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Neuronal surface antibody-mediated autoimmune encephalitis (NSAE) occurs across a wide age range. However, few studies focused on the onset age and their related characteristics. We aimed to explore the age-dependent profile of NSAE. A total of 134 patients with a definite diagnosis of NSAE were retrospectively enrolled from 3 tertiary hospitals between July 2014 and August 2020. Demographic, clinical, therapeutic, and prognostic data were collected and compared between the late- (≥45) and younger-onset (

Seizure is one of the manifestations of central nervous system inflammatory demyelinating diseases, which mainly include multiple sclerosis (MS), aquaporin 4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Acute symptomatic seizures secondary to MS/AQP4-NMOSD/MOGAD occur in the acute phase of the diseases, and are more frequent in MOGAD. In contrast, recurrent nonprovoked seizures, mainly attributed to autoimmune-associated epilepsy, occur in the nonacute phase of the diseases. Seizures in MS/AQP4-NMOSD/MOGAD mostly have a focal onset. MS patients with concomitant systemic infections, earlier onset, and greater disease activity are more likely to have seizures, whereas factors such as greater MS severity, the presence of status epilepticus, and cortical damage indicate a greater risk of developing epilepsy. In MOGAD, cerebral cortical encephalitis and acute disseminated encephalomyelitis (ADEM)-like phenotypes (predominately ADEM and multiphasic disseminated encephalomyelitis) indicate a greater seizure risk. Multiple relapses with ADEM-like phenotypes predict epilepsy in pediatrics with MOGAD. Pathophysiologically, acute symptomatic seizures in MS are associated with neuronal hyperexcitability secondary to inflammation and demyelination. Chronic epilepsy in MS is largely due to gliosis, neuronal dysfunction, and synaptic abnormalities. The mainstay of treatment for seizures secondary to MS/AQP4-NMOSD/MOGAD consists of immunotherapy along with antiseizure medications. This critical review discusses the most-updated evidence on epidemiology, clinical correlates, and inflammatory mechanisms underlying seizures and epilepsy in MS/AQP4-NMOSD/MOGAD. Treatment cautions including drug-drug interactions and the impact of treatments on the diseases are outlined. We also highlight pitfalls and challenges in managing such patients and future research perspectives to address unsolved questions.

Peripheral neuropathies, especially those with atypical features, remain a diagnostic challenge. In this case, a 60-year-old patient presented with acute-onset weakness starting in the right hand then sequentially involving the left leg, left hand, and right leg over 5 days. The asymmetric weakness was accompanied by persistent fever and elevated inflammatory markers. Subsequent development of rashes combined with careful review of the history led us to the final diagnosis and targeted treatment. This case highlights clinical pattern recognition with the help of electrophysiologic studies in peripheral neuropathies, which provide shortcuts to narrow the differential diagnosis. We also illustrate the important pitfalls from history taking to ancillary testing in diagnosing the rare but treatable cause of peripheral neuropathy (eFigure 1,links.lww.com/WNL/C541).

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.

We aimed to evaluate the assessment and management of epilepsy with anxiety and depression, and their clinical practice based on a survey.A cross-sectional survey of epilepsy health professionals was undertaken in Zhejiang Province using the modified International League Against Epilepsy (ILAE) Psychology Task Force questionnaire. We recorded the characteristics of participants and the practice of screening, referral, and treatment for depression and anxiety disorders. A total of 146 participants joined in the survey, of which 76.0% were neurologists, and 69 participants were the member of the Zhejiang Association Against Epilepsy (ZAAE).This survey revealed that almost all participants (87.7%) agreed that screening for depression and anxiety in patients with epilepsy (PWEs) was very important; however, the frequency of screening was very low (41.1% of participants screened less than 10% of patients, and 34.2% participants screened between 10% and 30% of patients). A higher frequency of screening was reported in the member group and compared with that in the non-member group (P = 0.025). The main barrier to screening was the lack of time during clinic visits: 81.5% participants included screening questions as part of their clinical review. When anxiety/depression was diagnosed, the next step should be to refer patients to a psychiatrist (78.1%). No standardized procedures and lack of mental health specialists trained to assess and/or manage PWEs, were the main barriers to follow-up assessment and management. Lack of appropriately trained mental health specialists was also the main barrier to psychological treatment for depression and anxiety.This survey highlighted that epilepsy healthcare professionals in Zhejiang province agreed on the importance of screening for psychiatric comorbidities in PWEs; however, the screening and management were actually insufficient. Certain barriers to screening, referral, and treatment were presented and improvements were recommended.

The Kelch-like protein 11 antibody-associated paraneoplastic neurological syndrome (KLHL 11-PNS) was first identified in 2019. This novel antibody, targeting the intracellular KLHL 11 antigen, can be detected in serum and cerebrospinal fluid using tissue-based and cell-based assays. It is thought to be a biomarker for a T-cell autoimmunity response. The most likely immunopathogenesis of KLHL 11-PNS appears to be linked to cytotoxic T-cell-mediated neuronal injury and loss. Patients have adult-male predilection, rhombencephalitis (brainstem and / or cerebellar involvement), and a robust oncological correlation with testicular germ cell tumors (predominately seminoma). Brain magnetic resonance imaging demonstrated T2 / fluid-attenuated inversion recovery hyperintensities and atrophy of the temporal lobe, cerebellum, and brainstem. Most patients responded poorly to immunotherapy and oncotherapy and thus had a poor long-term prognosis. We review the literature and provide an update of current knowledge regarding KLHL 11-PNS, including epidemiology, underlying mechanism, clinical presentations, paraclinical and oncological findings, diagnostic workup, and treatment approaches.

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

Background: 4-Hydroxybenzyl alcohol (4-HBA), one of the major active phenolic constituents of Gastrodia elata Blume, has been shown to be a neuroprotective agent. Previous studies have demonstrated the anticonvulsive effect of Gastrodia elata, while no studies have investigated the antiepileptogenic effect of 4-HBA. Methods: We examined the effect of 4-HBA (25 mg/kg, 50 mg/kg or 100 mg/kg i.p.) on amygdaloid kindled seizures. Fully kindled seizures were achieved by daily electrical stimulation of the amygdala. Seizure stage and afterdischarge duration (ADD) were assessed daily. The effects of 4-HBA on neuronal loss were observed before kindling and 20 days after kindling by Nissl staining. Results: We found that treatment with 50 mg/kg 4-HBA delayed seizure stage progression, and 25 mg/kg and 50 mg/kg 4-HBA shortened the corresponding ADD. Rats pretreated with 50 mg/kg 4-HBA needed more kindling stimulations to reach stages 4-5 and exhibited more cumulative ADD to stage 5. Pretreatment with 50 mg/kg 4-HBA shortened the number of days in stages 4–5 and decreased the incidence of generalized seizures. Pretreatment with 4-HBA showed no effect on fully kindled rats. Moreover, 50 mg/kg 4-HBA attenuated neuronal loss in the ipsilateral CA1 and the bilateral entorhinal cortex. Conclusion: Our data suggests that 4-HBA can protect against epileptogenesis by preventing the after-discharge propagation in amygdaloid kindled seizures. In addition, the anti-epileptogenic activity may be related to the neuroprotective function of 4-HBA in the late stage of kindling.

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.

Radiation-induced necrosis is commonly seen after radiotherapy for nasopharyngeal carcinoma (NPC), but a post-irradiation brain abscess is rarely encountered and easily overlooked, which may lead to a dismal outcome. We describe two Chinese men with cerebral herniation caused by temporal lobe abscess within a radio-necrotic lesion presenting only with headache and neurological defects. Cranial magnetic resonance imaging (MRI) or computed tomography (CT) showed cystic lesions in the temporal lobe with a severe mass effect. Both patients had brain herniation before emergency operations. Therefore, our findings suggest that a post-irradiation brain abscess may insidiously develop into disastrous herniation, and regular multi-modality neuroimaging follow-up should be carried out to help avoid this situation.

To evaluate the small fiber function in patients with type 2 diabetes mellitus of the early stage by measuring the sensory threshold with the quantitative temperature testing technology.Twenty cases of patients with type 2 diabetes with no neurological deficit (DM group) and twenty age and sex-matched healthy controls underwent the detecting of cold sensory threshold (CST), warm sensory threshold (WST), cold pain threshold (CPT), heat pain threshold (HPT) in both inside of their hands.There was no significant difference in CST, WST, CPT and HPT between left and right inside of hand of the same sample among all the testers. But the four kinds of threshold showed significant difference in the right inside of hand between patients and healthy people ( P0.05). In addition, the CST and WST differed significantly in the left inside of hand between the patients and healthy controls while the CPT and HPT showed no significant difference in the left inside of hand between them. Patients group and control group with CST and WST on the left side of the comparison difference was statistically significant (P0.05).Quantitative analysis of temperature sense threshold can not only reflect increase of the pain threshold value, also can reflect its decrease, i. e. hyperalgesia, which may help to diagnose small fibrous peripheral neuropathy recognition, especially in early diabetic peripheral neuropathy.

Carnosine (beta-alanyl-l-histidine) has been characterized as a putative neurotransmitter. However, so far, understanding of the role of carnosine in the brain is very limited. The objective of this study was to examine the effects of carnosine on the development of pentylenetetrazol (PTZ) kindling seizures and protection against the PTZ kindled seizures in rats. Chemical kindling was elicited by repeated intraperitoneal injection of PTZ (35 mg/kg) once every 48 h until the occurrence of Stage 4-5 seizures, and the seizure activity of kindling was recorded for 30 min. In an acute PTZ challenge study, 60 mg/kg PTZ was used to induce kindled seizure. Injection of carnosine (200, 500 mg/kg, i.p.) significantly decreased seizure stage, and prolonged the latencies for myoclonic jerks, in a dose- and time-dependent manner. In the seizure development process, 500 mg/kg carnosine also significantly delayed the onset of PTZ kindled seizures. In addition, carnosine significantly reversed decreased histamine levels induced by PTZ kindled seizure in the hippocampus. These results indicate that carnosine can protect against PTZ-induced seizures in both the development of kindling and the challenge process in rats. The results suggest that carnosine might be an endogenous anticonvulsant factor in the brain and can be used as a new antiepileptic drug in future.

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.

Histamine H(3) receptor antagonists have been considered as potential drugs to treat central nervous system diseases. However, whether these drugs can inhibit epileptogenesis remains unclear. This study aimed to investigate the effects of thioperamide, a selective and potent histamine H(3) receptor antagonist, on the seizure development and memory impairment induced by pentylenetetrazole (PTZ)-kindling epilepsy in rats.Chemical kindling was elicited by repeated intraperitoneal (ip) injections of a subconvulsant dose of PTZ (35 mg/kg) once every 48 hours for 12 times, and seizure activity of kindling was recorded for 30 minutes. Control rats were ip injected with saline instead of PTZ. Morris water maze was used to evaluate the spatial memory. Phosphorylated cyclic adenosine monophosphate response element binding protein (p-CREB) was tested by Western blotting in hippocampus.Intracerebroventricular (icv) injections with thioperamide (10 µg, 20 µg) 30 minutes before every PTZ injections, significantly prolonged the onset of PTZ-kindling and inhibited the seizure stages. PTZ-kindling seizures led to the impairment of spatial memory in rats, and thioperamide ameliorated the impairment of spatial learning and memory. Compared to non-kindling rats, there was a significant decrease in p-CREB level in hippocampus of the PTZ-kindling rats, which was reversed by thioperamide.Thioperamide plays a protective role in seizure development and cognitive impairment of PTZ-induced kindling in rats. The protection of thioperamide in cognitive impairment is possibly associated with the enhancement of CREB-dependent transcription.

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 evaluate the effects of administration of hyperbaric oxygenation(HBO) when initiated at different time after acute transient ischemia. Apoptosis in the ischemic penumbra was further investigated to search for the possible mechanism.The male SD rats were randomly assigned to the following groups: control, HBO therapy initiated 3 h after ischemia, HBO therapy initiated 6 h after ischemia, HBO therapy initiated 12 h after ischemia. All animals were subjected to 90 min intraluminal middle cerebral artery occlusion (MCAO) with the regional cerebral blood flow monitored in vivo by laser Doppler flowmetry. HBO treatment was performed in a pressure chamber with 100% O2, 3 arm for 1 h. Neurological deficits and infarct volumes were assessed at 24 hours after ischemia. The immunohistochemical changes of apoptosis in the penumbra were evaluated by detecting the expression of cleaved Caspase-3, cleaved Caspase-9, Bcl-2, Bax and TUNEL staining.HBO therapy initiated at 3 and 6 hours after ischemia significantly improved the neurological function and reduced infarct volume. Meanwhile, it increased the expression of Bcl-2 protein and decreased the expression of activated Caspase-3, activated Caspase-9 and TUNEL-positive cells. However, HBO therapy administrated 12 hours after ischemia aggravated the neurological deficits and enlarged infarct volume, while it showed no significant reduction of apoptotic change compared with control.There is a therapeutic window for the use of HBO in acute transient cerebral ischemia in rats. HBO-treatment is highly effective in reducing infarct volume when initiated up to 6h after the onset of ischemia. Inhibition of apoptotic cell death in the penumbra appears to be the underlying protective effect of early therapy.

To observe the intracellular calcium ion spatio-temporal and dynamic changes in the hippocampal neuronal culture model of epilepsy induced by low magnesium ion medium, and to explore the relationship between calcium ion and epilepsy.Applying both laser scanning confocal microscope and patch clamp to timely observe the changes of [Ca2+]i and electrophysiological in the hippocampal neuronal culture model of epilepsy, and the influence of NMDA receptor-gated channels retarder and non-NMDA receptor-gated channels retarder.After the hippocampal nerve cell broken into epileptiform discharges, [(Ca2+]i rapidly ascended to (620 +/- 70) nmol/L, NMIDA acceptor retarder (MK-801, 10 micromol/L) and non-NMDA acceptor retarder (NBQX, 10 micromol/L) reduced [Ca2+]i ascendance. Recovery of the elevated [Ca2+]i was obviously delay, after 90 min and 150 min epileptiform discharges, it took (114.8 +/- 5.2) min and (135.0 +/- 22.7) min (P0.05) respectively.In vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons

Hydrocephalus is a common medical condition characterized by abnormalities in the secretion,circulation or resorption of cerebrospinal fluid (CSF), resulting in ventricular dilatation. The pathogenetic mechanism for the hydrocephalus is attributed to: the overproduction of CSF by the choroid plexus; the defect in CSF absorption and obstruction of CSF flow in the cerebral ventricles. However, the underlying etiology is poorly understood. With the development of genetic engineering, a growing body of evidence indicates that genetic factors play an essential role in the pathogenesis of hydrocephalus. It is the aim of this review to summarize these findings.

To investigate whether the selective AT1 receptor antagonist irbesartan exerts neuroprotective effect on focal cerebral ischemia in normotensive rats.Cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion, with the monitoring of laser Doppler flowmetry. To avoid the interaction with peripheral AT1 receptors, irbesartan was infused intracerebroventricularly (ICV) at a dose which effectively inhibited brain- but not vascular AT1 receptors. Neurological status was evaluated daily after MCAO. Rats were killed and brain samples were collected for the measurement of infarct size and immunohistochemical evaluation of apoptosis by deoxynucleotidyltransferase-mediated biotinylated UTP nick end labeling (TUNEL) and expression of activated Caspase-3 and the cleavage fragment of poly (ADP-ribose) polymerase (PARP).Treatment with irbesartan improved significantly the neurobehavioral functions after cerebral ischemia. The infarct size was reduced about 42% on day 7 after MCAO (P0.05). Meanwhile,irbesartan treatment significantly decreased the number of TUNEL-positive cells in the penumbra. The expression of activated Caspase-3 and the downstream cleavage fragment of poly (ADP-ribose) polymerase in the penumbra were also inhibited by irbesartan therapy on day 3 after transient cerebral ischemia.Angiotensin AT1 receptor antagonist exhibits neuroprotection against transient cerebral ischemia in the brain. The neuroprotective effects in ischemic tissue may be associated with its inhibition of apoptotic cell death in the penumbra.

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.