I. Commonly used drugs against Parkinson’s disease (a) Levodopa Levodopa is widely used in the treatment of patients with various types of Parkinson’s disease, and has good effect on 75% of patients, which can significantly improve the patient’s symptoms and improve the quality of life. It is more effective in muscle tonicity and dyskinesia and less effective in tremor; it is more effective in mild cases and younger patients and less effective in severe cases and old and frail patients; it is more effective in primary Parkinson’s disease and less effective in elderly and post-encephalitis secondary Parkinson’s syndrome; it is not effective in those caused by taking antipsychotic drugs. The effect of levodopa is slow, with improvement of symptoms appearing only 2 to 3 weeks after administration, and maximum efficacy is obtained only after 1 to 6 months or more. This drug must be taken for a long time, and after several months to a year of continuous use, some patients can maintain satisfactory results with a reduced dose. In the first few years of levodopa treatment, the effect is stable and satisfactory. Commonly used compound preparations include: methyldopa, restorative, etc. (ii) Anticholinergic drugs play a therapeutic role in Parkinson’s disease by blocking central cholinergic receptors and weakening the effect of acetylcholine in the striatum, which can help restore the relative balance of the two transmitter systems of DA and acetylcholine in Parkinson’s disease from another perspective. Anticholinergic drugs are effective for tremor and tonicity, but less effective for bradykinesia, and are indicated for patients with prominent tremor and younger age. The traditional anticholinergic drugs atropine and scopolamine were the first such drugs used in the treatment of Parkinson’s disease, but their peripheral anticholinergic effects cause large adverse effects. (iii) dopamine-releasing agents Currently the most commonly used is amantadine. The mechanism of action of this product against Parkinson’s disease is more complex, the main mechanism of action is to enhance presynaptic synthesis and release of DA, reduce DA reuptake, and also have a direct agonistic effect on DA receptors. In addition, there is a weak anti-acetylcholine effect. It has a synergistic effect with levodopa. Less effective than levodopa, but better than cholinergic receptor blockers. Fast onset and short duration of action, with peak effect after 48 h. However, the efficacy of some patients gradually decreases after 5 to 12 weeks of continuous use, and may be restored after a period of discontinuation. The effect of the drug can generally be maintained for about 1 year, and then weakened. Amantadine is effective in reducing tremor, and also has some effect on dyskinesia. 90% of the drug is excreted by the kidneys in its original form, so it should be prohibited for people with severe kidney disease. (iv) Dopamine agonists These drugs are less effective than levodopa in the control of Parkinson’s disease and have more adverse effects, such as psychoneurological symptoms and upright hypotension. The dopamine receptor agonists can be divided into two groups: ergometrine, bromocriptine, pergolide (Xie Liang Xing), ergot urea, etc.; medical `education network collection of apomorphine, apomorphine, piribedil (Tesudal), etc. In recent years, a variety of new DA agonists have emerged, such as carte blanche, ropinirole and pramipexole. The mechanism of action of therapeutic drugs (a) anticholinergic drugs These drugs mainly inhibit the excitatory function of the acetylcholine (Ach) system in the central striatum, so that the length of dopamine and Ach tends to be relatively balanced, thus relieving the symptoms. This class of drugs has a certain effect on tremor and tonicity, especially on relieving tremor, and has a weak effect on hypokinesis. (ii) Drugs to improve DA function in the brain DA replacement drugs, directly increase the concentration of DA in the brain, levodopa preparations are still the most effective and basic drugs for the treatment of Parkinson’s disease. All other drugs play further adjuvant therapeutic role on the basis of this drug. It has a strong effect on myotonia and hypokinesia and a weak effect on tremor. DA receptor agonists act directly and selectively on DA receptors, thereby enhancing DA function. The main DA metabolizing enzymes in the brain are monoamine oxidase (MAO) and catecholamine oxygen-site methyltransferase (COMT), which ultimately degrade DA to homovanillic acid. Inhibition of the activity of these two enzymes reduces the degradation of DA and thus enhances the effect of DA. (iii) Selection of therapeutic drugs Once the diagnosis of Parkinson’s disease is clear, clinicians need to select the appropriate drug for treatment from a wide range of anti-PD drugs. Given the differences in intrinsic activity, potential impact on disease progression, and safety characteristics of different drugs, the choice of therapeutic agents varies greatly from patient to patient. The choice of medication must be individualized, taking into account the patient’s age, intellectual status, and primary symptoms, as well as the severity of disruption to daily activities. Younger patients may have more severe symptoms, but younger patients usually have a more benign disease process and better intellectual status than older patients, and younger patients are often expected to be treated for 20 to 30 years, so extra attention should be paid to the treatment of these populations. Therefore, the avoidance of adverse effects of long-term levodopa application and the provision of neuroprotection to avoid disease progression are the first considerations in the selection of drug therapy for this group of patients. Less consideration is given to neuroprotection and the complications of long-term levodopa use. Carbidopa/levodopa, among all antiparkinsonian drugs, is the most effective one that can relieve the signs and symptoms of PD patients. It is characterized by a rapid onset of action and initial treatment is generally well tolerated. Currently, many experts in motor diseases believe that reducing the dosage of levodopa reduces the incidence of its long-term adverse effects. Therefore, the use of levodopa in younger patients (<60 years of age) must first be delayed as much as possible, and once levodopa is used, the lowest effective amount must be used. Carbidopa/levodopa extended-release dosage forms produce a more continuous receptor stimulation and may therefore be preferred over shorter-acting, conventional generic dosage forms. Bromocriptine and pergolide have been used for many years as adjuncts to levodopa in the treatment of Parkinson's disease. It is effective alone or as an adjunct to levodopa. Dopamine receptor agonists are generally considered less effective than levodopa in controlling the signs and symptoms of PD. However, because of the ability to reduce the dosage of levodopa and the potential for intrinsic neuroprotective effects, these drugs may be considered early in the course of the disease. If a dopamine agonist is to be changed, it is recommended that the agonist dose be tapered over a period of 1 to 2 weeks. Another selected dopamine receptor agonist is then started and gradually increased to the desired dose.