After knowing the symptoms of Parkinson's, how should we proceed and what tests should we conduct? What tests should be done for Parkinson's disease?
http://www.mingyihui.net/article_390.html
Laboratory Tests:
1. Reduced serum renin activity, decreased tyrosine content; reduced NE and 5-HT content in substantia nigra and striatum, glutamate decarboxylase (GAD) activity is 50% lower than the control group.
2. Decreased GABA in cerebrospinal fluid (CSF), significantly reduced HVA content, a metabolic product of DA and 5-HT in CSF.
3. Biochemical testing shows reduced somatostatin content in CSF detected by radioimmunoassay. Urinary DA and its metabolic products, 3-methoxytyramine, 5-HT, adrenaline, and NE are also reduced.
Imaging Studies:
1. CT, MRI imaging findings: As Parkinson's disease is a degenerative disease of the central nervous system, pathological changes mainly occur in the substantia nigra, striatum, globus pallidus, caudate nucleus, and cerebral cortex. Therefore, CT imaging shows general brain atrophy, sometimes with calcification of the basal ganglia. MRI can show enlarged ventricles due to brain atrophy, and T2-weighted images often reveal multiple high signal spots in the basal ganglia and white matter regions.
2. SPECT Imaging Findings:
(1) Dopamine receptor (DAR) functional imaging: Dopamine receptors are widely distributed along the dopaminergic pathway in the central nervous system, mainly in the substantia nigra and striatal system. DAR(DL) is located on the cell bodies of non-cholinergic interneurons in the striatum; DAR(D2) is located on the cell bodies of dopaminergic neurons in the substantia nigra and striatum.
SPECT involves injecting radioactive isotopes, primarily 123I-IBZM and 131I-IBZM, specific D2 receptor markers, intravenously into the body. By measuring the radioactivity ratio in the basal ganglia region relative to the frontal lobe, occipital lobe, or cerebellum, it reflects the number and function of DAR receptors to diagnose early-stage Parkinson's disease. If patients receive early treatment with dopamine preparations, there will be an upregulation of DAR(D2) on the contralateral side of the brain where the disease began. In mid-to-late stage Parkinson's disease patients who have been taking dopamine preparations long-term, the basal ganglia/occipital lobe and basal ganglia/frontal lobe ratios decrease. Although SPECT functional imaging can only detect the number of DAR receptors, it cannot confirm whether the disease is primary Parkinson's but can distinguish certain secondary Parkinson's diseases and serve as an indicator for monitoring disease progression and drug treatment effects.
(2) Dopamine transporter (DAT) functional imaging: The mechanism by which 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 DAT content and the severity of Parkinson's disease. A significant reduction in DAT in the basal ganglia is evident in early-stage Parkinson's disease patients.
SPECT uses 11C-WIN35428 and 123I-CIT, injected intravenously into the body, to measure the basal ganglia/cerebellum activity ratio and the thalamus/cerebellum activity ratio, reflecting the number of DATs in different regions of the central nervous system. In early-stage Parkinson's disease patients, the number of DATs in the basal ganglia region is significantly reduced.
3. PET Functional Imaging: Positron emission tomography (PET) diagnosis of Parkinson's disease has a working principle and method similar to SPECT. It currently relies mainly on brain glucose metabolism imaging, generally using 18F-fluorodeoxyglucose (18FDG). In the early stages of Parkinson's disease, the local glucose metabolism rate in the striatum moderately decreases, and further decreases in later stages. Many PET receptor imaging agents exist, with PET neurotransmitter functional imaging agents primarily using 18F-dopa-PET (18FD-PET) isotopes, following the same basic principles as SPECT. PET can perform early diagnosis of Parkinson's disease, early diagnosis in high-risk populations for Parkinson's disease, and serve as an objective indicator for assessing disease severity.
After confirming the diagnosis through testing, how should we proceed with treatment? Precautions before treating Parkinson's disease?
Prevention: To date, the exact cause of Parkinson's disease remains unclear, so preventive measures lack precise targeting. However, many studies have confirmed that various risk factors mentioned above have a certain causal relationship with the degeneration and death of dopaminergic neurons in the midbrain substantia nigra. If preventive measures are taken against these risk factors, they will certainly be beneficial in preventing the onset of Parkinson's disease and slowing its progression.
Primary Prevention (Preventing Disease):
1. Individuals with a family history of Parkinson's disease and relevant gene carriers, as well as those exposed to toxic chemicals, should be considered high-risk groups. Close monitoring and follow-up, regular health check-ups, and enhanced health education are necessary, emphasizing self-protection.
2. Strengthen environmental protection efforts in industrial and agricultural production, reducing emissions of harmful gases, wastewater, and pollutants. Protective measures should be strengthened for workers in hazardous environments.
3. Improve rural and urban water supply facilities, protect water resources, reduce pollution in rivers, reservoirs, ponds, and wells, ensuring the population has access to safe and hygienic drinking water.
4. Elderly people should use phenothiazines, reserpine, and butyrophenones cautiously.
5. Pay attention to the prevention and treatment of geriatric diseases (hypertension, hyperlipidemia, hyperglycemia, cerebral arteriosclerosis, etc.), strengthen physical fitness, delay aging, prevent atherosclerosis, all of which play a positive role in preventing Parkinson's disease.
Secondary Prevention (Early Detection, Early Diagnosis, Early Treatment):
1. Early diagnosis. Parkinson's disease has a long subclinical phase. If clinical pre-diagnostic techniques such as olfactory dysfunction, PET scanning, mitochondrial DNA, dopamine antibodies, cerebrospinal fluid chemistry, electro-physiology, etc., are conducted early, subclinical Parkinson's disease may be detected sooner. Treatment with neuroprotective agents (such as vitamin E, SOD, glutathione, glutathione peroxidase, neurotrophic factors, selegiline) might delay the entire clinical course of the disease, contributing to health management.
2. In the early stages of Parkinson's disease, although the number of neurons in the substantia nigra and striatum decreases, dopamine secretion increases compensatorily. At this point, dopamine levels in the brain do not significantly decrease, referred to as the compensation phase. Generally, medication is not recommended during this phase. Physical therapy, medical sports, Tai Chi, hydrotherapy, massage, Qigong, acupuncture, etc., can be used to maintain daily work and life, delaying the application of antiparkinsonian drugs as much as possible. Some advocate for early use of low-dose levodopa to reduce complications, depending on individual circumstances, choosing the optimal option.
3. During the decompensation phase of Parkinson's disease, drug treatment should be used.
Tertiary Prevention (Slowing Disease Progression, Preventing Disability, Improving Quality of Life):
1. Actively pursue comprehensive treatments including physiotherapy, occupational therapy, acupuncture, massage, traditional Chinese and Western medicine, or surgery to slow disease progression.
2. Emphasize psychological counseling, emotional support, ensure adequate sleep, avoid emotional tension and excitement, thereby reducing factors that exacerbate muscle tremors.
3. Encourage active movement among patients, such as eating, dressing, washing, etc. Patients with speech disorders can practice vocalization loudly in front of a mirror. Strengthen joint and muscle strength activities and labor training to maintain limb mobility as much as possible, being cautious about falling and preventing limb deformities or disabilities.
4. For long-term bedridden patients, enhance daily care, maintain cleanliness, frequently turn them over and tap their backs to prevent pneumonia and bedsores. Most Parkinson's disease patients die from infections in the lungs or other systems like the urinary system. Pay attention to dietary nutrition, provide nasogastric feeding if necessary, keep bowel movements regular, continuously enhancing physical strength, improving immune function, and lowering mortality rates.
http://www.mingyihui.net/article_390.html