依达拉奉联合奥扎格雷钠治疗急性脑梗死的临床分析

目的观察依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效和安全性。方法36例急性脑梗死患者给予依达拉奉和奥扎格雷钠,并与应用奥扎格雷钠和三七总甙注射液治疗的34例患者进行比较。结果治疗后依达拉奉组和三七总甙组ESS评分均有改善(P<0.05),但依达拉奉组改善更明显,且与三七总甙组有显著性差异(P<0.05)。结论依达拉奉联合奥扎格雷钠治疗急性脑梗死能有效改善神经功能,安全性高。     

依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效观察

目的研究依达拉奉、奥扎格雷钠联合应用治疗急性脑梗死的临床疗效。方法选择120例急性脑梗死患者,随机分为对照组60例和治疗组60例。对照组应用红花,治疗组依达拉奉、奥扎格雷钠联合应用,2组其他内科治疗相同。结果14d和30d评定神经功能缺损的有效率对照组分别为16.7%和28.3%,依达拉奉、奥扎格雷钠联合治疗组40.0%和53.3%,2组比较有显著性差异(P=0.041和P=0.030);14d和30d日常生活能力的有效率,对照组分别为20.0%和40.0%,依达拉奉、奥扎格雷钠联合治疗组分别为43.3%和76.7%,2组比较差异有显著性(P=0.033和P=0.019)。结论依达拉奉联合奥扎格雷钠能有效改善急性期脑梗死患者近期的神经功能缺损评分和日常生活能力。     

依达拉奉联合奥扎格雷钠治疗进展性缺血性脑卒中疗效观察

目的探讨依达拉奉联合奥扎格雷钠治疗进展性缺血性脑卒中的疗效。方法将88例进展性缺血性脑卒中患者随机分为治疗组和对照组,治疗组应用依达拉奉联合奥扎格雷钠治疗,对照组应用奥扎格雷钠,其余常规抗血小板治疗及辅助治疗均相同。结果分别在治疗前、治疗后7、14、30d,评估神经功能缺损程度和有效率:与治疗前比较,2组神经功能缺损评分均降低,但治疗组降低更明显,治疗7、14、30d后治疗组总有效率明显高于对照组。结论依达拉奉联合奥扎格雷钠治疗进展性缺血性脑卒中疗效显著。     

奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效观察

目的：观察奥扎格雷钠联合依达拉奉治疗急性脑梗死的临床疗效。方法126例急性脑梗死患者随机分为治疗组63例和对照组63例,治疗组应用奥扎格雷钠与依达拉奉联合治疗,对照组应用奥扎格雷钠治疗,比较2组疗效。结果治疗组总有效率与基本痊愈率均高于对照组,差异有统计学意义（ P＜0.05）。结论奥扎格雷钠联合依达拉奉治疗急性脑梗死效果显著,疗效安全,值得临床推广应用。     

依达拉奉联合奥扎格雷钠治疗老年糖尿病并发急性脑梗死临床观察

目的评价依达拉奉联合奥扎格雷钠治疗老年糖尿病患者急性脑梗死的疗效和安全性。方法 64例老年急性脑梗死患者,以往确诊2型糖尿病,随机分为依达拉奉联合奥扎格雷钠治疗组和对照组,分别在治疗前,治疗后1、2、3周,采用日常生活能力（ADL）量表、欧洲卒中评分（ESS）等神经心理分析工具对患者的疗效进行评价,并观察有无出血或转氨酶升高等不良反应,进行安全性评估。结果依达拉奉联合奥扎格雷钠治疗组的ESS及ADL评分较对照组均有明显改善（P〈0.05分别）。在研究期间,1例患者出现轻度转氨酶升高,不良事件发生率为3.1%。依达拉奉的安全性和依从性良好。结论依达拉奉联合奥扎格雷钠治疗老年糖尿病患者急性脑梗死安全有效。     

依达拉奉联合奥扎格雷钠治疗急性脑梗死疗效观察

目的研究依达拉奉联合奥扎格雷治疗急性脑梗死的效果。方法将我院2009年住院的90例急性脑梗死患者随机分为3组,分别采用依达拉奉、奥扎格雷及依达拉奉联合奥扎格雷治疗。结果单用依达拉奉组有效率73.3%,单用奥扎格雷钠组有效率70.0%,联合治疗组有效率86.7%。联合治疗组总有效率分别高于奥扎格雷组和依达拉奉组,差异均有统计学意义（P〈0.05）,依达拉奉组与奥扎格雷钠组比较差异无统计学意义（P〉0.05）。结论依达拉奉联合奥扎格雷治疗急性脑梗死效果好,值得临床推广应用。     

依达拉奉联合奥扎格雷钠治疗2型糖尿病并发急性脑梗死疗效

目的探讨依达拉奉联合奥扎格雷钠治疗2型糖尿病并发急性脑梗死的有效性及安全性。方法选取我院收治的52例2型糖尿病并发急性脑梗死患者,分为单一组(n=26)和联合组(n=26),单一组单纯使用奥扎格雷钠治疗,联合组应用依达拉奉和奥扎格雷钠治疗,比较2组治疗效果及不良反应发生情况。结果联合组神经功能缺损评分、日常生活活动能力评分明显优于单一组(P0.05);联合组有效率为88.46%,明显高于单一组的73.08%,差异有统计学意义(P0.05);2组不良反应率比较,差异无统计学意义(P0.05)。结论依达拉奉联合奥扎格雷钠治疗2型糖尿病并发急性脑梗死具有一定的有效性和安全性,可促进患者神经功能康复和提高生活质量,值得推广应用。     

依达拉奉联合奥扎格雷钠治疗急性脑梗死的疗效观察

目的 探讨依达拉奉联合奥扎格雷钠治疗急性脑梗死的有效性和安全性.方法 将90例急性脑梗死患者随机分为2组,治疗组45例,常规治疗基础上应用依达拉奉30mg加生理盐水100ml,静滴,2次/d,奥扎格雷钠80mg加生理盐水100ml,静滴,2次/d.对照组45例,常规治疗基础上只应用奥扎格雷钠80mg加生理盐水100ml,静滴,2次/d.2周后行疗效评定.结果 治疗组有效率91%,对照组有效率80%.结论 依达拉奉联合奥扎格雷钠治疗急性脑梗死疗效肯定,有效改善急性脑梗死的神经功能缺失.     

奥扎格雷钠和依达拉奉联合治疗急性脑梗死疗效观察

目的探讨奥扎格雷钠联合依达拉奉治疗急性脑梗死的疗效。方法将80例急性进展型脑梗死患者随机分为治疗组(40例)和对照组(40例)。对照组应用低分子右旋糖酐、复方丹参液、胞二磷胆碱治疗。治疗组在对照组基础上加用奥扎格雷钠和依达拉奉治疗。2组于治疗前及治疗后3个月时进行神经功能缺损评分、疗效评定和生活能力评定。结果治疗组神经功能缺损评分下降明显优于对照组,总有效率明显高于对照组。治疗组生活能力评定显著优于对照组。结论奥扎格雷钠联合依达拉奉治疗急性脑梗死疗效好,无明显不良反应。     

依达拉奉联合奥扎格雷钠治疗进展性脑梗死临床观察

目的 观察依达拉奉联合奥扎格雷钠治疗进展性脑梗死的疗效和安全性.方法 符合进展性脑梗死标准的82例患者随机分为观察组42例和对照组40例.对照组患者给予常规治疗+奥扎格雷钠;观察组给予常规治疗+奥扎格雷钠+依达拉奉.2组疗程均为21 d.2组患者于治疗前后进行NIHSS神经功能缺损评分、日常生活能力(ADL)评分和hs-CRP、D-二聚体的测定.结果 治疗21 d后,观察组痊愈率和总有效率均显著高于对照组(χ2=4.0397,4.8308,P均＜0.05).在hs-CRP、D-二聚体、NIHSS评分、ADL评分四项指标方面,治疗后观察组均显著优于对照组(t=2.4486,2.5964,2.1936,7.0401,P＜0.05).结论 依达拉奉与奥扎格雷钠联合治疗进展性脑梗死有协同效果,优于奥扎格雷钠单药治疗,无明显不良反应.     

Modulation of glutamatergic synaptic transmission in the bed nucleus of the stria terminalis

Glutamate, catecholamine and neuropeptide signaling within the bed nucleus of the stria terminalis (BNST) have all been identified as key participants in anxiety-like behaviors and behaviors related to withdrawal from exposure to substances of abuse. The BNST is thought to serve as a key relay between limbic cognitive centers and reward, stress and anxiety nuclei. Human studies and animal models have demonstrated that stressors and drugs of abuse can result in long term behavioral modifications that can culminate in psychological diseases such as addiction and post-traumatic stress disorder. The ability of catecholamines and neuropeptides to influence synaptic glutamatergic transmission (stemming from cognitive centers) within the BNST may have profound consequences over these behaviors. In this review we highlight studies examining synaptic plasticity and modulation of excitatory transmission within the BNST, emphasizing how such modulation may result in alterations in anxiety and reward related behavior.     

替加环素联合药物治疗泛耐药鲍曼不动杆菌中枢神经系统感染临床观察

目的探讨替加环素(TGC)联合药物治疗泛耐药鲍曼不动杆菌(PDR-Ab)中枢神经系统感染的效果。方法选取2017-02—2020-02驻马店市第一人民医院收治的108例PDR-Ab中枢神经系统感染患者为研究对象,根据随机数表法分为TGC-头孢哌酮/舒巴坦(CPZ/SB)组(TGC-CPZ/SB组)和TGC-异帕米星(ISM)组(TGC-ISM组),比较2组患者入院后24 h内及治疗10 d炎性指标、急性生理功能与慢性健康状况Ⅱ(APACHEⅡ)评分、细菌清除率、不良反应发生情况及临床总有效率。结果治疗10 d后TGC-CPZ/SB组和TGC-ISM组白细胞数(14.33±2.16 vs 12.59±3.10)、C反应蛋白(75.85±16.27 vs 63.16±15.33)、脂多糖(15.58±4.23 vs 12.11±2.34)、降钙素原(2.26±0.77 vs 1.43±0.57)、白细胞介素-6(39.84±5.25 vs 31.42±4.29)比较差异有统计学意义(P<0.05),且均显著低于治疗前(P<0.05);治疗10 d后TGC-ISM组APACHEⅡ评分(11.57±3.28)分,显著低于TGC-CPZ/SB组的(13.66±4.25)分(P<0.05);TGC-ISM组细菌清除率(74.07%)显著高于TGC-CPZ/SB组(55.56%)(P<0.05);2组恶心呕吐、听力减退、头痛、关节痛、视力模糊等不良反应发生率比较差异无统计学意义(P>0.05);TGC-ISM组临床总有效率88.89%,显著高于TGC-CPZ/SB组的70.37%,差异有统计学意义(P<0.05)。结论TGC联合ISM方案治疗PDR-Ab中枢神经系统感染的临床疗效良好,抑炎效果更好,且安全性高。     

Heterogenous distribution of peptide-containing nerve fibres within the circular muscle layer of the human pylorus

The distribution of nerve fibres immunoreactive for vasoactive intestinal polypeptide (VIP), substance P (SP), methionine-enkephalin (ENK), calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) within the circular muscle layer was examined histochemically in the human pylorus, adjacent antrum and duodenum. Longitudinal cryostat sections of the pyloric and surrounding regions were stained by an indirect immunofluorescence method, and the total length of each type of peptidecontaining fibre per unit sectional area (µm/mm²) was measured using an image-analysing system. The narrow region of the circular muscle layer bordering the submucosa in the pylorus contained a rich supply of VIP, SP, ENK and CGRP immunoreactive fibres; VIP fibres were most prominent with less SP and ENK fibres and moderate amounts of CGRP. These peptide-containing nerve fibres were more dense than in the pyloric circular muscle, the longitudinal muscle layer and also the adjacent muscle layer. NPY-immunoreactive fibres were sparsely distributed throughout the pyloric region. These results suggest that the inner edge of the circular muscle, lying adjacent to the submucosa and densely innervated with peptidecontaining fibres, may be a characteristic feature of the human pyloric sphincter.     

Update of the original HDLS kindred: divergent clinical courses

Sundal C, Ekholm S, Nordborg C, Jönsson L, Börjesson‐Hanson A, Lindén T, Zetterberg H, Viitanen M, Andersen O. Update of the original HDLS kindred: divergent clinical courses.
Acta Neurol Scand: 2012: 126: 67–75.
© 2011 John Wiley & Sons A/S. Background – Hereditary diffuse leukoencephalopathy with spheroids (HDLS) was first identified among a Swedish kindred with 17 cases. The average age of onset was 36 years. Autopsy in four cases revealed the presence of axonal spheroids. The causative gene is unknown. Methods – We performed genealogical and longitudinal observations of the original kindred. Forty members were examined, five telephone‐interviewed, and one of the original HDLS cases from 1984 was neuropathologically examined. The clinical course was documented. The cerebrospinal fluid (CSF) findings of two recently affected cases were examined, and one of those autopsied. Results – Of those examined, two developed HDLS during our survey and 38 were healthy. Those interviewed by telephone were healthy. One had symptoms suggestive of HDLS in 1984, but autopsy during our survey showed no spheroids. This patient, two relatives healthy at our examination and one without symptoms at telephone interview had HDLS diagnoses in the 1984 report. Thus, four HDLS diagnoses were unconfirmed. The number of identified patients amounts to 15 among 75 individuals in four generations, including two recent cases who demonstrated a subacute multisystem encephalopathy in Case 1 and an insidious course in Case 2. CSF showed signs of neurodegeneration without inflammation, and autopsy verified HDLS in Case 1. Conclusions – Some HDLS cases were misdiagnosed with unspecified psychiatric diagnoses in affected relatives from the original 1984 publication. However, HDLS is an encephalopathy dominated by a frontal lobe syndrome with an inexorably progressive and fatal course, where the different symptomatology in two recent cases confirmed the existence of acute and chronic variants.     

The role of the prefrontal cortex in the development of muscle fatigue in Charcot–Marie–Tooth 1A patients

This study aimed at comparing both peripheral and central mechanisms of muscle fatigue between Charcot–Marie–Tooth 1A patients and healthy individuals during a fatiguing voluntary task by simultaneous electromyographic and electroencephalographic recordings. Six Charcot–Marie–Tooth 1A patients (3 females, 40 ± 11 years) and 6-matched healthy individuals performed four blocks of sub-maximal isometric knee extensions. At the beginning of the session and after each block, electrically-evoked maximal single-twitch, maximal voluntary contraction and surface-electromyography of the vastus lateralis muscle were measured. The movement-related-cortical potentials were averaged in early (block 1–2) and late (block 3–4) stages of fatigue. The effect of fatigue was demonstrated at peripheral level by the decline of maximal voluntary contraction, maximal twitch and surface electromyography amplitude and at central level by the larger amplitude of movement-related-cortical-potentials during late than early stage of fatiguing sub-maximal contractions. Charcot–Marie–Tooth 1A patients showed lower motor cortex activity during motor planning, with earlier onset and larger prefrontal cortex activity during the late stage of the fatiguing task than healthy controls. These data demonstrate the key role of the prefrontal cortex in the development of fatigue in Charcot–Marie–Tooth 1A patients, which may be activated as a compensatory mechanism for the low motor cortex activation, thus reflecting high awareness of movement complexity.     

Photically evoked potentials and afterpotentials recorded from the visual cortex of the unanesthetized hedgehog

Evoked potentials to visual stimuli (VEP) were recorded from the visual cortex of the enanesthetized hedgehog (Erinaceus europaeus), a primitive placental mammal with relatively little differentiation of cortex and thalamus. The VEPs consisted of several distinct positive and negative voltage deflections. Reproducibility of the response was high, as indicated from the small intrasession and intersession response variability. Rhythmic afterpotentials (AP), previously reported for higher mammals, were readily elicited. They had a lower frequency (3/sec) than APs observed in other mammals. The use of the hedgehog in electrophysiological and psychophysiological research is suggested because data obtained from this primitive placental mammal may shed light on CNS functions of higher mammals, as well as mammalian forms ‘lower’ on the evolutionary scale.     

Bisphenol A exposure disrupts the development of the locus coeruleus‐noradrenergic system in mice

It has been reported that bisphenol A (BPA), a widespread xenoestrogen employed in the production of polycarbonate plastics, affects brain development in both humans and rodents. In the present study employing mice, we examined the effects of exposure to BPA (500 μg/kg/day) during fetal and lactational periods on the development of the locus coeruleus (LC) at the age of embryonic day 18 (E18), postnatal 3 weeks (P3W), P8W and P16W. The number of tyrosine hydroxylase‐immunoreactive cells (TH‐IR cells) in females exposed to BPA was decreased, compared with the control females at P3W. At P8W, the number of TH‐IR cells in females exposed to BPA was significantly decreased, compared with the control females, whereas the number of TH‐IR cells in males exposed to BPA was significantly increased, compared with the control males, which resulted in reversed transient sexual differences in the numbers of TH‐IR cells observed in the controls at P8W. However, no significant changes were demonstrated at E18 or P16W. Next, we examined the density of the fibers containing norepinephrine transporter (NET) in the anterior cingulate cortex (ACC) and prefrontal cortex, at P3W, P8W and P16W, because NET would be beneficial in identifying the targets of the LC noradrenergic neurons. There were no significant differences shown in the density of the NET‐positive fibers, between the control and the groups exposed to BPA. These results suggested that BPA might disrupt the development of physiological sexual differences in the LC‐noradrenergic system in mice, although further studies are necessary to clarify the underlying mechanisms.     

Certoparin versus UFH to prevent venous thromboembolic events in the very elderly patient: an analysis of the CERTIFY study

Introduction

There is an exponential rise of thromboembolic risk with age because of co-morbidities, immobility and pharmacotherapy. We aimed to investigate the benefits and risks of heparin prophylaxis in very elderly patients ≥ 80 years and the type of heparin used in a subgroup analysis of the CERTIFY trial.

Patients/methods

3,239 patients were randomized to 3,000 U aXa o.d. certoparin or 5,000 IU t.i.d. unfractionated heparin (UFH) for 8-20 days.

Results

Patients ≥ 80 years (n = 1,365) were more likely to be female, had a lower mean bodyweight, were more frequently using antiplatelets and had a GFR below 30 ml/min/1.73 m² more often than patients < 80 years (n = 1,875). The combined endpoint of proximal DVT, symptomatic non-fatal PE and VTE related death was experience by 5.26% of patients ≥ 80 years versus 3.51% in younger patients (OR 1.53; 95%CI 1.05-2.21; p = 0.03). There were no significant differences in both minor (OR 1.11; 95%CI 0.75-1.62) and major (OR 2.53; 95%CI 0.93-6.86) bleeding risks. Certoparin and UFH were equally effective in reducing thromboembolic risk in either age group. The risk of any (OR 0.45; 95%CI 0.26-0.79) and minor bleeding (OR 0.42; 95%CI 0.23-0.78) was reduced with certoparin in the very elderly only. There were more adverse events in elderly patients (OR 1.26; 95%CI 1.1-1.46), but rates were otherwise comparable.

Conclusions

The analysis confirmed the increased thromboembolic risk in very elderly patients, but demonstrated no increased bleeding risk. Certoparin and UFH were equally effective and safe with a reduced risk of minor bleeding complications with certoparin in the very elderly.     

Three-layer model with absorption for conservative estimation of the maximum acoustic transmission coefficient through the human skull for transcranial ultrasound stimulation

Transcranial ultrasound stimulation (TUS) has been shown to be a safe and effective technique for non-invasive superficial and deep brain stimulation. Safe and efficient translation to humans requires estimating the acoustic attenuation of the human skull. Nevertheless, there are no international guidelines for estimating the impact of the skull bone. A tissue independent, arbitrary derating was developed by the U.S. Food and Drug Administration to take into account tissue absorption (0.3 dB/cm-MHz) for diagnostic ultrasound. However, for the case of transcranial ultrasound imaging, the FDA model does not take into account the insertion loss induced by the skull bone, nor the absorption by brain tissue. Therefore, the estimated absorption is overly conservative which could potentially limit TUS applications if the same guidelines were to be adopted. Here we propose a three-layer model including bone absorption to calculate the maximum pressure transmission through the human skull for frequencies ranging between 100 kHz and 1.5 MHz. The calculated pressure transmission decreases with the frequency and the thickness of the bone, with peaks for each thickness corresponding to a multiple of half the wavelength. The 95th percentile maximum transmission was calculated over the accessible surface of 20 human skulls for 12 typical diameters of the ultrasound beam on the skull surface, and varies between 40% and 78%. To facilitate the safe adjustment of the acoustic pressure for short ultrasound pulses, such as transcranial imaging or transcranial ultrasound stimulation, a table summarizes the maximum pressure transmission for each ultrasound beam diameter and each frequency.     

Localisation of pre- and postsynaptic cholinergic markers in the human brain

The cholinergic neurotransmission in the central nervous system plays an important role in modulating cognitive processes such as learning, memory, arousal and sleep as well as in modulating locomotor activity. Dysfunction of the central cholinergic system is involved in numerous neuropsychiatric diseases. This review will provide a synopsis on the regional localisation of cholinergic and cholinoceptive structures within the adult human brain. On the cholinergic site data based on the distribution of choline acetyltransferase-immunoreactive structures are in the focus, complemented by data from acetylcholinesterase and vesicular acetylcholine transporter studies. On the cholinoceptive site, the distribution and localisation of receptors that transduce the acetylcholine message, i.e. the muscarinic and the nicotinic acetylcholine receptors is summarized. In addition to these data obtained on post mortem brain an overview of markers which allow for the in vivo monitoring of the cholinergic system in the brain is given. The detailed knowledge on the distribution and localisation of cholinergic markers in human brain will provide further information on the cholinergic circuits of neurotransmission — a prerequisite for the interpretation of in vivo imaging data and the development of selective diagnostic and therapeutic compounds.