Parkinson’s disease (Parkinson’s disease) is a common degenerative disease of the nervous system in middle and old age, mainly characterized by progressive degeneration of dopaminergic neurons in the substantia nigra and pathological changes in the formation of Lewy bodies, biochemical changes in the striatal region with reduced dopamine transmission and imbalance between dopamine and acetylcholine transmitters, tremor, myotonia, bradykinesia, postural The disease is characterized by motor symptoms such as tremor, bradykinesia, bradykinesia, postural disturbances and non-motor symptoms such as hyposmia, constipation, abnormal sleep behavior and depression.
The overall prevalence rate of people over 65 years of age in China is 1700/100,000, and increases with age, posing a heavy burden to both families and society. In recent years, there have been significant advances in the understanding of the pathogenesis of Parkinson’s disease and the discovery of biological markers for early diagnosis, as well as the exploration of therapeutic methods and tools. The guidelines for the treatment of Parkinson’s disease in foreign countries, especially in Europe and the United States, have given us good insight and help.
The first and second editions of the Chinese Parkinson’s Disease Treatment Guidelines were formulated by the Parkinson’s Disease and Movement Disorders Group of the Chinese Medical Association Neurology Branch in 2006 and 2009, respectively, which have played an important role in standardizing and optimizing the treatment behavior of Parkinson’s disease and improving the treatment effect in China. In the past 5 years, there have been some updates of treatment concepts and advances in treatment methods in China and abroad in this treatment area.
In order to better adapt to its development and better guide clinical practice, we are now making the necessary changes and updates to the second edition of the Chinese Parkinson’s disease treatment guidelines.
1. Treatment principles
1.1 Comprehensive treatment
Every patient with Parkinson’s disease can exhibit motor and non-motor symptoms sequentially or simultaneously, but they are accompanied by both types of symptoms throughout the course of the disease, sometimes producing multiple non-motor symptoms. Not only do motor symptoms affect the patient’s ability to work and perform daily activities, but non-motor symptoms also significantly interfere with the patient’s quality of life. Therefore, we should adopt a comprehensive and integrated treatment for both motor and non-motor symptoms of Parkinson’s disease.
Treatment methods and tools include pharmacotherapy, surgery, exercise therapy, psychological guidance and care nursing. Drug therapy is preferred and is the main treatment throughout the treatment process, while surgery is an effective supplement to drug therapy. The currently applied treatments, whether pharmacological or surgical, can only improve the patient’s symptoms, but cannot stop the development of the disease, let alone cure it. Therefore, treatment should not only be based on the present, but also requires long-term management to achieve long-term benefits.
1.2 Principles of medication administration
Both motor and non-motor symptoms of the disease can affect the patient’s ability to work and live in daily life, therefore, the principle of medication should be aimed at achieving effective improvement of symptoms, work ability and quality of life. We advocate early diagnosis and early treatment, not only to improve the symptoms, but also to slow down the disease progression.
We should adhere to the principle of “dose titration” to avoid acute side effects of drugs, and strive to achieve the principle of “achieving satisfactory clinical effects with small doses as much as possible”, so as to avoid or reduce the incidence of motor complications, especially xerokinesis, which has been proved that the incidence of xerokinesis in patients with Parkinson’s disease in China is significantly higher. The incidence of atopic disorders in patients with Parkinson’s disease in China has been shown to be significantly lower than that in foreign patients with Parkinson’s disease.
Treatment should follow the evidence of evidence-based medicine and also emphasize individualized characteristics. The selection of medication for different patients needs to take into account the patient’s disease characteristics (whether the tremor is predominant or tonic hypokinesia) and disease severity, the presence or absence of cognitive impairment, age of onset, employment status, the presence or absence of co-morbidities, possible side effects of medication, the patient’s willingness, affordability and other factors to avoid, delay or reduce as much as possible side effects and motor complications of medications.
When performing anti-Parkinson’s disease drug therapy, especially when using levodopa, the drug should not be stopped suddenly to avoid withdrawal malignant syndrome.
2. Drug therapy
Depending on the severity of clinical symptoms, the course of Parkinson’s disease can be divided into early and intermediate to late stages, i.e. Hoehn-Yahr levels 1~2.5 are defined as early stage and Hoehn-Yahr levels 3~5 are defined as intermediate to late stage. In the following, we propose specific treatment recommendations for early and intermediate to late stage Parkinson’s disease.
2.1 Treatment of early stage Parkinson’s disease
Once the disease occurs, it will progressively worsen over time, and there is evidence that the disease progresses more rapidly in the early stages of the disease than in the later stages. Therefore, once early diagnosis is made, treatment should be started as early as possible in order to master the timing of disease modification, which plays a key role in the success or failure of the entire treatment of Parkinson’s disease in the future.
Early treatment can be divided into non-pharmacological treatment (including awareness and understanding of the disease, supplemental nutrition, strengthening exercise, firm confidence in overcoming the disease, as well as social and family understanding, care and support for patients) and pharmacological treatment. Generally, monotherapy is given in the early stage of the disease, but the combination of multiple drugs (embodying multiple targets) in optimized small doses can also be used to achieve the goal of optimal efficacy, longer maintenance time and lowest incidence of exercise complications.
Pharmacological treatments include disease-modifying therapeutic agents and symptomatic therapeutic agents. In addition to their potential disease-modifying effects, disease-modifying drugs also have a symptom-modifying effect; symptomatic drugs, in addition to significantly improving disease symptoms, also have some disease-modifying effects.
The goal of disease-modifying therapy is to delay the progression of the disease. Among the MAO-B inhibitors, selagiline + vitamin E (DATATOP) and resagiline (ADAGIO) have been clinically tested for their potential to delay disease progression; among the DR agonists, pramipexole CALM- PD study and ropinirole REAL-ET study suggest a possible disease-modifying effect. Clinical trials with high doses (1200 mg/d) of coenzyme Q10 also suggest a possible disease-modifying effect.
2.1.1 Preferred drug principles
1. Patients with early onset disease, in the absence of hypo-intelligence, may have the following options.
Non-ergot DR agonists;
MAO- inhibitors;
Amantadine;
Levodopa complex;
Covalently administered levodopa + catechol-O methyltransferase (COMT) inhibitors.
The drugs of choice are not in the above order, but are chosen according to the individual patient. If the patient cannot afford the high cost of the drug for financial reasons, then regimen ③ is preferred; if the patient has a special job, seeks to significantly improve motor symptoms, or has cognitive impairment, then regimen ④ or ⑤ is preferred; or regimen ④ can be used in combination with a low dose of regimen ①, ②, or ③. In cases where tremor is evident and other anti-Parkinsonian drugs are ineffective, anticholinergic drugs such as benzhexol may be used.
In patients with late onset or with concomitant hypo-intelligence, compound levodopa therapy is generally preferred. DR agonists, MAO-B inhibitors, or COMT inhibitors may be added as symptoms worsen and efficacy decreases. Anticholinergic drugs are not used as much as possible, especially for elderly male patients, because they have more side effects.
2.1.2 Therapeutic drugs
Anticholinergic drugs: Currently, benzhexol is mainly used in China at a dose of 1-2 mg 3 times/d. It is mainly used for patients with tremor, but not recommended for patients without tremor. Patients <60 years old should be informed that long-term application of this class of drugs may lead to cognitive decline, so cognitive function should be reviewed regularly and discontinued as soon as cognitive decline is detected; for patients ≥60 years old, it is best not to apply anticholinergic drugs. It is contraindicated in patients with narrow-angle glaucoma and prostatic hypertrophy.
Amantadine: 50~100mg, 2~3 times/d, last dose should be taken before 4pm. It has been shown to improve hypokinesia, tonicity, tremor, and is helpful in improving isokinesia (Level C evidence). Use with caution in patients with renal insufficiency, epilepsy, severe gastric ulcer, hepatic disease, and contraindicated in nursing mothers.
Compound levodopa (benserazide levodopa, carbidopa levodopa): The initial dosage is 62.5~125.0mg, 2~ times /d, gradually increase the dosage to the appropriate dose for satisfactory efficacy and maintenance without side effects, 1h before or 1.5h after meals.
Previously, it was advocated to postpone the application as much as possible because the early application could induce orexia; the available evidence suggests that the early application of small doses (≤400mg/d) does not increase the occurrence of orexia. The rapid onset of action of compounded levodopa in regular release and the relatively long maintenance time of controlled release, but the slow onset of action and low bioavailability, require attention when using, especially when switching between the 2 different dosage forms. It should be used with caution in patients with active peptic ulcers and is contraindicated in patients with narrow-angle glaucoma and psychiatric disorders.
DR agonists: Non-ergot DR agonists are currently preferred, especially in the early stages of early-onset Parkinson’s disease. These long half-life agents prevent or reduce motor complications by avoiding “pulse” stimulation of the DR in the striatal postsynaptic membrane. Agonists should be started at small doses and gradually increased until satisfactory efficacy is achieved without side effects.
The side effects of DR agonists are similar to those of compounded levodopa, except that they have a low incidence of fluctuating symptoms and dyskinesia and a high incidence of postural hypotension, ankle edema, and psychiatric abnormalities (hallucinations, hyperphagia, hypersexuality, etc.). – Dihydroergocryptine, cabergoline, and lisuride; non-ergot agonists include pramipexole, ropinirole, piribedil, rotigotine, and atropine. The DR agonists of the ergot class can be used for the treatment of the disease. Ergot DR agonists can lead to heart valve lesions and pulmonary pleural fibrosis, therefore, their use is no longer advocated, among which pergolide is no longer used in China.
Non-ergot DR agonists that have been available in China for many years are
Piribedil extended-release: The initial dose is 50mg once daily, which can be changed to 25mg twice daily for patients prone to side effects, and increased to 50mg twice daily in the second week, with an effective dose of 150mg/d, divided into 3 oral doses, with the maximum dose not exceeding 250mg/d;
Pramipexole: There are 2 dosage forms: regular release and extended release. The use of normal release: the initial dose is 0.125mg 3 times daily (1-2 times for individual patients prone to side effects), increasing by 0.125mg 3 times a day every week, and the effective dose is generally 0.50-0.75mg 3 times a day, with the maximum dose not exceeding 4.5mg/d. The use of extended release: the daily dose is the same as normal release, but is taken once a day.
Upcoming non-ergot DR agonists are
Ropinirole: The initial dose is 0.25mg 3 times daily, increasing by 0.75mg per week to 3mg daily, with a general effective dose of 3-9mg per day in 3 divided doses and a maximum daily dose of 24mg;
Rotigotine: initial dose of 2mg once daily, increasing by 2mg per week, the effective dose is generally 6~8mg per day for early stage patients and 8~16mg per day for middle and late stage patients.
Ergot DR agonists that have been available in China for many years include
Bromocriptine: 0.625mg once daily, increasing by 0.625mg every 5 days, effective dose 3.75~15.00mg/d, divided into 3 oral doses;
a- Dihydroergot cryptothecin: 2.5mg twice daily, increasing by 2.5mg every 5 days, effective dose 30~50mg/d in 3 oral doses. The dose conversion between the above 5 drugs is: piribedil: pramipexole: ropinirole: bromocriptine: α- dihydroergotocriptine = 100:1:5:10:60), which is only for reference due to individual differences.
MAO-B inhibitors: The main ones are selagiline and rasagiline, of which selagiline is available as a normal-release agent and an oral mucosal disintegrant. The usage of selegiline (normal release) is 2.5~5.0mg twice a day in the morning and noon, not in the evening or night to avoid insomnia, or combined with vitamin E2000U (DATATOP program); the absorption, action and safety of oral mucosal disintegration agent are better than selegiline normal release, the dosage is 1.25~2.50mg/d. The dosage of rasagiline is 1mg, 1 day. The dosage is 1mg once a day, taken in the morning. It should not be used in combination with 5-hydroxytryptamine reuptake inhibitors (SSRI).
COMT inhibitors: Combination levodopa + COMT inhibitors such as entacapone bidopa tablets (a combination of entacapone/levodopa/carbidopa, divided into 4 dosage forms according to levodopa dose) are preferred in the early stage of the disease, not only to improve the patient’s symptoms, but also to prevent or delay the occurrence of motor complications.
However, the FIRST-STEP and STRIDE-PD studies suggest that early application of entacapone bidopa does not delay motor complications and increases the incidence of isokinetic disorders, which is still controversial and needs to be further validated.
In the mid to late stages of the disease, entacapone or tolcapone can be added to the treatment to further improve symptoms when the efficacy of compounded levodopa is diminished. The dosage of entacapone is 100~200mg per dose, and the number of doses is the same as that of levodopa, or less than the number of doses of levodopa if the number of doses of levodopa per day is higher. Tolcapone is 100mg per dose, 3 times a day, the first dose is taken together with levodopa and thereafter at 6h interval, it can be used alone, the maximum daily dose is 600mg.
Side effects include diarrhea, headache, excessive sweating, dry mouth, elevated transaminases, abdominal pain, and yellowing of urine. Tolcapone may cause hepatic impairment and requires close monitoring of liver function, especially during the first 3 months after dosing.
2.2 Treatment of mid- to late-stage Parkinson’s disease
The clinical manifestations of intermediate to advanced Parkinson’s disease, especially advanced Parkinson’s disease, are extremely complex, with the progression of the disease itself, as well as the involvement of drug side effects or motor complications. The treatment of patients with mid- to late-stage Parkinson’s disease should, on the one hand, continue to strive to improve the motor symptoms of patients; on the other hand, some motor complications and non-motor symptoms should be properly managed.
2.2.1 Treatment of motor complications
Motor complications (symptom fluctuations and dyskinesia) are common in the middle and late stages of Parkinson’s disease. Adjusting the type, dose and frequency of medication can improve symptoms, and surgical treatment such as deep brain electrical stimulation (DBS) is also effective.
Treatment of symptom fluctuations (Figure 2): Symptom fluctuations mainly include endofdosedeterioration and on-offphenomenon. The treatment of end-of-dosedeterioration is
2. treatment of atopic movement disorders (Figure 3): atopic movement disorders (AIMs), also known as dyskinesia, include dose peak atopic movement disorder, biphasic atopic movement disorder, and dystonia (dystonia).
The management of dose peak isokinesia is as follows
Decrease the dose of compounded levodopa for each dose;
If the patient is on compounded levodopa alone, reduce the dose appropriately and add a DR agonist or add a COMT inhibitor;
Add amantadine (Level C evidence);
Addition of atypical antipsychotics such as clozapine;
If a compounded levodopa controlled-release agent is used, it should be replaced with a regular-release agent to avoid the cumulative effects of the controlled-release agent.
The management of biphasic heteronegativity (both early and late dose heteronegativity) is as follows.
If a compounded levodopa controlled-release agent is being used, it should be switched to a regular-release agent, preferably with aqueous solvent, which can effectively alleviate the initial dose ochronosis;
The addition of a long half-life DR agonist or COMT inhibitor that extends the levodopa blood paddle clearance half-life may alleviate the end-dose anisotropy and may also help to improve the first-dose anisotropy. Continuous infusion of a DR agonist or levodopa methyl or ethyl ester by microchestnut may improve both ochronosis and symptom fluctuations, and oral preparations are being tested to see if the same effect can be achieved. Clinical trials related to the therapeutic efficacy of other agents for the treatment of athetoid disorder such as adenosine A2A receptor antagonists that act on non-DAergic aspects of the basal ganglia are ongoing.
The management of morning dystonia is as follows.
The treatment of morning dystonia is the same as the treatment of atopic dystonia in the “on” phase, with the addition of a combination of levodopa controlled-release tablets or a long-acting DR agonist at bedtime, or a combination of levodopa normal-release or aqueous solution before waking. Surgical treatment, mainly DBS, may be beneficial.
Instead of increasing the total daily dose of compounded levodopa, it is appropriate to increase the number of daily doses and reduce the dose per dose (provided that it is still effective in improving motor symptoms), or to increase the total daily dose (if the original dose is not large), with the same dose per dose and an increase in the number of doses;
Switching from regular release to controlled release to prolong the duration of action of levodopa is preferable for early end-of-dose deterioration, especially at night, and requires a 20%-30% increase in dose (US guidelines consider that the “off” period cannot be shortened, level C evidence, while UK NICE guidelines recommend it for use in patients with advanced disease, but not as a first choice, level B evidence). B as the first choice);
Add DR agonists with long half-lives, with pramipexole and ropinirole as level B evidence, cartegolide and apomorphine as level C evidence, and bromocriptine as level C evidence as it does not shorten the “off” period, and try switching to another DR agonist if the efficacy of the DR agonist has diminished;
Add a COMT inhibitor that produces sustained DA stimulation in the striatum, with entocapone as Class A evidence and tolcapone as Class B evidence;
Addition of MAO-B inhibitors, with resagiline as Class A evidence and slegiline as Class C evidence;
Avoiding dietary (protein-containing) effects on levodopa absorption and blood-brain barrier, preferably 1 h before or 1.5 h after meals, and adjusting the protein diet may be effective;
Surgical treatment with DBS mainly in the thalamic nucleus (STN) may be beneficial and is a level C evidence. The management of the on-off phenomenon is more difficult, and oral DR agonists can be used, or a continuous infusion of levodopa methyl or ethyl ester or DR agonists (e.g., ergocalciferol) can be used in microchestnuts.
2.2.2 Treatment of postural balance disorder
Postural balance disorder is the most common cause of falls in patients with Parkinson’s disease, and is likely to occur when changing positions such as turning, rising and bending. There is a lack of effective treatment measures, and adjusting drug doses or adding drugs occasionally works. Active body weight adjustment, stepping, striding, listening to commands, walking to music or clapping, or crossing objects (real or imaginary) may be beneficial. Use a walker or even a wheelchair if necessary and be well protected.
2.2.3 Treatment of non-motor symptoms
Non-motor symptoms of Parkinson’s disease involve many types, mainly including sensory disorders, psychiatric disorders, autonomic dysfunction and sleep disorders, which need to be treated actively and accordingly.
Treatment of psychiatric disorders: The most common psychiatric disorders include depression and/or anxiety, hallucinations, cognitive impairment or dementia. The first step is to screen whether the patient’s mental disorder is induced by anti-Parkinson’s disease medications or caused by the disease itself.
If the former is the case, the following anti-Parkinsonian drugs should be reduced or discontinued sequentially according to the probability of triggering the patient’s mental disorder: anticholinergics, amantadine, MAO-B inhibitor DR agonists; if the patient’s symptoms still exist after taking the above measures, the compound levodopa can be gradually reduced without significantly aggravating the motor symptoms of Parkinson’s disease.
If the effect of medication adjustment is not satisfactory, it suggests that the patient’s mental disorder may be caused by the disease itself, and symptomatic medication should be considered. For treatment of hallucinations and delusions, clozapine or quetiapine is recommended, the former being slightly more effective than the latter, but clozapine has a 1% to 2% chance of causing granulocyte deficiency, so blood counts need to be monitored.
For the treatment of depression and/or anxiety, selective SSRIs can be used, as well as DR agonists, especially pramipexole, which can improve both motor symptoms and depressive symptoms. Lorazepam and diazepam are very effective in relieving irritable states.
For the treatment of cognitive impairment and dementia, cholinesterase inhibitors such as rivastigmine (rivastigmine), donepezil (donepezil), and meperidine (mementine) can be applied, with rivastigmine having the stronger evidence.
Treatment of autonomic dysfunction: The most common autonomic dysfunctions include constipation, urinary disorders, and positional hypotension. For constipation, intake of adequate fluids, fruits, vegetables, fiber and lactulose (10-20g/d) or other mild laxative drugs can improve constipation symptoms, such as lactulose, dragon aloe pills, rhubarb tablets and senna; gastric motility drugs, such as domperidone and mosapride, can also be added. Anticholinergics need to be stopped and exercise increased.
For the treatment of urinary frequency, urgency and urge incontinence in urinary disorders, peripheral anticholinergics such as oxybutynin, propantheline, tolterodine and hyoscyamine can be used.
In contrast, cholinergic preparations are given to those with no reflexes in the forced urinary muscles (but need to be used with caution, as it can aggravate the motor symptoms of Parkinson’s disease). If urinary retention occurs, intermittent clean catheterization should be taken, and if caused by prostatic hypertrophy, patients with severe positional hypotension should increase salt and water intake if necessary.
Elevated head position during sleep, do not lie flat; may wear elastic pants; do not rise quickly from the prone or sitting position; a- adrenergic agonist midodrine (midodrine) is preferred for treatment and is most effective; selective peripheral dopamine receptor antagonist domperidone may also be used.
Treatment of sleep disorders: The main sleep disorders include insomnia, abnormal rapid eye movement sleep behavior (RBD), and excessive daytime sleepiness (EDS). The most common problem with insomnia is difficulty maintaining sleep (also known as sleep fragmentation). Frequent awakenings may allow tremor to reappear during light sleep, or the patient may have difficulty turning over at night due to inability to move at night because the concentration of dopaminergic drugs taken during the day has been depleted during the night, or increased nocturnal urination.
If associated with nocturnal symptoms of Parkinson’s disease, the addition of a levodopa controller, DR agonist, or COMT inhibitor may be effective. If you are taking Slegiline or Amantadine, especially in the evening, you should first correct the time of day by taking Slegiline in the morning or at noon and Amantadine before 4:00 p.m. If there is no significant improvement, you should reduce or even discontinue the medication or use a short-acting sedative sleeper.
EDS may be related to the severity of Parkinson’s disease and cognitive decline, as well as to the use of anti-Parkinsonian DR agonists or levodopa. If patients experience drowsiness after each dose, this may indicate an overdose, and reducing the dose may help improve EDS; levodopa controlled-release agents may also be given instead of regular-release agents, which may help avoid or reduce post-dose drowsiness.
Treatment of sensory disorders: The most common sensory disorders include hyposmia, pain or numbness, and restless legs syndrome (RLS). Olfactory hyposmia is quite common in patients with Parkinson’s disease and occurs years before the onset of motor symptoms, but there are no clear measures to improve olfactory impairment.
Pain or numbness is common in Parkinson’s disease, especially in patients with advanced Parkinson’s disease, and can be caused by the disease or by concomitant bone and joint pathology. If the pain or numbness decreases or disappears during the “open phase” of anti-Parkinson’s disease medication and returns during the “closed phase,” then it may be caused by Parkinson’s disease and treatment can be adjusted to prolong the “open phase. Conversely, if the pain or numbness is caused by other diseases or other causes, the appropriate treatment can be chosen.
For patients with Parkinson’s disease with RLS, DR agonists such as pramipexole within 2 h before bedtime are very effective, or a combination of levodopa can also be effective.
3. surgical treatment
Surgery can be considered in patients with significant effects of early drug therapy, significantly reduced efficacy of long-term treatment, or severe motor fluctuations and dyskinesia, as described in the Chinese Expert Consensus on Deep Brain Electrical Stimulation for Parkinson’s Disease. It is important to emphasize that surgery can significantly improve motor symptoms, but cannot cure the disease.
Surgery requires strict control of its indications, and patients with Parkinson’s superposition syndrome in non-primary Parkinson’s disease are a contraindication to surgery. Surgery has a good effect on limb tremor and/or myotonicity, but has no significant effect on somatic mid-axis symptoms such as postural balance disorders.
Surgical approaches include nerve nucleus destruction and DBS, with DBS being the primary choice because of its relative noninvasiveness, safety, and modifiability. The targets include the medial pallidum (GPi), ventral intermediate nucleus of the thalamus (VIM), and thalamic nucleus (STN), with DBS in the STN being the most effective in improving tremor, tonicity, bradykinesia, and anisokinesia.
Preoperative levodopa sensitivity may be an indicator of prognosis for STNDBS treatment (level B evidence), age and duration of disease may be indicators of prognosis for STNDBS, and young patients with a short duration of disease may improve more than those with a longer duration and older age (level C evidence), however, there is insufficient evidence to make any recommendations regarding prognostic factors for GPi and VIMDBS (level U evidence).
4. Rehabilitation and exercise therapy
Rehabilitation and exercise therapy may be helpful in improving the symptoms of Parkinson’s disease and even in slowing the progression of the disease. Patients with Parkinson’s disease mostly have gait disorders, postural balance disorders, speech and/or swallowing disorders, etc. Rehabilitation or exercise training can be performed according to the different mobility disorders.
Exercises such as aerobics, tai chi, jogging, etc.; speech disorder training, gait training, postural balance training, etc. can be carried out. If adhered to daily, it will help to improve the patient’s self-care ability, improve motor function, and prolong the validity of medication.
5. Psychological guidance
Patients with Parkinson’s disease mostly have depression and other psychological disorders. Depression can occur before and after the appearance of motor symptoms in Parkinson’s disease, and is one of the main risk factors affecting patients’ quality of life, as well as affecting the effectiveness of anti-Parkinson’s disease drug therapy. Therefore, the treatment of Parkinson’s disease should not only focus on improving patients’ motor symptoms, but also pay attention to improving patients’ depression and other psychological disorders, and give equal importance to effective psychological guidance and antidepressant drug treatment, so as to achieve more satisfactory treatment results.
6. Care and attention
In addition to professional drug treatment, scientific care is also very important to maintain the quality of life of patients with Parkinson’s disease. Scientific care is often an adjunct to effective control of the disease and improvement of symptoms; it can also effectively prevent possible accidents such as accidental aspiration or falls.
In conclusion, there is no absolute fixed pattern for the treatment of Parkinson’s disease, as there may be differences in symptoms and sensitivity to treatment among different patients. The need for treatment varies from patient to patient, and the same patient’s need for treatment varies at different stages of the disease.
Therefore, this guideline may apply to the general rule, but in clinical practice, care should be taken to understand in detail the patient’s condition (severity of disease, type of symptoms, etc.), response to treatment (whether it is effective, duration of onset of action, duration of maintenance of action, prolongation of the “on” period and “off” period When applying the drug, we should pay attention to the patient’s condition (severity of disease, type of symptoms, etc.), treatment response (whether it is effective, onset of action, duration of maintenance of action, prolongation of “on” and “off” period, and whether there are side effects or complications), and combine with your own treatment experience to follow the guidelines and reflect the principle of individualization in order to achieve more ideal treatment results.