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Conditions · Head and neck

Parkinson disease !

Parkinson disease is a slowly progressive brain disease from loss of dopamine-making cells; it causes slow movement, tremor and stiffness.

Updated 2026-10-29

Structures involved

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In biochemistry

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Why it happens

What it is

A progressive neurodegenerative disease caused mainly by loss of dopamine-producing neurones in the substantia nigra. It causes slowness of movement with tremor or rigidity, plus many non-motor symptoms.

Who gets it

The second most common neurodegenerative disease after Alzheimer disease. Onset is usually after age 60 and it is somewhat more common in men; early-onset forms are often genetic. Cases are increasing as Latin American populations age.

Causes

  • Mostly sporadic, from a combination of ageing, genetic susceptibility and environmental factors
  • Genetic forms in a minority (e.g. LRRK2, PRKN, GBA variants)
  • Exposure to pesticides and some toxins has been associated

Risk factors

  • Older age
  • Male sex
  • Family history
  • Pesticide exposure and rural farm work
  • Head injury (association)

Pathophysiology

Dopaminergic neurones of the substantia nigra pars compacta degenerate, with Lewy bodies of misfolded alpha-synuclein. Loss of dopamine in the striatum (caudate nucleus and putamen) unbalances the basal ganglia circuits, increasing inhibitory output to the thalamus and motor cortex. Motor signs appear only after many neurones are lost; changes elsewhere explain non-motor symptoms.

Symptoms and signs

  • Bradykinesia: slowness and progressive reduction of repetitive movements (required for diagnosis)
  • Rest tremor, often pill-rolling, usually asymmetric at onset
  • Rigidity (lead-pipe or cogwheel)
  • Shuffling gait with reduced arm swing, stooped posture; postural instability later
  • Reduced facial expression, small handwriting, soft voice
  • Non-motor: loss of smell, constipation, REM sleep behaviour disorder, depression, orthostatic hypotension, cognitive decline

Diagnosis

Clinical
Clinical diagnosis: bradykinesia plus rest tremor or rigidity, using accepted criteria (e.g. Movement Disorder Society), supported by a clear response to dopaminergic treatment and absence of features of other causes.
Tests
No blood test confirms it. Tests exclude mimics when indicated (e.g. thyroid function, copper studies in young patients for Wilson disease). Genetic testing in selected early-onset cases.
Imaging
Brain MRI is usually normal and is used to exclude other causes. Dopamine transporter imaging (SPECT) can help when the diagnosis is uncertain, for example versus essential tremor.

Differential diagnosis

  • Essential tremor
  • Drug-induced parkinsonism
  • Vascular parkinsonism
  • Atypical parkinsonism (progressive supranuclear palsy, multiple system atrophy, dementia with Lewy bodies)
  • Normal pressure hydrocephalus
  • Wilson disease (young patients)

Goal of treatment

Control symptoms and preserve function and quality of life; no current treatment stops progression.

Treatment

Medical
Levodopa combined with a peripheral decarboxylase inhibitor: the most effective drug for motor symptoms.
Medical
Other options: dopamine agonists, MAO-B inhibitors, COMT inhibitors and amantadine, chosen by age, symptoms and side effects.
Medical
Treatment of non-motor symptoms: constipation, orthostatic hypotension, depression, sleep problems and psychosis.
Surgical
Deep brain stimulation of the subthalamic nucleus or globus pallidus for selected patients with motor fluctuations or tremor not controlled by drugs.
Rehabilitation
Physiotherapy, exercise, occupational therapy and speech and swallowing therapy throughout the disease.

Drugs for this condition

Complications

  • Motor fluctuations (wearing off) and dyskinesias with long-term levodopa
  • Falls and fractures
  • Dysphagia and aspiration pneumonia
  • Dementia, psychosis and depression
  • Impulse control disorders with dopamine agonists
  • Parkinsonism-hyperpyrexia syndrome if medication is stopped suddenly

Prognosis

Slowly progressive over many years. Most patients respond well to treatment at first; disability later comes from fluctuations, falls, swallowing problems and cognitive decline.

Test yourself

Think of the answer, then tap the question to see it.

Which neurones are lost in Parkinson disease?

Dopaminergic neurones of the substantia nigra pars compacta, which project to the striatum.

Which motor sign is required for the diagnosis of parkinsonism?

Bradykinesia, plus rest tremor or rigidity.

What protein forms Lewy bodies?

Misfolded alpha-synuclein.

Why is levodopa given with a peripheral decarboxylase inhibitor?

To stop its conversion to dopamine outside the brain, increasing brain delivery and reducing nausea and other peripheral effects.

Which features suggest an atypical parkinsonism rather than Parkinson disease?

Early falls, rapid progression, symmetric onset, early autonomic failure, gaze palsy or poor response to levodopa.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Parkinson Disease (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.

Substantia nigra highlighted on the Durgical 3D model