Parkinson’s disease itself is not a fatal disease and generally does not affect life expectancy. With the continuous innovation and improvement of treatment methods and levels, more and more patients are able to maintain a high level of motor function and quality of life for life. Of course, if patients do not receive timely and reasonable treatment, it can easily lead to a decline in physical function and even inability to take care of themselves, and eventually various complications, such as pneumonia and urinary tract infections.
Who is prone to Parkinson’s disease?
Parkinson’s disease is a degenerative disease of the nervous system commonly seen in middle-aged and elderly people. It is mainly characterized by slow movements, tremors in the hands, feet or other parts of the body, and loss of flexibility and stiffness in the body. It is called the “third killer” of middle-aged and elderly people because it is caused by the degeneration of neurons at the base of the brain, resulting in insufficient dopamine secretion from the nerve cells. But what causes neuronal degeneration? This is a question that is still not well understood and is being actively studied by scientists around the world.
It is believed that the following factors are involved.
① Age
Parkinson’s disease is a disease of brain capacity decline, mostly in the 50 years of age or older, some famous figures such as Pope John Paul II, boxer Ali, etc. are Parkinson’s disease patients.
②Family genetic predisposition
Medical doctors in long-term practice found that Parkinson’s disease seems to have a tendency to gather in families, families with Parkinson’s disease patients have a higher incidence of their relatives than the normal population.
③Environmental factors
Epidemiological findings have revealed regional differences in the prevalence of Parkinson’s disease, so it is suspected that there may be some toxic substances in the environment that damage neurons in the brain. The main environmental factors are now thought to be the damage caused by chemicals such as herbicides, pesticides, carbon monoxide, mercury and manganese poisoning, which may be the main cause of Parkinson’s disease.
④Drug factors
Taking high doses of sedatives and antipsychotics, which block dopamine receptors and dopamine binding so that dopamine cannot exert its inhibitory effects, and rifampicin, which depletes dopamine in the brain in large amounts, causing dopamine depletion.
In summary, no single factor can fully explain the etiology of Parkinson’s disease. Most researchers prefer that the etiology of Parkinson’s disease is the result of a combination of these factors. That is, after middle age, individuals who are susceptible to environmental toxins develop subclinical nigrostriatal damage after exposure to toxins due to their detoxification dysfunction, which worsens with age, and dopaminergic neurons progressively continue to die and degenerate, eventually losing compensation and developing clinical symptoms of Parkinson’s disease.
What symptoms suggest Parkinson’s disease (a)
Parkinson’s disease has a slow onset and the initial symptoms often go unnoticed. However, older adults who develop the following symptoms should seek prompt consultation with a neurologist to determine if they have Parkinson’s disease
Resting tremor: Tremor (trembling) is often the earliest manifestation of Parkinson’s disease and occurs in most patients during the course of the disease. It usually starts in the distal part of one upper limb, mainly in the thumb, index finger and middle finger, and is manifested as the fingers appearing to move as if they are rolling pills or counting bills. It then gradually extends to the ipsilateral lower extremity and the contralateral extremity, and in later stages may spread to the jaw, lips, tongue and head. In the early stages of the disease, many patients do not pay much attention to the tremor, which often appears when the fingers or limbs are in a particular position and disappears when the position is changed. Later, the tremor develops only when the limb is at rest, for example, when watching TV or talking with others, the limb suddenly appears to tremble involuntarily, and the tremor decreases or stops when changing position or movement, so it is called resting tremor, which is the most important feature of tremor in Parkinson’s disease. The tremor intensifies when the patient is emotionally or mentally stressed and can disappear completely during sleep. Another characteristic of tremor is its rhythmical nature, where the frequency of the vibrations is 4 – 7 times per second. This feature can also help to distinguish tremors caused by other diseases such as chorea, cerebellar disorders, and hyperthyroidism.
Muscle rigidity: In Parkinson’s disease, the limbs and trunk usually lose their flexibility and become rigid. The development of this muscle stiffness is very slow, and the early stages of the disease tend to begin in one limb. Initially, the inflexibility and stiffness of one limb is felt, and it gradually worsens, resulting in motor retardation and difficulty in performing even the movements of daily life. If you pick up the patient’s arm or leg and help him to move the joint, you will obviously feel the stiffness of the limb, and it is difficult to move the joint, like bending a lead pipe back and forth. If the affected limb has tremor at the same time, there is a feeling of intermittent pause, like the feeling of two biting gears turning, called “gear-like muscle ankylosis”. This phenomenon is not felt by the patient, but is easily detected by the doctor during an examination.
What symptoms indicate Parkinson’s disease?
Parkinson’s disease starts slowly and the first symptoms often go unnoticed. However, older adults who experience the following symptoms should visit a neurologist promptly to determine if they have Parkinson’s disease.
Slow movement: The third major clinical symptom of Parkinson’s disease is slow movement, which refers to the gradual slowing down of the movements that the patient wants to make and also means that each movement starts slowly. In the early stages, due to the straightening of the upper arm muscles and finger muscles, the patient’s upper limbs are often unable to perform fine movements, such as untying shoelaces and buttoning, which become much slower than before, or cannot be completed successfully at all. Writing also gradually becomes difficult, and the handwriting becomes curved and smaller, which is known as “microcapitalism” in medical science. The facial muscle movements are reduced, the patient rarely blinks, the eyes turn less, and the expression is dull, as if wearing a mask. Once the patient starts walking, the body leans forward, the center of gravity shifts forward, the pace becomes smaller and faster, and the patient cannot stop in time, i.e. “panic gait”. During walking, the coordinated swing of the affected upper limb is reduced or even disappears; it is difficult to turn around, and it takes several consecutive small steps to turn around. The patient is unable to swallow saliva naturally due to the impaired movement of the mouth, tongue, palate and pharynx muscles, resulting in profuse salivation. Speech decreases, speech becomes slower, and pronunciation becomes increasingly unclear, with a low, monotonous voice. In severe cases, it may lead to choking and coughing when eating and drinking. Jiangyang Xu, Department of Neurology, Huaian Third People’s Hospital
Special posture: Although all muscles of the patient’s body can be involved and muscle tone is increased, flexor muscle tone is higher than extensor muscle at rest, so the patient has special posture: head tilted forward, trunk slightly flexed, upper arm inward, elbow joint bent, wrist slightly extended, finger metacarpal joint bent and interphalangeal joint straightened, thumb to palm, hip and knee joint mildly bent.
Other symptoms: There may be plant nervous disorders, such as increased secretion of saliva and sebaceous glands, increased or decreased sweat secretion, difficulty in excreting stool and urine, and upright hypotension. A small number of patients may have a combination of dementia or depression and other psychiatric symptoms.
Older people with Parkinson’s disease should not be afraid, because Parkinson’s disease itself is not a fatal disease and does not generally affect life expectancy. As treatment methods and levels continue to improve, more and more patients are able to maintain their quality of life for life. Of course, if patients do not receive timely and reasonable treatment, they are also prone to decline in physical functions and even become unable to take care of themselves, and eventually develop various complications, such as pneumonia and urinary tract infections.
The progression of the disease is different for each person and varies greatly among individuals. A few patients progress rapidly to disability within a few years, while most patients have a relatively slow progression of the disease and can maintain good function 15 to 20 years after the disease with reasonable treatment. In addition to Parkinson’s disease itself, this depends to a large extent on the patient’s own psychological quality, medical conditions and family care. Those patients who maintain an optimistic mood, strong will, harmonious family relationships and good home care, together with reasonable and timely medical treatment, most patients are able to maintain long-lasting self-care abilities and their disease progresses relatively slowly.
How is Parkinson’s disease diagnosed?
Diagnosis is not difficult for a patient with typical symptoms of Parkinson’s disease. If a person has any two of the symptoms of resting tremor, rigidity and bradykinesia, and other clinical symptoms of Parkinson’s syndrome are ruled out, and the symptoms improve significantly after taking levodopa preparations, the diagnosis of Parkinson’s disease can be made clinically. However, a true diagnosis of Parkinson’s disease requires a pathologic diagnosis of brain tissue, and the specific pathology of Parkinson’s disease, Lewy bodies, can be found in sections of brain tissue, which unfortunately cannot be done in patients before surgery.
Currently, the diagnosis of Parkinson’s disease is based on clinical signs and symptoms. In general, the approximate time from onset of Parkinson’s disease to a definitive clinical diagnosis is 2-5 years. There is no instrument or laboratory test that can diagnose Parkinson’s disease, and some tests that doctors have patients undergo in the clinic, such as CT scans or MRIs of the brain, are designed to rule out other diseases that can cause Parkinson’s disease syndrome.
One instrument that may be useful for early diagnosis is positron emission scanning, or PET, and current research has found that applying a [18F]-fluorodopa reagent injected into the body and followed by a PET scan can confirm the diagnosis of a patient with early Parkinson’s disease. Because [18F]-fluorodopa is a similar compound of levodopa, it can cross the blood-brain barrier and be taken up by nigrostriatal neurons, and its uptake can reflect the activity of presynaptic dopa decarboxylase, thus indirectly reflecting the number of nigrostriatal dopamine neurons and the severity of the disease. The site of Parkinson’s disease is located in a part of the human brain called the midbrain. There is a group of nerve cells called nigrostriatal neurons, which synthesize a neurotransmitter called dopamine, and their nerve fibers project to other areas of the brain, such as the striatum, to regulate motor function in the brain. When more than 80% of these nigrostriatal neurons degenerate and die, the neurotransmitter dopamine in the brain decreases to the point where it cannot maintain the normal function of the regulatory nervous system, and the symptoms of Parkinson’s disease appear.
Some studies have shown that the accumulation of [18F]-fluorodopa in the striatum of Parkinson’s disease patients is significantly lower than normal, and the contralateral nucleus accumbens of patients with lateral Parkinson’s disease is only 57%-80% of normal. However, the test is very expensive and is largely not used clinically to diagnose Parkinson’s disease.
Drug treatment for Parkinson’s disease
Drug therapy is still the main method of treatment for Parkinson’s disease.
The principles of drug therapy for Parkinson’s disease.
1, fine water, not to seek full effect”. That is to say, strive to use the smallest dose of drugs so that the symptoms are basically controlled, so that patients can maintain 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 the same effect as normal people.
2, slowly increase the dose 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 to increase, to achieve the “ideal efficacy” when the dose to maintain.
3, dose individualization, that is, according to the titration to determine the dose of each person, rather than uniformly all patients with the same dose. The fourth is: small and precise variety, 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 dosage and finally stop the drug. The “ideal outcome” can be basically normal or close to normal, but does not require complete normalcy.
Generally speaking, there are three levels of treatment goals.
1. For young early-stage patients, the goal is to maintain or restore the ability to work
2. The minimum treatment goal for patients in the middle and late stages is to restore the ability to care for themselves
3. The minimum treatment goal for patients with advanced disease is to reduce pain and prolong life
Drug therapy for Parkinson’s disease has evolved to the third generation. The first generation is anticholinergic drugs, the second generation is levodopa, and the third generation is the receptor agonist of DA.
Some of the more commonly used drugs for Parkinson’s disease are divided into eight categories in order.
(1) Anticholinergic drugs: such as Antan.
(2) Dopamine replacement agents: such as levodopa.
(3) levodopa and extracerebral dopamine carboxylase inhibitors: e.g. dobutamine, carbidopa
(4) Dopaminergic receptor agonists: e.g. bromoxynil, xylazine
(5) L-dopa potentiators: e.g., amantadine
(6) Monoamine oxidase inhibitors: such as sulforaphane.
(7) COMT inhibitors: such as tolcapone.
(8) Others.
Although all of the above are currently used to treat Parkinson’s disease, the treatment mechanism is different, so under what circumstances which drug should be used, which one should be used first, which one should be used later, the dosage of the drug should be how much, etc., should follow the guidance of the doctor, do not take the drug without permission, so as not to bring trouble to the future treatment.