Overview In the 17th and 18th centuries, medical experts identified a disease characterized by tremor of the limbs, with a forward tilt of the trunk and a panic gait. The disease was first described by Dr. James Parkinson in England in 1817 as a condition in which the patient had involuntary tremors, decreased muscle strength, a forward tilt of the trunk when walking, and a running gait after starting, but normal sensation and intelligence. Since the disease was rare at that time, it did not attract the attention of other physicians. It was not until the 1918-1924 pandemic of sleeping encephalitis that the symptoms and signs of the patients were so similar to those described by Parkinson’s doctors that a group of diseases with similar symptoms and signs was officially named “Parkinson’s disease”. The research on Parkinson’s disease also began, but limited by the conditions at the time, the research progressed slowly until the last 40-50 years, especially in recent years, the research on Parkinson’s disease, both pathogenesis and drug treatment have made rapid progress. The pathological basis of Parkinson’s disease: dopaminergic neurons in the dense part of the substantia nigra are reduced by more than 50%, resulting in a decrease in the production of dopamine and a relative increase in its antagonistic transmitter, acetylcholine, which is hyperfunctional. Etiology of Parkinson’s disease: mainly related to ageing, environmental factors, genetic factors, etc. Genetic factors increase the susceptibility to the disease, but only the combined effect of environmental factors and aging leads to a large number of degeneration of nigrostriatal neurons leading to the onset of the disease. Clinical manifestations of Parkinson’s disease I. Motor symptoms: 1. Tremor: first appears in the distal limbs, such as fingers → ipsilateral lower limbs → contralateral upper and lower limbs → jaw, lips, tongue, head. The tremor is mostly resting (pill rubbing) with a frequency of 4~6Hz, and the disease progresses to a certain degree with resting + action tremor. The tremor may increase during emotional excitement, disappear during sleep, and may be temporarily suppressed by strong willful effort. 2, ankylosis: increased muscle tone of the limb lead tube-like, gear-like. Muscle ankylosis can cause pain in the limbs, which can be easily misdiagnosed as “rheumatic pain, frozen shoulder disease, lumbago”. 3. Movement disorders (reduction): slowed movement, lower case syndrome, gait disorder (panic gait), loss of joint movement, mask face, swallowing difficulty, salivation. Non-motor symptoms: 1. Autonomic symptoms: urinary frequency, intractable constipation, profuse sweating, seborrhea, postural hypotension (upright dizziness). 2, psychiatric symptoms: depression, hallucinations, cognitive dysfunction, dementia. 3, sleep disorders: difficulty falling asleep, difficulty maintaining sleep, early awakening, excessive daytime sleepiness. The diagnosis of Parkinson’s disease is based on the British Brain Bank’s diagnostic criteria: reduced movement (slower initiation of voluntary movements and a progressive decrease in the speed and amplitude of repetitive movements) and one of the following: (1) muscle rigidity; (2) resting tremor of 4-6 Hz; (3) postural instability (not due to visual, vestibular, cerebellar or proprioceptive disorders). Treatment of Parkinson’s disease I. Drug therapy: Currently, drug therapy is still the mainstay. No special treatment is needed in the early stages of the disease, and patients should be encouraged to do more active exercises. If the disease affects the patient’s ability to perform daily tasks and live, medication will be used. (i) Protective therapy: monoamine oxidase B inhibitors selagiline and resagiline (evidence-based evidence of protective effect on nigrostriatal neurons); coenzyme Q10 and vitamin E, dopamine receptor agonists (may have protective effect). (ii) Pharmacological treatment: The following drugs can be chosen: (i) anticholinergic drugs: such as Antan; (ii) amantadine; (iii) compound levodopa: such as methyldopa, Xanax; (iv) dopamine agonists: such as Senfuro (pramipexole hydrochloride), Tamsulosin (piribedil); (v) monoamine oxidase B inhibitors: selagiline hydrochloride, resagiline, etc.; (vi) catecholamine oxygen transferase (COMT) inhibitors: such as entocapone (Kodan), tolterodine, etc. (6) catecholamine oxygen transferase (COMT) inhibitors: such as entocapone (Kodan), tolcapone, etc. Surgery: When drug therapy fails, is not tolerated, or when anomia (a complication of dyskinesia) occurs, surgery can be considered, but postoperative drug therapy is still required, only at a reduced dose. Surgical methods used: ① pallidum destruction; ② thalamic destruction; ③ deep brain electrical stimulation (DBS) III. Rehabilitation: As an adjunct to improve symptoms also play a role. Guidance on language, eating, walking and various daily life training and guidance is very important to improve the quality of life of patients. Parkinson’s disease is a chronic progressive disease, and there is no cure. In the late stages of the disease, patients become bedridden due to severe muscle tonus and generalized muscle stiffness. Parkinson’s disease itself is not life-threatening, and the immediate causes of death are various complications such as pneumonia and fractures.