Wu Li’e, Department of Neurology, The First Affiliated Hospital of Baotou Medical College, 19th World Parkinson’s Day
China has 2-2.5 million people, accounting for 1/2 of the world’s population. young, adolescents account for 10% (environmental pollution, drug addiction, head trauma). This year’s theme is: “scientific treatment, rhythmical life” Parkinson’s disease is a common disease in neurology, and there are more Parkinson’s patients in China. Many patients come to neurology when they have hand tremors, but most of them are not Parkinson’s disease. Hand tremor in neurology is usually called tremor, common resting tremor (when the muscles are relaxed), postural tremor (during activity, especially fine movements), idiopathic tremor (senility – fine movements, destination hand tremor, often apparently genetic, Prenalol -心得安) Parkinson’s disease is mainly based on movement disorders, in addition should pay attention to non-motor symptoms of Parkinson’s (sensory, sleep, mental, autonomic symptoms – Lipofan, postural hypotension, intractable constipation, etc.).
I. The main manifestations of Parkinson’s disease
Parkinson’s disease starts slowly and the initial symptoms often go unnoticed. Moreover, patients usually do not know when they start to develop the disease, and family members find that patients walk more and more slowly and move more and more clumsily. The disease most often presents with the following manifestations.
1. Resting tremor: This is a clinical manifestation unique to Parkinson’s patients. It manifests as shaking of the limbs when at rest. The tremor usually starts in the distal part of the upper limb (hand), mainly in the thumb, index finger and middle finger, and manifests itself as if the fingers are rolling pills or counting bills. The tremor worsens during tension and disappears during sleep.
2. Increased muscle tone and bradykinesia: the muscles of the extremities are tense, with a lead pipe or gear-like appearance.
The patient’s upper and lower limb movements gradually become slow and stiff and inflexible, writing becomes smaller and smaller, buttoning is very slow, arms do not swing when walking, mask face (little facial expression), slow or slurred speech, and much drooling.
3. Abnormal posture and gait: the body is in a forward leaning and forward bending posture. Difficulty in starting to move, panic gait (that is, it is very difficult to start activities, difficult to start, often feel that the feet stick to the ground can not step, but after starting to walk, it will be small steps, and the faster you walk, the feeling that you can not brake, we call this gait panic gait). In addition, patients with this disease will turn with one foot as the axis, and the other foot will follow in small steps to turn the body. 4.
4. Other symptoms: (1) Phytodysfunctional manifestations: fatty face, salivation, persistent constipation, increased frequency of nocturnal urination, etc.; (2) Neuropsychological disorders: depression and anxiety, manifesting distraction, inability to sleep, poor appetite, general weakness, etc. (less dopamine, more acetylcholine).
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II. Etiology and pathogenesis
Etiology: There is no definite conclusion on the etiology, considering that it may be related to a combination of ageing, genetic factors (10%), environmental factors (20%, industrial and agricultural pollution, indoor decoration pollution, cell phone and computer radiation) exposure, and viral infection. Adolescents who develop Parkinson’s often have a family genetic background of Parkinson’s disease. Alcoholism, trauma, overexertion and certain psychiatric factors may be risk factors for the disease.
Mechanism: Parkinson’s disease is a degenerative disease of the central nervous system, mainly due to pathological changes in the cells located in the midbrain “substantia nigra”, which reduces the synthesis of dopamine, reduces the function of acetylcholine inhibition, and increases the excitatory effect of acetylcholine. The result of the imbalance between the two is “tremor palsy. —- dopamine in the brain is reduced and acetylcholine is increased.
Diagnosis
Diagnosis is sometimes difficult, and there is no effective blood marker or test as a diagnostic criterion for Parkinson’s (Movement Disorders, Mount Sinai Medical Center), and the diagnosis is based on clinical manifestations and signs, with no special auxiliary tests.
IV. Differentiation
Secondary Parkinson’s disease (infection, drugs – phenothiazines (chlorpromazine, endothiazide) and butylphenols (haloperidol), poisoning (Mn, CO, CS2), atherosclerosis, trauma, rifampin, gastroflucan, flunarizine, methyldopa, lithium). Parkinson’s superimposed syndrome (multisystem atrophy, progressive supranuclear palsy, Lewy body dementia, corticobasal ganglion degeneration), idiopathic tremor
V. Treatment.
Medication, surgery (pallidum, thalamic disruption, deep brain stimulation, cell transplantation), and drugs are the main treatments. It can be supplemented by rehabilitation, psychotherapy, etc.
The drug treatment of Parkinson’s disease is very individualized and there is no absolute plan. The kind of plan used needs to be combined with the patient’s age, specific symptoms, drug efficacy, economic conditions, etc. The treatment must be under the guidance of a physician, and in principle, it should be “long term, not full effect”.
Dopamine agonists and dopamine metabolism blockers are effective in the treatment of motor symptoms fluctuations; clozapine is effective in hallucinations; cholinesterase inhibitors may improve dementia symptoms; antidepressants and pramipexole may improve depressive symptoms; tolcapone crosses the blood-brain barrier and blocks the degradation of levodopa and dopamine; entacapone does not cross the blood-brain barrier.
1. Pharmacotherapy: There are four main types of drugs in common use: one is dopamine preparations, which are directly used to replenish the dopamine underproduced in the brain (levodopa preparations – methyldopa, xylazine); the second is drugs that inhibit dopamine degradation, so that the already insufficient dopamine consumption is reduced a bit (amantadine); the third is anti-acetylcholine drugs (Antan), and the fourth is dopamine receptor agonists (pramipexole – Senfuro, bromocriptine) that enhance the brain’s uptake and utilization of dopamine. There are also adjuvant dopamine potentiators (A is US – liver damage, diarrhea; Kotan)
Principle: Slow incremental doses in small doses, selection of drugs based on patient age, type of symptoms, severity, employment status, drug price, and financial ability. Long-term medication can produce diminished efficacy, symptom fluctuations, and movement disorders.
① Anticholinergic drugs – mainly for young tremor patients: Antan (not used for glaucoma, prostatic hypertrophy, psychiatric disorders, affects memory – used sparingly in the elderly).
② Amantadine: abnormal gait and dyskinesia, in addition to affecting NMDA glutamate receptors, also promotes DA release at nerve endings (not used for poor renal function, epilepsy, liver disease, severe gastric ulcer).
③ (Compound) levodopa: the most basic and effective drug for PD. Medopa, Xanax, good effect on an empty stomach (amino acids affect L-DA absorption, 0.5-1 hour before meals, 2 hours after meals) – side effects: nausea, vomiting, hypotension, arrhythmias. Can be taken with vitamin B6, if levodopa alone, not with vitamin B6.
④ Dopamine receptor agonists bromocriptine, pergolide (xylazine), Tysudar, pramipexole.
⑤ Monoamine oxidase inhibitors: reduce DA degradation.
⑥ Catechol-oxo-site – methyltransferase COMT inhibitors: Ada ism, Kodan (inhibits L-DA metabolism in the periphery, increases the amount into the brain and reduces DA degradation). Must be used in combination with L-DA, ineffective alone.
2. Surgical treatment: pallidum, thalamic disruption, deep brain stimulation. — Patients who have failed pharmacological treatment, are intolerant or develop motor deficits. It is effective in young, predominantly tremor tonic and partial to one side.
There are two main types of surgical treatment: “cell knife” surgery and “brain pacemaker” surgery, especially “brain pacemaker” surgery can not only improve all the symptoms of Parkinson’s, but also eliminate the side effects of long-term medication. In particular, the pacemaker surgery can not only improve all the symptoms of Parkinson’s and eliminate the side effects of long-term medication, but can also effectively slow down the progression of the disease. The best time for surgical treatment is in the middle of the disease, and it is not necessary to do it if the disease is very mild.
3. cell transplantation and gene therapy: autologous adrenal medulla and allogeneic nigrostriatal cells are transplanted into the striatum of the patient – the long-term efficacy is not certain.
4. rehabilitation therapy: adjuvant therapy.
5. neuropsychological treatment: most likely to combine depression and anxiety symptoms, thus making the original symptoms more prominent.