As of 2025, no disease-modifying therapies exist that reverse or slow neurodegeneration. Management typically 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 pharmacological treatment is debated, but initial dopamine agonist and MAO-B inhibitor treatment and later levodopa therapy are common. Invasive procedures such as
deep brain stimulation may be used when medications are ineffective.
Medications Levodopa pills contain a cocktail of the dopamine precursor levodopa and
COMT and
AAAD inhibitors.
Levodopa is the most widely used and most effective therapy—the
gold standard—for PD 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 in parkinsonism. Despite its efficacy, levodopa poses several challenges. Its administration has been called the "pharmacologist's nightmare". Its metabolism outside the brain by
aromatic L-amino acid decarboxylase and
catechol-O-methyltransferase can cause nausea and vomiting; inhibitors such as
carbidopa,
entacapone, and
benserazide are usually taken with levodopa to mitigate these effects. 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.
Dopamine agonists Dopamine agonists are an alternative or complement to 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 PD. The agonist
apomorphine is often used for drug-resistant OFF time in later-stage PD. After five years of use, impulse-control disorders may occur in over 40% of those 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 at any disease stage. Common side effects are nausea, dizziness, insomnia, sleepiness, and 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 a risk exists of
serotonin syndrome with the SSRI or SNRI antidepressants.
Doxepin and rasagiline may reduce physical fatigue in PD.
Invasive interventions Surgery for PD 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 levodopa for PD treatment 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 is rare as of 2025. DBS involves the implantation of
electrodes called
neurostimulators, which send 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 long-term 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 Although pharmacological therapies can improve symptoms, autonomy, and the 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. 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. Aerobic exercise, resistance training, and balance- and task-specific training have been found to improve strength,
VO2 max and balance. While flexibility training is commonly used, it has a lower strength of recommendation compared to aerobic and resistance training. ride of this PD patient, is often recommended. 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 bradykinesia, shuffling, and decreased arm swing include
pole walking,
treadmill walking, and
marching exercises. 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.
Speech therapies such as the
Lee Silverman voice treatment may reduce the effect of speech disorders associated with PD.
Occupational therapy as a rehabilitation strategy 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.
Diet PD poses digestive problems such as 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 intakes are used to treat constipation.
Palliative care As PD 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, and fear, as well as existential concerns. 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. == Prognosis ==