Parkinson's disease

Parkinson's disease, also known as Parkinson's syndrome, is an elderly disease characterized by tremors. There are many causative factors for Parkinson's syndrome. In addition to age, genetics, environmental toxins, etc. can also cause the disease. Because the current treatment options are quite limited, we need to know the causes and symptoms, respond proactively, and seek timely treatment when we discover the disease.

The cause of PD is still unclear, but previous studies have shown that it may be related to many factors. Some people have proposed several hypotheses, all of which have some evidence, but also have many differences. Some scholars pointed out that it may be "multiple causes for one result", such as the interaction between individual susceptibility and environmental factors, and the influence of environmental toxins on the basis of aging. In recent years, with the rapid development of science and technology, the research level of basic theories has been continuously improved, which is of great benefit to further clarify the pathogenesis of PD. The most popular ones are: aging, genetic factors, environmental toxins, infection, oxidative stress and free radical formation, etc. ① One of the most common causes of aging. The prevalence of PD changes with age. Glutathione peroxidase and catalase decrease in the aging process and PD; monoamine oxidase increases with age, iron, copper, calcium accumulate, and melanin accumulates. The incidence rate increases with age, with the peak age being 61 to 70 years old, and then decreases. Degenerative changes occur in the dopamine neurons in the substantia nigra and striatum, and pigment granules and nerve cells are lost. The PD group is significantly more serious than the normal group of the same age. The motor symptoms of PD will appear clinically. Symptoms of this disease usually occur between the ages of 51 and 60. Based on this age, if aging is the only cause, dopamine levels have not yet reached a low enough level. Therefore, aging is only a triggering factor for PD. ②Genetic factors Through detailed investigation of the families of PD patients, it has been widely recognized that at least part of the disease is caused by genetic factors in terms of etiology. ③ Environmental toxins People have long noticed that manganese poisoning, carbon monoxide poisoning, phenothiazines, and butyrophenone drugs can produce PD symptoms. ④ PD often occurs after infection with type A encephalitis. Some authors believe that PD is related to viral infection. It has not been clearly confirmed. ⑤ Oxidative stress and free radical formation The metabolism of living substances cannot be separated from oxygen, and the cell metabolism requires the gradual reduction of molecular oxygen to produce energy. The whole process occurs in the mitochondria. In addition, many other enzymes, such as tyrosine hydroxylase, monoamine oxidase, NADPH-cytochrome P450 degrading enzyme and xanthine oxidase, are also mediators for the production or utilization of reactive oxygen. Reduced oxygen plays a positive role in many normal biological processes, but excessive formation can also damage nerve cells. In conclusion, PD is not caused by a single factor, but may be caused by multiple factors. Genetic factors can increase susceptibility to disease, but only under the combined effects of environmental factors and aging, through oxidative stress. Mitochondrial dysfunction and other factors lead to massive degeneration of substantia nigra dopaminergic neurons and cause the disease.

Clinical manifestations: The onset age of this disease is between 40 and 70 years old, with the peak onset before 50 to 60 years old. It is more common in males than in females. Cases in young families have also been reported. Trauma, depression, overwork, and cold can induce this disease. The onset is insidious and progresses slowly, with less movement, dullness or posture changes often being the first symptoms. The main symptoms that gradually worsen include resting tremor, increased muscle tension, bradykinesia or slow movements, and autonomic nervous system disorders. 1. Symptoms (1) Early symptoms The earliest symptoms of a patient are often difficult to detect and are easily ignored. Some people call it a subclinical state. The patient lacks flexibility in movement, moves less, and gradually has difficulty bending the spine and limbs. As the disease progresses, the stride becomes smaller, the voice becomes smaller when leaning forward, and there is pain and fatigue in the neck, back, shoulders and buttocks. The palpebral fissures become slightly widened, and the patient becomes staring. (2) Typical symptoms: ① Tremor is often the first symptom, accounting for 80% of PD. The characteristic tremor is resting tremor which is not obvious during active movement. It usually starts from the distal fingers of one upper limb and then gradually spreads to the ipsilateral lower limb and the contralateral upper and lower limb. The mandible, lips, tongue and head are usually the last to be affected. The tremor is relatively coarse, with a frequency of 4-8 times/s4-8Hz, which can be temporarily controlled by consciousness but is not persistent. It worsens with excitement and fatigue and disappears during sleep. ② Myotonia The muscle rigidity of PD patients is due to increased extrapyramidal muscle tension. The muscle tension of both agonist and antagonist muscles is increased. When the joints are passively moved, the resistance is always increased, similar to the feeling of bending a soft lead pipe, so it is called "lead pipe rigidity". If some patients have tremors, they may feel intermittent pauses in the uniform resistance when flexing and extending the limbs, like gears turning, which is called "gear rigidity". Due to increased muscle tension and imbalance, abnormal posture is often manifested: the head is tilted forward, the torso is bent forward, the upper limbs and forearms are adducted, the elbows are flexed, the wrists are straight, and the metacarpophalangeal joints are flexed. Myotonia can cause joint pain in elderly patients because increased muscle tension obstructs blood supply to the joints. ③ Bradykinesia is a characteristic symptom of basal ganglia dysfunction in PD, which manifests as akinesia in severe cases. Various movements are slow, such as tying shoelaces, dressing, shaving and brushing teeth, etc., which are slow or difficult. Facial expressions with few or even no blinking movements are called "mask face". Difficulty in starting, reduced ability to overcome inertia, difficulty in stopping movement, difficulty in changing movement posture. Once you take small steps, your feet scrape the ground, which is called "short gait". Walking faster and faster, lacking the accompanying swing of the arms, the torso rushes forward, and cannot stop immediately is called "panicked gait". When encountering an obstacle, the person hesitates or stops, and turns with small steps together with the head and torso. Language disorders can manifest as low pronunciation, unclear articulation, stuttering or repetitive speech, which is called "panic speech". Trembling and distortion of handwriting, uneven line spacing, and smaller and smaller writing are called "micrographia". These characteristic motor disorders may also manifest as difficulty in swallowing. Slow chewing may indicate nervousness or excitement. A sudden cessation of all movements, as if frozen, is called the freezing phenomenon, which is short-lived. On the contrary, abnormal movement, that is, the temporary relief of hypoactivity and the performance of normal activities, and in rare circumstances such as emergency situations, there are also significant and effective movements, which are called paradoxical movements. On-off phenomenon is the sudden inability to move and sudden freedom of movement. Special signs may include repeated tapping on the upper edge of the eyebrow arch to induce more than one blink, and the two eyeballs' upward gaze and convergence movement are limited, that is, oculomotor crisis, which is more common in post-encephalitis and drug-induced Parkinson's syndrome.

④Autonomic dysfunction is often caused by excessive saliva secretion, which leads to excessive secretion of sebaceous glands and increased sweating, making the skin, especially the facial skin, greasy. Low blood pressure can easily lead to postural hypotension, but syncope rarely occurs. It is more common in elderly patients. Biochemical examinations have found that reduced tyrosine content is related to low plasma renin and aldosterone levels. However, the serum sodium level was normal, suggesting a peripheral sympathetic nerve defect. Patients may suffer from intractable constipation, incomplete urination, dribbling urine, urinary incontinence, etc. The pathological basis is damage to the dorsal nucleus of the vagus nerve and sympathetic nerve dysfunction. ⑤The most common mental disorder is depression, which is usually mild to moderate and suicide is rare. About 40% of PD patients experience depression during the course of their illness, characterized by anorexia, sleep disorders, and lack of sexual desire. The second is dementia, the incidence of which is 12% to 20% in PD, and the risk of first-degree relatives suffering from dementia is extremely high. Other symptoms include emotional indifference, slow thinking, personality changes, loneliness, autism, etc. 2. Signs (1) The early characteristic is a decrease in blinking rate. Normally, the blinking frequency of healthy people is 15 to 20 times per minute, while that of PD patients can be reduced to 5 to 10 times per minute. (2) Typical signs ① “Striate hand” presents with metacarpophalangeal joint flexion, proximal interphalangeal joint extension and distal interphalangeal joint flexion; foot deformity may also occur at the same time. ②Myerson disease cannot inhibit the blink reaction by tapping the bridge of the nose or between the eyebrows. ③ Oculomotor crisis: Tonic spasm between the two eyeballs in the direction of gaze, usually common in those with both eyes looking upward, rarely in those looking sideways or downward, recurrent attacks, often accompanied by neck, mouth and muscle spasms. ④ Involuntary inhibition of the levator palpebrae muscle and the orbicularis oculi muscle due to disuse of eyelid opening and closing. (3) Atypical signs: The knee reflex varies greatly. It can be normal, difficult to elicit, or active. It is limited to PD patients with single testing. The bilateral knee reflexes are symmetrical and flexion-type. The inferior frontal and frontal reflexes are rarely increased.

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