Parkinson’s disease is a neurological disorder commonly seen in middle and old age. Its pathology is characterized by the degenerative death of dopaminergic neurons in the nigrostriatal system of the midbrain, resulting in a decrease in dopamine neurotransmission in the brain and clinical manifestations such as resting tremor, muscle rigidity and motor retardation. Although its cause is not fully understood and cannot be cured, patients can still maintain their ability to work and live independently for a longer period of time through reasonable treatment. Currently, early Parkinson’s disease can be treated symptomatically with medications. Most of the drugs have some adverse effects in the early stage of application, the most common being gastrointestinal symptoms, such as nausea and vomiting. Therefore, each anti-Parkinson’s drug should be titrated: starting with a small dose and slowly increasing the dose to achieve optimal efficacy within the tolerable range of adverse drug reactions, and maintaining treatment at that dose. The “optimal efficacy” should be based on the patient’s specific situation to set the desired treatment goals. In general, there are three levels of treatment goals: 1. The goal of treatment for young, early-stage Parkinson’s disease patients is to maintain or restore work capacity, the first goal. These patients are mostly in stages I and II according to Hoehn-Yahr staging. 2. The minimum treatment goal for patients with intermediate and advanced Parkinson’s disease is to maintain or restore the ability to care for themselves, i.e., the second goal. These patients are mostly in stage III and IV according to Hoehn-Yahr staging. 3. The minimum treatment goal for patients with advanced stages is to relieve pain and prolong life, i.e., the third goal. These patients are mostly in stage V according to Hoehn-Yahr stage. Parkinson’s disease drug treatment principles: the first is: “fine water, do not seek full effect”. In other words, strive to use the smallest dose of drugs so that the symptoms are basically controlled, so that patients can maintain a normal life and work ability, in order to less or late side effects, do not blindly increase the dose of drugs in order to force completely like normal people as the effect of treatment. The second is: add the dose slowly and carry out titration. In other words, each use of a drug should be slowly increased from the smallest dose, within the tolerable range of adverse drug reactions, little by little increase, to achieve the “ideal effect” when the dose is maintained. The third is: individualized dose, which means that the dose for each individual is determined according to titration, rather than the same dose for all patients across the board. The fourth is: reduce the variety and stop the drug slowly. In other words, do not add a variety of anti-Parkinsonian drugs at once, and if you want to withdraw a drug, you should not withdraw it at once, but slowly reduce the dose and finally stop the drug. The “ideal outcome” can be basically normal or close to normal, but does not require complete normalcy. The development of a treatment plan for Parkinson’s disease is governed by age, severity of the disease, the patient’s financial ability and response to the drug. Patients whose function has not been affected in the early stages can start without medication and enhance functional exercise. Patients whose symptoms have affected motor function should be given appropriate medication. First of all, it should be determined whether the patient has cognitive dysfunction, if so then the compounded levodopa preparation should be used directly, if not age is the first factor we should consider. For patients under 65 years of age, non-dopaminergic drugs such as: amantadine can be considered first, which has an ameliorating effect on various major symptoms in most patients and a slightly worse effect on tremor. The duration of efficacy is relatively short, ranging from several months to more than 1 year. The drug is suitable for monotherapy in mild early stage patients. Anticholinergic agents are commonly used, and this drug is more effective in tremor, thus suitable for early patients with predominantly tremor. The application of this drug requires attention to the age and cognitive function of the patient. It should usually be avoided in patients over 70 years of age or in those with cognitive impairment. If, after the above-mentioned treatment, the formulated desired goals are not achieved or the patient’s progression significantly affects function, the application of compounded levodopa preparations and dopa agonists should be considered. Compounded levodopa preparations are the most efficacious and well-tolerated drugs for the treatment of Parkinson’s disease. The starting dose should be as low as 1/4 tablet of medroxyprogesterone three times a day and then gradually “titrated” to be effective. In the early stages of treatment, a fixed dose of 3 or 4 times a day with 1 1/2 to 2 1/2 tablets or less per day of medroxyprogesterone is preferable to pulsed dosing. The use of controlled-release tablets in the early phase is generally not advocated. Doba receptor agonists: Although they are less effective than levodopa, they are currently preferred for the treatment of early patients, especially for young patients with onset before the age of 40, because of their ability to delay the application of levodopa and possible neuroprotective effects. The available domestic receptor agonists are pergolide, piribedil, α-dihydroergotin and bromocriptine. Pergolide has good efficacy on various symptoms of Parkinson’s disease, especially on nocturnal urinary frequency. In the initial application, it is necessary to start with 0.025 mg once a day and increase 0.025 mg every 3-5 days until the intended goal is achieved. For our patients, it is safer to use 0.1-0.3mg 3 times a day. The effect of Tysudar on tremor is better, and it also has a certain improvement effect on rigidity and bradykinesia, which can be used 50mg 1-3 times a day. As for dopa agonists and levodopa preparations, which one should be used first should be considered according to the patient’s condition. For relatively young patients with mild disease, dope-agonists can be considered, and conversely, levodopa preparations can be considered. If the drugs alone do not work well, a combination of drugs can be considered instead of just increasing the dose of a particular drug. Patients aged 65 years or older with severe symptoms and significantly impaired function may be treated directly with levodopa preparations, and later, depending on the situation, a combination of dopa agonists or other drugs may be considered. Patients respond to levodopa in five phases: Phase I: a “honeymoon period” with a stable and long-lasting effect; Phase II: decreasing effect at noon; Phase III: sleep disturbance, “morning stiffness”, possible foot spasms or abnormalities in muscle tone. Stage 4: Predictable “end-of-dose phenomenon”; Stage 5: Frequent decompensation, “switch phenomenon”, and marked “ochronosis The fifth stage: Frequent loss of efficacy, “switching phenomenon”, and significant “isokinetic syndrome”. Generally speaking, the “honeymoon period” of levodopa is about 5 years, after which complications such as reduced efficacy, fluctuating symptoms and ochronosis occur. For a long time, it was suspected that the motor fluctuations and ochronosis after levodopa application might be caused by its toxicity, and it was advocated to use levodopa late or sparingly. Although, late or sparing use may have reduced the development of motor fluctuations and isokinetic disorders, it has significantly reduced the quality of life of patients. Recent studies have shown that motor fluctuations and isokinetic disorders arise mainly due to a progressive decrease in dopaminergic neurons in the brain, with diminished ability to convert levodopa and to store and release dopamine. Levodopa may improve the survival of patients. In contrast, motor fluctuations and allodynia arise mainly because of the short half-life of levodopa and the rapid changes in its plasma concentration, reflected by dopamine receptors being activated too high or too low. Clinical studies have also found that intestinal infusion of levodopa improves symptoms and reduces the time off and isokinesia in patients with advanced PD.