The association of cortical dysplasia and anterior horn arthrogryposis: a case report

We describe a 21-year-old woman with neurogenic congenital contractures (arthrogryposis) of the lower limbs, normal intelligence, hyper-reflexia and partial epilepsy. MRI revealed bilateral opercular (perisylvian) cortical dysplasia with infolding of cerebral cortex, a focal neuroblast migrational disorder. This type of migrational disorder is known to have a prenatal onset after the 20th fetal week, whereas the anterior horn cell degeneration responsible of neurogenic arthrogryposis originates at 12–14 weeks of gestation. A prenatal viral infection along the neural axis during both these gestational periods or a genetic defect could be responsible for both lesions in this case.     

Possible Relation of Hemin-Induced HO-1 Expression to the Upregulation of VEGF and BDNF mRNA Levels in Rat C6 Glioma Cells

Glial cells are generally considered to contribute to retaining the integrity of neural function through the protection of neuronal cells against neurodegenerative insults and also expected to play a potential role in the protection of cerebrovascular systems from various toxic insults of hemorrhaged blood, thus proposing a possible implication of glial cells in the recovery of brain function from the damage caused by cerebral hemorrhage. Based on this hypothetical idea, the direct effect of hemin on the expression of genes encoding heme oxygenase-1 (HO-1), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF) in glial cells was examined using rat C6 glioma cells as an in vitro model system. Hemin elevated both HO-1 and VEGF mRNA levels in the glioma cells at the concentration causing no critical damage to the cells, and the elevation of BDNF mRNA levels was also observed by exposing the cells to hemin under the same conditions. Furthermore, the elevation of VEGF and BDNF mRNA levels induced by hemin was blocked by pretreatment of the cells with the agents inhibiting not only HO-1 gene expression but also its enzymatic activity. These pharmacological studies indicate that hemin can induce the enhancement of VEGF and BDNF gene expression probably through the mechanism mediated by HO-1 activity in the glioma cells, proposing the possibility that glial cells are capable of contributing to the recovery of brain function from the damage caused by cerebral hemorrhage through the production of neurogenic and angiogenic factors.     

重症手足口病神经源性肺水肿的诊治

重症手足口病可并发神经源性肺水肿,严重者导致死亡.应早期识别神经系统表现,密切关注交感神经亢进表现及神经源性肺水肿的高危因素,监测呼吸频率,及时发现呼吸困难、紫绀和肺部啰音等危重症前兆或表现.严格控制液体负荷、降低颅内压、抑制交感神经功能、保护心脏功能、积极呼吸支持、加强呼吸道管理是治疗神经源性肺水肿的关键.     

小趾展肌神经与神经源性跟痛症关系的解剖学基础

目的　探讨小趾展肌神经的局部解剖特点及其与神经源性跟痛症的关系,为临床诊断治疗提供解剖学依据。 方法　32侧防腐成人尸体下肢标本,解剖观察小趾展肌神经的起源、分支、走行和分布特点。 结果　小趾展肌神经81.25%起源于足底外侧神经,起点59.38%位于后上象限;起点与参考线的垂直深度,左侧（10.81±0.96）mm,右侧（10.24±1.10）mm;小趾展肌神经发出1～3支骨膜支到达跟骨结节内侧突的骨膜;小趾展肌神经与跟骨结节内侧突该的水平距离左侧（19.95±1.82）mm,右侧（20.89±2.48）　mm 。 结论　小趾展肌神经行经　展肌和足底方肌内侧头之间,跟骨结节内侧突前可能被卡压,卡压或病变（特别是骨膜支）可能与足底腱膜炎发生有关;跟骨骨刺不一定会造成神经源性跟痛症。     

Ultrasound of oral and masticatory muscles: Why every neuromuscular swallow team should have an ultrasound machine

Patients with neuromuscular disorders often present with swallowing difficulties due to oral phase problems and pharyngeal residue after swallow. It is important to assess the underlying pathology and cause of the swallowing disturbance in this patient group, such as dystrophic changes in oral and masticatory muscles. This allows for more patient‐tailored recommendations, for example optimal compensation strategies to maintain function for longer. Ultrasound can show structural changes caused by dystrophy or denervation of muscles, detect involuntary movements such as fasciculations, and provide dynamic video images of tongue motion during swallowing attempts. This article, based on the authors' extensive experience with ultrasound in neuromuscular disease, explains the concepts of oral muscle ultrasound and its proven value in assessing neuromuscular mastication and swallowing problems. As a patient‐friendly and portable technique, we advocate its use as a standard tool for analyzing neuromuscular dysphagia. Clin. Anat. 30:183–193, 2017. © 2017 Wiley Periodicals, Inc.     

神经原性血浆外渗法测量皮肤的神经再支配

目的：观察皮瓣埋入神经后不同时间获得神经再支配的范围。方法：兔耳大神经埋入转移到耳背的颈肩部失神经皮瓣,用神经原性血浆外渗和图像分析法测量皮瓣的染色面积。结果：３．０ｃｍ直径圆形皮瓣下埋入１．５ｃｍ长神经,术后１个月为１０３．５ｍｍ＾２,３个月为３１２．３ｍｍ＾２,５个月为４５９．０ｍｍ＾２,８个月为５８５．５ｍｍ＾２,分别占皮瓣总面积的１６．８％、５０．７％、７４．６％和９５．０％。结论：兔３．     

Endostitch‐assisted endoscopic Zenker's diverticulostomy: a tried approach for difficult cases

The aim was to describe a tried approach to endoscopic Zenker's diverticulostomy, especially in those patients with unfavorable anatomy or smaller pouches who may otherwise be relegated to open repair. The study design was a retrospective case series The setting was an urban, tertiary care university medical center There were seven patients, both inpatient and outpatient, with chief complaints of dysphagia. All had a documented Zenker's diverticulum (ZD) on barium swallow. All of the patients were deemed by the primary surgeon to have some anatomic factor that limited exposure of the diverticulum. The patients underwent Endostitch‐assisted endoscopic Zenker's diverticulostomy. Records were retrospectively reviewed, including preoperative and postoperative swallowing status, radiographic findings, operative findings, and follow‐up results. Seven patients were reviewed, each of whom had successful endoscopic treatment of ZD. Notably, in each case, an anatomical factor precluded the seating of the gastrointestinal anastomosis (GIA) stapler on the cricopharyngeal bar without the use of endoscopic retention sutures. The majority of the patients were discharged on postoperative day one. All but one patient noted a marked improvement in swallowing function immediately following the procedure and at their outpatient follow‐up visit. Endoscopic Zenker's diverticulostomy has been well‐described and established as a reliable technique in a majority of cases. We report on our experience using a previously described technique specifically for difficult, unfavorable, or contraindicated cases and suggest the employment of this technique as an alternative method to facilitate endoscopic repair and possibly limit the need for an open approach.     

Involvement of capsaicin-sensitive afferents and the Transient Receptor Potential Vanilloid 1 Receptor in xylene-induced nocifensive behaviour and inflammation in the mouse

The inflammatory actions of xylene, an aromatic irritant and sensitizing agent, were described to be predominantly neurogenic in the rat, but the mechanism and the role of the Transient Receptor Potential Vanilloid 1 (TRPV1) capsaicin receptor localized on a subpopulation of sensory nerves has not been elucidated. This paper characterizes the involvement of capsaicin-sensitive afferents and the TRPV1 receptor in nociceptive and acute inflammatory effects of xylene in the mouse. Topical application of xylene on the paw induced a short, intensive nocifensive behaviour characterized by paw liftings and shakings, which was more intensive in Balb/c than in C57Bl/6 mice. Genetic deletion of the TRPV1 receptor as well as destroying capsaicin-sensitive nerve terminals with resiniferatoxin (RTX) pretreatment markedly reduced, but did not abolish nocifensive behaviours. In respect to the xylene-induced plasma protein extravasation detected by Evans blue leakage, significant difference was neither observed between the Balb/c and C57Bl/6 strains, nor the ear and the dorsal paw skin. These inflammatory responses were diminished in the RTX pretreated group, but not in the TRPV1 gene-deleted one. Injection of the antioxidant N-acetylcysteine 15 min prior to xylene smearing significantly reduced plasma protein extravasation at both sites. These results demonstrate that xylene-induced acute nocifensive behaviour is mediated by capsaicin-sensitive afferents via TRPV1 receptor activation in mice. Neurogenic inflammatory components play an important role in xylene-induced plasma protein extravasation, but independently of the TRPV1 ion channel. Reactive oxygen or carbonyl species participate in this process presumably via stimulation of the TRPA1 channel.