Variaciones de los plexos coroideos y las barreras cerebrales en la hipertensión arterial y el envejecimiento

IntroductionThe choroid plexuses, blood vessels, and brain barriers are closely related both in terms of morphology and function. Hypertension causes changes in cerebral blood flow and in small vessels and capillaries of the brain. This review studies the effects of high blood pressure (HBP) on the choroid plexuses and brain barriers.DevelopmentThe choroid plexuses (ChP) are structures located in the cerebral ventricles, and are highly conserved both phylogenetically and ontogenetically. The ChPs develop during embryogenesis, forming a functional barrier during the first weeks of gestation. They are composed of highly vascularised epithelial tissue covered by microvilli, and their main function is cerebrospinal fluid (CSF) production. The central nervous system (CNS) is protected by the blood-brain barrier (BBB) and the blood–CSF barrier (BCSFB). While the BBB is formed by endothelial cells of the microvasculature of the CNS, the BCSFB is formed by epithelial cells of the choroid plexuses. Chronic hypertension induces vascular remodelling. This prevents hyperperfusion at HBPs, but increases the risk of ischaemia at low blood pressures. In normotensive individuals, in contrast, cerebral circulation is self-regulated, blood flow remains constant, and the integrity of the BBB is preserved.ConclusionsHBP induces changes in the choroid plexuses that affect the stroma, blood vessels, and CSF production. HBP also exacerbates age-related ChP dysfunction and causes alterations in the brain barriers, which are more marked in the BCSFB than in the BBB. Brain barrier damage may be determined by quantifying blood S-100β and TTRm levels.     

Endovascular deep brain stimulation: Investigating the relationship between vascular structures and deep brain stimulation targets

BackgroundEndovascular delivery of current using ‘stentrodes’ – electrode bearing stents – constitutes a potential alternative to conventional deep brain stimulation (DBS). The precise neuroanatomical relationships between DBS targets and the vascular system, however, are poorly characterized to date.ObjectiveTo establish the relationships between cerebrovascular system and DBS targets and investigate the feasibility of endovascular stimulation as an alternative to DBS.MethodsNeuroanatomical targets as employed during deep brain stimulation (anterior limb of the internal capsule, dentatorubrothalamic tract, fornix, globus pallidus pars interna, medial forebrain bundle, nucleus accumbens, pedunculopontine nucleus, subcallosal cingulate cortex, subthalamic nucleus, and ventral intermediate nucleus) were superimposed onto probabilistic vascular atlases obtained from 42 healthy individuals. Euclidian distances between targets and associated vessels were measured. To determine the electrical currents necessary to encapsulate the predefined neurosurgical targets and identify potentially side-effect inducing substrates, a preliminary volume of tissue activated (VTA) analysis was performed.ResultsSix out of ten DBS targets were deemed suitable for endovascular stimulation: medial forebrain bundle (vascular site: P1 segment of posterior cerebral artery), nucleus accumbens (vascular site: A1 segment of anterior cerebral artery), dentatorubrothalamic tract (vascular site: s2 segment of superior cerebellar artery), fornix (vascular site: internal cerebral vein), pedunculopontine nucleus (vascular site: lateral mesencephalic vein), and subcallosal cingulate cortex (vascular site: A2 segment of anterior cerebral artery). While VTAs effectively encapsulated mfb and NA at current thresholds of 3.5 V and 4.5 V respectively, incremental amplitude increases were required to effectively cover fornix, PPN and SCC target (mean voltage: 8.2 ± 4.8 V, range: 3.0–17.0 V). The side-effect profile associated with endovascular stimulation seems to be comparable to conventional lead implantation. Tailoring of targets towards vascular sites, however, may allow to reduce adverse effects, while maintaining the efficacy of neural entrainment within the target tissue.ConclusionsWhile several challenges remain at present, endovascular stimulation of select DBS targets seems feasible offering novel and exciting opportunities in the neuromodulation armamentarium.     

临床实习生对患者隐私的认知及保护情况调查

目的了解临床实习生对患者隐私的认知以及在临床实践中对患者隐私的保护情况,探讨患者隐私教育及临床实习中存在的问题,分析成因并提出加强患者隐私教育、引导实习生合理获取患者隐私的具体建议,以改善临床医学教育过程中存在的薄弱环节。方法随机选取海军军医大学等5所医学院校的572名临床医学实习生为调查对象,发放调查问卷。主要内容包括实习生隐私教育评分、对于隐私保护法及隐私具体范围的知晓情况、临床实践中是否泄露隐私、隐私与临床诊疗等方面,调查结果采用SPSS 21.0软件进行分析。结果27.6%实习生曾发生过泄露患者隐私的情况,58.9%实习生不了解隐私相关法律法规及隐私具体范围,95.4%实习生认为出于诊疗目的而获取患者隐私信息很有必要,但仍有56.6%实习生曾回避涉及患者隐私的医疗活动。结论临床医学实习生的教育中患者隐私教育相对欠缺并有待进一步加强。实习生应当自觉保护患者隐私,维护患者利益,并树立对于患者隐私的合理认知,从患者隐私中提取有价值的信息。     

1 H-MRS对低级别和高级别脑胶质瘤鉴别诊断的作用及病理级别相关性的研究

目的 分析脑胶质瘤的氢质子磁共振波谱（proton magnetic resonance spectroscopy，^1H—MRS）表现及其临床意义；探讨脑胶质瘤的^1H—MRS特点与其病理级别相关性。资料与方法 搜集经临床手术、病理证实的脑胶质瘤36例，按照WHO诊断标准分成两组：低级别脑胶质瘤组、高级别脑胶质瘤组。所有患者在术前行^1H—MRS检查。均在MR非增强成像的基础上获得。使用Siemens Sonata 1．5T超导磁共振扫描仪，多体素扫描，点分辨表面线圈法，检测不同区域代谢物变化。结果 脑胶质瘤的^1H—MRS表现：肌酸（Cr）轻度下降，N-乙酰天门冬氨酸（NAA）显著下降。胆碱（Cho）显著增高。低级别、高级别脑胶质瘤的肿瘤组织分别和对侧正常脑组织的NAA／Cr、Cho／Cr、NAA／Cho比值存在非常显著性差异（P〈0．01）；低级别脑胶质瘤和高级别脑胶质瘤的肿瘤组织的NAA／Cr、Cho／Cr、NAA／Cho比值存在显著性差异（P〈0．05）。脑胶质瘤的NAA／Cho、Cho／Cr、NAA／Cr比值与病理级别相关，其中NAA／Cho和Cho／cr比值反映肿瘤级别较稳定；NAA／Cr、NAA／Cho比值存在负相关关系（相关系数rs分别为-0．663，-0．851），Cho／Cr比值存在正相关关系（相关系数rs为0．858）。结论 ^1H—MRS与MRI相结合能提高脑胶质瘤术前诊断的准确性。^1H-MRS可评价脑胶质瘤的分级，反映脑胶质瘤代谢特性以及肿瘤生长潜能。     

脑静脉畸形的MRI表现及其诊断价值

目的 探讨脑静脉畸形的MRI表现，评价各成像序列的诊断价值。资料与方法 搜集经临床手术证实的脑静脉畸形8例进行回顾性分析，所有患者均进行了常规MRI平扫及3D-MOTSA MRA检查。6例行Gd-DTPA增强T1WI，其中3例行3D-MOTSA增强MRA检查。结果 小脑4例，额叶、顶叶、枕叶共4例。5例MRI平扫引流静脉为长T1短T2流空信号，3例呈长T1低信号、长T2高信号。扩张的髓静脉为网状及条状长T1低信号、长T2高信号，增强扫描呈“海蛇头”样改变，即多条髓静脉呈辐射状汇入粗大的引流静脉。3D-MOTSA MRA检查显示部分引流静脉，髓静脉显示较少。3D-MOTSA增强MRA检查引流静脉全程显示，髓静脉显示数目多。结论 MRI能明确诊断脑静脉畸形的合并症，弥补脑血管造影的不足，3D-MOTSA增强MRA检查可取代脑血管造影。     

重型颅脑损伤的手术治疗

目的探讨重型颅脑损伤梯度减压的手术方法对预防术中脑膨出、降低死亡率及致残率的效果。方法对100例重型颅脑损伤患者采用分次减压手术方式及去骨瓣后，硬膜与颞肌筋膜瓣减张缝闭硬膜切口方法。结果40例脑肿胀患者术中脑嘭出6例占15．0％，死亡19例占47．5％；60例脑内血肿病人未发生脑膨出，死亡12例占20％。结论脑外伤后脑血管调节麻痹及血肿压迫继发脑水肿易造成脑膨出.术中分次减压降低了骨窗部位脑组织的顺应性，从而降低了局部的压力梯度，避免脑血管急性扩张，能有效防止脑膨出，降低死亡率及致残率。     

A case of acute heart failure associated with Guillain-Barré syndrome

Abstract Guillain-Barré syndrome (GBS) is a disease of the peripheral nervous system, which is caused by aberrant immune responses directed against some components of peripheral nerves. GBS is rarely accompanied by cardiovascular involvement. We describe a case of acute neuropathy complicated by sudden heart failure and left ventricular dysfunction which had a presumably neurogenic origin. Pathogenesis of acute heart failure is probably due to transitorial stunned myocardium and neurogenic cardiac injury. We show a rare case of transitorial and acute cardiac dysfunction by echocardiography and laboratory markers of heart failure.     

深低温对全脑缺血性损伤的保护作用

国际上把低温划分为轻度低温(33～35℃),中度低温 (28～32℃),深度低温(17～27℃)和超深度低温(2～16℃)。低温已经被大量动物试验和临床实践证实具有脑保护作用,但同时也存在心律失常,凝血功能障碍,免疫抑制等全身多系统副作用,产且温度越低,副作用越明显。日前国内外已经有大量的试验证实深低温对全脑缺血的脑保护作用,它能明显增加脑组织对缺血的耐受性,本文将就深低温对全脑缺血性损