Parkinson's disease: an animated, cited guide
This page needs JavaScript for its animations. The outline and key answers are below, and every claim in the full version carries a numbered citation.
Not medical advice. Parkinson's Companion is an educational synthesis of published literature. It does not replace a clinician.
What is in it
- What Parkinson's is Parkinsonism versus Parkinson's disease, who it affects, the numbers.
- The dopamine pathway Substantia nigra to striatum, the go and brake loops, and what losing dopamine does.
- Alpha-synuclein and Lewy bodies From a small synaptic protein to a Lewy body, and how it may spread.
- How it spreads: Braak stages Six stages from the brainstem to the cortex, and the body-first debate.
- Genes and inheritance LRRK2, GBA1, SNCA and parkin, founder populations, and what a test means.
- Before the tremor Dream enactment, smell, constipation and the prodromal criteria.
- Stages and symptoms Hoehn and Yahr, motor and non-motor symptoms, and how fast it moves.
- Diagnosis and the MDS criteria The clinical criteria as a calculator, DaT scans and synuclein tests.
- The differential Essential tremor, drug-induced parkinsonism, MSA, PSP and Lewy body dementia.
- Levodopa and carbidopa From the pill to the striatum, step by step.
- Levodopa over time Wearing-off, dyskinesia, the narrowing window and what smooths it.
- The other medicines Agonists, MAO-B and COMT inhibitors, amantadine and the order of use.
- Deep-brain stimulation Targets, the stimulation field, the beta rhythm and what the trials found.
- Beyond movement Mood, hallucinations, dementia, sleep and blood pressure.
- Risk and protection Pesticides, solvents, head injury, smoking, coffee and exercise.
- Living with Parkinson's Exercise, therapy, falls, speech, work, caregiving and the end of life.
- Nursing care Medicines on time, drugs to avoid, swallowing, assessment, documentation.
- Toward a cure Synuclein antibodies, GLP-1 drugs, LRRK2 and GBA1, cells and genes.
- History and people From James Parkinson's 1817 essay to the synuclein test.
- Flashcards and mnemonics Flip cards by topic.
- Quiz Questions with explanations.
- Glossary Every term, searchable.
- Sources Every reference behind the guide.
Common questions
What is the difference between Parkinson's disease and parkinsonism?
Parkinsonism is a pattern of signs: slowness of movement (bradykinesia) together with a rest tremor, stiffness (rigidity) or both. Parkinson's disease is one cause of it, a disease in which dopamine-making neurons in the substantia nigra are lost and the protein alpha-synuclein collects in Lewy bodies. In a Minnesota population study, 42 percent of new cases of parkinsonism were Parkinson's disease and 20 percent were caused by drugs.
How many people have Parkinson's disease?
The WHO reports over 8.5 million people with Parkinson's disease worldwide in 2019, and says prevalence has doubled in the past 25 years. The Global Burden of Disease study counted 6.1 million in 2016, up from 2.5 million in 1990. One 2025 projection reaches 25.2 million by 2050, mostly because populations are ageing.
What are the early signs of Parkinson's?
Changes can begin years before the movement signs. Loss of smell may start more than 20 years before, and constipation 10 to 16 years before, in one prospective study. Acting out dreams (REM sleep behaviour disorder) is a strong warning sign: in an international cohort, 31 percent had developed a neurodegenerative disease after 5 years and 74 percent after 12. Not everyone with these signs develops Parkinson's.
How is Parkinson's disease diagnosed?
Mainly by examination, using the 2015 Movement Disorder Society criteria: parkinsonism must be present, then exclusions, red flags and supportive features are weighed. A DaT scan can show loss of dopamine nerve endings but cannot separate Parkinson's from some similar diseases. A spinal-fluid alpha-synuclein seed amplification test detected 87.7 percent of people with Parkinson's in a large 2023 study, less often in LRRK2 carriers; it is not a stand-alone diagnosis.
What is levodopa wearing-off?
Early on, each dose of levodopa seems to last all day. After some years, the benefit of each dose fades before the next one is due, and symptoms return. A pooled analysis found motor fluctuations in about 40 percent of people after 4 to 6 years of levodopa, and dyskinesia (extra, involuntary movements) in slightly fewer.
Does starting levodopa early make Parkinson's worse?
No. In the LEAP trial, people who started levodopa 40 weeks earlier did no worse after 80 weeks, and rates of dyskinesia and fluctuations did not differ. In the earlier ELLDOPA trial, people taking levodopa had worsened less than those on placebo after a two-week washout.
What is deep-brain stimulation and how well does it work?
Thin electrodes are placed in the subthalamic nucleus or globus pallidus and connected to a stimulator in the chest. In a 2006 randomised trial in people under 75 with advanced disease, stimulation improved quality of life (PDQ-39) by 9.5 points more and off-medication motor scores by 19.6 points more than medicines alone over 6 months. It helps mainly the symptoms that levodopa helps, and tremor.
Is Parkinson's disease genetic?
Usually not in a simple way. In large testing programmes, 13 to 15 percent of people with Parkinson's carried a relevant variant, most often in GBA1 or LRRK2, and the share is higher in Ashkenazi Jewish and North African Berber ancestry. Most carriers never develop the disease: for the LRRK2 G2019S variant, estimates of the risk by age 80 range from about 26 to 74 percent depending on the study.