worth treating actively — bad constipation can worsen levodopa absorption. Increase fluids and fibre; your GP can advise on osmotic laxatives (such as polyethylene glycol). Available at any Australian pharmacy.

Diet and levodopa

Levodopa competes with protein for absorption. If you find your medication isn’t working consistently after meals, try taking it 30–60 minutes before food, or shifting protein intake to evening meals. Discuss with your neurologist before changing the timing.

VIII.

Allied health — the team beyond your neurologist

Parkinson’s care works best as a team. Most of the team is coordinated through your GP, who can refer you under a chronic disease management plan when appropriate.

  • Parkinson’s-experienced physiotherapist — for movement, balance, and falls prevention. Programs such as LSVT BIG use deliberately large, high-amplitude movements to retrain motor patterns.
  • — for the soft voice that frequently develops in Parkinson’s. LSVT LOUD is an evidence-supported program; ask for a certified clinician.
  • Occupational therapist — for handwriting, kitchen and bathroom adaptations, dressing aids, and home-safety assessment.
  • Parkinson’s nurse specialist — free telephone support is available through Parkinson’s NSW (1800 644 189). They run education sessions, peer support groups, and help you navigate the wider system.
  • Dietitian — helpful for swallowing problems, weight loss, or medication-protein interactions.
  • Social worker / counsellor — for the emotional and practical adjustments that come with the diagnosis.

We don’t hold a fixed in-house allied-health network at CURA. Your GP is best placed to refer locally — they know who is taking new patients in your area and can match the referral to your specific needs.

IX.

Advanced therapies — when DBS, apomorphine, and Duodopa become relevant

Most people with Parkinson’s do well on oral medication for many years. A meaningful minority eventually reach a stage where standard tablets stop providing smooth control — with motor fluctuations (“wearing off” before the next dose), troublesome dyskinesia, or both. At that point, three advanced options are considered.

  • — thin electrodes are placed in specific deep brain structures and connected to a small generator under the skin, similar to a pacemaker. Programmed correctly, DBS reduces motor fluctuations and dyskinesia in well-selected patients. Not every patient is a candidate; assessment is done at a movement-disorders centre.
  • Apomorphine pump — a continuous subcutaneous infusion of a powerful dopamine agonist, delivered during waking hours via a small pump. Useful for severe motor fluctuations.
  • Duodopa (levodopa intestinal gel) — a continuous gel infusion of levodopa delivered directly into the small intestine via a surgically placed tube and pump. Provides very smooth medication delivery.

How CURA fits in. When advanced therapies become relevant, your neurologist will refer you to a tertiary movement-disorders centre for assessment. We continue to share care where appropriate — for example, with ongoing oral-medication adjustments or follow-up between visits to the centre. Your neurologist will discuss the specific referral pathway with you at the time.

X.

Driving with Parkinson’s in Australia

Australian driving standards are set by Austroads’ Assessing Fitness to Drive.

A Parkinson’s diagnosis does not always mean stopping driving on day one. It usually means moving to a conditional licence, ongoing review, and sometimes a formal on-road OT-DRIVE assessment (an occupational therapist who specialises in driver fitness). Many people with Parkinson’s drive safely for years.

Two specific risks worth knowing about:

  • Dopamine agonists can cause sudden onset of sleep — in some cases without warning drowsiness beforehand. If you’re on pramipexole, ropinirole, or rotigotine, tell your neurologist about any daytime sleepiness.
  • Parkinson’s can affect reaction time and visuospatial judgement in subtle ways before it shows up on testing. An on-road assessment can catch this.

In NSW, the driver is legally required to notify Transport for NSW of the diagnosis. Doctors are protected when reporting in good faith.

XI.

Capacity, Enduring Power of Attorney, and advance care planning

For most people with Parkinson’s, capacity to make your own decisions is preserved for many years. But cognitive change is part of the long-term picture for a meaningful minority, and these conversations are best had early, while the person can take part in them fully.

  • Enduring Power of Attorney (financial) — appoint someone you trust to make financial decisions if you can’t.
  • Appointment of Enduring Guardian (NSW) — appoint someone for lifestyle and medical decisions.
  • Advance Care Directive — record your wishes for future medical care.
  • Will review.
XII.

Caring for the carer

If you’re reading this because someone you love has Parkinson’s, you’re carrying a long-term load. Carer burnout is real, common, and treatable.

Two things worth doing this week:

  • Call Parkinson’s NSW on 1800 644 189 — free, confidential, weekday hours. They have nurse specialists and can connect you with local peer support.
  • See your own GP for a Mental Health Care Plan — this opens up Medicare-rebated psychology sessions for you, the carer.

Other resources: Carers Australia (1800 422 737), Lifeline (13 11 14) for crisis support, and My Aged Care for in-home support packages.

You’ll be a better carer if you take care of yourself first.

Q&A

Frequently asked questions

How is Parkinson’s disease diagnosed?

Parkinson’s is a clinical diagnosis. A neurologist takes a careful history and performs a movement examination, looking for the combination of slowness of movement (bradykinesia) with rest tremor and/or stiffness. Where appropriate, the neurologist may use a structured motor scoring system (MDS-UPDRS) and a brief cognitive screen (MoCA). An MRI is sometimes ordered to rule out other causes; specialised dopamine imaging (DAT-SPECT) is reserved for cases where the diagnosis is genuinely unclear.

Will I need a brain scan?

Not always. Most people are diagnosed clinically without imaging. An MRI is typically arranged when other causes need to be excluded — vascular changes, normal-pressure hydrocephalus, or structural lesions. DAT-SPECT (a dopamine-system scan) is used selectively when the picture is uncertain, particularly to separate Parkinson’s from essential tremor or drug-induced parkinsonism. Imaging is arranged via a separate referral; it is not part of the consultation visit.

Is the consultation one appointment or two?

One. The first Parkinson’s consultation at CURA is a single 60-minute appointment. Any imaging (MRI or DAT-SPECT), formal cognitive testing, or further investigations are arranged afterwards via a separate referral. You won’t have a scan on the day. We’ll explain what’s being arranged before you leave, and a follow-up appointment is booked once results are available.

What’s the first medication usually?

There is no single right starting medication — the choice depends on age, severity, what’s bothering you most, and other health conditions. The three main first-line options are levodopa (the most effective symptomatic treatment, and gentler than older teaching suggested), dopamine agonists (often used in younger patients), and MAO-B inhibitors (used for milder symptoms). Your neurologist will discuss the trade-offs and choose with you. Medications are introduced gradually and titrated over weeks.

Will I need to give up driving?

Usually not on day one. Australian driving standards (Austroads, Assessing Fitness to Drive) require a conditional licence and ongoing review for people with Parkinson’s disease. Many people drive safely for years. A formal on-road OT-DRIVE assessment is sometimes requested. Two specific risks to know: dopamine agonists can cause sudden onset of sleep, and Parkinson’s itself can affect reaction time and visuospatial judgement. In NSW you are legally required to notify Transport for NSW of the diagnosis.

What about clinical trials and stem-cell therapy?

Parkinson’s research is moving fast — alpha-synuclein-targeting drugs, gene therapies, and cell-based approaches are all in active trials. Most clinical trials in Australia run through movement-disorders centres at major teaching hospitals. Be cautious of overseas “stem-cell clinics” that charge large fees for unproven treatments — these are not part of any recognised Parkinson’s pathway. Parkinson’s Australia and Parkinson’s NSW publish trial information; ask your neurologist about specific options.

Does Medicare cover the consultation?

Yes. Specialist neurology consultations attract Medicare rebates with a valid GP referral (12 months) or specialist-to-specialist referral (3 months). Please call our reception for current gap fees. Telehealth follow-ups are also Medicare-rebated and are commonly used for medication reviews once you are established with us.

XIII.

Patient and carer resources

CURA Medical Specialists is a general neurology practice in Drummoyne, Sydney’s Inner West. We see and manage Parkinson’s patients, and refer to a movement-disorders centre when advanced therapies become relevant — book a consultation.