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Deep brain stimulation is a primary treatment method that improves motor and motor complications in patients with advanced Parkinson's disease. Delirium is a common and serious complication following deep brain stimulation. However, the clinical attention toward this complication remains insufficient. Advanced age, cognitive decline, and the severity of the disease may all be risk factors for delirium. The presence of delirium may also affect cognitive function and disease prognosis. Neurotransmitters such as acetylcholine and dopamine may be involved in the occurrence of delirium. Furthermore, inflammation, the effects of microlesioning of local nuclei, and brain atrophy may also play roles in the onset of delirium. Nonpharmacological therapy appears to be the primary treatment for postoperative delirium in Parkinson's disease. The current article reviews the pathogenesis, epidemiology, prognosis, and treatment of delirium following deep brain stimulation in Parkinson's disease to help clinicians better understand this common complication and to prevent, identify, and treat it as soon as possible, as well as to provide more accurate treatment for patients.
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Parkinson's disease (PD) is a clinically common neurodegenerative disease of the central nervous system (CNS) characterized by loss of dopamine neurons in the substantia nigra. Microglia (MG), as an innate immune cell in the CNS, are involved in a variety of immunity and inflammatory responses in the CNS. A number of studies have shown that the overactivation of MG is one of the critical pathophysiological mechanisms underlying PD. MicroRNAs (miRNAs) are considered to be an important class of gene expression regulators and are involved in a variety of physiological and pathological mechanisms, including immunity and inflammation. In addition, miRNAs can affect the progress of PD by regulating the expression of various MG genes and the polarization state of the MG. Here, we summarize recent articles and describe the important role of MG pathological polarization in the progression of PD, the diverse mechanisms responsible for how miRNAs regulate MG, and the potential therapeutic prospects of miRNAs for PD. We also propose that the regulation of miRNAs may be a novel protective approach against the pathogenesis of PD.
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Multiple system atrophy (MSA) is an adult onset, fatal disease, characterized by an accumulation of alpha-synuclein (α-syn) in oligodendroglial cells. MicroRNAs (miRNAs) are small non-coding RNAs involved in post-translational regulation and several biological processes. Disruption of miRNA-related pathways in the central nervous system (CNS) plays an important role in the pathogenesis of neurodegenerative diseases, including MSA. While the exact mechanisms underlying miRNAs in the pathogenesis of MSA remain unclear, it is known that miRNAs can repress the translation of messenger RNAs (mRNAs) that regulate the following pathogenesis associated with MSA: autophagy, neuroinflammation, α-syn accumulation, synaptic transmission, oxidative stress, and apoptosis. In this review, the metabolism of miRNAs and their functional roles in the pathogenesis of MSA are discussed, thereby highlighting miRNAs as potential new biomarkers for the diagnosis of MSA and in increasing our understanding of the disease process.
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BACKGROUND: Lower urinary tract (LUT) dysfunction is very common in Parkinson's disease (PD) patients. However, the number of studies conducted on LUT dysfunction and its related factors in Chinese PD patients is very limited, and there is no international consensus concerning the results. METHODS: This cross-sectional study enrolled 100 Chinese PD patients. The patients were classified based on their overactive bladder symptom score (OABSS) and then assigned to either a PD with overactive bladder (PD-OAB) group or a PD with no overactive bladder (PD-NOAB) group. A binary logistic regression analysis was performed to identify the accompanying factors for overactive bladder (OAB). Next, correlations between the OABSS and patient sex, age, age of onset, disease duration, MDS-UPDRS-III, H-Y stage, PD subtype, treatment, education, and nonmotor symptoms were analyzed to identify factors correlated with LUT dysfunction. RESULTS: Eighty nine (89%) of the PD patients suffered from LUT dysfunction, and OAB was diagnosed in 45 (45%) of those PD patients. The most common lower urinary tract (LUT) symptom in the PD patients was nighttime frequency (86%), followed by urgency (50%), urge incontinence (34%), and daytime frequency (17%). Patients in the PD-OAB group had an older age and age of onset, were at a more advanced Hoehn-Yahr stage, and had more severe motor symptoms and nonmotor symptoms, including worse cognition, and a greater incidence of REM sleep behavior disorder (RBD). A binary logistic regression analysis showed that a lower Frontal Assessment Battery (FAB) score, higher H-Y stage, and RBD accompanied with a higher prevalence of OAB in PD patients. A multiple linear regression analysis showed that the OABSS was significantly influenced by the FAB score, H-Y stage, RBD, and age. CONCLUSIONS: The FAB score, H-Y stage, and RBD are accompanying factors for OAB. A higher OABSS in PD patients was related to a lower FAB score for frontal lobe executive dysfunction, a higher H-Y stage for severity of motor disorders, RBD, and an older age.
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OBJECTIVE: To investigate the diagnostic value of MHC-I expression in PM. METHODS: Analyzing the results of clinical and pathological findings and the immunohistochemical findings of MHC-I expression of 54 cases. RESULTS: Among the 16 patients with PM, 63 percent patients showed inflammatory infiltration, 94 percent showed MHC-I expression; Among 19 patients with progressive muscular dystrophy, 9 percent patients showed inflammatory infiltration, 11 percent showed MHC-I expression. The other 19 patients showed no inflammatory infiltration and MHC-I expression. CONCLUSION: MHC-I expression as a diagnostic index of PM was appropriate, which had ideal sensitivity, specificity and negative likelihood ratio.