What Are the Symptoms of Rickets?

Parkinson's disease, also known as idiopathic Parkinson's disease (PD), referred to as Parkinson's disease, also known as paralysis agitans (shaking palsy), is a common neurological degenerative disease in the elderly and middle-aged and elderly people. The most common extrapyramidal disease in humans. The prevalence of people over the age of 65 is 1000 / 100,000, with increasing age, slightly more men than women. The main clinical characteristics of the disease are: resting tremor, slow and reduced movement, increased muscle tone, and unstable posture.

Symptoms of Parkinson's disease

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nickname: Idiopathic parkinson disease
TCM disease name: Tremor paralysis
English name: idiopathic Parkinson's disease
English alias: PD
Multiple groups: Middle-aged and elderly

Common locations: Limbs
Common causes: Neurological degenerative diseases
Common symptoms: Tremor paralysis
Contagious: no
way for spreading: no

1. General information ^[1]

1. What foods are good for elderly Parkinson's disease:

The food is diverse and soft. The food throughout the day should be varied, including cereals, vegetables, fruits, milk or beans, and meat. A variety of foods can satisfy the body's various nutritional needs and make the diet fun. At the same time, the food should be soft, easy to digest, easy to chew and swallow, and can be supplied as semi-liquid or soft food.

Eat more cereals and vegetables. Usually eat 300 to 500 grams of cereals every day. Carbohydrates usually do not affect the efficacy of the drug. Eat about 300 grams of vegetables and 1 to 2 medium-sized fruits every day to get vitamins A, B, C, and a variety of minerals and dietary fiber.

Eat milk and beans often. Milk is rich in calcium. Calcium is an important element of bone formation, so for elderly Parkinson's patients prone to fractures and osteoporosis, a glass of milk or yogurt per day is an excellent way to supplement calcium. However, the protein content of milk may have a certain effect on the efficacy of levodopa drugs. In order to avoid affecting the effect of medication during the day, it is recommended to arrange milk to drink at night before going to bed. In addition, soy products such as tofu and dried tofu can also be supplemented with calcium.

Drink 6 to 8 glasses of water and drinks every day. Water is the best drink. Sufficient water can soften and excrete feces, prevent constipation, and relieve the symptoms of dry mouth, thirst and dry eyes caused by use.

Pay attention to the interval between meals and medications. Meals are usually taken half an hour after taking levodopa for better absorption of the drug. However, if the symptoms of nausea are obvious after taking the medicine, you can eat some low-protein foods such as biscuits, fruits, ginger juice or fruit juice while taking the medicine. A small number of patients will have symptoms of involuntary movement after taking the drug, and can be taken at meals to reduce the symptoms by delaying drug absorption.

2. What foods should not be eaten in elderly Parkinson's disease:

Limit meat. Because some amino acid components in food protein can affect the function of levodopa drugs into the brain, it is necessary to limit protein intake. Eat about 50 grams of meat a day and choose lean poultry, livestock or fish. One egg contains 25 grams of lean meat. Meat can be distributed in the morning, evening, or lunch and dinner. In order to improve the efficacy of the day, you can also try to arrange protein-rich foods only for dinner during the day.

Try not to eat fatty meat, emu oil and animal offal. Excessive fat in the diet can also delay the absorption of levodopa drugs and affect the efficacy.

Idiopathic Parkinson's disease is a common neurological degenerative disease in the elderly, and there is no effective prevention method. Early diagnosis and treatment and strengthening the care of patients can effectively improve the quality of life of patients.

1. Differentiated from secondary tremor paralysis syndrome

(1) Cerebrovascular tremor palsy syndrome: It often occurs after lacunar infarction or acute stroke, and has hypertension, arteriosclerosis, pyramidal tract signs, and pseudobulbar paralysis. CT scans of the brain are helpful for diagnosis.

(2) Post-encephalitis tremor paralysis syndrome: there is a history of encephalitis before the disease, seen at any age, common eye movement crisis (onset involuntary eye muscle spasm with binocular upwards), sebum overflow, increased salivation.

(3) Drug-induced tremor palsy syndrome: caused by a history of taking antipsychotic drugs such as phenothiazines or antihypertensive drugs such as rudolwood, which interfered with the metabolism of catecholamines at different stages, and the symptoms disappeared after drug withdrawal.

(4) Toxic tremor paralysis syndrome: It is mainly diagnosed based on poisoning diseases, such as a history of carbon monoxide poisoning before the disease.

2. Differentiate from tremors caused by various reasons

(1) Idiopathic tremor: Although tremor is similar to this disease, it has no symptoms of muscle rigidity and bradykinesia. It may have a family genetic history, benign course, and a few may develop into tremor paralysis.

(2) Senile tremor: seen in the elderly, the tremor is thin and fast, and appears during voluntary movement without muscle rigidity.

(3) Hysterical tremor: there are mental factors before the illness, the form, amplitude and speed of tremor are variable, the concentration becomes worse when concentrated, and there are other manifestations of rickets.

(4) Post-encephalitis tremor paralysis syndrome has a history of encephalitis, common eye movement crisis, sebum overflow and increased salivation.

(5) Vascular tremor syndrome seen in the lacunar state is caused by lacunar stroke in the striatum. The gait disorder is prominent, and dementia and pyramidal tract signs may be present, while tremor and bradykinesia are rare and can be confirmed by MRI or CT scan.

(6) Those who are caused by brain injury, tumors and poisoning can make a diagnosis based on relevant medical history and findings.

(7) Those with basal ganglia calcification must find out the cause of calcification. Basal ganglia calcification may not all appear tremor paralysis.

(8) The tremor of alcoholism, anxiety, and hyperthyroidism is not difficult to identify based on medical history.

3. Differentiate from some central nervous system degeneration diseases with tremor paralysis symptoms such as hepatolenticular degeneration, primary orthostatic hypotension, cerebellar pontine olive atrophy, etc. In addition to the symptoms of tremor and paralysis, these diseases also have other neurological symptoms corresponding to various diseases, such as cerebellar symptoms, pyramidal tract signs, ophthalmoplegia, involuntary movements, orthostatic hypotension, motor neuron disease, and dementia.

Laboratory inspection:

1. Serum renin activity decreased and tyrosine content decreased; NE and 5-HT content in substantia nigra and striatum decreased, and glutamate decarboxylase (GAD) activity was reduced by 50% compared with the control group.

2. GABA in CSF decreased, and HVA content of DA and 5-HT metabolites in CSF decreased significantly.

3. The biochemical detection of CSF somatostatin decreased by radioimmunoassay. Urine DA and its metabolites 3-methoxytyramine, 5-HT and epinephrine, NE are also reduced.

Other auxiliary checks:

1. CT and MRI imaging manifestations Because Parkinson's disease is a degenerative disease of the central nervous system, pathological changes are mainly in the substantia nigra, striatum, pallidum, caudate nucleus, and cerebral cortex. Therefore, CT imaging manifestations In addition to universal brain atrophy, calcification of the basal ganglia is sometimes seen. In addition to MRI showing cerebral atrophy such as ventricular enlargement, T2-weighted images often have multiple high-signal spots in the basal ganglia and white matter.

2.SPECT image performance

(1) Functional images through dopamine receptors (DAR): Dopamine receptors are widely distributed on the dopaminergic pathway in the central nervous system, mainly the substantia nigra and striatum systems, and DAR (DL) is distributed in non-striatum Cholinergic interneuron cell bodies; DAR (D2) is located in the substantia nigra, striatum dopaminergic neuron cell bodies.

SPECT is a radionuclide, currently mainly 123I-IBZM, 131I-IBZM, specific D2 receptor markers. After intravenous injection into the human body, radioactivity in the basal ganglia area and radioactivity in the frontal, occipital or cerebellum The ratio reflects the number and function of DAR receptors to diagnose early Parkinson's disease. If patients are treated early with dopa, the onset contralateral brain DAR (D2) is upregulated. In patients with intermediate-to-advanced Parkinson's disease who have been taking dopa for a long time, the basal ganglia / occipital lobe and basal ganglia / frontal lobe ratios in the brain are reduced. SPECT functional imaging can only detect the number of DAR receptors and cannot help determine whether it is primary Parkinson Disease, but can distinguish some secondary Parkinson's disease, can also be used as an indicator of the evolution of Parkinson's disease disease and drug treatment.

(2) Functional imaging by dopamine transporter (DAT): How dopamine transporter (DAT) transports dopamine (DA) is unclear. DAT is mainly distributed in the basal ganglia and thalamus, followed by the frontal lobe. There is a positive correlation between the content of DAT and the severity of Parkinson's disease. DAT in the basal ganglia is reduced, which is significant in patients with early Parkinson's disease.

SPECT uses 11C-WIN35428 and 123I-CIT. After intravenous injection into the human body, the basal ganglia / cerebellum activity ratio and thalamus / cerebellum activity ratio are measured to reflect the number of DAT in different regions of the center. In patients with early Parkinson's disease, the number of DAT in the basal ganglia area was significantly reduced.

3. PET functional imaging positron emission tomography (PET) diagnosis of Parkinson's disease, its working principle and method are basically similar to SPECT. At present, it is mainly dependent on cerebral glucose metabolism imaging. 18F deoxyglucose (18FDG) is generally used. Because in the early stage of Parkinson's disease, the local glucose metabolism rate of the striatum is moderately reduced, and the glucose metabolism rate is further reduced in the later stage. There are many receptor imaging agents for PET. PET neurotransmitter imaging agents mainly use nuclide such as 18F-dopa-PET (18FD-PET). The basic principle is the same as SPECT. PET can be used for early diagnosis of Parkinson's disease, and it can be used for early diagnosis in high-risk groups of Parkinson's disease. It is an objective indicator to judge the severity of the disease. Hair Parkinson's disease has a great effect.

May be accompanied by symptoms of autonomic nervous dysfunction, such as easy sweating, sebaceous glands secrete more and greasy, saliva more and thick, fear of heat and cold, urine dripping, dry stool, a few cases may have lower extremity edema. Most patients also have symptoms of advanced neurological dysfunction, such as dementia, depression, hyposexuality, sleep disorders, poor appetite, and fatigue and pain throughout the body.

PD is a chronic progressive disease. At present, there is no cure. Most patients can continue to work for several years after the onset of disease, and they can also develop disability quickly. The late stage of the disease can be bedridden due to severe muscle rigidity and general stiffness. Causes of death are often complications such as pneumonia and fractures.

1. Very complex and may be related to the following factors.

(1) Ageing: PD mainly occurs in middle-aged and elderly people, and the incidence is rare before the age of 40, suggesting that ageing is related to the incidence. Studies have found that after 30 years of age, DA neurons, tyrosine hydroxylase (TH), and dopa decarboxylase (DDC) activity, striatum DA transmitters have decreased year by year, and DAD1 and D2 receptor density have decreased. But elderly people suffer from PD after all, indicating that physiological DA neuron degeneration is not enough to cause the disease. In fact, only when the nigral DA neurons are reduced by more than 50% and the striatum DA transmitters are reduced by more than 80% can PD symptoms appear clinically, and aging is only a contributing factor to PD.

(2) Environmental factors: Epidemiological investigation shows that long-term exposure to pesticides, herbicides or certain industrial chemicals may be a risk factor for PD. In the early 1980s, some drug addicts in California in the United States appeared to be primary due to the misuse of a neurotoxic substance, a pyridine derivative, 1-methyl 4-phenyl1,2,3,6-tetrahydropyridine (MPTP). Some pathological changes, biochemical changes, symptoms, and drug response to PD in PD have similar effects in monkeys injected with MPTP. Neurophilic MPTP and certain insecticides and herbicides may inhibit the activity of NADH-CoQ reductase (complex I) in the nicotinic mitochondrial respiratory chain, reduce ATP production, increase free radical generation, and cause DA neurons to degenerate and die. There is obvious lipid peroxidation in the substantia nigra region of PD, and the reduced glutathione is significantly reduced, suggesting that antioxidant mechanism disorders and oxidative stress may be related to PD.

(3) Genetic factors: About 10% of patients have family history, showing incompletely autosomal dominant or recessive inheritance, and the rest are sporadic PD. Twin consistency studies have shown that genetic factors may play an important role in certain younger (<40 years) patients. So far, 10 single genes such as PARK 1 10 have been identified as being related to PD. Among them, three gene products have been confirmed to be related to familial PD: -synuclein is a mutation of PARK1 gene, and the gene is located on the long arm of chromosome 4q21 23, -synuclein may increase the sensitivity of DA energy nerve cells to neurotoxins; Parkin is a mutation in the PARK2 gene and is located on the long arm of chromosome 6 625.2-27; C-terminal hydroxylase of ubiquitin- L1 is a mutation of the PARK5 gene and is located on the short arm 4p14 of chromosome 4. Cytochrome P45O2D6 gene and some mitochondrial DNA mutations may be one of the susceptibility factors for PD, which may reduce the P450 enzyme activity, impair liver detoxification function, and easily cause toxins such as MPTP to damage the nigrostriatal body.

(4) Oxidative stress and free radical generation: Free radicals can cause unsaturated fatty acids to undergo lipid peroxidation (LPO), which can oxidatively damage proteins and DNA, causing cell degeneration and death. PD patients with increased B-type monoamine oxidase (MAO-B) activity can produce excess OH groups and damage cell membranes. At the same time of oxidation, DA oxidation products in the substantia nigra cells polymerize to form neuromelanin, which combines with iron to produce Fenton reaction to form OH. Under normal circumstances, there are enough antioxidants in the cell, such as glutathione (GSH), glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) in the brain. DA Free radicals generated by oxidation will not produce oxidative stress, which is guaranteed to avoid free radical damage. In patients with PD, the reduced GSH and LPO in the substantia nigra area are reduced, the iron ion (Fe2) concentration is increased, and the ferritin content is reduced, making the substantia nigra area susceptible to oxidative stress.

(5) Mitochondrial dysfunction: In recent years, it has been found that mitochondrial dysfunction plays an important role in the pathogenesis of PD. Understanding of mitochondrial dysfunction in PD patients stems from the study of the mechanism of action of MPTP. MPTP causes Parkinson's disease by inhibiting the activity of nigromitochondrial respiratory chain complex . In vitro experiments confirmed that MPTP active ingredient MPP can cause the mitochondrial membrane potential (m) of MES 23.5 cells to decrease and increase the generation of oxygen free radicals. In patients with PD, the activity of nicotinic mitochondrial complex can be reduced by 32% to 38%, and the decrease in the activity of complex can significantly increase the sensitivity of nigroblasts to free radical damage. No change in complex I activity was found in the substantia nigra of patients with multiple system atrophy and progressive supranuclear palsy, indicating that the decrease in PD substantia nigra complex I activity may be a relatively specific change in PD. The existence of mitochondrial function defects in PD patients may be related to genetic and environmental factors. Studies suggest that mitochondrial DNA mutations exist in PD patients. Complex is encoded by the genome of the nucleus and mitochondria, and any fragment of the two groups of genes can affect the function of complex . .

(6) Excitatory toxicity: The authors found that the content of excitatory amino acids (glutamic acid, aspartic acid) in striatum of PD monkey model prepared by MPTP was significantly increased by microdialysis and HPLC detection. If the glutamate concentration in the extracellular space is abnormally high, it will over-stimulate the receptor and have a significant toxic effect on the CNS. Animal experiments have found that microinjection of glutamic acid into the brain can cause necrosis of large neurons. The neurotoxicity of glutamate is through receptors. NMDA receptors mediate excitatory neurotoxicity and are related to degeneration of DA neurons. Glutamate can damage nerve cells by activating NMDA receptors to produce nitric oxide (NO), and release more excitatory amino acids, further aggravating neuronal damage.

(7) ^[2] Human aging may be accompanied by an increase in free Ca2 concentration in nerve cells, a decrease in Ca2 / Mg2-ATPase activity, and a decrease in mitochondrial calcium storage capacity. Changes in intracellular Ca2 concentration affect many important neuronal functions, such as cytoskeleton maintenance, neurotransmitter function, protein synthesis, and Ca2-mediated enzyme activity. Calcium-binding proteins, especially 28KD vitamin D-dependent calcium-binding protein (Calbindin-D28K) May play an important role, related to calcium / magnesium-ATPase activation, and has neuroprotective effects. Icopini and Christakos et al. Reported that Calbindin-D28K content and mRNA expression in substantia nigra, hippocampus and dorsal raphe nucleus of PD patients were significantly lower than those in normal subjects, suggesting that decreased calbinin gene expression can also lead to cytotoxicity.

(8) Immunological abnormalities: Abramsky (1978) proposed that the incidence of PD is associated with immune abnormalities. Clinical studies have shown that the cellular immune function of PD patients is reduced, and the activity of interleukin-1 (IL-1) is significantly reduced. McRae-Degueurce et al. Reported the presence of anti-DA neuron antibodies in the cerebrospinal fluid (CSF) of PD patients. Cell culture showed that PD plasma and CSF inhibited DA neuron function and growth in rat midbrain. Injecting the blood IgG from PD patients stereotactically into the substantia nigra of rats, the substantia nigra tyrosine hydroxylase (TH) and DA energy neurons were significantly reduced, suggesting that it may initiate or participate in immune-mediated substantia nigra damage. Tumor necrosis factor- (TNF-), IL-6, epithelial growth factor (EGF), metastatic growth factor- (TGF-) and 2-microglobulin (2-MG) may be related to the pathogenesis of PD.

(9) Apoptosis: Studies have shown that there are apoptosis, lack of free radicals, neurotoxins and neurotrophic factors in the pathogenesis of PD. Agid (1995) examined the morphological and biochemical characteristics of apoptosis in nigrosinergic DA neurons in PD patients. It was found that about 5 energy neurons in PD patients had apoptosis-specific lesions and the presence of TNF- receptor (-TN- FR) and bcl-2 proto-oncogene expression, and apoptosis may be the basic steps of DA neuron degeneration.

At present, it is generally believed that PD is not caused by a single factor, and multiple factors may be involved. Genetic factors increase the susceptibility to disease. Under the combined effects of environmental factors and aging, the nigra DA neurons degenerate through mechanisms such as oxidative stress, mitochondrial failure, calcium overload, excitatory amino acid toxicity, and apoptosis. Causes illness.

2. Pathological changes The main pathological changes of PD are degeneration and loss of pigmented neurons, and DA neurons in dense substantia nigra are most significant. Microscopically, neurons were reduced, melanin in melanocytes disappeared, and melanin particles were dispersed in tissues and macrophages, with different degrees of glial proliferation. Normal human substantia nigra cells decrease with age. At 80 years of age, substantia nigra cells have decreased from 425,000 to 200,000. PD patients have fewer than 100,000. DA symptoms neurons are lost by more than 50% when symptoms occur. Blue spots The nucleus raphe, dorsal vagus nucleus, pale globus, putamen, caudate nucleus, and subthalamic nucleus were also slightly changed.

The presence of eosinophilic inclusion bodies Lewy bodies in the cytoplasm of residual neurons is an important pathological feature of the disease. Lewy bodies are glass-like masses composed of cytoplasmic proteins with a dense core in the center and a filamentous halo around it. . A cell sometimes sees multiple Lewy bodies of different sizes. It is found in about 10% of the remaining cells. The substantia nigra is obvious. Pale spheres, striatum and blue spots are also visible. Alpha-synuclein and ubiquitin are Lewy small An important component of the body.

3. Neurochemical changes DA and acetylcholine (Ach) are two important neurotransmitters in the striatum. Their functions antagonize each other. Maintaining balance between them plays an important role in regulating basal ganglia circuit activity. The DA neurotransmitter pathway in the brain is mainly the nigro-striatum system. DA neurons in the dense substantia nigra take up L-tyrosine from the blood stream and form L-poly under the action of intracellular tyrosine hydroxylase (TH). L-dopa; Dopamine (DA) is generated by dopamine decarboxylase (DDC); through the nigrostriatal bundle, DA acts on post-synaptic neurons in the putamen and caudate nucleus, and is finally broken down into High vanillic acid (HVA).

What Are the Symptoms of Rickets?

Symptoms of Parkinson's disease

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