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To evaluate the therapeutic effectiveness and cost-efficiency of first-line immunotherapies on neuronal surface antibody-mediated autoimmune encephalitis (AE) based on a real-world observational study in China.Our study retrospectively collected the clinical and paraclinical data of patients with definite neuronal surface antibody-mediated AE between July 2014 and July 2020. Regular follow-up was performed after administering standard regimens of first-line immunotherapies, including intravenous methylprednisolone (IVMP) and / or intravenous immunoglobulin (IVIG). Therapeutic effectiveness was reflected by modified Rankin Scale scores. The health resource utilization and direct medical costs were extracted to analyze the cost-efficiency.Among the 78 eligible patients, 48 (61.5%) were males with a median age of 40 years. More than half (56, 71.8%) were treated with combination therapy, with the rest receiving IVMP and IVIG monotherapy (both of 11, 14.1%). Related objective variables, i.e., sex, onset age, disease course, onset symptoms, antibody types, abnormal paraclinical results, disease severity, and the health insurance, showed insignificant differences on the selection of therapy. Each therapy showed similar short-term (4-week) and long-term (1-year) therapeutic effects. Yet the single or combination of IVIG had a slightly better effectiveness but higher cost than the monotherapy of IVMP.The combination of IVMP and IVIG was used more frequently than either alone, which may be associated with neurologist's personal experience and patient's wishes. Though with similar therapeutic effectiveness, the use of IVMP alone might be a better choice with a better cost-efficiency.

Background Accumulating data have suggested seizures occur frequently in patients with neuronal surface antibody‐mediated autoimmune encephalitis. We aimed to evaluate seizure outcomes and potential factors associated with the development of epilepsy in patients with anti‐N‐methyl‐D‐aspartate receptor (NMDAR), anti‐leucine‐rich glioma‐inactivated 1 (LGI1), and anti‐gamma‐aminobutyric‐acid B receptor (GABABR) encephalitis. Methods Patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis were prospectively recruited from 2014 to June 2019, with a median follow‐up period of 30.5 months (range 8–67 months). Seizure outcomes were assessed and risk factors of epilepsy were analyzed. Results A total of 119 patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis were included, and 83 (69.7%) of them developed new‐onset seizures. By the end of follow‐up, 17 (21.3%) of 80 patients had seizure relapses after intermittent seizure remission or exhibited uncontrolled seizure episodes, contributing to epilepsy. Immunotherapy delay and interictal epileptic discharges (IEDs) were identified to be associated with the development of epilepsy in patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis, particularly anti‐NMDAR encephalitis. Furthermore, multivariate logistic regression analysis demonstrated that immunotherapy delay was an independent predictor for epilepsy. Conclusion Our study suggested that immunotherapy delay and IEDs were associated with the development of epilepsy in patients with anti‐NMDAR, anti‐LGI1, and anti‐GABABR encephalitis. Early diagnosis and treatment were required, and particular consideration should be given to patients with these risk factors.

PurposeThe comorbidity of depression in patients with epilepsy is common and treatment is still controversial. This pilot study was aimed at evaluating the efficacy and safety of Xylaria nigripes for treating depressive symptoms in patients with epilepsy during 12 weeks of treatment.MethodsA multicenter, double-blind, placebo-controlled, randomized superiority study was performed. A total of 104 patients with epilepsy who fulfilled the study criteria were randomized 1:1 to receive Xylaria nigripes (the Wu Ling group) or placebo (the placebo group) treatment in the 12-week period of study. The participants were visited on weeks 0, 2, 4, 8, and 12 of the treatment course.ResultsEighty-one patients finished all of the visits. The primary efficacy endpoint in this study was the total effective rate for depression, which was significantly greater in the Wu Ling group (51.3%, n=39) than in the placebo group (35.7%, n=42, 0.51–0.36=0.15, 95% CI −0.06 to 0.37, U=2.83, P=0.002) after 12 weeks of treatment. No differences in seizure frequency or changes in severity were found between the Wu Ling and the placebo groups. In addition, the quality of life and seizure worry subscale scores in patients with epilepsy were also improved more notably in the Wu Ling group than in the placebo group (P

Paroxysmal kinesigenic dyskinesia is associated with macrostructural and microstructural abnormalities in the thalamus.To examine functional and structural connectivity of thalamocortical networks in paroxysmal kinesigenic dyskinesia and to further investigate the effect of mutation of the proline-rich transmembrane protein 2 on thalamocortical networks.Patients with paroxysmal kinesigenic dyskinesia (n = 20), subdivided into proline-rich transmembrane protein 2-mutated (n = 8) and nonmutated patients (n = 12) and healthy controls (n = 20) underwent resting-state functional MRI and diffusion imaging scan. The functional properties of correlations in neural activity (functional connectivity) and the structural properties of white matter probabilistic tractography (structural connectivity) were analyzed to characterize thalamocortical networks. Furthermore, the effect of proline-rich transmembrane protein 2 mutation on functional and structural connectivity of thalamocortical networks were examined using one-way analysis of variance among three groups.Patients had increased functional and structural connectivity between ventral lateral/anterior thalamic nuclei and a lateral motor area, as compared to controls. This functional connectivity positively correlated with disease duration. Interestingly, proline-rich transmembrane protein 2-mutated patients showed decreased functional connectivity and preserved structural connectivity, between mediodorsal nucleus and prefrontal cortex, compared to nonmutated patients and controls.Thalamomotor/premotor hyperconnectivity suggests abnormal communication between thalamus and motor cortex in patients. Furthermore, thalamoprefrontal hypoconnectivity in proline-rich transmembrane protein 2-mutated patients might indicate that proline-rich transmembrane protein 2 mutations result in inefficient thalamoprefrontal integration. Our findings facilitate a deeper understanding of the crucial role of thalamocortical dysconnectivity in the pathophysiological mechanisms of paroxysmal kinesigenic dyskinesia. © 2017 International Parkinson and Movement Disorder Society.

Background and Purpose— Cerebral microbleeds (CMB) and white matter lesions (WML) are cerebral small vessel diseases. Hypertension is considered the most important risk factor. Its mechanism is not yet clarified. Our study assessed the association of blood pressure variability (BPV) with CMB and WML progression. Methods— Patients with a history of ischemic stroke within 1 to 6 months were consecutively recruited and followed-up for 12 to 18 months. Blood pressure was measured monthly and controlled to a target level. BPV was quantified by the maximum, standard deviation, coefficient of variation, successive variation, standard deviation independent of mean, and successive variation independent of mean. Magnetic resonance imaging was performed at baseline and the end of the study. CMB and WML were rated using Microbleed Anatomic Rating Scale and Age-Related White Matter Changes scales, respectively. Multiple logistic analyses assessed BPV associations with CMB and WML development. Results— Of 720 patients recruited, 500 and 584 had follow-up results for CMB and WML, respectively; 13.2% and 48.1% showed CMB and WML progression, respectively, over a median of 14 months. Patients with CMB had a higher mean, maximum, standard deviation, coefficient of variation, successive variation, standard deviation independent of the mean, and successive variation independent of the mean in either systolic blood pressure or diastolic blood pressure ( P Conclusion— BPV independently predicts CMB progression in deep and infratentorial regions. Clinical Trial Registration Information— URL: http://www.clinicaltrials.gov . Unique identi-fier: NCT00202020.

To survey the features and its impact of neuropathic pain in neurological outpatients.A total of 106 patients with neuropathic pain were selected from Neurology Clinic of the Second Affiliated Hospital of Zhejiang University. General status instrument, SF-36 Quality of Life Scale and Hamilton Anxiety Scale (HAMA) were used in the survey.Trigeminal neuralgia (23.6%), nerve root pain (21.7%), and post-herpetic neuralgia (13.2%) were the most common causes of neuropathic pain. The sequence of impairments in life quality of the patients was role-physical (21.2), bodily pain (39.9), role-emotional (41.2), general health (50.0), physical functioning (55.1), vitality (60.0), mental health (68.5), and social functioning (70.9). Pearson correlation coefficients were statistically significant between bodily pain and other dimensions of life quality (P0.05). Western medication (45.3%) was the most common treatment adopted by physicians.The prevalence of neuropathic pain is common in elderly patients. The three major types of neuropathic pain seriously affect the quality of life in patients. Although western medicine is the first choice of treatment, clinical drug selection should be standardized with efforts of both doctors and patients.

Delayed post-anoxic encephalopathy has rarely been reported, and has most commonly been associated with carbon monoxide poisoning. The underlying pathophysiological mechanism is unknown. We describe a patient with a delayed neurologic decline after a good initial recovery from a hypoxic-ischemic event precipitated by acute blood loss. MRI revealed early globus pallidus necrosis followed by delayed substantia nigra damage and leukoencephalopathy. We suggest that anemia might play a role in this pattern of hypoxic-ischemic brain injury.

To compare the safety of intravenous thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) in ischemic patients under the guidance of CT and multi-mode MRI.The clinical, laboratory, and radiologic data from 113 consecutive hyperacute ischemic patients who received intravenous rtPA therapy from June 2009 to October 2011 was retrospectively reviewed. The rate of hemorrhagic transformation (HT) and the clinical outcome between CT and multi-mode MRI was compared. Etiological subgroups were classified according to Chinese ischemic stroke subclassification (CISS).Among 113 patients treated with intravenous rtPA, the mean age was 66 ±12 years, 74(65.5%) were man, the pretreatment National Institutes of Health Stroke Scale score (NIHSS) was 12.4 ±6.5, and time from symptom onset to therapy was 259.7 ±131.7 min. Postlytic radiological HT was found in 34 patients (30.1%). Symptomatic ICH occurred in 9 patients (8%). Logistic regression analysis suggested that multi-mode MRI was an independent predictor of reduced risk of HT.The risk of hemorrhagic complications is lower in patients receiving intravenous thrombolytic therapy with rtPA guided by multi-mode MRI than those guided by CT scan.

Comparing the characteristics of cognitive impairment of patients with single subcortical lesion stroke of four different areas, we are to explore the cognitive function of the thalamus and basal ganglia and this is help for early identification of vascular cognitive impairment (VCI).63 patients with single subcortical lesion stroke (including 14 left thalamic stoke group, 17 left basal ganglia stroke group, 15 right thalamic stroke group, 17 right basal ganglia stroke group) and 34 healthy subjects participated in the current study, whose age, sex and education were matched. A comprehensive neuropsychological battery was used for evaluation.Compared to the normal control group, there was an overall decline of cognitive functions in patients with single subcortical lesion stroke in memory, attention/executive function, language, and visuospatial ability (P0.05). The scores of the left thalamic stroke group were worse than the other three stroke groups in language (BNT16.6 ± 2.6), auditory verbal learning test-immediate recall (12.8 ± 4.4), auditory verbal learning test-delayed recall (2.4 ± 2.3), listening recognition (19.1 ± 3.1), structure delayed recall (9.1 ± 4.7) and symbol digit modalities test-recall (0.9 ± 1.1) (P0.05). However, the left basal ganglia stroke group did better in tests manipulated by the right hand [including Trial making test (part A) score (75 ± 22), Trail making test (part B) score (204 ± 81), Clock drawing test (23.5 ± 4.6), Symbol digit modalities test (24 ± 9)] than other three stroke group, as good as the normal group (P0.05).Single subcortical stroke patients may have general, non-selective cognitive impairment. But, different stroke areas have their own characteristics. The scores of the left thalamic stroke group were worse than the other three stroke groups.

To investigate the change of latency and interpeak latency of each component of BAEP (brainstem auditory evoked potential, BAEP) and its correlation with PV/PFV (pontine volume/posterior fossa volume, PV/PFV) ratio in OPCA (olivopontocerebellar atrophy, OPCA).We used Keypoint EMG/EP to determine waves I PL (peak latency, PL), III PL, V PL and I - III IPL (interpeak latency, IPL), III - V IPL, I - V IPL and used 1.5TMR 3D volume rendering software to determine PV (pontine volume, PV), CV(cerebellar volume, CV) and PFV (posterior fossa volume,PFV). Then calculated PV/PFV ratio, CV/PFV ratio and PV/ CV ratio in OPCA group and control group.Compared with control group, in OPCA group wave IIII PL, I - III IPL were significantly elongated (P0.05), III - V IPL was significantly shorten (P0.05), PV/PFV ratio was significantly decreased (P0.01); there was a positive correlation between III-V IPL and PV/PFV ratio (r = 0.83, P0.01).In patients with OPCA, III PL, I - III IPL of BAEP were elongated and III - V IPL of BAEP was shorten. III - V IPL became shorter when the volume of pontine decreased.

To investigate the influence of location and size of acute insular infarct on stroke-related electrocardiogram (ECG) changes and cardiovascular events.Ninety-nine cases admitted to hospital from October 2007 to June 2009, who were diagnosed as acute middle cerebral artery territory infarct within 48 h after onset and without the history of cardiac diseases, were included in the study. The patients were further divided into three groups: major insular infarct, minor insular infarct and control group, according to the infarct size on MRI diffusion-weighted image. The clinical data, ECG changes and cardiovascular events were compared between left and right insular infarct. Logistic regression was applied to determine the independent risk factors of ECG changes and cardiovascular events.Large artery atherosclerosis was the main cause of acute insular infarct (71.8 %), which was associated with higher NIHSS score compared to the control group (P0.01). Comparing the left and right insular infarct, the frequencies of sinus bradycardia and sudden cardiac death were significantly higher in left insular infarct (P0.01 and P0.05), while there was a trend that the frequency of atrial fibrillation was higher in right insular infarct (P = 0.079). With the larger size of insular infarct, the frequency of sinus bradycardia, new atrial fibrillation and sudden cardiac death (P0.01, P0.05 and P0.05, respectively) became much higher. Logistic regression analysis showed that major insular infarct was related to the higher frequency of sinus bradycardia (OR = 4.660, 95% CI: 1.646 ~ 13.195; P = 0.004).Acute insular infarct is associated with the stroke-related ECG changes and sudden cardiac death. Left insular infarct is related to sinus bradycardia, possibly due to the enhanced parasympathetic tone. It deserves clinical attention that the incidence of cardiac autonomic disturbance becomes higher with the enlarged insular infarct size.

To develop and validate a Chinese version of the Patient-Weighted Quality of Life in Epilepsy Questionnaire (QOLIE-31-P).The original English version of the QOLIE-31-P was translated into the Chinese language. The inventory was then completed by 200 adult patients with epilepsy; and 49 patients also completed the scale twice within three weeks. Test retest, internal consistency reliabilities, construct validity, and some influential factors for quality of life in adults with epilepsy were assessed.Test retest reliability (Pearson's correlation coefficient) for the Chinese version of the QOLIE-31-P ranged from 0.725 to 0.912 (P0.001), and the internal consistency reliability (Cronbach's alpha coefficient) ranged from 0.627 to 0.898. Factor analysis showed that there were seven factors, which explained the total variance for 64.9%. The coefficient of seizure frequency with the quality of life was -0.81(P0.05). The QOLIE-31-P score of the patients with tonic clonic seizure was 55.7 +/-16.6, and that of other seizure type was 61.4 +/-18.7(t=-2.568, P0.05).The psychometric properties of the Chinese version of the QOLIE-31-P have satisfactory reliability and validity, and can be applied to assess quality of life in Chinese adult patients with epilepsy.

To investigate the effects of puerarin with aspirin on the markers of damaged vascular endothelial cells, as von Willebrand factor (vWF), and thrombomodulin (TM) in patients with acute cerebral infarction (ACI).Forty-five patients with ACI were included in this study and divided into basic treatment and puerarin groups, meanwhile 26 healthy persons selected as control group. The serum vWF and sTM concentrations were measured by enzyme-linked immunosorbant assay (ELISA) and national institute health stroke scale (NIHSS) score was evaluated at admission and 14 days later after treatment.The level of serum vWF significantly increased in patients with ACI compared to control and major stroke had higher vWF level than minor stroke (P0.01), but the serum level of sTM had no obviously differences respectively. Correlation analysis showed that there is a positive correlation between the level of vWF and NIHSS score (P0.05, r = 0.368), while the significant correlations between the level of vWF and sTM, sTM and NIHSS score were not observed. After 14 days treatment, the level of serum vWF and NIHSS score were obviously decreased in patients treated with puerarin and aspirin, not in basic treated patients. The level of sTM was increased in patients after 14 d, while puerarin treated patient has lower sTM level than patients with basic treatment (P0.05).Patients with ACI cotreated with puerarin and aspirin improved the neurological function, decreased the levels of serum vWF and sTM, indicating puerarin with aspirin had the protective effects on the damaged vascular endothelial cells.

To investigate the clinical manifestations and to make genetic analysis in a pedigree with myotonic dystrophy disease.The proband and available family members were identified by neurological examination. The clinical manifestation of 8 patients (including the proband) was analyzed; the electromyographic data of 5 patients were compared with 6 other family members. Blood samples were obtained from the 7 patients of the family (excepting II6). DM(1) and DM(2) gene were amplified by PCR, tested by agarose electrophoresis, then analyzed by genetic analyzer.Myotonia and muscle weakness were the main manifestations associated with heart block (7/8) and cataract(6/7). Electromyologram showed myopathic abnormalities not only in patients but also in other members of the family (5/6). The CTG repeats in DM1 and CCTG repeats in DM2 were all in normal range.There likely to be new mutants in this DM pedigree and further study is needed.

To report a Chinese Charcot-Marie-Tooth disease type 2 (CMT2) family.All the members in the family were studied clinically,and 6 patients were studied electrophysiologically. Sural nerve biopsy was performed in the proband. PMP22 gene duplications were detected by highly polymorphic short tandem repeat. Point mutation analysis of PMP22, MPZ and NEFL gene was screened by PCR-SSCP combined with DNA direct sequencing. A genome-wide screening was carried out to the family.Except 2 who had weakness and atrophy in both proximal and distal muscles of the lower limbs, all patients presented muscle wasting and a predominating weakness of distal parts of the lower limbs, and mild to moderate sensory impairments. In 6 patients who were subjected to elctrophysiological examinations, median-nerve conduction velocity (NCV) of the median nerve was normal. Electromyograms (EMGs) revealed signs of denervation with large motor unit potentials, fibrillation potentials and positive sharp waves. Sural nerve biopsy of the proband confirmed the presence of axonal neuropathy with an important loss of large myelinating fibers and a large number of clusters with mostly thinly myelinated axons. PMP22, MPZ and NEFL gene mutations were not found. The results of genome-wide screening revealed a linkage of CMT2 to a locus at chromosome 12q24.The results are consistent with the diagnosis of CMT2. This family represents a rare genetic type of CMT2 which can be designated as CMT2L.

To assess the safety and efficacy of gabapentin in treatment of refractory epilepsy.Sixty-six patients with refractory epilepsy were treated with gabapentin 200 mg/d and 72 patients with placebo, totally 138 patients in five hospitals in different cities in China. Double-blind study was performed to observe the times of seizure, and Mini-Mental State Examination (MMSE) and Activities of Daily Life (ADL) assessment were conducted every 4 weeks.In comparison with the control group, the seizure times at any time point in the GB group all decreased with significant differences at the 12th and 20th weeks. The significant efficacy rates, with the seizure times decreasing by more than 75%, in the gabapentin group were higher than those in the control group, with significant differences in the 4, 8, 16, and 20th weeks. Both the MMSE scores of the 2 groups were raised with a significant difference between the 2 groups at the 16 weeks. There was no significant difference in ADL between these 2 groups. No serious side effect was found in these 2 groups.Gabapentin at a dosage of 1200 mg/d is safe and effective in treatment of epilepsy.

To investigate the relationship between X chromosome and obligatory gene of a pedigree with congenital nystagmus,we used the following markers: DXS1214, DXS1068, DXS993, DXS8035, DXS1047, DXS8033, DXS1192 and DXS1232. Genome screening and genotyping were conducted in this pedigree of congenital nystagmus, and linkage analysis by LINKAGE package was used to determine the potential location. The linkage was not found on the Xp (All LOD score-1) but on Xq (the maximum LOD score=2). The related gene of this pedigree was located on the long arm of X chromosome. We demonstrate that Xq26-Xq28 is a common locus for CMN. It bring us closer to the identification of a gene responsible for X-linked CMN.

To identify mutations of keratin 9 (KRT9) gene in a big Chinese family with epidermolytic palmoplantar keratoderma(EPPK) combined with knuckle-pad-like lesions and nail lesions.Genomic DNA from peripheral blood of all available members in this family and 50 unrelated healthy individuals was used for amplification of the whole coding sequence and the intron-exon boundaries of KRT9 gene by PCR; The mutation was detected by direct sequence analysis and identified by restriction endonuclease Dde I.A mutation of AATAGT at codon 160 (N160S) was found in all patients but not in unaffected family members and 50 controls.The mutation of AATAGT at codon 160 (N160S) is the disease-causing mutation in this Chinese pedigree with EPPK.

To investigate the possible role of valproic acid therapy in the development of the weight gain and hyperinsulinemia of epileptic patients.The weight and fasting insulin levels were measured in 43 epileptic patients treated with valproic acid (VPA) alone and 39 patients with carbamazepine (CBZ) alone for at last 2 years. The body mass index (BMI) and homeostasis model assessment (HOMA) index were studied in the two groups.BMI was higher in the VPA-treated group (23.47+/-1.45) than that in the CBZ-treated group (22.27+/-2.10, P0.05). Fasting insulin level and HOMA index in the VPA group were also higher [(6.64+/-0.79)mU/L and 1.33+/-0.21] than those in the CBZ group [(5.52+/- 0.52)mU/L, P0.01; 1.15+/-0.12, P0.01]. While BMI in the VPA group showed no significant correlation with plasma concentration and dose of valproate.VPA therapy is associated with significantly greater weight gain and hyperinsulinemia, suggesting development of insulin resistance.

Tuberous sclerosis complex (TSC) is an autosomal dominant disease characterized by unusual tumor-like growth, termed hamartomas that develop in a variety of tissues and organs. Clinical findings characteristic of TSC include facial angiofibroma, epilepsy and mental retardation. In the last decade, two genes (TSC1 and TSC2) responsible for this disease were identified and both of them are speculated to be a kind of tumor suppressor gene. TSC1 and TSC2 are located on 9q34 and 16p13.3, respectively. This study was designed to detect gene mutations in patients with TSC.All the exons of TSC1 and TSC2 were analyzed by using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) in DNA separated from peripheral blood of 28 patients with TSC and 100 normal controls. Of the 28 patients, 17 were male and 11 were female, the age of the patients was 1 - 48 years.The mutations were not clustered on a particular exon in either of the genes. Four TSC1 mutations found in 28 cases were on exons (1 nonsense, 2 missense and 1 frameshift); 13 mutations were found in TSC2 gene (2 nonsense, 2 frameshift, 1 deletion and 8 missense). Both TSC1 and TSC2 mutations were detected in 2 cases respectively. The same missense mutation (Q654E) was found in 2 unrelated patients. There was no obvious relationship between the location of the mutation and the clinical symptoms.Mutations found in this study were distributed on various exons and there was no clustering of the mutations, the widespread distribution of TSC1/TSC2 mutations hinders the development of a simple diagnostic test, and the identification of individual mutations does not provide prediction of prognosis.

To measure the urokinase-type plasminogen activator (UPA) and its receptor (UPAR) in the plasma of patients with cerebral infarction and to study the effects of UPA and UPAR on cerebral infarction.ELISA sandwich method was used to measure the plasma levels of UPA and UPAR in 89 patients with acute cerebral infarction, subdivided into mild, moderate and severe subgroups according to the modified Edinburgh-Scandinavia stroke scale (mESSS), and 30 patients with other disease and 30 healthy persons as controls.Within 2 days after the onset of cerebral infarction the UPA and UPAR levels were (1663.7 +/- 384.2) ng/L and (1 375.3 +/- 303.0) ng/L respectively, both significantly higher than those of the patients with other diseases [(1 033.0 +/- 122.7) ng/L and (978.3 +/- 120.0) ng/L respectively (P = 0.038 and P = 0.000)] and those of the normal control group [(1 005.0 +/- 128.9) ng/L and (904.7 +/- 158.6) ng/L respectively, both P = 0.000]. Two weeks after the onset of stroke, the plasma UPA level was (1 185.5 +/- 384.6) ng/L, not significantly different from those of the 2 control groups (both P0.05); while the plasma UPAR level in the cerebral infarction was (1 159.3 +/- 261.2) ng/L, significantly higher than those in the 2 control groups (P0.01). Within 2 days after the onset of infarction the plasma UPA and UPAR levels of the severe subgroup were (1 938.9 +/- 256.5) ng/L and (1 510.8 +/- 378.7) ng/L respectively, both significantly higher than those of the moderate subgroup [(1 593.7 +/- 204.8) ng/L and (1 296.6 +/- 151.2) ng/L respectively, both P0.01] and those of the mild subgroup [1 358.5 +/- 175.9] ng/L and (1 226.8 +/- 98.3) ng/L respectively, both P0.01], Two weeks after the onset of stroke,the plasma UPA and uPAR levels of the severe subgroup remained significantly higher than those of the mild subgroup [(1 152.6 +/- 170.3) ng/L vs (1 041.9 +/- 187.0) ng/L, (P0.05)] and [(1 186.4 +/- 158.3) ng/L vs (1 053.9 +/- 109.4) ng/L, (P0.01)]. In addition, the plasma UPA and UPAR levels of the patients who died from cerebral infarction at last were the highest among all the groups.The plasma levels pf UPA and UPAR increase in patients with cerebral infarction and may be related with the severity of disease. The UPA and UPAR genes may play an important role via proteolytic degradation of the extracellular matrix and basement membrane during the development of cerebral infarction.