Parkinson's disease

"Parkinson's" redirects here. For the medical journal, see Parkinson's Disease (journal). For other uses, see Parkinson's (disambiguation).

Parkinson's disease
Other names	Idiopathic or primary parkinsonism, hypokinetic rigid syndrome, paralysis agitans, shaking palsy
A. 1880s illustration of Parkinson's disease (PD) B. Mild motor-predominant PD C. Intermediate PD D. Diffuse malignant PD
Specialty	Neurology
Symptoms	Main: Tremor, bradykinesia, rigidity, postural instability (collectively known as parkinsonism) Other: Dysautonomia, depression, anxiety, sleep abnormalities
Complications	Falls, dementia, aspiration pneumonia
Usual onset	Age over 60
Duration	Long-term
Risk factors	Family history, dyspepsia, general anesthesia, pesticide exposure, head injuries
Diagnostic method	Symptomatic, medical imaging
Differential diagnosis	Dementia with Lewy bodies, progressive supranuclear palsy, essential tremor, antipsychotic use, fragile X-associated tremor/ataxia syndrome, Huntington's disease, dopamine-responsive dystonia, Wilson's disease
Prevention	Physical activity, nicotine, caffeine
Treatment	Physical therapy, deep brain stimulation
Medication	L-DOPA, COMT inhibitors, AAAD inhibitors, dopamine agonists, MAO-B inhibitors
Prognosis	Near-normal life expectancy
Frequency	8.5 million (2019)
Named after	James Parkinson

Parkinson's disease (PD), or simply Parkinson's, is a neurodegenerative disease primarily of the central nervous system, affecting both motor and non-motor systems. Symptoms typically develop gradually, with non-motor issues becoming more prevalent as the disease progresses. Common motor symptoms include tremors, bradykinesia (slowness of movement), rigidity, and balance difficulties, collectively termed parkinsonism. In later stages, Parkinson's disease dementia, falls, and neuropsychiatric problems such as sleep abnormalities, psychosis, mood swings, or behavioral changes may arise.

Most cases of Parkinson's disease are sporadic, though contributing factors have been identified. Pathophysiology involves progressive degeneration of nerve cells in the substantia nigra, a midbrain region that provides dopamine to the basal ganglia, a system involved in voluntary motor control. The cause of this cell death is poorly understood but involves the aggregation of alpha-synuclein into Lewy bodies within neurons. Other potential factors involve genetic and environmental influences, medications, lifestyle, and prior health conditions.

Diagnosis is primarily based on signs and symptoms, typically motor-related, identified through neurological examination. Medical imaging techniques like neuromelanin MRI can support the diagnosis. Parkinson's typically manifests in individuals over 60, with about one percent affected. In those younger than 50, it is termed "early-onset PD".

No cure for Parkinson's is known, and treatment focuses on alleviating symptoms. Initial treatment typically includes L-DOPA, MAO-B inhibitors, or dopamine agonists. As the disease progresses, these medications become less effective and may cause involuntary muscle movements. Diet and rehabilitation therapies can help improve symptoms. Deep brain stimulation is used to manage severe motor symptoms when drugs are ineffective. There is little evidence for treatments addressing non-motor symptoms, such as sleep disturbances and mood instability. Life expectancy for those with PD is near-normal but is decreased for early-onset.

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. It is classified as a synucleinopathy due to the abnormal accumulation of the protein alpha-synuclein, which aggregates into Lewy bodies within affected neurons.

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

The four cardinal motor symptoms of Parkinson's—bradykinesia (slowed movements), postural instability, rigidity, and tremor—are called parkinsonism. These four symptoms are not exclusive to Parkinson's and can occur in many other conditions, including HIV infection and recreational drug use. Neurodegenerative diseases that feature parkinsonism but have distinct differences are grouped under the umbrella of Parkinson-plus syndromes or, alternatively, atypical parkinsonian disorders. Parkinson's disease can result from genetic factors or be idiopathic, in which there is no clearly identifiable cause. The latter, also called sporadic Parkinson's, makes up some 85–90% of cases.

Signs and symptoms

Main article: Signs and symptoms of Parkinson's disease

Motor

See also: Parkinsonism

Motor symptoms include a stooping posture, the "Parkinsonian gait", and jagged, diminutive handwriting.

Although a wide spectrum of motor and non-motor symptoms appear in Parkinson's, the cardinal features remain tremor, bradykinesia, rigidity, and postural instability, collectively termed parkinsonism. Appearing in 70–75 percent of PD patients, tremor is often the predominant motor symptom. Resting tremor is the most common, but kinetic tremors—occurring during voluntary movements—and postural tremor—preventing upright, stable posture—also occur. Tremor largely affects the hands and feet: 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.

Bradykinesia describes difficulties in motor planning, beginning, and executing, resulting in overall slowed movement with reduced amplitude that affects sequential and simultaneous tasks. Bradykinesia can also lead to hypomimia, reduced facial expressions. Rigidity, also called rigor, refers to a feeling of stiffness and resistance to passive stretching of muscles that occurs in up to 89 percent of cases. Postural instability typically appears in later stages, leading to impaired balance and falls. Postural instability also leads to a forward stooping posture.

Beyond the cardinal four, other motor deficits, termed secondary motor symptom, commonly occur. 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. Most PD patients experience speech problems, including stuttering, hypophonic, "soft" speech, slurring, and festinating speech (rapid and poorly intelligible). Handwriting is commonly altered in Parkinson's, decreasing in size—known as micrographia—and becoming jagged and sharply fluctuating. Grip and dexterity are also impaired.

Non-motor

Neuropsychiatric and cognitive

Neuropsychiatric symptom prevalence in Parkinson's disease

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

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

Cognitive impairments rank among the most prevalent and debilitating non-motor symptoms. These deficits may emerge in the early stages or before diagnosis, 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.

Autonomic

Dysphagia—an autonomic failure—and subsequent complications like aspiration pneumonia (pictured) reduce quality of life.

Autonomic nervous system failures, known as dysautonomia, can appear at any stage of Parkinson's. They are among the most debilitating symptoms and greatly reduce quality of life. Although almost all PD patients suffer cardiovascular autonomic dysfunction, only some are symptomatic. 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.

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

Other non-motor symptoms

Sensory deficits appear in up to 90 percent of patients and are usually present at early stages. Nociceptive and neuropathic pain are common, with peripheral neuropathy affecting up to 55 percent of individuals. Visual impairments are also common, including deficits in visual acuity, color vision, eye coordination, and visual hallucinations. An impaired sense of smell is also common. PD patients can experience difficulty visually interpreting spaces and objects, as well as a reduced ability to recognize faces and emotions. Difficulty reading and double vision are commonly reported.

Sleep disorders are common in PD, affecting up to 98% according to a seminal 1988 study. They comprise 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.

PD is also associated with a variety of skin disorders that include melanoma, seborrheic dermatitis, bullous pemphigoid, and rosacea. 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.

Causes

Main article: Causes of Parkinson's disease

The protein alpha-synuclein aggregates into Lewy bodies and neurites, stained brown at right.

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

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

Genetic

Ribbon diagram of parkin

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

As of 2024, around 90 genetic risk variants across 78 genomic loci have been identified. Notable risk genes include SNCA (which encodes alpha-synuclein), LRRK2, and VPS35 for autosomal dominant inheritance, and PRKN, PINK1, and DJ1 for autosomal recessive inheritance. LRRK2 is the most common autosomal dominant variant and is estimated to be responsible for 1–2 percent of all cases of PD and 40 percent of familial cases. Parkin variants cause nearly half of recessive, early onset monogenic PD. Mutations in the GBA1 gene, linked to Gaucher's disease, are found in 5–15 percent of PD cases. The GBA1 variant of PD more frequently involves cognitive cognitive decline.

Environmental

See also: Environmental health and Exposome

Environmental toxicants like pesticides are believed to be a trigger for Parkinson's.

The limited heritability of Parkinson's strongly implies environmental factors, but identifying these risk factors and causality is difficult due to PD's often decade-long prodromal period. However, environmental toxicants such as air pollution, pesticides, and industrial solvents like trichloroethylene are strongly linked to Parkinson's.

Certain pesticides—like paraquat, glyphosate, and rotenone—are the most established environmental toxicants for Parkinson's, and are likely causal. PD prevalence is strongly associated with local pesticide use, and many pesticides harm mitochondria. Paraquat, for instance, structurally resembles metabolized MPTP, which selectively kills dopaminergic neurons by inhibiting mitochondrial complex 1 and is widely used to model PD. Pesticide exposure after diagnosis may also accelerate disease progression. Without pesticide exposure, an estimated 20 percent of all PD cases would be prevented.

Hypotheses

Prionic hypothesis

See also: Prion

The hallmark of Parkinson's is the formation of protein aggregates, initially alpha-synuclein fibrils and then Lewy bodies and Lewy neurites. The prion hypothesis holds that alpha-synuclein aggregates are pathogenic: they can travel to neighboring, healthy neurons and seed new aggregates. Some suggest that the heterogeneity of PD may be due to different "strains" of alpha-synuclein aggregates and different anatomical sites of origin. 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. However, therapeutic efforts to clear alpha-synuclein have failed. Additionally, postmortem brain tissue analysis shows that alpha-synuclein pathology does not progress through clearly progress through the nearest neural connections.

Braak's hypothesis

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

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

Catecholaldehyde hypothesis

Main article: Catecholaldehyde hypothesis

The catecholaldehyde hypothesis argues that the dopamine metabolite DOPAL (pictured) triggers alpha-synuclein aggregation.

The enzyme monoamine oxidase (MAO) play a central role in the metabolism of the neurotransmitter dopamine and other catecholamines. The catecholaldehyde hypothesis argues that the oxidation of dopamine by MAO into 3,4-dihydroxyphenylacetaldehyde (DOPAL) and hydrogen peroxide and the subsequent abnormal accumulation thereof leads to neurodegeneration. The theory posits that DOPAL interacts with alpha-synuclein and causes it to aggregate.

Mitochondrial dysfunction

Whether mitochondrial dysfunction is a cause or consequence of PD pathology remains unclear. Impaired ATP production, increased oxidative stress, and reduced calcium buffering may contribute to neurodegeneration. The finding that MPP⁺—a respiratory complex I inhibitor and MPTP metabolite—caused parkinsonian symptoms strongly implied that mitochondria contributed to PD pathogenesis. Alpha synuclein and toxicants like rotenone similarly disrupt respiratory complex I. Additionally, faulty genes variants involved in familial Parkinson's—including PINK1 and Parkin—prevent the elimination of dysfunctional mitochondria through mitophagy.

Neuroinflammation

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

Pathophysiology

Main article: Pathophysiology of Parkinson's disease

Parkinson's results from the death of dopamine-releasing neurons in the substantia nigra pars compacta, seen by the loss of dark neuromelanin in the lower inset.

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. The death of these neurons reduces available dopamine in the striatum, which in turn affects circuits controlling movement in the basal ganglia. By the time motor symptoms appear, 50–80 percent of all dopaminergic neurons in the substantia nigra have degenerated.

However, cell death and Lewy pathology are not limited to the substantia nigra. 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. In the third Braak stage, lewy body pathology appears in the substantia nigra, and, by the sixth step, lewy pathology has spread to the limbic and neocortical regions. Although Braak staging offers a strong basis for PD progression, the Lewy pathology around 50 percent patients do not adhere to the predicted model. Indeed, lewy pathology is highly variable and may be entirely absent in some PD patients.

Alpha synuclein pathology

Further information: Protein aggregation and Lewy body

Lewy bodies and Lewy neurites stained brown in PD brain tissue

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

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. 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.

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. High risk gene variants also impair all three of these processes. 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. Risky gene variants, chiefly GBA, further compromise lysosomal function. 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. Microglial activation, possibly caused by alpha-synuclein, is also strongly indicated.

Risk factors

Positive 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. 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. Traumatic brain injury significant increases PD risk, especially if recent. Dairy consumption is associated with a higher risk, possibly due to contaminants like heptachlor epoxide. Although the connection is unclear, melanoma diagnosis is associated with an approximately 45 percent risk increase. There is also an association between methamphetamine use and PD risk.

Negative risk factors

Higher blood concentration of urate—a potent antioxidant—are associated with a lower risk of Parkinson's.

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

Although findings have varied, usage of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen may be neuroprotective. Calcium channel blockers may also have a protective effect, with a 22% risk reduction reported. Higher blood concentrations of urate—a potent antioxidant—have been proposed to be neuroprotective. 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.

Diagnosis

Pars compacta neuron with Lewy body (arrowhead) and alpha-synuclein-positive Lewy neurite (right)

A physician's initial assessment is typically based on medical history and neurological examination. They assess motor symptoms (bradykinesia, rest tremors, etc.) using clinical diagnostic criteria. The finding of Lewy bodies in the midbrain on autopsy is usually considered final proof that the person had PD. The clinical course of the illness over time may diverge from PD, requiring that presentation is periodically reviewed to confirm the accuracy of the diagnosis.

Multiple causes can occur for Parkinsonism or diseases that look similar. Stroke, certain medications, and toxins can cause "secondary parkinsonism" and need to be assessed during a visit. Parkinson-plus syndromes, such as progressive supranuclear palsy and multiple system atrophy, must be considered and ruled out appropriately to begin a different treatment and disease progression (anti-Parkinson's medications are typically less effective at controlling symptoms in Parkinson-plus syndromes). Faster progression rates, early cognitive dysfunction or postural instability, minimal tremor, or symmetry at onset may indicate a Parkinson-plus disease rather than PD itself.

Medical organizations have created diagnostic criteria to ease and standardize the diagnostic process, especially in the early stages of the disease. The most widely known criteria come from the UK Queen Square Brain Bank for Neurological Disorders and the U.S. National Institute of Neurological Disorders and Stroke. The Queen Square Brain Bank criteria require slowness of movement (bradykinesia) plus either rigidity, resting tremor, or postural instability. Other possible causes of these symptoms need to be ruled out. Finally, three or more of the following supportive symptoms are required during onset or evolution: unilateral onset, tremor at rest, progression in time, asymmetry of motor symptoms, response to levodopa for at least five years, the clinical course of at least ten years and appearance of dyskinesias induced by the intake of excessive levodopa. If a suspected case of PD does not respond to levodopa then the diagnosis should be reconsidered. Assessment of sudomotor function through electrochemical skin conductance can be helpful in diagnosing dysautonomia.

When PD diagnoses are checked by autopsy, movement disorders experts are found on average to be 79.6% accurate at initial assessment and 83.9% accurate after refining diagnoses at follow-up examinations. When clinical diagnoses performed mainly by nonexperts are checked by autopsy, the average accuracy is 73.8%. Overall, 80.6% of PD diagnoses are accurate, and 82.7% of diagnoses using the Brain Bank criteria are accurate.

Imaging

Computed tomography (CT) scans of people with PD usually appear normal. Magnetic resonance imaging has become more accurate in diagnosis of the disease over time, specifically through iron-sensitive T2* and susceptibility weighted imaging sequences at a magnetic field strength of at least 3T, both of which can demonstrate absence of the characteristic 'swallow tail' imaging pattern in the dorsolateral substantia nigra. In a meta-analysis, absence of this pattern was highly sensitive and specific for the disease. A meta-analysis found that neuromelanin-MRI can discriminate individuals with Parkinson's from healthy subjects. Diffusion MRI has shown potential in distinguishing between PD and Parkinson-plus syndromes, as well as between PD motor subtypes, though its diagnostic value is still under investigation. CT and MRI are used to rule out other diseases that can be secondary causes of parkinsonism, most commonly encephalitis and chronic ischemic insults, as well as less-frequent entities such as basal ganglia tumors and hydrocephalus.

The metabolic activity of dopamine transporters in the basal ganglia can be directly measured with positron emission tomography and single-photon emission computed tomography scans. It has shown high agreement with clinical diagnoses of PD. Reduced dopamine-related activity in the basal ganglia can help exclude drug-induced Parkinsonism. This finding is nonspecific and can be seen with both PD and Parkinson-plus disorders. In the United States, DaTSCANs are only FDA approved to distinguish PD or Parkinsonian syndromes from essential tremor.

Iodine-123-meta-iodobenzylguanidine myocardial scintigraphy can help locate denervation of the muscles of the heart which can support a PD diagnosis.

Differential diagnosis

Secondary parkinsonism – The multiple causes of parkinsonism can be differentiated through careful history, physical examination, and appropriate imaging. Other Parkinson-plus syndromes can have similar movement symptoms but have a variety of associated symptoms. Some of these are also synucleinopathies. Lewy body dementia involves motor symptoms with early onset of cognitive dysfunction and hallucinations that precede motor symptoms. Alternatively, multiple systems atrophy or MSA usually has early onset of autonomic dysfunction (such as orthostasis), and may have autonomic predominance, cerebellar symptom predominance, or Parkinsonian predominance.

Other Parkinson-plus syndromes involve tau, rather than alpha-synuclein. These include progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS). PSP predominantly involves rigidity, early falls, bulbar symptoms, and vertical gaze restriction; it can be associated with frontotemporal dementia symptoms. CBS involves asymmetric parkinsonism, dystonia, alien limb, and myoclonic jerking. Presentation timelines and associated symptoms can help differentiate similar movement disorders from idiopathic Parkinson disease.

Vascular parkinsonism is the phenomenon of the presence of Parkinson's disease symptoms combined with findings of vascular events (such as a cerebral stroke). The damaging of the dopaminergic pathways is similar in cause for both vascular parkinsonism and idiopathic PD and present with similar symptoms. Differentiation can be made with careful bedside examination, history evaluation, and imaging.

Hot Cross Bun sign that is commonly found in MRI of multiple system atrophy

Parkinson-plus syndrome – Multiple diseases can be considered part of the Parkinson's plus group, including corticobasal syndrome, multiple system atrophy, progressive supranuclear palsy, and dementia with Lewy bodies. Differential diagnosis can be narrowed down with careful history and physical exam (especially focused on the sequential onset of specific symptoms), progression of the disease, and response to treatment. Some key symptoms:

• Corticobasal syndrome – levodopa-resistance, myoclonus, dystonia, corticosensory loss, apraxia, and non-fluent aphasia
• Dementia with Lewy bodies – levodopa resistance, cognitive predominance before motor symptoms, and fluctuating cognitive symptoms, (visual hallucinations are common in this disease)
• Essential tremor – This can at first look like Parkinsonism, but has key differentiators. In essential tremor, the tremor gets worse with action (improves in PD), a lack of other symptoms is common in PD, and normal DatSCAN is seen.
• Multiple system atrophy – levodopa resistance, rapidly progressive, autonomic failure, stridor, present Babinski sign, cerebellar ataxia, and specific MRI findings
• Progressive supranuclear palsy – levodopa resistance, restrictive vertical gaze, 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, processes respectively termed neurorestoration and neuroprotection. Patients are typically managed with a holistic approach that combines lifestyle modifications with physical therapy. Current pharmacological interventions purely target symptoms, by either increasing endogenous dopamine levels or directly mimicking dopamine's effect on the patient's brain. These include dopamine agonists, MAO-B inhibitors, and levodopa: the most widely used and effective drug. The optimal time to initiate pharamacological treatment is debated, but initial dopamine agonist and MAO-B inhibitor treatment and later levodopa therapy is common. Invasive procedures such as deep brain stimulation may be used for patients that do not respond to medication.

Medications

Levodopa

LCE pills contain levodopa and COMT and AAAD inhibitors.

Levodopa (L-DOPA) is the most widely used and the most effective therapy—the gold standard—for Parkinson's treatment. The compound occurs naturally and is the immediate precursor for dopamine synthesis in the dopaminergic neurons of the substantia nigra. Levodopa administration reduces the dopamine deficiency, decreasing parkisonian symptoms.

Despite its efficacy, levodopa poses several challenges and has been called the "pharmacologist's nightmare". 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. Symptoms may become unresponsive to levodopa, with sudden changes between a state of mobility ("ON time") and immobility ("OFF time"). Longterm 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.

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. Ergot dopamine agonists were commonly used, but have been largely replaced with non-ergot compounds due to severe adverse effects like pulmonary fibrosis and cardiovascular issues. Non-ergot agonists are efficacious in both early and late stage Parkinson's, The agonist apomorphine is often used for drug-resistant OFF time in later-stage PD. However, after five years of use, impulse control disorders may occur in over 40 percent of PD patients taking dopamine agonists. A problematic, narcotic-like withdrawal effect may occur when agonist use is reduced or stopped. Compared to levodopa, dopamine agonists are more likely to cause fatigue, daytime sleepiness, and hallucinations.

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. 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. When used with levodopa, time spent in the off phase is reduced. Selegiline has been shown to delay the need for initial levodopa, suggesting that it might be neuroprotective and slow the progression of the disease. Common side effects are nausea, dizziness, insomnia, sleepiness, and (in selegiline and rasagiline) orthostatic hypotension. MAO-Bs are known to increase serotonin and cause a potentially dangerous condition known as serotonin syndrome.

Other drugs

Treatments for non-motor symptoms of PD have not been well studied and many medications are used off-label. A diverse range of symptoms beyond those related to motor function can be treated pharmaceutically. Examples include cholinesterase inhibitors for cognitive impairment and modafinil for excessive daytime sleepiness. 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. Doxepin and rasagline may reduce physical fatigue in PD. Other treaments have received government approval, such as the first FDA-approved treatment for PD psychosis, pimavanserin. Although its efficacy is inferior to off-label clozapine, it has significantly fewer side effects.

Invasive interventions

Further information: Deep brain stimulation

Placement of an electrode into the brain for deep brain stimulation.

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). The discovery of L-DOPA for PD treament caused ablative therapies to largely disappear. Ablative surgeries experienced a resurgence in the 1990s but were quickly superseded by newly-developed deep brain stimulation (DBS). Although gamma knife and high-intensity focused ultrasound surgeries have been developed for pallidotomies and thalamotomies, their use remains rare.

DBS involves the implantation of electrodes called neurostimulators, which sends electrical impulses to specific parts of the brain. 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. DBS typically targets rigidity and tremor, and is recommended for PD patients who are intolerant or do not respond to medication. Cognitive impairment is the most common exclusion criteria.

Rehabilitation

Further information: Management of Parkinson's disease § Rehabilitation

Exercise, like the tricycle ride of this PD patient, is a common recommendation.

Although pharmacological therapies can improve symptoms, patients' autonomy and ability to perform everyday tasks is still reduced by PD. As a result, rehabilitation is often useful. However, the scientific support for any single rehabilitation treatment is limited.

Exercise programs are often recommended, with preliminary evidence of efficacy. Regular physical exercise with or without physical therapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life. Aerobic, mind-body, and resistance training may be beneficial in alleviating PD-associated depression and anxiety. Strength training may increase manual dexterity and strength, facilitating daily tasks that require grasping objects.

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. Deep diaphragmatic breathing may also improve chest-wall mobility and vital capacity decreased by the stooped posture and respiratory dysfunctions of advanced Parkinson's. Rehabilitation techniques targeting gait and the challenges posed by braykinesia, shuffling, and decreased arm swing include pole walking, treadmill walking, and marching exercises.

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

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. 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. 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. Increased water and fiber intake is used to treat constipation.

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. Early integration of palliative care into the disease course is recommended, rather than delaying until later stages. Palliative care specialists can help with physical symptoms, emotional factors such as loss of function and jobs, depression, fear, as well as existential concerns. Palliative care team members also help guide patients and families on 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.

Prognosis

See also: Unified Parkinson's disease rating scale

Prognosis of PD subtypes

Parkinson's subtype	Mean years post-diagnosis until:
	Severe cognitive or movement abnormalities	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. On average, life expectancy is reduced in those with Parkinson's, with younger age of onset resulting in greater life expectancy decreases. 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.

Around 30% of Parkinson's patients develop dementia, and is 12 times more likely to occur in elderly patients of those with severe PD. Dementia is less likely to arise in patients with tremor-dominant PD. 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.

The incidence rate of falls in Parkinson's patients 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. Around 90% of those with PD develop hypokinetic dysarthria, which worsens with disease progression and can hinder communication. Additionally, over 80% of PD patients develop dysphagia: consequent inhalation of gastric and oropharyngeal secretions can lead to aspiration pneumonia. Aspiration pneumonia is responsible for 70% of deaths in those with PD.

Epidemiology

Agricultural areas are associated with higher Parkinson's prevalence, possibly due to exposure to pesticides and industrial waste.

As of 2024, Parkinson's is the second most common neurodegenerative disease and the fastest-growing in total number of cases. As of 2023, global prevalence was estimated to be 1.51 per 1000. Although it is around 40% more common in men, age is the dominant predeterminant of Parkinson's. 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. The total number is predicted to rise to over 12 million patients by 2040. Some label this a pandemic.

This increase may be due to a number of global factors, including prolonged life expectancy, increased industrialisation, and decreased smoking. 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%. The influence of multiple genetic and environmental factors complicates epidemiological efforts.

Relative to Europe and North America, disease prevalence is lower in Africa but similar in Latin America. Although China is predicted to have nearly half of the global Parkinson's population by 2030, estimates of prevalence in Asia vary. Potential explanations for these geographic differences include genetic variation, environmental factors, health care access, and life expectancy. 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. 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". The association between rural residence and Parkinson's has been hypothesized to be caused by environmental factors like herbicides, pesticides, and industrial waste.

History

Main article: History of Parkinson's disease

In 1877, Jean-Martin Charcot (left) named the disease for James Parkinson, credited as the first to comprehensively describe it. Patient Pierre D. (right) served as the model for William Gowers' widely distributed illustration 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. He presented six clinical cases, including three he had observed on the streets near Hoxton Square in London. 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.

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. In 1877, Charcot renamed the disease after Parkinson, as not all patients displayed the tremor suggested by "shaking palsy". Subsequent neurologists who made early advances to the understanding of Parkinson's include Armand Trousseau, William Gowers, Samuel Kinnier Wilson, and Wilhelm Erb.

The Internal Classic (c. 425–221 BC), a Chinese text credited to the Yellow Emperor (pictured), details a disease with strikingly parkinsonian symptoms.

Although Parkinson is typically credited with the first detailed description of PD, many previous texts reference some of the disease's clinical signs. In his essay, Parkinson himself acknowledged partial descriptions by Galen, William Cullen, Johann Juncker, and others. 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. 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. 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.

In 1912, Frederic Lewy described microscopic particles in affected brains, later named Lewy bodies. In 1919, Konstantin Tretiakoff reported that the substantia nigra was the main brain structure affected, corroborated by Rolf Hassler in 1938. The underlying changes in dopamine signaling were identified in the 1950s, largely by Arvid Carlsson and Oleh Hornykiewicz. In 1997, Polymeropoulos and colleagues at the NIH discovered the first gene for PD, 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. Anticholinergics and surgery were the only treatments until the use of levodopa, which, although first synthesized by Casimir Funk in 1911, did not enter clinical use until 1967. By the late 1980s, deep brain stimulation introduced by Alim Louis Benabid and colleagues at Grenoble, France, emerged as an additional treatment.

Society and culture

The reduced ability to facially express emotions—as depicted here by French anatomist Paul Richer in 1888—can harm social well-being.

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. 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. 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.

Cost

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

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. 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. However, as of 2022, no rigorous economic surveys had been performed for low or middle income nations. Regardless, preventative care has been identified as crucial to prevent the rapidly increasing incidence of Parkinson's from overwhelming national health systems.

Advocacy

Scottish rugby player Gavin Hastings signs a pledge from the World Parkinson Congress

The birthday of James Parkinson, 11 April, has been designated as World Parkinson's Day. 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.

Advocacy organizations include the National Parkinson Foundation, which has provided more than $180 million in care, research, and support services since 1982, 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; the American Parkinson Disease Association, founded in 1961; and the European Parkinson's Disease Association, founded in 1992.

Notable cases

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

Actor Michael J. Fox and boxer Muhammad Ali (center) are pictured in 2002 speaking before the US Senate to urge increased funding for Parkinson's research.

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

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

Several historical figures have been theorized to have had Parkinson's, often framed in the industriousness and inflexibility of the so-called "Parkinsonian personality". For instance, English philosopher Thomas Hobbes was diagnosed with "shaking palsy"—assumed to have been Parkinson's—but continued writing works such as Leviathan. Adolf Hitler is widely believed to have had Parkinson's, and the condition may have influenced his decision making. Mao Zedong was also reported to have died from the disorder.

Clinical research

Main article: Research in Parkinson's disease

Astronaut Alexander Gerst conducts Parkinson's research aboard the International Space Station in 2018

As of 2024, no disease-modifying therapies exist that reverse or slow the progression of Parkinson's. Active research directions include the search for new animal models of the disease and studies of the potential usefulness of gene therapy, stem cell transplants, and neuroprotective agents. Improved treatments will likely use a combination of therapeutic strategies to improve PD symptoms and maximize outcomes. Reliable biomarkers for Parkinson's are also needed for early diagnosis. Research criteria for their identification have been established.

Neuroprotective treatments

See also: Anti-α-synuclein drug

Anti-alpha-synuclein drugs that prevent alpha-synuclein oligomerization and aggregation or promote their clearance are being heavily explored, and potential therapeutic strategies include small molecules and immunotherapies like vaccines and monoclonal antibodies. Although immunotherapies have shown promise, their effiacy is often inconsistent. Anti-inflammatory drugs that target NLRP3 and the JAK-STAT signaling pathway are another possible therapeutic strategy.

As the gut microbiome in PD is often disrupted and may produce toxic compounds, fecal microbiota transplants may restore a healthy microbiome and improve various motor and non-motor symptoms. Although neurotrophic factors—peptides that enhance the growth, maturation, and survival of neurons—have shown modest results and require invasive surgical administration, less invasive routes such as viral vectors are being explored. Calcium channel blockers may restore the calcium imbalance present in Parkinson's, and are being investigated as a neuroprotective treatment. Other therapies, like deferiprone, may reduce the abnormal accumulation of iron in PD.

Cell-based therapies

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

Researchers at Argonne National Laboratory examine induced pluripotent stem cells (iPSCs) for use in Parkinson's and other diseases: the action potentials of one such iSPC differentiated into a dopaminergic neuron are visible at right.

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. Although most initial research sought to generate dopaminergic neuron precursor cells from fetal brain tissue, pluripotent stem cells—particularly induced pluripotent stem cells (iPSCs)—have become an increasingly popular tissue source.

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

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. This material may deilver a functional, wildtype version of a gene, or knockdown a pathological variants. Experimental gene therapies for PD have aimed to increase the expression of growth factors or enzymes involved in dopamine synthesis, like tyrosine hydroxylase. The one-time delivery of genes circumvents the recurrent invasive administration required to administer some peptides and proteins to the brain. MicroRNAs are an emerging PD gene therapy platform that serve as an alternative to viral vectors.

Notes and references

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