Objective To investigate the incidence rate, onset time and electrophysiological characteristics of rapid eye movement sleep behavior disorder (RBD) and the relationship between RBD and synucleinopathies as well as the electrophysiological diagnostic criteria of RBD in Parkinson' s disease (PD) and multiple system atrophy (MSA). Methods Sleep survey and night video-polysomnography (NPSG)were used to study sleep disturbance of PD and MSA. (1) Subjective sleep assessments: All subjects,including 66 PD patients, 65 age and sex matched healthy controls and 30 MSA patients, completed the sleep questionnaires, and the RBD incidence rate and onset time were got. (2) Objective sleep assessments: 8 PD patients, 13 MSA patients, and 15 age and sex matched healthy controls underwent video-NPSG recording on two consecutive nights. Sleep architect were analyzed. The NPSG characteristics of RBD accompany with PD and MSA were analyzed, and the electrophysiological diagnostic varameters of it were determined. Results Patients with PD or MSA had a higher prevalence of RBD. RBD was found in 59. 1% (39/66) PD patients and 86. 6% (26/30) MSA patients, among those, 46. 2% ( 18/39 ) and 84.6% (22/26) had the waking symptoms of MSA and PD. The main NPSG characteristics of RBD of PD or MSA were chin REM without atonia (RWA) and increased movement. Conclusions The relatively higher RBD prevalence in MSA and PD patients indicates that RBD has close relationship with PD and MSA.Part of patients with RBD preceding neurology disease indicates that RBD may be the early marker of PD and MSA. The main NPSG characteristics of RBD accompany with PD and MSA are chin RWA and the motor manifestations. RWA and phasic EMG activity density are supposed to be the NPSG diagnostic parameters.

Objective To study a possible correlation between the duration of reproductive period ( from puberty to menopause) and the prognosis of ischemic stroke. Methods Female in-patients with acute ischemic stroke confirmed by CT/MRI in the Neurology Department of the First Affiliated Hospital of Zhengzhou University from 09/03/2006 to 08/30/2008 were enrolled in this study. The probable risk factors of prognosis were analyzed and recovery was assessed by modified Rankin score (MRS) at 6 months followup. Multivariate Logistic regression was used for statistic analysis. Results 371 female patients were enrolled. The average age was (66. 2 ± 10. 0) years; average menopause age was (48. 5 ± 3.9 ) years and average duration of reproductive period was (33.3 ± 4. 3) years. There is a negative correlation between the duration and MRS (OR =0. 285, 95% CI: 0. 095-0. 850, P =0.024). There is no correlation between menopause age and prognosis of stroke. Conclusions Duration of reproductive period is a predictor for prognosis of ischemic stroke. Patients with longer reproductive period have better prognosis.

Objective To investigate the percentage of Th17 cells and regulatory T cells in patients with myasthenia gravis (MG) and observe the effects of methylprednisolone infusion on these cells.Methods The circulating Th17 cells and CD4+ CD25highT cells of 66 MG patients and 35 healthy controls were detected using four colour cytometry. The relationship between these cells and MGFA score in 18 MG patients and in 8 MG patients after methylprednisolone was infusion were also analyzed in this study. Results There was significant difference in the percentage of circulating Th17 cells between MG patients (2. 61% ±0. 28% ) and the healthy controls (0. 94% ± 0. 12%, Z = 4. 059, P = 0. 0001 ). Methylprednisolone therapy significantly reduced the percentage of circulating Th17 cells from 4. 72% ± 1.21% to 1.81% ± 0. 69%(Z = 1. 995,P = 0. 0460). In addition, the percentage of Th17 cells showed a positive correlation with MGFA score(r =0. 5359, P =0. 0219). Conclusions Circulating Th17 cells are elevated in MG patients.Methylprednisolone therapy can reduce such elevation, and this may be important in mediating symptomatic improvement in MG patients.

Objective To quantitatively estimate upper motor neuron (UMN) lesion with the triple stimulation technique (TST) in amyotrophic lateral sclerosis (ALS). Methods Fifty ALS patients and 22 normal controls were enrolled in the study. Patients were examined clinically with conventional transcranial magnetic stimulation (TMS) and TST at abductor digiti minimi. Central motor conduction time (CMCT),motor evoked potential ( MEP), resting motor threshold ( RMT), compound muscle action potential ( CMAP), modified ashworth scale ( MAS), Medical Research Council scale and modified ALS scale were assessed and their correlation to disease progress was analyzed. Results The TST amplitude ratio was significantly decreased in ALS patients with UMN signs(28 cases 62. 0% (40. 7%, 75.9% ) ), compared with controls ( 96. 9% ± 2. 6% ) and ALS patients without UMN signs ( 22 cases 95.6% ( 85.4%,100. 0% ) ;Z = -4. 827, -5.435, both P =0. 000). The abnormal rates of the TST amplitude in ALS with UMN signs, ALS without UMN signs and controls were 89. 3%, 27.3% ,9. 1% respectively. The abnormal rates of the TST amplitude, the latency of MEP, CMCT, RMT in detecting UMN lesions were 89. 3%,64. 3%, 53.6%, 64. 3% , 78. 6%, respectively. The TST amplitude was significantly correlated to tendon reflex in right arm ( r = 0. 690, P = 0. 000), with modified ashworth scale ( MAS, r = - 0. 772,P = 0. 000),with diagnostic degree ( r = 0. 483, P = 0. 000), with RMT ( r = - 0. 774,P = 0. 000), the latency of MEP (r = - 0. 444, P = 0. 005 ), motor evoked potential/compound muscle action potential of erb' s ( MEP/ CMAPerb, r = 0. 685, P = 0. 000 ), MEP/CMAPerb in facilitation ( r = 0. 770, P = 0. 000). Conclusions TST appears to be a more accurate and sensitive measure of detecting and quantifying UMN abnormality in ALS patients than the other parameters. TST may reveal the subclinical UMN impairment in ALS and provide an accurate diagnosis assessment for UMN loss in ALS and an objective scale for monitoring the progression of disease.

Objective To investigate the diffusion changes in ipsilateral substantia nigra after a chronic striatum infarction with diffusion tensor imaging ( DTI ) and its connotation for clinical lecture.Methods Participators underwent a DTI scan and were divided into three groups. The striatum infarction (SI) group consisted of twenty patients with chronic basal ganglia infarction with striatum involved, while the non striatum infarction (NSI) group consisted of another twenty patients with chronic basal ganglia infarctions without striatum involved. The control group consisted of twenty healthy volunteers. Before the DTI scan all patients underwent a clinical evaluation with Modified Rankin Scale (mRS) and Barthol Index,and the four patients of SI group with symptoms like Parkinson disease underwent an additional evaluation with the third subscale of Unified Parkinson' s Disease Rating Scale ( UPDRS Ⅲ ). Results Compared with NSI and control groups, the infarct side substantia nigra MD of SI group increased by 30. 86 percent (t =40.07,P=0.000) and 31.42 percent (t =42. 64,P =0.000). The FA values from the three groups were not different. There were four patients with some symptoms like Parkinson disease in SI group. Compared with those patients without symptom like Parkinson disease in SI group, the infarct side substantia nigra MD of these four patients increased by 22 percent(t = 18.03, P =0. 01 ). Moreover, the infarct side substantia nigra MD of these four patients was correlated with their UPDRS Ⅲ positively ( r = 0. 97, P = 0. 03 ).Conclusions The secondary degeneration in the ipsilateral side substantia nigra after striatum infarction could be detested quantitatively with diffusion tensor imaging. The secondary degeneration in substantia nigra may be responsible for the symptoms like Parkinson disease in striatum infarction patients.

Objective To study the locations of P-glycoprotein(P-gp),multi-drug resistanceassociated protein (MRP) and lung resistance.related protein(LRP)in brain tissue of focal cortical dysplasia (FCD) and to compare the quantity of these proteins in different brain tissues in an effort to study the mechanism of refractory epilepsy and to provide theoretical basis for medical treatment in patients with epilepsy.Methods The brain tissues of 16 cases with refractory epilepsy were collected during surgery,including 8 cases of focal cortical dysplasia type Ⅰ(FCD Ⅰ)and 8 cases of focal cortical dysplasia type Ⅱ (FCD Ⅱ) Five cases of glioma without history of epilepsy were included as the control group.Envision method was used to observe the location and intensity of expression of these three proteins.Western-Blot was used to analyze these proteins quantitatively.Results In brain tissue,the locations of P-glycoprotein,multi-drug resistance-associated protein and lung resistance-related protein were difierent.P-gp located mainly in capillary endothelial cells;MRP in neurons components;the location of LRP included capillary endothelial cells,balloon cells and the matrix of lesions.The expressions of three proteins in brain tissue of FCD were significantly higher than in control group(P-gp:0.520 ±0.121,MRP:0.132±0.018,LRP:0.092.±0.018,U=0.000,P<0.01).The expressions of P-gp and LRP in lesions of FCD Ⅱ(3.809 ±0.842 and 0.655±0.303,respectively)were higher than that in surrounding regions(2.636 ±0.622 and 0.290±0.096,U value were 6.000 and 4.500,both P<0.01).Conclusions P-gp,MRP and LRP expressed at different position of focal cortical dysplasia,suggesting that their roles were distinctive.

Objective To investigate whether there are different effects of electric stimulation of vagus nerve,peripheral nerve(sciatic nerve and trigeminal nerve),and motor cortex on pentylenetetrazol (PTZ)induced convulsion in rats.Methods The vagus nerve and sciatic nerve were exposed in rats.The stimulation electrodes were placed on the vagus nerve,sciatic nerve,trigeminal nerve,and motor cortex,respectively.After electric stimulation,PTZ(50 mg/kg)was intraperitoneally injected into the rats.The pattern and latency of the convulsion seizure were observed and recorded.Results Racine's grade Ⅰ-Ⅴ grade convulsion seizure Was present in 9 rats(9/10)in the control group after the injection of PTZ.However,this intensity Was reduced to Ⅰ-Ⅲ grade differentially in all the rats by electric stimulation of the vagus nerve(5/10)or peripheral nerve(6/10 and 5/10).Furthermore,in the group of rats stimulated at motor cortex,there Was completely no convulsion.On the other hand,when pathological changes appeared in cortex or hippocampus(i.e.epileptic model was set up by 7 weeks stimulation),the same stimulation of motor cortex was not able to inhibit the convulsion seizure induced by injection of PTZ and all these rats showed Ⅳ-Ⅴ grade seizure(10/10).Conclusions In physiological condition,all of the four types of stimulation differentially reduced intensity of convulsion seizure triggered by PIZ injection and motor cortex stimulation has the best effect.However.when rats were in pathological status and epileptic nidus appeared in their brains.stimulatiion of motor cortex has no effect on PTZ induced convulsion seizure.

objective To examine nuclear transIocation of peroxisome proliferator-activated receptor γ(PPARγ)in rats following focal cerebral ischemia/reperfusion(I/R),and to explore the significance of altered PPARγ,nuclear translocation in ischemic brain injury.Methods Healthy adult male SD rats underwent 60-min cerebral artery occlusion followed by reperfusion of 4,8,or 24 h,respectively.The cytoplasmic-to-nuclear shuttling of PPARγ was characterized by Western blot,immunohistochemical and immunofluoreseence staining.The effects of PPARγ agonist rosiglitazone (Ros) and antagonist GW9662 on I/R-induced PPARγ nuclear translocation were also examined in the present study. Furthermore,TTC staining war adopted to determine the change in cerebral infarction volume. Results (1)Western blot analysis revealed an increase of PPARγ in the nucleus and a simultaneous reduction in the cytosol following ischemia and reperfusion for 4 h(tcytosol=9.03,tmuclear=27.19,P=0.00).Prolonged the reperfusion further enhanced this I/R induced PPARγ translocation in a time-dependent manner.Using immunohistochemistry and immunofluorescence,nuclear PPAR γ positive staining increased from 48.3%in the sham control to 80.3% following ischemia and reperfusion for 24 h.(2)Western blot analysis revealed that PPARγ agonist Ros further increased I/R-induced nuclear enrichment of PPARγ,whereas PPARγ antagonist GW9662inhibited I/R-stimulated change in PPARγ.(3)When compared to the L/R group using TTC staining,Ros treatment significantly decreased the infarction volume by 48.40%(15.46±4.94 versus 29.96±3.39,t=5.93.P=0.00),whereas GW9662 increased by 58.95%(47.62±4.93 versus 29.96±3.39,t=7.23,P=0.00).Conclusions Cerebral I/R injury induces PPARγ translocation from the cytosol to the nucleus.This change may represent an intrinsic neuroprotective response against brain I/R injury.

Objective To study the tortuosity coefficient (TC) values of basilar arteries in the adult,and its change in cerebral basilar artery infarction.Methods TC values of basilar arteries was prospectively analyzed using the magnetic resonance angiography images of 135 controls(19-80 years of age,male 90,female 45)and 42 patients with cerebral infarction(5l-70 years of age,male 28,female 14).The relationship between TC values and posterior circulation infarction was statistically evaluated.Results Differences of TC between age groups were statistically significant except group B (31-50 years)and C(51-70 years)(F=10.31,P<0.01).The infarction group had greater TC value(2.497±1.200)than the control group(1.939±0.850,t=2.39,P=0.0195).Conclusions (1)Basilar artery tortuosity is positively related to age,reflecting the degree of arteriosclerosis;(2)Basilar artery tortuosity increases in patients with posterior circulation infarction.

Objective To identify disease-causing mutations in a large panel of Chinese Han patients with hereditary spastic paraplegia(HSP).Methods The coding sequence of the SPG11 gene in the probands of 28 families with ARHSP and 14 sporadic HSP patients was analyzed,and the identified changes in the sequence were tested to exclude being a benign polymorphism by sequencing 200 chromosomes from normal controls.Results Identified 13 causative mutations in SPG11 gene in 7 ARHSP and 3 sporadic HSP The mutations were:c.5977C>T/p.Q1993X、c.4668T>A/p.Y1556X、c.6898_6899delCT/p.L2300AfsX23.38、c.3719_3720delTA/p.11240VfsX263、c.733_734delAT/p.M245VfsX246、c.7088_7089insATTA/p.Y2363X、c.2163_2164insT/p.1722Yfsx731、c.7101-7102insT/p.K2368X、c.6790_6791insC/p.12264PfsX2339、c.654_655delinsG/p.S218RfsX219、c.7151+4_7151+7delAGTA/p.K2384fsX2386、c.6355-21_6355-18delTCT、c.3004C>T/p.G1002X.Among them,12 were novel mutations.The rate of mutation in the SPG11 gene was 25.0%(7/28)in ARHSP,6/6 in ARHSP-TCC and 3/14 in sporadic cases.Conclusions In Chinese Han population,patients with ARHSP-TCC and sporadic HSP-TCC should be screened for SPG11.Sequencing of the SPG11 gene in these patients with is valuable for clinical diagnostic testing.