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Objective:To investigate the impact of group-based rehabilitation exercise on motor and non-movement symptoms of Parkinson's disease(PD).Methods:A total of 88 patients from out-patient and in-patient services at our hospital were randomly assigned to an early exercise group(E-EG), a late exercise group(L-EG), and a control group(CG)using a randomized delayed-start design.Patients in the E-EG carried out a rigorous, formal group exercise program, one hour per session, twice per week, for 18 months(May 2018-November 2019). Patients in the L-EG took part in the exercise program in the final 6-12 months of the study.We assessed outcomes using the Unified Parkinson's Disease Rating Scale(UPDRS), Parkinson's disease questionnaire-39(PDQ-39 Q), trail-making test part A & B, nine-hole peg test(9-HPT), 30 second sit to stand test(30s SST), 10 m walk test(10 m W), mini-balance evaluation systems test(Mini-BEST), Fullerton Advanced Balance(FAB)Scale and time up and go(TUG)test.Results:Compared with pre-exercise levels, patients with PD in the E-EG had lower performance in UPDRS(17.5±8.3 vs.20.0±8.6, t=-2.2, P=0.02)and lower performance in PDQ-39(27.2±2.1 vs.29.0±9.8, t=-2.6, P=0.001)after exercise.Moreover, compared with pre-exercise levels, patients with PD in the E-EG showed decreased post-exercise performance in trail-making test part B(114.2±25.5 vs.129.8±28.4, t=-2.3, P=0.02)and in 9-HPT(33.7±7.3 vs.39.6±9.3, t=-2.6, P=0.001). Conclusions:The practice of group-based rehabilitation exercise can improve movement abilities and quality of life in PD patients, especially if implemented early.Targeted rehabilitation exercise should be taken as part of the treatment strategy for PD patients as early as possible to deliver the best benefits.
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Anti-Sry-like high mobility group box (SOX) 1 antibodies (abs) are partly characterized onconeural autoantibodies (autoabs) due to their correlation with neoplastic diseases. AntiSOX1 abs are associated with various clinical manifestations, including Lambert-Eaton myasthenic syndrome (LEMS) and paraneoplastic cerebellar degeneration (PCD). However, the clinical characteristics of patients with anti-SOX1 abs have not been described in detail. This review systematically explores the reported patients with anti-SOX1 abs and analyzes these cases for demographic characteristics, clinical features, coexisting neuronal autoabs, neuroimaging findings, treatment, and clinical outcomes. In addition, considering that PCD is the most common paraneoplastic neurological syndrome and that the association between PCD and anti-SOX1 abs remains unclear, we focus on the presence of autoabs in relation to PCD and associated tumors. PCD-associated autoabs include various intracellular autoabs (e.g., anti-Hu, anti-Yo, anti-Ri, and anti-SOX1) and cell-surface autoabs (anti-P/Q-type voltage-gated calcium channel). Commonly involved tumors in PCD are small-cell lung cancer (SCLC), gynecological, and breast tumors. LEMS is the most common clinical symptom in patients with antiSOX1 abs, followed by PCD, and multiple neuronal autoabs coexist in 47.1% of these patients.SCLC is still the predominant tumor in patients with anti-SOX1 abs, while non-SCLC is uncommon. No consistent imaging feature is found in patients with anti-SOX1 abs, and there is no consensus on either the therapy choice or therapeutic efficacy. In conclusion, the presence of anti-SOX1 abs alone is a potential predictor of an uncommon paraneoplastic neurological disorder, usually occurring in the setting of LEMS, PCD, and SCLC. The detection of anti-SOX1 abs contributes to an early diagnosis of underlying tumors, given the diversity of clinical symptoms and the absence of characteristic neuroimaging features.
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Nemaline myopathy is a common type of congenital myopathy,and various gene mutations of thin filaments and related components are the causes of the disease.In recent years,a total of 13 gene mutations have been found to be associated with the disease.We review the six new pathogenic genes discovered in the past five years,and summarize gene function,encoded protein,mutation type and clinical features of nemaline myopathy.The pathogenesis of nemaline myopathy is needed to be further explored.
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Parkinson's disease is characterized by progressive motor dysfunction owing to degeneration of dopaminergic neurons in the substantia nigra and other nuclei.Recently,the bilateral high frequency stimulation of the subthalamic nucleus deep brain stimula tion (STN-DBS) as the treatment of PD was famous with good curative effect.But postoperative apathy as its side-effect impact on the therapeutic effect and the quality of life of patients seriously,which drawn the attention of clinicians.In this article,we summarized the incidence,manifestation and treatment of postoperative apathy and tried to provide some ideas for clinicians.
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Objective To investigate the prevalence of cognitive and motor disorders as well as emotional and sleep abnormality in the veterans from military communities in Beijing. Methods The participants underwent a comprehensive in-person evaluation including detailed neuropsychological testing,Hospital Anxiety and Depression Scale and special questionnaires for movement and sleep disorders. Results The overall prevalence of cognitive impairment, extrapyramidal diseases was 32.7%, 8.8% . The prevalence of mild cognitive impairment, dementia, Parkinson disease, essential tremor, anxiety and depression was 26.2% , 6.5% , 2.0% , 6.1 % , 1.4% and 4.1% respectively. Prevalence of all kinds of sleep disorders ranged from 10. 3% to 53. 9%. The prevalence of cognitive impairment had no significant difference of sex, but were correlated to age and education, the correlation coefficient was 0. 326 and -0.221 ( P<0.01) . Conclusion Veterans from military communities had higher prevalence of cognitive impairment, extrapyramidal diseases and sleep disorders and lower that of anxiety and depression relatively.
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BACKGROUND:At present, some neurological imaging methods, including MRI, fMRI, 2-(1-(6-[(2-[18F]fluoroethyl)(methyl)amino]-2-naphthyi) ethylidene) malononitrile (18F-FDDNP) positron emission tomography (PET), are helpful but not specific for the diagnosis of Alzheimer disease (AD). 18F-FDG is a special marker of beta-amyloid (Aβ), thus AD can be diagnosed by 18F-FDDNP PET at early period.OBJECTIVE: To evaluate the role of 18F-FDDNP PET in the diagnosis of AD, and establish reliable clinical biological indexes for the diagnosis of AD patients.DESIGN: A controlled analysis.SETTINGS : Department of Geriatric Neurology and Department of Nuclear Medicine, the General Hospital of Chinese PLA. PARTICIPANTS: Patients visiting the General Hospital of Chinese PLA from May 2004 to March 2005 were selected. Informed consents were obtained from all the participants. ① AD group (n =7): (74.88±12.03) years old; Accorded with the criteria related to diagnosis of AD in NINCDS/ADRDA (National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer Disease and Related Disease Association) and revision of Diagnostic and statistical Manual (DSM-Ⅳ, 4th ed.); brain CT or magnetic resonance imaging (MRI) examination displayed that inter-uncus distance of temporal lobes was ≥ 30 mm. ② Vascular dementia group (n =6): (73.83±4.75) years old; Accorded with the diagnostic criteria of NINDS-AIREN (National Institute of Neurological Diseases and Stroke, USA) and DSM-Ⅳ for vascular dementia; Inter-uncus distance of temporal lobes ＜ 30 mm. ③ Control group (n =6): (71.17±3.71) years old; Without rarefaction of white matter; Intelligence examination was normal.METHODS: PET was performed in all the subjects. PET scanner type was SEIMENS ECAT EXACT HR. The tracer selected was 18F-FDDNP which had radiochemical purity higher than 95% and error of radioactivity measurement lower than 10%. The images were collected at 5, 25 and 45 minutes after injection of 18F-FDDNP. Horizontal and coronary tomograms of brain were obtained after reconstruction.MAIN OUTCOME MEASURES: Characteristics of 18F-FDDNP brain PET images.RESULTS: ① In the control group, signs of obvious atrophy of brain were not seen. At about 45 minutes, the radioactivity in cortex and subcortical nucleus groups was essentially cleared and the structures of brain could not be differentiated clearly. ② In the vascular dementia group, brain atrophy and enlargement of ventricular system to various degrees could be seen. The clearance of radioactivity at three time points was similar to that in the control images. ③ In the AD group, the brain was obviously atrophied and the ventricular system was enlarged. The clearance of radioactivity at the three time points was significantly different from the images of other two groups. The radioactivity in cortex and hippocampus was cleared slower. At 45 minutes, the gray matter could still be clearly differentiated from the white matter, but the radioactivity in corpus striatum and thalamus was not higher than that in cortex and much radioactivity retention could be seen in cortex and hippocampus.CONCLUSION: 18F-FDDNP PET brain images can differentiate AD and vascular dementia, and it is an effective imaging index for the diagnosis of AD.
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BACKGROUND: β-amyloid has been proved to be capable of inducing cell apoptosis and play a vital role in Alzheimer disease (AD).OBJECTIVE: To probe into olanzapine's protective effect and mechanism of PC12 cell apoptosis induced by β-amyloid 25-35.SETTING: Department of Neurology, Southern Building of the General Hospital of Chinese PLA.DESIGN: Randomized design.MATERIALS: This experiment was carried out in the Neuropsychopathic Research Institute, Medical College of the University of Saskatchewan(Canada), between May 2002 and March 2003.METHODS: P12 cells were cultured with RPMI1640 culture medium.100 μL cell suspension was inoculated in each well of 96-well culture plate, and 5 mL suspension was inoculated in 25 cm2 culture bottle covered with collagen and cultured for 24 hours, then with additional 50 μmol/L and 100 μmol/L olanzapine, respectively, for 24 hours, and β-amyloid 25-35 of different concentrations (0.01 μmol/L, 2 μmol/L and 20 μmol/L) for 24 hours. PC12 cell apoptosis was induced by β-amyloid 25-35 in 96-well culture plate and cells were harvested to assay their survival rate with MTF colorimetric assay. PC12 cells in 25-cm2 culture bottles were also harvested to detect the effect of olanzapine on Bax and caspase-3 expression in PC12 cells using Western blot assay.MAIN OUTCOME MEASURES: ① Cell survival rate; ② the expression of Bax and caspase-3 in PC12 cells.RESULTS: ① Cell survival rate: cell activity was found declined from 75% to 35% in PC12 cells induced by β-amyloid 25-35, but obviously increased in PC12 cells due to pretreatment with olanzapine of 50 μmol/L and 100 μmol/L. ② Olanzapine's effects on Bax expression in PC12 cell apoptosis induced by β-amyloid 25-35: Bax expression increased in PC12cells due to exposure to β-amyloid 25-35 of 0.01 μmol/L, 2 μmol/L and 20 μmol/L, but it could be suppressed if pretreated with olanzapine of 50 μmol/L. ③ Effect of olanzapine on caspase-3 expression in PC12apoptotic cells induced by β-amyloid 25-35: There was no change in PC12cells induced by 0.001 μmol/L or 0.01 μmol/L of β-amyloid, as well as in PC12 cells pretreated with 50 μmol/L olanzapine. However, caspase-3 expression obviously increased in PC12 cells exposed to 2 μmol/L and 20 μmol/L of β-amyloid 25-35, and it could be suppressed by pretreatment with 50 μmol/L of olanzapine.CONCLUSION: ① β-amyloid 25-35 can induce the high expression of cell apoptosis related Bax and caspase-3 in vitro cultured PC12 cells. ②Olanzapine can reduce the expression, thus enhancing the survival rate of PC 12 cells.
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Objective To evaluate the efficacy and safty of BaileMian capsulae on treatment of insomnia in aged people. Methods 40 aged people with insomnia were randomly divided into the research group (BaileMian capsule group,n= 20) and the control group (Zaorenanshen capsule group,n=20) treated for 14 days.The clinical effects were esti- mated with SDRS before and after 1 w and 2 w treatment.Results The total SDRS scores after treatments in both groups were significantly decreased comparing with scores before treatments respectively (P
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BACKGROUND: Many studies have indicated that amyloid beta-protein (Aβ) plays an important role in the pathophysiology of Alzheimer disease (AD), the reduction of production of Aβ can slow down the deterioration of AD, so to reduce Aβ production could become an important therapeutic target in AD. Many AD patients present behavioral disturbance and psychotic symptoms, and are treated with antipsychotics. Olanzapine and quetiapine can significantly improve the clinical global impressions(CGI) severity-of-Alzheimer scores, clinical studies suggest that early and prolonged intervention can improve long-term outcome.OBJECTIVE: To investigate the effect of olanzapine and quetiapine on the secretion of Aβ42 in Swedish amyloid precursor protein(APP) gene and presenilin 1 gene transfected murine N2a neuroblastoma cells.DESIGN: A completely randomized controlled trial based on N2a cells.MATERIALS: Setting was at Neuropsychiatry Research Institute of Medical College, University of Saskatchewan. The murine N2a and double transfected N2a cell was provided by department of neurology and neuroscience, Cornell university medical college.INTERVENTIONS: The double transfected murine N2a neuroblastoma cells were treated for 24 hours with 200 μmol/L olanzapine and 50 μ mol/L quetiapine respectively, then intracellular and extrocellular levels of Aβ were determined. The MTT assay was used to determine cell viability; the BCA assay was used to determine the protein content of cells; the western blot analysis was used to determine the APP expression; and the Enzyme-Linked-Immuno-Sorbent Assay(ELISA) was used to determine the Aβ produced by double transfected murine N2a neuroblastoma cells.MAIN OUTCOME MEASURES: The levels of intracellular and extracellullar Aβ 42 secreted by double transfected murine N2a neuroblastoma cells were detected using ELISA.RESULTS: The double transfected N2a cells produced more APPs than the naive N2a cells. The extracellular Aβ[ (4.78 ± 0.54) nmol/L] of cells treated with olanzapine decreased significantly comparing to the vehicle [(7.69±0.62) nmol/L] (t=3.52, P ＜0.05); and theextracellular Aβ[ (4. 09 ±0. 18) nmol/L] of cells treated with quetiapine decreased significantly comparing to the vehicle[ (7.50 ±0.50) nmol/L] ( t =5.61,P ＜ 0.05) . The intracellular Aβ of cells treated with olanzapine did not change significantly conpared with the vehicle ( P ＞ 0.05 ); the intracellular Aβ of cells treated with quetiapine did not change significantly compared with the vehicle ( P ＞ 0.05 ).CONCLUSION: The result suggests that olanzapine and quetiapine can decrease the production of Aβ42 in double transfected murine N2a neuroblastoma cells and clinically may be helpful in slowing down the progression of AD by decreasing the extrocellular secretion of Aβ42.
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Objective To investigate the pathogenesis of the syringomyelia in Chiari I malformation by measuring the posterior cranial fossa structures. Methods The posterior cranial fossa structures on mid sagittal MR image were measured in 50 normal subjects,and 24 Chiari I malformation patients associated with syringomyelia and 26 Chiari I malformation patients without syringomyelia. The t test was used for statistical analysis. Results In Chiari I malformation patients and normal subjects, the width of the CSF space anterior to the medulla oblongata was (4 2?1 8) mm and (6 6?1 4) mm respectively( t =7 30, P 0 05). In Chiari I malformation with syringomyelia group and without syringomyelia group, the width of the CSF space anterior to the medulla oblongata was (2 9?1 4) mm and (5 5?1 1) mm respectively( t =7 30, P
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Objective To explore histopathological features in the nigrostriatal tissues of Parkinson’s disease (PD)and Parkisonism plus syndrome. Methods The substantia nigra and the striatum of 5 PD cases, 3 progressive supralnuclear palsy (PSP) cases and 3 multiple system atrophy (MSA) cases, and 5 normal aging control cases were examined by routine neuropathological methods and Gallyas-Braak staining and tau, ubiquitin and ?-synuclein immunohistochemistry. Pigmented neurons in the substantia nigra of PD, PSP, MSA cases and normal aging control cases were counted. The neuronal and glial cytoplasmic inclusions in the nigrostriatal tissues were observed. Components of the abnormal proteins were identified. Results Nerve cells in the substantia nigra of PD,PSP and MSA groups showed severe loss in number,especially the ventrolateral zone and the ventromedial zone. Compared with those in the normal aging control group,numbers of nerve cells in the ventrolateral zone of PD, PSP and MSA groups decreased to 37.5%, 24.2%, 33.8% in the right side, and 48.0%, 25.8%, 33.9% in the left side respectively. There were ?-synuclein and ubiquitin-positive Lewy bodies in the substantia nigra of PD. A lot of tau-positive, argyrophilic globous neurofibrinary tangles, tuft-shaped astrocytes and coiled bodies in the substantia nigra and the striatum of PSP were observed.Severe loss of neurons and gliosis in the caudate nucleus and putamen of MSA were found. In addition, ?-synuclein and ubiquitin-positive glial cytoplasmic inclusions were found in the substantia nigra and striatal region of MSA. Conclusions Lewy bodies in PD and glial cytoplasmic inclusions in MSA are related to abnormal depositions of ?-synuclein and ubiquitin.Neuronal and glial cytoplasmic inclusions in PSP are related to abnormal aggregation of tau.
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60 years old) in a community of Beijing were investigated by telephone visit, physical examination and Doppler examination. The rates of hypertension, coronary artery disease, diabetes and stroke were evaluated according to the patient whether had PAOD. Results Among 1730 people, 263 cases were diagnosed as POAD. The prevalence of hypertension, coronary heart disease, diabetes and stroke in PAOD population (59.3%,40.3%,29.3% and 22.3%) was higher than those in non-PAOD population (48.1%,32.6%,23.0%and 15.2%)( P
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Objective To investigate the mechanism of the protective effects of olanzapine against apoptosis of PC12 cells induced by ?-amyloid peptide 25-35 (A?_ 25-35 ). Methods Based on the model of apoptosis of PC12 cells induced by A?_ 25-35 , cell viability was determined by MTT assay. The expressions of Bax, Caspase-3 of PC12 cells induced by A?_ 25-35 and olanzapine were assessed by Western blot. Results 10 -14 -10 -5 mol/L A?_ 25-35 lowered the cell viability of PC12 cells, 50?mol/L and 100?mol/L olanzapine pretreatment enhanced the cell viability of PC12 cells, and there was significant difference compared with olanzapine non-pretreated groups (P