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Classification and terminology

See also: Parkinsonism and Parkinson-plus syndrome

Parkinson's disease (PD) is a neurodegenerative disease affecting both the central and peripheral nervous systems, characterized by the loss of dopamine-producing neurons in the substantia nigra region of the brain.¹ It is classified as a synucleinopathy due to the abnormal accumulation of the protein alpha-synuclein, which aggregates into Lewy bodies within affected neurons.²

The loss of dopamine-producing neurons in the substantia nigra causes movement abnormalities, leading to Parkinson's further categorization as a movement disorder.³ In 30% of cases, disease progression leads to the cognitive decline, resulting in Parkinson's disease dementia (PDD).⁴ Alongside dementia with Lewy bodies, PDD is one of the two subtypes of Lewy body dementia.⁵

The four cardinal motor symptoms of Parkinson's—bradykinesia (slowed movements), postural instability, rigidity, and tremor—are called parkinsonism.⁶⁷ These four symptoms are not exclusive to Parkinson's and can occur in many other conditions,⁸ including HIV infection and recreational drug use.⁹¹⁰ Neurodegenerative diseases that feature parkinsonism but have distinct differences are grouped under the umbrella of Parkinson-plus syndromes or, alternatively, atypical parkinsonian disorders.¹¹¹² Parkinson's disease can be attributed to genetic factors, but most cases are sporadic, with no clearly identifiable cause.¹³

Signs and symptoms

Main article: Signs and symptoms of Parkinson's disease

Motor

See also: Parkinsonism

A wide spectrum of motor and non-motor symptoms appear in Parkinson's; the cardinal features are tremor, bradykinesia, rigidity, and postural instability, collectively termed parkinsonism.¹⁴ Appearing in 70–75 percent of those with PD,¹⁵¹⁶ tremor is often the predominant motor symptom.¹⁷ Resting tremor is the most common, but kinetic tremors—occurring during voluntary movements—and postural tremor—preventing upright, stable posture—also occur.¹⁸ Tremor largely affects the hands and feet:¹⁹ a classic parkinsonian tremor is "pill-rolling", a resting tremor in which the thumb and index finger make contact in a circular motion at 4–6 Hz frequency.²⁰²¹

Bradykinesia describes difficulties in motor planning, beginning, and executing, resulting in overall slowed movement with reduced amplitude that affects sequential and simultaneous tasks.²² Bradykinesia can also lead to hypomimia, reduced facial expressions.²³ Rigidity, also called rigor, refers to a feeling of stiffness and resistance to passive stretching of muscles.²⁴ Postural instability typically appears in later stages, leading to impaired balance and falls.²⁵ Postural instability also leads to a forward stooping posture.²⁶

Beyond the cardinal four, other motor deficits, termed secondary motor symptoms, commonly occur.²⁷ Notably, gait disturbances result in the Parkinsonian gait, which includes shuffling and paroxysmal deficits, where a normal gait is interrupted by rapid footsteps—known as festination—or sudden stops, impairing balance and causing falls.²⁸²⁹ Most people with PD experience speech problems, including stuttering, hypophonic, "soft" speech, slurring, and festinating speech (rapid and poorly intelligible).³⁰ Handwriting is commonly altered in Parkinson's, decreasing in size—known as micrographia—and becoming jagged and sharply fluctuating.³¹ Grip and dexterity are also impaired.³²

Neuropsychiatric and cognitive

Table featuring the prevalence of neuropsychiatric symptoms in PDNeuropsychiatric symptom prevalence in Parkinson's disease³³

Symptom
	Prevalence (%)
Anxiety	40–50
Apathy	40
Depression	20–40
Impulse control disorders	36–60
Psychosis	15–30

Neuropsychiatric symptoms like anxiety, apathy, depression, hallucination, and impulse control disorders occur in up to 60% of those with Parkinson's. They often precede motor symptoms and vary with disease progression.³⁴ Non-motor fluctuations, including dysphoria, fatigue, and slowness of thought, are also common.³⁵ Some neuropsychiatric symptoms are not directly caused by neurodegeneration but rather by its pharmacological management.³⁶

Cognitive impairments rank among the most prevalent and debilitating non-motor symptoms.³⁷ These deficits may emerge in the early stages or before diagnosis,³⁸³⁹ and their prevalence and severity tend to increase with disease progression. Ranging from mild cognitive impairment to severe Parkinson's disease dementia, these impairments include executive dysfunction, slowed cognitive processing speed, and disruptions in time perception and estimation.⁴⁰

Autonomic

Autonomic nervous system failures, known as dysautonomia, can appear at any stage of Parkinson's.⁴¹⁴² They are among the most debilitating symptoms and greatly reduce quality of life.⁴³ Although almost all individuals with PD have cardiovascular autonomic dysfunction, only some are symptomatic.⁴⁴ Chiefly, orthostatic hypotension—a sustained blood pressure drop of at least 20 mmHg systolic or 10 mmHg diastolic after standing—occurs in 30–50 percent of cases. This can result in lightheadedness or fainting: subsequent falls are associated with higher morbidity and mortality.⁴⁵⁴⁶

Other autonomic failures include gastrointestinal issues like chronic constipation, impaired stomach emptying and subsequent nausea, excessive salivation, and dysphagia (difficulty swallowing): all greatly reduce quality of life.⁴⁷ Dysphagia, for instance, can prevent pill swallowing and lead to aspiration pneumonia.⁴⁸ Urinary incontinence, sexual dysfunction, and thermoregulatory dysfunction—including heat and cold intolerance and excessive sweating—also frequently occur.⁴⁹

Other

Sensory deficits appear in up to 90 percent of people with PD and are usually present at early stages.⁵⁰ Nociceptive and neuropathic pain are common,⁵¹ with peripheral neuropathy affecting up to 55 percent of individuals.⁵² Visual impairments are also frequently observed, including deficits in visual acuity, color vision, eye coordination, and visual hallucinations.⁵³ An impaired sense of smell is also prevalent.⁵⁴ Individuals often struggle with spatial awareness, recognizing faces and emotions, and may experience challenges with reading and double vision.⁵⁵

Sleep disorders are highly prevalent in PD, affecting up to 98%.⁵⁶ These disorders include insomnia, excessive daytime sleepiness, restless legs syndrome, REM sleep behavior disorder (RBD), and sleep-disordered breathing, many of which can be worsened by medication. RBD may begin years before the initial motor symptoms. Individual presentation of symptoms varies, although most people affected by PD show an altered circadian rhythm at some point of disease progression.⁵⁷⁵⁸

PD is also associated with a variety of skin disorders that include melanoma, seborrheic dermatitis, bullous pemphigoid, and rosacea.⁵⁹ Seborrheic dermatitis is recognized as a premotor feature that indicates dysautonomia and demonstrates that PD can be detected not only by changes of nervous tissue, but tissue abnormalities outside the nervous system as well.⁶⁰

Causes

Main article: Causes of Parkinson's disease

As of 2024, the cause of neurodegeneration in Parkinson's is unclear,⁶¹ though it is believed to result from the interplay of genetic and environmental factors.⁶² The majority of cases are sporadic with no clearly identifiable cause, while approximately 5–10 percent are familial.⁶³ Around a third of familial cases can be attributed to a single monogenic cause.⁶⁴

Molecularly, abnormal aggregation of alpha-synuclein is considered a key contributor to PD pathogenesis,⁶⁵ although the trigger for this aggregation is debated.⁶⁶ Proteostasis disruption and the dysfunction of cell organelles, including endosomes, lysosomes, and mitochondria, are implicated in pathogenesis.⁶⁷ Additionally, maladaptive immune and inflammatory responses are potential contributors.⁶⁸ The substantial heterogeneity in PD presentation and progression suggests the involvement of multiple interacting triggers and pathogenic pathways.⁶⁹

Genetic

Parkinson's can be narrowly defined as a genetic disease, as rare inherited gene variants have been firmly linked to monogenic PD, and the majority of sporadic cases carry variants that increase PD risk.⁷⁰⁷¹⁷² PD heritability is estimated to range from 22 to 40 percent.⁷³ Around 15 percent of diagnosed individuals have a family history, of which 5–10 percent can be attributed to a causative risk gene mutation. Carrying one of these mutations may not lead to disease. Rates of familial PD vary by ethnicity: monogenic PD occurs in up to 40% of Arab-Berber and 20% of Ashkenazi Jewish people with PD.⁷⁴

As of 2024, around 90 genetic risk variants across 78 genomic loci have been identified.⁷⁵ Notable risk variants include SNCA (which encodes alpha-synuclein), LRRK2, and VPS35 for autosomal dominant inheritance, and PRKN, PINK1, and DJ1 for autosomal recessive inheritance.⁷⁶⁷⁷ LRRK2 is the most common autosomal dominant variant, responsible for 1–2 percent of all PD cases and 40 percent of familial cases.⁷⁸⁷⁹ Parkin variants are associated with nearly half of recessive, early-onset monogenic PD.⁸⁰ Mutations in the GBA1 gene, linked to Gaucher's disease, can cause monogenic PD,⁸¹ and are associated with cognitive decline.⁸²

Environmental

See also: Environmental health and Exposome

The limited heritability of Parkinson's strongly suggests environmental factors are involved, though identifying these risk factors and establishing causality is challenging due to PD's decade-long prodromal period.⁸³

Environmental toxicants such as air pollution, pesticides, and industrial solvents like trichloroethylene are strongly linked to Parkinson's.⁸⁴ Certain pesticides—like paraquat, glyphosate, and rotenone—are the most established environmental toxicants for Parkinson's and are likely causal.⁸⁵⁸⁶⁸⁷ PD prevalence is strongly associated with local pesticide use, and many pesticides are mitochondrial toxins.⁸⁸ Paraquat, for instance, structurally resembles metabolized MPTP,⁸⁹ which selectively kills dopaminergic neurons by inhibiting mitochondrial complex 1 and is widely used to model PD.⁹⁰⁹¹ Pesticide exposure after diagnosis may also accelerate disease progression.⁹² Without pesticide exposure, an estimated 20 percent of all PD cases would be prevented.⁹³

Hypotheses

Prionic

The hallmark of Parkinson's is the formation of protein aggregates, beginning with alpha-synuclein fibrils and followed by Lewy bodies and Lewy neurites.⁹⁴ The prion hypothesis suggests that alpha-synuclein aggregates are pathogenic and can spread to neighboring, healthy neurons and seed new aggregates. Some propose that the heterogeneity of PD may stem from different "strains" of alpha-synuclein aggregates and varying anatomical sites of origin.⁹⁵⁹⁶ Alpha-synuclein propagation has been demonstrated in cell and animal models and is the most popular explanation for the progressive spread through specific neuronal systems.⁹⁷ However, therapeutic efforts to clear alpha-synuclein have failed.⁹⁸ Additionally, postmortem brain tissue analysis shows that alpha-synuclein pathology does not clearly progress through the nearest neural connections.⁹⁹

Braak's

Main article: Parkinson's disease and gut-brain axis § Braak's hypothesis

In 2002, Heiko Braak and colleagues proposed that Parkinson's disease begins outside the brain and is triggered by a "neuroinvasion" of some unknown pathogen.¹⁰⁰¹⁰¹ The pathogen enters through the nasal cavity and is swallowed into the digestive tract, initiating Lewy pathology in both areas.¹⁰²¹⁰³ This alpha-synuclein pathology may then travel from the gut to the central nervous system through the vagus nerve.¹⁰⁴ This theory could explain the presence of Lewy pathology in both the enteric nervous system and olfactory tract neurons, as well as clinical symptoms like loss of smell and gastrointestinal problems.¹⁰⁵ It has also been suggested that environmental toxicants might be ingested in a similar manner to trigger PD.¹⁰⁶

Risk factors

As 90 percent of Parkinson's cases are sporadic, the identification of the risk factors that may influence disease progression or severity is critical.¹⁰⁷¹⁰⁸ The most significant risk factor in developing PD is age, with a prevalence of 1 percent in those aged over 65 and approximately 4.3 percent in age over 85.¹⁰⁹ Traumatic brain injury significantly increases PD risk, especially if recent.¹¹⁰¹¹¹ Dairy consumption correlates with a higher risk, possibly due to contaminants like heptachlor epoxide.¹¹² Although the connection is unclear, melanoma diagnosis is associated with an approximately 45 percent risk increase.¹¹³ There is also an association between methamphetamine use and PD risk.¹¹⁴

Protective factors

Although no compounds or activities have been mechanistically established as neuroprotective for Parkinson's,¹¹⁵¹¹⁶ several factors have been found to be associated with a decreased risk.¹¹⁷ Tobacco use and smoking is strongly associated with a decreased risk, reducing the chance of developing PD by up to 70%.^118119120 Various tobacco and smoke components have been hypothesized to be neuroprotective, including nicotine, carbon monoxide, and monoamine oxidase B inhibitors.¹²¹¹²² Consumption of caffeine as an ingredient of coffee or tea is also strongly associated with neuroprotection.¹²³ Prescribed adrenergic antagonists like terazosin may reduce risk.¹²⁴

Although findings have varied, usage of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen may be neuroprotective.¹²⁵¹²⁶ Calcium channel blockers may also have a protective effect, with a 22% risk reduction reported.¹²⁷ Higher blood concentrations of urate—a potent antioxidant—have been proposed to be neuroprotective.¹²⁸¹²⁹ Although longitudinal studies observe a slight decrease in PD risk among those who consume alcohol—possibly due to alcohol's urate-increasing effect—alcohol abuse may increase risk.¹³⁰

Pathophysiology

Main article: Pathophysiology of Parkinson's disease

Parkinson's disease has two hallmark pathophysiological processes: the abnormal aggregation of alpha-synuclein that leads to Lewy pathology, and the degeneration of dopaminergic neurons in the substantia nigra pars compacta.¹³¹¹³² The death of these neurons reduces available dopamine in the striatum, which in turn affects circuits controlling movement in the basal ganglia.¹³³ By the time motor symptoms appear, 50–80 percent of all dopaminergic neurons in the substantia nigra have degenerated.¹³⁴

However, cell death and Lewy pathology are not limited to the substantia nigra.¹³⁵ The six-stage Braak system holds that alpha-synuclein pathology begins in the olfactory bulb or outside the central nervous system in the enteric nervous system before ascending the brain stem.¹³⁶ In the third Braak stage, Lewy body pathology appears in the substantia nigra,¹³⁷ and, by the sixth step, Lewy pathology has spread to the limbic and neocortical regions.¹³⁸ Although Braak staging offers a strong basis for PD progression, around 50 percent of individuals do not adhere to the predicted model.¹³⁹ Lewy pathology is highly variable and may be entirely absent in some persons with PD.¹⁴⁰¹⁴¹

Alpha-synuclein pathology

Further information: Protein aggregation and Lewy body

Alpha-synuclein is an intracellular protein typically localized to presynaptic terminals and involved in synaptic vesicle trafficking, intracellular transport, and neurotransmitter release.¹⁴²¹⁴³ When misfolded, it can aggregate into oligomers and proto-fibrils that in turn lead to Lewy body formation.^144145146 Due to their lower molecular weight, oligomers and proto-fibrils may disseminate and be transmitted to other cells more rapidly.¹⁴⁷

Lewy bodies consist of a fibrillar exterior and granular core. Although alpha-synuclein is the dominant proteinaceous component, the core contains mitochondrial and autophagosomal membrane components, suggesting a link with organelle dysfunction.¹⁴⁸¹⁴⁹ It is unclear whether Lewy bodies themselves contribute to or are simply the result of PD pathogenesis: alpha-synuclein oligomers can independently mediate cell damage, and neurodegeneration can precede Lewy body formation.¹⁵⁰

Pathways involved in neurodegeneration

See also: Neurodegeneration § Mechanisms

Three major pathways—vesicular trafficking, lysosomal degradation, and mitochondrial maintenance—are known to be affected by and contribute to Parkinson's pathogenesis, with all three linked to alpha-synuclein.¹⁵¹ High risk gene variants also impair all three of these processes.¹⁵² All steps of vesicular trafficking are impaired by alpha-synuclein. It blocks endoplasmic reticulum (ER) vesicles from reaching the Golgi—leading to ER stress—and Golgi vesicles from reaching the lysosome, preventing alpha-synuclein degradation and leading to its build-up.¹⁵³ Risky gene variants, chiefly GBA, further compromise lysosomal function.¹⁵⁴ Although the mechanism is not well established, alpha-synuclein can impair mitochondrial function and cause subsequent oxidative stress. Mitochondrial dysfunction can in turn lead to further alpha-synuclein accumulation in a positive feedback loop.¹⁵⁵ Microglial activation, possibly caused by alpha-synuclein, is also strongly indicated.¹⁵⁶¹⁵⁷

Mitochondrial dysfunction

See also: Mitochondrial disease

Mitochondrial dysfunction is well-established in Parkinson's.¹⁵⁸ Increased oxidative stress and reduced calcium buffering may contribute to neurodegeneration.¹⁵⁹ The finding that MPP+—a respiratory complex I inhibitor and MPTP metabolite—caused parkinsonian symptoms strongly implied that mitochondria contributed to PD pathogenesis.¹⁶⁰ Additionally, faulty gene variants involved in familial Parkinson's—including PINK1 and Parkin—prevent the elimination of dysfunctional mitochondria through mitophagy.¹⁶¹

Neuroinflammation

Some hypothesize that neurodegeneration arises from a chronic neuroinflammatory state created by local activated microglia and infiltrating immune cells.¹⁶² Mitochondrial dysfunction may also drive immune activation, particularly in monogenic PD.¹⁶³ Some autoimmune disorders increase the risk of developing PD, supporting an autoimmune contribution.¹⁶⁴ Additionally, influenza and herpes simplex virus infections increase the risk of PD, possibly due to a viral protein resembling alpha-synuclein.¹⁶⁵ Parkinson's risk is also decreased with immunosuppressants.¹⁶⁶

Diagnosis

Diagnosis of Parkinson's disease is largely clinical, relying on medical history and examination of symptoms, with an emphasis on symptoms that appear in later stages.¹⁶⁷¹⁶⁸ Although early stage diagnosis is not reliable,¹⁶⁹¹⁷⁰ prodromal diagnosis may consider previous family history of Parkinson's and possible early symptoms like rapid eye movement sleep behavior disorder (RBD), reduced sense of smell, and gastrointestinal issues.¹⁷¹ Isolated RBD is a particularly significant sign as 90% of those affected will develop some form of neurodegenerative parkinsonism.¹⁷² Diagnosis in later stages requires the manifestation of parkinsonism, specifically bradykinesia and rigidity or tremor. Further support includes other motor and non-motor symptoms and genetic profiling.¹⁷³

A PD diagnosis is typically confirmed by two of the following criteria: responsiveness to levodopa, resting tremor, levodopa-induced dyskinesia, or with dopamine transporter single-proton emission computed tomography.¹⁷⁴ If these criteria are not met, atypical parkinsonism is considered.¹⁷⁵ Definitive diagnoses can only be made post-mortem through pathological analysis.¹⁷⁶ Misdiagnosis is common, with a reported error rate of near 25 percent, and diagnoses often change during follow-ups.¹⁷⁷¹⁷⁸ Diagnosis can be further complicated by multiple overlapping conditions.¹⁷⁹

Imaging

Diagnosis can be aided by molecular imaging techniques such as magnetic resonance imaging (MRI), positron emission tomography (PET), and single-photon emission computed tomography (SPECT).¹⁸⁰ As both conventional MRI and computed tomography (CT) scans are usually normal in early PD, they can be used to exclude other pathologies that cause parkinsonism.¹⁸¹¹⁸² Diffusion MRI can differentiate PD from multiple systems atrophy (MSA).¹⁸³ Emerging MRI techniques of at least 3.0 T field strength—including neuromelanin-MRI, 1H-MRSI, and resting state fMRI—may detect abnormalities in the substantia nigra, nigrostriatal pathway, and elsewhere.¹⁸⁴

Unlike MRI, PET and SPECT use radioisotopes for imaging.¹⁸⁵ Both techniques can aid diagnosis by characterizing PD-associated alterations in the metabolism and transport of dopamine in the basal ganglia.¹⁸⁶¹⁸⁷ Largely used outside the United States, iodine-123-meta-iodobenzylguanidine myocardial scintigraphy can assess heart muscle denervation to support a PD diagnosis.¹⁸⁸

Differential diagnosis

See also: Parkinson-plus syndrome

Differential diagnosis of Parkinson's is among the most difficult in neurology.¹⁸⁹ Differentiating early PD from atypical parkinsonian disorders is a major difficulty. In their initial stages, PD can be difficult to distinguish from the atypical neurodegenerative parkinsonisms, including MSA, dementia with Lewy bodies, and the tauopathies progressive supranuclear palsy and corticobasal degeneration.¹⁹⁰¹⁹¹ Other conditions that may present similarly to PD include vascular parkinsonism, Alzheimer's disease, and frontotemporal dementia.¹⁹²¹⁹³

The International Parkinson and Movement Disorder Society has proposed a set of criteria that, unlike the standard Queen's Square Brain Bank Criteria, includes non-exclusionary "red-flag" clinical features that may not suggest Parkinson's.¹⁹⁴ A large number of "red flags" have been proposed and adopted for various conditions that might mimic the symptoms of PD.¹⁹⁵ Diagnostic tests, including gene sequencing, molecular imaging techniques, and assessment of smell may also distinguish PD.¹⁹⁶ MRI is particularly powerful due to several unique features for atypical parkinsonisms.¹⁹⁷

Disorder	Distinguishing symptoms and features198199200
Corticobasal syndrome	Levodopa resistance, myoclonus, dystonia, corticosensory loss, alien limb phenomenon, apraxia, and non-fluent aphasia
Dementia with Lewy bodies	Levodopa resistance, cognitive predominance before motor symptoms, and fluctuating cognitive symptoms
Essential tremor	Tremor that worsens with action, normal SPECT scan
Multiple system atrophy	Levodopa resistance, rapidly progressive, autonomic failure, stridor, present Babinski sign, cerebellar ataxia, and specific MRI findings like the "Hot Cross Bun"
Progressive supranuclear palsy	Levodopa resistance, restrictive vertical gaze, pseudobulbar crying, eyelid twitching, specific MRI findings, and early and different postural difficulties

Management

Main article: Management of Parkinson's disease

As of 2024, no disease-modifying therapies exist that reverse or slow neurodegeneration.²⁰¹²⁰² Management typically combines lifestyle modifications with physical therapy.²⁰³ Current pharmacological interventions purely target symptoms, by either increasing endogenous dopamine levels or directly mimicking dopamine's effect on the patient's brain.²⁰⁴²⁰⁵ These include dopamine agonists, MAO-B inhibitors, and levodopa: the most widely used and effective drug.²⁰⁶²⁰⁷ The optimal time to initiate pharmacological treatment is debated,²⁰⁸ but initial dopamine agonist and MAO-B inhibitor treatment and later levodopa therapy is common.²⁰⁹ Invasive procedures such as deep brain stimulation may be used when medication is ineffective.²¹⁰²¹¹

Medications

Levodopa

Levodopa is the most widely used and the most effective therapy—the gold standard—for Parkinson's treatment.²¹² The compound occurs naturally and is the immediate precursor for dopamine synthesis in the dopaminergic neurons of the substantia nigra.²¹³ Levodopa administration reduces the dopamine deficienciency in parkinsonism.²¹⁴²¹⁵

Despite its efficacy, levodopa poses several challenges and its administration been called the "pharmacologist's nightmare".²¹⁶²¹⁷ Its metabolism outside the brain by aromatic L-amino acid decarboxylase (AAAD) and catechol-O-methyltransferase (COMT) can cause nausea and vomiting; inhibitors like carbidopa, entacapone, and benserazide are usually taken with levodopa to mitigate these effects.^218219220 Long-term levodopa use may also induce dyskinesia and motor fluctuations. Although this often causes levodopa use to be delayed to later stages, earlier administration leads to improved motor function and quality of life.²²¹

Dopamine agonists

Dopamine agonists are an alternative or complement for levodopa therapy. They activate dopamine receptors in the striatum, with reduced risk of motor fluctuations and dyskinesia, and are efficacious in both early and late stage Parkinson's,²²² The agonist apomorphine is often used for drug-resistant OFF time in later-stage PD.²²³²²⁴ After five years of use, impulse control disorders may occur in over 40 percent of those taking dopamine agonists.²²⁵ A problematic, narcotic-like withdrawal effect may occur when agonist use is reduced or stopped.²²⁶²²⁷ Compared to levodopa, dopamine agonists are more likely to cause fatigue, daytime sleepiness, and hallucinations.²²⁸

MAO-B inhibitors

MAO-B inhibitors—such as safinamide, selegiline and rasagiline—increase the amount of dopamine in the basal ganglia by inhibiting the activity of monoamine oxidase B, an enzyme that breaks down dopamine.²²⁹ These compounds mildly alleviate motor symptoms when used as monotherapy but can also be used with levodopa and can be used at any disease stage.²³⁰ Common side effects are nausea, dizziness, insomnia, sleepiness, and orthostatic hypotension.²³¹ MAO-Bs are known to increase serotonin and cause a potentially dangerous condition known as serotonin syndrome.²³²

Other drugs

Treatments for non-motor symptoms of PD have not been well studied and many medications are used off-label.²³³ A diverse range of symptoms beyond those related to motor function can be treated pharmaceutically.²³⁴ Examples include cholinesterase inhibitors for cognitive impairment and modafinil for excessive daytime sleepiness.²³⁵ Fludrocortisone, midodrine and droxidopa are commonly used off label for orthostatic hypotension related to autonomic dysfunction. Sublingual atropine or botulinum toxin injections may be used off-label for drooling. SSRIs and SNRIs are often used for depression related to PD, but there is a risk of serotonin syndrome with the SSRI or SNRI antidepressants.²³⁶ Doxepin and rasagline may reduce physical fatigue in PD.²³⁷

Invasive interventions

Surgery for Parkinson's first appeared in the 19th century and by the 1960s had evolved into ablative brain surgery that lesioned the basal ganglia, thalamus or globus pallidus (a pallidotomy).²³⁸ The discovery of levadopa for PD treatment caused ablative therapies to largely disappear.²³⁹²⁴⁰ Ablative surgeries experienced a resurgence in the 1990s but were quickly superseded by newly-developed deep brain stimulation (DBS).²⁴¹ Although gamma knife and high-intensity focused ultrasound surgeries have been developed for pallidotomies and thalamotomies, their use is rare as of 2025.²⁴²²⁴³

Deep brain stimulation (DBS) involves the implantation of electrodes called neurostimulators, which sends electrical impulses to specific parts of the brain.²⁴⁴ DBS for the subthalamic nucleus and globus pallidus interna has high efficacy for up to 2 years, but longterm efficacy is unclear and likely decreases with time.²⁴⁵ DBS typically targets rigidity and tremor,²⁴⁶ and is recommended for PD patients who are intolerant or do not respond to medication.²⁴⁷ Cognitive impairment is the most common exclusion criteria.²⁴⁸

Rehabilitation

Further information: Management of Parkinson's disease § Rehabilitation

Although pharmacological therapies can improve symptoms, autonomy and ability to perform everyday tasks is still reduced by PD. Rehabilitation is often useful, but the scientific support for any single rehabilitation treatment is limited.²⁴⁹

Exercise programs are often recommended, with preliminary evidence of efficacy.^250251252 Regular physical exercise with or without physical therapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life.²⁵³ Aerobic, mind-body, and resistance training may be beneficial in alleviating PD-associated depression and anxiety.²⁵⁴²⁵⁵ Strength training may increase manual dexterity and strength, facilitating daily tasks that require grasping objects.²⁵⁶ Aerobic exercise, resistance training, balance and task-specific training have been found to improve strength, VO2 Max and balance. While flexibility training is commonly used, but it has a lower strength of recommendation compared to aerobic and resistance training.²⁵⁷

In improving flexibility and range of motion for people experiencing rigidity, generalized relaxation techniques such as gentle rocking have been found to decrease excessive muscle tension. Other effective techniques to promote relaxation include slow rotational movements of the extremities and trunk, rhythmic initiation, diaphragmatic breathing, and meditation.²⁵⁸ Deep diaphragmatic breathing may also improve chest-wall mobility and vital capacity decreased by the stooped posture and respiratory dysfunctions of advanced Parkinson's.²⁵⁹ Rehabilitation techniques targeting gait and the challenges posed by bradykinesia, shuffling, and decreased arm swing include pole walking, treadmill walking, and marching exercises.²⁶⁰ Long-term physiotherapy (greater than six months) reduces the need for antiparkinsonian medication; multidisciplinary rehabilitation programs combined with physiotherapy can result in reduction in the levodopa-equivalent dose.²⁶¹

Speech therapies such as the Lee Silverman voice treatment may reduce the effect of speech disorders associated with PD.²⁶² Occupational therapy is a rehabilitation strategy that can improve quality of life by enabling people with PD to find engaging activities and communal roles, adapt to their living environment, and improve domestic and work abilities.²⁶³

Diet

Parkinson's poses digestive problems like constipation and prolonged emptying of stomach contents, and a balanced diet with periodical nutritional assessments is recommended to avoid weight loss or gain and minimize the consequences of gastrointestinal dysfunction. In particular, a Mediterranean diet is advised and may slow disease progression.²⁶⁴²⁶⁵ As it can compete for uptake with amino acids derived from protein, levodopa should be taken 30 minutes before meals to minimize such competition. Low protein diets may also be needed by later stages.²⁶⁶ As the disease advances, swallowing difficulties often arise. Using thickening agents for liquid intake and an upright posture when eating may be useful; both measures reduce the risk of choking. Gastrostomy can be used to deliver food directly into the stomach.²⁶⁷²⁶⁸ Increased water and fiber intake is used to treat constipation.²⁶⁹

Palliative care

As Parkinson's is incurable, palliative care aims to improve the quality of life for both the patient and family by alleviating the symptoms and stress associated with illness.^270271272 Early integration of palliative care into the disease course is recommended, rather than delaying until later stages.²⁷³ Palliative care specialists can help with physical symptoms, emotional factors such as loss of function and jobs, depression, fear, as well as existential concerns.²⁷⁴ Palliative care team members also help guide difficult decisions caused by disease progression, such as wishes for a feeding tube, noninvasive ventilator or tracheostomy, use of cardiopulmonary resuscitation, and entering hospice care.²⁷⁵²⁷⁶

Prognosis

See also: Unified Parkinson's disease rating scale

Prognosis of PD subtypes²⁷⁷²⁷⁸

Parkinson's subtype	Mean years post-diagnosis until:
	Severe cognitive or movement abnormalities279	Death
Mild-motor predominant	14.3	20.2
Intermediate	8.2	13.1
Diffuse malignant	3.5	8.1

As Parkinson's is a heterogeneous condition with multiple etiologies, prognostication can be difficult and prognoses can be highly variable.²⁸⁰²⁸¹ On average, life expectancy is reduced in those with Parkinson's, with younger age of onset resulting in greater life expectancy decreases.²⁸² Although PD subtype categorization is controversial, the 2017 Parkinson's Progression Markers Initiative study identified three broad scorable subtypes of increasing severity and more rapid progression: mild-motor predominant, intermediate, and diffuse malignant. Mean years of survival post-diagnosis were 20.2, 13.1, and 8.1.²⁸³

Around 30% of individuals with Parkinson's develop dementia, which is 12 times more likely to occur in the elderly with severe PD.²⁸⁴ Dementia is less likely to arise in tremor-dominant PD.²⁸⁵ Parkinson's disease dementia is associated with a reduced quality of life in people with PD and their caregivers, increased mortality, and a higher probability of needing nursing home care.²⁸⁶

The incidence rate of falls is approximately 45 to 68%, thrice that of healthy individuals, and half of such falls result in serious secondary injuries. Falls increase morbidity and mortality.²⁸⁷ Around 90% of those with PD develop hypokinetic dysarthria, which worsens with disease progression and can hinder communication.²⁸⁸ Over 80% develop dysphagia: consequent inhalation of gastric and oropharyngeal secretions can lead to aspiration pneumonia.²⁸⁹

Epidemiology

As of 2024, Parkinson's is the second most common neurodegenerative disease and the fastest-growing in total cases.²⁹⁰²⁹¹ As of 2023, global prevalence was estimated to be 1.51 per 1000.²⁹² Although it is around 40% more common in men,²⁹³ age is the dominant predeterminant of Parkinson's.²⁹⁴ Consequently, as global life expectancy has increased, Parkinson's disease prevalence has also risen, with an estimated increase in cases by 74% from 1990 to 2016.²⁹⁵ The number is predicted to rise to over 12 million by 2040.²⁹⁶

This increase may be due to a number of global factors, including prolonged life expectancy, increased industrialisation, and decreased smoking.²⁹⁷ Although genetics is the sole factor in a minority of cases, most cases of Parkinson's are likely a result of gene-environment interactions: concordance studies with twins have found Parkinson's heritability to be just 30%.²⁹⁸ The influence of multiple genetic and environmental factors complicates epidemiological efforts.²⁹⁹

Relative to Europe and North America, disease prevalence is lower in Africa but similar in Latin America.³⁰⁰ Although China is predicted to have nearly half of the global Parkinson's population by 2030,³⁰¹ estimates of prevalence in Asia vary.³⁰² Potential explanations for these geographic differences include genetic variation, environmental factors, health care access, and life expectancy.³⁰³ Although PD incidence and prevalence may vary by race and ethnicity, significant disparities in care, diagnosis, and study participation limit generalizability and lead to conflicting results.³⁰⁴³⁰⁵ Within the United States, high rates of PD have been identified in the Midwest, the South, and agricultural regions of other states: collectively termed the "PD belt".³⁰⁶ The association between rural residence and Parkinson's has been hypothesized to be caused by environmental factors like herbicides, pesticides, and industrial waste.³⁰⁷

History

Main article: History of Parkinson's disease

In 1817, English physician James Parkinson published the first full medical description of the disease as a neurological syndrome in his monograph An Essay on the Shaking Palsy.³⁰⁸³⁰⁹ He presented six clinical cases, including three he had observed on the streets near Hoxton Square in London.³¹⁰ Parkinson described three cardinal symptoms: tremor, postural instability and "paralysis" (undistinguished from rigidity or bradykinesia), and speculated that the disease was caused by trauma to the spinal cord.³¹¹³¹²

There was little discussion or investigation of the "shaking palsy" until 1861, when Frenchman Jean-Martin Charcot—regarded as the father of neurology—began expanding Parkinson's description, adding bradykinesia as one of the four cardinal symptoms.^313314315 In 1877, Charcot renamed the disease after Parkinson, as the tremor suggested by "shaking palsy" is not present in all.³¹⁶³¹⁷ Subsequent neurologists who made early advances to the understanding of Parkinson's include Armand Trousseau, William Gowers, Samuel Kinnier Wilson, and Wilhelm Erb.³¹⁸

Although Parkinson is typically credited with the first detailed description of PD, many previous texts reference some of the disease's clinical signs.³¹⁹ In his essay, Parkinson himself acknowledged partial descriptions by Galen, William Cullen, Johann Juncker, and others.³²⁰ Possible earlier but incomplete descriptions include a Nineteenth Dynasty Egyptian papyrus, the ayurvedic text Charaka Samhita, Ecclesiastes 12:3, and a discussion of tremors by Leonardo da Vinci.³²¹³²² Multiple traditional Chinese medicine texts may include references to PD, including a discussion in the Yellow Emperor's Internal Classic (c. 425–221 BC) of a disease with symptoms of tremor, stiffness, staring, and stooped posture.³²³ In 2009, a systematic description of PD was found in the Hungarian medical text Pax corporis written by Ferenc Pápai Páriz in 1690, some 120 years before Parkinson. Although Páriz correctly described all four cardinal signs, it was only published in Hungarian and was not widely distributed.³²⁴³²⁵

In 1912, Frederic Lewy described microscopic particles in affected brains, later named Lewy bodies.³²⁶ In 1919, Konstantin Tretiakoff reported that the substantia nigra was the main brain structure affected, corroborated by Rolf Hassler in 1938.³²⁷ The underlying changes in dopamine signaling were identified in the 1950s, largely by Arvid Carlsson and Oleh Hornykiewicz.³²⁸ In 1997, Polymeropoulos and colleagues at the NIH discovered the first gene for PD,³²⁹ SNCA, which encodes alpha-synuclein. Alpha-synuclein was in turn found to be the main component of Lewy bodies by Spillantini, Trojanowski, Goedert, and others.³³⁰ Anticholinergics and surgery were the only treatments until the use of levodopa,³³¹³³² which, although first synthesized by Casimir Funk in 1911,³³³ did not enter clinical use until 1967.³³⁴ By the late 1980s, deep brain stimulation introduced by Alim Louis Benabid and colleagues at Grenoble, France, emerged as an additional treatment.³³⁵

Society and culture

Social impact

For some people with PD, masked facial expressions and difficulty moderating facial expressions of emotion or recognizing other people's facial expressions can impact social well-being.³³⁶ As the condition progresses, tremor, other motor symptoms, difficulty communicating, or mobility issues may interfere with social engagement, causing individuals with PD to feel isolated.³³⁷ Public perception and awareness of PD symptoms such as shaking, hallucinating, slurring speech, and being off balance is lacking in some countries and can lead to stigma.³³⁸

Cost

The economic cost of Parkinson's to both individuals and society is high.³³⁹ Globally, most government health insurance plans do not cover Parkinson's therapies, requiring expenses to be paid out-of-pocket.³⁴⁰ Indirect costs include lifetime earnings losses due to premature death, productivity losses, and caregiver burdens.³⁴¹ The duration and progressive nature of PD can place a heavy burden on caregivers:³⁴² family members like spouses dedicate around 22 hours per week to care.³⁴³

In 2010, the total economic burden of Parkinson's across Europe, including indirect and direct medical costs, was estimated to be €13.9 billion (US $14.9 billion) in 2010.³⁴⁴ The total burden in the United States was estimated to be $51.9 billion in 2017, and is project to surpass $79 billion by 2037.³⁴⁵ As of 2022, no rigorous economic surveys had been performed for low or middle income nations.³⁴⁶ Preventative care has been identified as crucial to prevent the rapidly increasing incidence of Parkinson's from overwhelming national health systems.³⁴⁷

Advocacy

The birthday of James Parkinson, 11 April, has been designated as World Parkinson's Day.³⁴⁸ A red tulip was chosen by international organizations as the symbol of the disease in 2005; it represents the 'James Parkinson' tulip cultivar, registered in 1981 by a Dutch horticulturalist.³⁴⁹

Advocacy organizations include the National Parkinson Foundation, which has provided more than $180 million in care, research, and support services since 1982,³⁵⁰ Parkinson's Disease Foundation, which has distributed more than $115 million for research and nearly $50 million for education and advocacy programs since its founding in 1957 by William Black;³⁵¹³⁵² the American Parkinson Disease Association, founded in 1961;³⁵³ and the European Parkinson's Disease Association, founded in 1992.³⁵⁴

Notable cases

Main article: List of people diagnosed with Parkinson's disease

In the 21st century, the diagnosis of Parkinson's among notable figures has increased the public's understanding of the disorder.³⁵⁵ Actor Michael J. Fox was diagnosed with PD at 29 years old,³⁵⁶ and has used his diagnosis to increase awareness of the disease.³⁵⁷ To illustrate the effects of the disease, Fox has appeared without medication in television roles and before the United States Congress without medication.³⁵⁸ The Michael J. Fox Foundation, which he founded in 2000, has raised over $2 billion for Parkinson's research.³⁵⁹

Boxer Muhammad Ali showed signs of PD when he was 38, but was undiagnosed until he was 42; he has been called the "world's most famous Parkinson's patient". ³⁶⁰ Whether he had PD or parkinsonism related to boxing is unresolved.³⁶¹ Cyclist and Olympic medalist Davis Phinney, diagnosed with Parkinson's at 40, started the Davis Phinney Foundation in 2004 to support PD research.³⁶²³⁶³

Adolf Hitler is believed to have had Parkinson's, and the condition may have influenced his decision making.^364365366

Clinical research

Main article: Research in Parkinson's disease

As of 2024, no disease-modifying therapies exist that reverse or slow the progression of Parkinson's.³⁶⁷³⁶⁸ Active research directions include the search for new animal models of the disease and development and trial of gene therapy, stem cell transplants, and neuroprotective agents.³⁶⁹ Improved treatments will likely combine therapeutic strategies to manage symptoms and enhance outcomes.³⁷⁰ Reliable biomarkers are needed for early diagnosis, and research criteria for their identification have been established.³⁷¹³⁷²

Neuroprotective treatments

See also: Anti-α-synuclein drug

Anti-alpha-synuclein drugs that prevent alpha-synuclein oligomerization and aggregation or promote their clearance are under active investigation, and potential therapeutic strategies include small molecules and immunotherapies like vaccines and monoclonal antibodies.^373374375 While immunotherapies show promise, their effiacy is often inconsistent.³⁷⁶ Anti-inflammatory drugs that target NLRP3 and the JAK-STAT signaling pathway offer another potential therapeutic approach.³⁷⁷

As the gut microbiome in PD is often disrupted and produces toxic compounds, fecal microbiota transplants might restore a healthy microbiome and alleviate various motor and non-motor symptoms.³⁷⁸ Neurotrophic factors—peptides that enhance the growth, maturation, and survival of neurons—show modest results but require invasive surgical administration. Viral vectors may represent a more feasible delivery platform.³⁷⁹ Calcium channel blockers may restore the calcium imbalance present in Parkinson's, and are being investigated as a neuroprotective treatment.³⁸⁰ Other therapies, like deferiprone, may reduce the abnormal accumulation of iron in PD.³⁸¹

Cell-based therapies

Main article: Cell-based therapies for Parkinson's disease

In contrast to other neurodegenerative disorders, many Parkinson's symptoms can be attributed to the loss of a single cell type. Consequently, dopaminergic neuron regeneration is a promising therapeutic approach.³⁸² Although most initial research sought to generate dopaminergic neuron precursor cells from fetal brain tissue,³⁸³ pluripotent stem cells—particularly induced pluripotent stem cells (iPSCs)—have become an increasingly popular tissue source.³⁸⁴³⁸⁵

Both fetal and iPSC-derived DA neurons have been transplanted into patients in clinical trials.³⁸⁶³⁸⁷ Although some individuals see improvement, the results are highly variable. Adverse effects, such as dyskinesia arising from excess dopamine release by the transplanted tissues, have also been observed.³⁸⁸³⁸⁹

Gene therapy

Main article: Gene therapy in Parkinson's disease

Gene therapy for Parkinson's seeks to restore the healthy function of dopaminergic neurons in the substantia nigra by delivering genetic material—typically through a viral vector—to these diseased cells.³⁹⁰³⁹¹ This material may deilver a functional, wildtype version of a gene, or knockdown a pathological variants.³⁹² Experimental gene therapies for PD have aimed to increase the expression of growth factors or enzymes involved in dopamine synthesis, like tyrosine hydroxylase.³⁹³ The one-time delivery of genes circumvents the recurrent invasive administration required to administer some peptides and proteins to the brain.³⁹⁴ MicroRNAs are an emerging PD gene therapy platform that may serve as an alternative to viral vectors.³⁹⁵

Notes and references

Notes

Citations

Works cited

Books

• Bhattacharyya KB (2017). "Chapter One – Hallmarks of Clinical Aspects of Parkinson's Disease Through Centuries". In Bhatia KP, Chaudhuri KR, Stamelou M (eds.). Parkinson's Disease. International Review of Neurobiology. pp. 1–23.
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• Ferri FF (2010). "Chapter P". Ferri's differential diagnosis: a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders (2nd ed.). Elsevier/Mosby. ISBN 978-0-3230-7699-9.
• Lanska DJ (2010). "Chapter 33: The history of movement disorders". Handbook of Clinical Neurology. 3. Vol. 95. History of Neurology. pp. 501–546. doi:10.1016/S0072-9752(08)02133-7. ISBN 978-0-444-52009-8. PMID 19892136.
• O'Sullivan SB, Schmitz TJ (2007). "Parkinson's Disease". Physical Rehabilitation (5th ed.). F.A. Davis. ISBN 978-0-8036-1247-1.
• Simon RP, Greenberg D, Aminoff MJ (2017). Lange Clinical Neurology (10th ed.). McGraw-Hill. ISBN 978-1-2598-6172-7.
• Stoker TB, Greenland JC, eds. (December 2018). Parkinson's Disease: Pathogenesis and Clinical Aspects. Codon Publications. ISBN 978-0-9944-3816-4.
  • Greenland JC, Barker RA (2018). "Chapter 6: The Differential Diagnosis of Parkinson's Disease". In Stoker TB, Greenland JC (eds.). Parkinson's disease: Pathogenesis and Clinical Aspects. Codon Publications. pp. 109–128. doi:10.15586/codonpublications.parkinsonsdisease.2018.ch6. ISBN 978-0-9944-3816-4. PMID 30702839. S2CID 80908095.
• The National Collaborating Centre for Chronic Conditions, ed. (2006). "Non-motor features of Parkinson's disease". Parkinson's Disease. London: Royal College of Physicians. pp. 113–133. ISBN 978-1-8601-6283-1. Archived from the original on 24 September 2010.

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