Parkinson’s disease (PD) is a clinically common extrapyramidal degenerative disease that used to be called tremor palsy and occurs in the middle-aged and elderly population. The cause of the disease is not well understood, but the main clinical manifestations are slowly progressive resting limb tremor, myotonia, bradykinesia and impaired postural reflexes. The main manifestations of the disease can also occur during the development of certain diseases such as cerebrovascular, encephalitis, hypoxic encephalopathy, tumors, metabolic abnormalities and some genetic degenerative diseases, so it is often referred to as Parkinson’s syndrome or Parkinson’s superimposed syndrome for the convenience of differentiation. With the development of medical research, there have been great advances in the understanding of PD. It is now found that PD patients with familial features present with autosomal dominant or recessive characteristics, and at least five mutated genes PARK1, PARK2, PARK5, PARK6, and PARK7 have been identified. Of course genetic factors do not play a dominant role in patients with disseminated PD, but they can increase the susceptibility of patients to the disease. Among the environmental factors, the most studied are 1-methyl-4-phenyl-1,2,3,5-tetrahydropyridine (MPTP), pesticides herbicides and other chemical toxicants may cause the onset of the disease, increasing age and metabolic decline also Ageing and metabolic decline may also act as pathogenic factors for the onset of the disease. In the presence of pathogenic factors, oxidative stress, mitochondrial damage, calcium overload, excitatory amino acid toxicity, and increased free radicals occur within dopaminergic neurons located in the basal ganglia region, leading to neuronal degeneration and apoptosis. This process can be slow, so there is no effective means to inhibit the progression of the disease. Pathologically, PD is mainly characterized by atrophy of the striatal substantia nigra in the basal ganglia area, and there are also structural changes in the cortex, midbrain, blue spot, and dorsal nucleus of the vagus nerve. The main clinical manifestations of PD are tremor, increased muscle tone (tonicity), motor retardation and postural balance disorders, which can be accompanied by dementia in the late stage. Symptoms mostly start from one limb and gradually expand to other limbs as the disease develops, although most patients have asymmetrical symptoms. (1) Tremor is characterized by regular alternating contractions of the active and antagonistic muscles of the affected limb at a frequency of about 4-6 times/second. The affected muscles are obvious when they are quiet, accelerated in frequency and amplitude when they are excited, and disappear after sleep. It is usually seen in the mouth, lips, head, neck, limbs and other parts of the body, and there is a characteristic back and forth movement of the fingers with slight flexion, which is similar to “pill rolling”. In the early stage of tremor, the patient can suppress the consciousness for a short time, but in the late stage, it becomes persistent and the consciousness cannot be controlled. (2) Tonicity is another characteristic manifestation of PD patients. The muscle tone of both active and antagonistic muscles is significantly increased, which makes it difficult for patients to move. Due to the continuous tension of the head, neck, trunk and limb muscles, they often show special postures, such as head tilting forward, bending, hunching, bending of both upper limbs and inability to swing naturally, walking in small steps, difficulty in starting and stopping, and dull and rigid facial expressions. (3) Dyskinesia refers to the inability of PD patients to perform many random movements, such as difficulty in fine motor movements, dysgraphia, procrastination, difficulty in turning, slow movement and balance disorders. In addition, persistent constipation, excessive sweating, impotence, increased sebaceous secretion, and salivation may occur due to dysfunction of the vegetative nerves. (4) Depression and dementia are common in patients, accounting for about 30%. They are characterized by slow thinking, difficulty in expression, slow thinking, labored speech and hollow words. Patients are often emotionally unstable, mainly depressed, lacking interest in things, unwilling to communicate with others actively, often with palpitations, chest tightness, dizziness, headache, insomnia, numbness and swelling of the limbs and other physical discomfort, but generally memory impairment appears later. The diagnosis of PD is mainly based on clinical manifestations, and can be diagnosed by the presence of two of the three main items of resting tremor, myotonia, and postural dyskinesia. For example, relatively young patients need to check copper blue protein to exclude Wilson’s disease; MRI and CT to exclude cerebrovascular disease, tumor, inflammatory demyelinating disease, etc.; PET or SPECT can reflect dopamine metabolism may be useful for diagnosis, but currently it is expensive and cannot be used as a routine test. 3.Treatment and prognosis The current treatment of PD cannot achieve a cure, but can only improve the symptoms, delay the development of the disease and improve the quality of life. Among the various treatments used, drug therapy is often the first choice, and surgical stereotactic surgery, radiation surgery and rehabilitation are only auxiliary means, used in specific occasions. Drugs that effectively increase dopamine levels are preferred, while anti-acetylcholine drugs are used as an adjunct. The latest treatment philosophy is that dopamine-based drugs should be used as early as possible when a certain number of dopamine receptors are still available to obtain the maximum benefit. (1) Dopaminergic neuropharmacological agents include dopamine replacement agents, dopamine receptor agonists, and dopamine metabolizing enzyme inhibitors. Levodopa preparations are commonly used clinically as replacement agents and act to compensate for the dopamine deficit in the substantia nigra and striatum. The initial dose of levodopa is 125 mg tid, gradually increasing to 250 mg tid, which has been used less frequently because of the excessive gastrointestinal reactions it causes, and a combination of levodopa and peripheral decarboxylase such as methyldopa and benzodiazepines is used. It is usually better to start with half a tablet daily and gradually increase the dosage until the symptoms are well controlled. Long-term use of levodopa preparations is associated with fluctuations in symptoms, 1 being end of deterioration and 2 being on-off pheomenon. The former is characterized by a shortening of the effective interval between doses and the need to increase the number of doses; the latter is characterized by a sudden reduction (end of deterioration) or worsening (end of off) of symptoms, similar to a “switch”. In the latter case, the symptoms are suddenly reduced (on period) or worsened (off period), similar to a “switch”. (2) Dopamine receptor agonists are widely used drugs, whose pharmacological mechanism is to improve the sensitivity to dopamine by binding to receptors, and can be used as both early treatment drugs and combination drugs for severe patients, which can effectively solve the problem of symptom fluctuation caused by prolonged use of levodopa. The former is represented by bromocriptine, with an initial dose of 0.625 mg taken in the morning, increasing by 0.625 mg every 3-5 days to a therapeutic dose of 7.5~15 mg daily. The effect of Pergolide (Xie Liang Xing) is similar to that of bromocriptine and has a stronger anti-PD ability, treatment should be started from 0.025mg and gradually increased to 0.375~1.5mg. However, the side effects of these drugs are larger, some patients may develop cardiovascular toxicity, postural hypotension or psychiatric symptoms, which limits the use to some extent. The latter clinically used are piribedil (Tesudal), which can act on D1 and D2 receptors, 25~50mg bid or tid. pramipexole is also an agonist of multiple dopamine receptors, the receptor affinity order is D3>D2>D4, can start from small doses, the average effective dose is 1.5~4.5mg/day, the effect of medication for about 3 weeks. (3) Anticholinergic drugs can inhibit the action of acetylcholine and improve the responsiveness of dopamine receptors, which has certain effect on tremor and tonicity. The side effects of these drugs include dry mouth, blurred vision, constipation, difficulty urinating, hallucinations, delusions, etc. They are contraindicated in patients with glaucoma and prostatic hypertrophy. In addition, the drugs used in clinical practice include the antiviral drug amantadine, which can promote the synthesis and release of dopamine in nerve endings, 50~100mg tid; the monoamine oxidase B inhibitor selagiline (Sigfranc) 2.5~5mg qd or bid; the catechol-oxygen-position-methyltransferase entacapone (Kotan) 100~200mg tid, etc., which are increasingly widely used. For the treatment of Parkinson’s combined with dementia, drugs related to Alzheimer’s treatment can be chosen. The regression and prognosis of the disease varies from person to person, with most patients having good drug control and a disease duration of more than 10 years. In a few patients, the disease progresses more rapidly and can be incapacitating within a few years. Early diagnosis and treatment is therefore essential.