Pharmacological treatment of Parkinson’s disease can be divided into six major groups: anticholinergics, amantadine, dopamine replacement therapy, dopamine receptor agonists, monoamine oxidase-B inhibitors, and COMT inhibitors. They achieve the treatment of Parkinson’s disease through different pharmacological mechanisms. 1. Anticholinergic drugs: They can inhibit the action of acetylcholine and correct the imbalance of acetylcholine and dopamine. It is suitable for patients with early mild disease, and has some effect on tremor and muscle rigidity. Commonly used drug is Antan, 2-4mg orally, 3 times daily. Side effects include dry mouth, blurred eyes, absence of sweating, flushing, nausea, insomnia, constipation, urinary retention and, hallucinations and delusions. They disappear after stopping the drug and reducing the dose. Contraindicated in people with glaucoma or prostatic hypertrophy. In the elderly, it can cause mental retardation. For patients over 60 years of age, it is now more advocated not to use. 2, amantadine: can promote the release of dopamine, and has a mild agonistic effect on dopamine receptors. Commonly used dose is 100m, 3 times a day. The effect is good for mild disease, the drug has few side effects. 3, dopamine replacement therapy: supplementation of dopamine in the brain is currently the most common and effective method. Exogenous dopamine cannot enter the brain through the blood-brain barrier (BBB), but levodopa, its precursor, can enter the brain through the BBB and be decarboxylated into dopamine by dopa decarboxylase, thus playing the role of replenishing dopamine in the brain. However, the decarboxylase enzyme that can decarboxylate levodopa is widely present in peripheral organs and blood vessel walls, so during its absorption and transmission, most of it has been converted into dopamine, which can stimulate peripheral dopamine receptors and cause various peripheral side effects. Such as nausea, vomiting, anorexia and other gastrointestinal symptoms and cardiovascular symptoms such as reduced blood pressure and heart rate disorders. Extracerebral dopamine decarboxylase inhibitors such as benserazide and methyldopamine, which do not pass the BBB, only inhibit the decarboxylation of levodopa outside the brain when applied in small doses. Therefore, combined application with levodopa can block the formation of peripheral dopamine, thus reducing the dosage of levodopa, enhancing its efficacy and reducing its peripheral side effects. Therefore, L-dopa alone is not used for treatment, and it is mostly used in combination with benserazide or methyldopa hydrazide. Commonly used drugs include: (1) Madopar: a 4:1 mixture of levodopa and benserazide. For patients with early lesions, the starting dose can be 125mg, taken 3 times a day. This drug significantly reduces the peripheral side effects of levodopa, but does not improve the central side effects. (2) Sinemet-CR: It is a controlled-release tablet of levodopa and methyldopa hydrazide complex, which can make levodopa blood concentration more stable and reach more than 4-6 hours, and help to reduce the end-of-dose phenomenon, switch phenomenon and dose peak hyperactivity of levodopa. The initial dose can be 125mg, taken 3 times a day. The dose should be increased gradually according to the condition. 4.Dopamine agonists: Because of the risk of pulmonary and cardiac valve fibrosis caused by ergot receptor agonists (Sniffer’s stop, Xelianxing), they are now used sparingly. The recommended non-ergot agonists include: (1) Trastal: a dopamine D2 agonist that stimulates D3 receptors in the midbrain cortical and limbic pathways, improving the patient’s intellectual and emotional impairment, and reducing glutamine and free radical levels. (2) Senfuro (Pramipexole) is a new generation non-ergot dopamine receptor agonist, which can avoid neurological damage caused by long-term use of levodopa and reduce the dose of levodopa. It can also selectively act on D2/D3 receptors, which can control tremor and other movement-related symptoms, while relieving psychiatric symptoms, and is a new drug for the treatment of Parkinson’s disease. 5. Monoamine oxidase-B inhibitor: Dopamine is degraded in the brain through MAO-B oxidation and a large number of oxygen free radicals are generated during its metabolism to damage neurons. Therefore, inhibiting the activity of MAO-B can both prolong the residence time of dopamine in the brain, enhance the therapeutic effect, reduce the dosage of levodopa and its side effects, and indirectly play a role in protecting neurons. Commonly used drugs Midodopy (Silegiline), Sigfranc. 6.COMT inhibitor (entacapone): This drug can stabilize the concentration of levodopa in the blood, thus reducing the dosage and its side effects. It can prolong the half-life of levodopa, prevent or delay the appearance of motor fluctuations and “isokinetic” phenomenon, and the common dose is 200mg, taken 3 times a day.