The Effect of Tizanidine on Chronic Vasospasm in Rats

Summary ? Background. Cerebral vasospasm after subarachnoid hemorrhage (SAH) has remained a major cause of morbidity and mortality in patients with SAH. Excitatory neurotransmitters are gathered in the extracellular space during ischemia due to cerebral vasospasm and initiate or stimulate a series of pathophysiological biochemical processes which consequently lead to neuronal death. Tizanidine (Sandoz compound DS 103–282, 5-chloro-4,2 (2-imidazolin-2-yl-amino)-2,1,3-benzothiazol hydrochloride) is a centrally-acting muscle relaxant and a selective α 2 adrenoreceptor agonist which shows its effect by stimulating presynaptic α 2 adrenoreceptors in central ASPergic and GLUergic system by inhibiting aspartic acid and glutamic acid release. In this study, the effect of Tizanidine on vasospasm was evaluated.  Methods. We used a femoral artery vasospasm model in rats which has been described by Okada et al. 60 rats were examined in three groups. The first group was used as control group (Control) (n=20), in the second group subarachnoid hemorrhage was performed (SAH) (n=20), in the third group Tizanidine was administered in addition to SAH (SAH+Tizanidine administration) (n=20). Animals in SAH+Tizanidine administration group received 0,3 mg/kg/day intraperitoneally for 7 days. Seven days after the experiment, after perfusion-fixation, 10 mm segments of both femoral arteries were removed and the femoral artery was prepared for light microscope examination, scanning and transmission electron microscopy and for morphometric analysis.  Results. There was a statistically significant difference between the electron, scanning and light microscopic observations and morphometric analysis of SAH+Tizanidine administration group and SAH group, and no statistically significant difference between SAH+Tizanidine administration group and control group.  Conclusion. This study has disclosed that Tizanidine administration before the vasospasm reduces ultrastructural and morphometric vasospastic insult significantly. However, the clinical application of Tizanidine as a protective and therapeutic agent in cerebral vasospasm needs further studies including the employment of clinically more relevant SAH models.     

Delayed Administration of the K+ Channel Activator Cromakalim Attenuates Cerebral Vasospasm after Experimental Subarachnoid Hemorrhage

Summary ? Background. Delayed cerebral vasospasm remains an unpredictable and inadequately treated complication of aneurysmal subarachnoid hemorrhage (SAH). Recent evidence indicates that the potassium channel activator cromakalim is capable of limiting cerebral vasospasm in rabbits when administered immediately after experimental SAH (i.e. before spastic constriction has been initiated). However, the ultimate clinical value of cromakalim for treating vasospasm will depend in part on its effectiveness when administered after SAH-induced constriction has already been initiated. The present study examined the effects of cromakalim on vasospasm when treatment was initiated after SAH-induced constriction was underway.  Methods. New Zealand white rabbits were subjected to experimental SAH by injecting autologous blood into the cisterna magna. Cromakalim (0.03, 0.1 or 0.3 mg/kg) or vehicle was injected intravenously at 8 hour intervals beginning 24 hours post-SAH. Animals were killed by perfusion fixation 48 hours after SAH. Basilar arteries were removed and sectioned, and cross-sectional area was measured.  Findings. The average cross sectional areas of basilar arteries were reduced by 64% and 68% in the SAH-only and SAH+vehicle groups, respectively. Treatment with cromakalim dose-dependently attenuated SAH-induced constriction. The groups treated with 0.03, 0.1, and 0.3 mg/kg cromakalim exhibited average decreases in cross-sectional area of 57%, 42%, and 19%, respectively.  Interpretation. These findings indicate that cromakalim dose-dependently attenuates cerebral vasospasm when administered 24 hours after experimental SAH in the rabbit. The results suggest K_ATP channel activators, such as cromakalim, could be of benefit for reversing cerebral vasospasm after aneurysmal SAH.     

小骨窗开颅加尿激酶治疗高血压脑出血

目的　探讨微创小骨窗血肿清除加用尿激酶溶解血肿治疗高血压脑出血的效果。方法　将 32例入院的高血压脑出血病例在头颅CT片指导下行颞部直切口 ,小骨窗 2 0～ 3 0cm ,直视下吸除大部血肿 ,活动性出血予以电凝止血。血肿腔放置硅胶管 ,手术后 3d引流管注入 1万U尿激酶 ,再引流陈旧溶解的血肿液 ,并与大骨瓣开颅血肿清除术的效果相比较。结果　 32例中 ,18例完全恢复 ,半自理 8例 ,优良率 81 3% ,偏瘫 4例 ,无植物生存 ,死亡 2例 ,病死率 6 %。与前期大骨瓣开颅血肿清除术相比较有良好的效果。结论　小骨窗微创血肿清除加尿激酶血肿腔溶解血肿的结合 ,最佳化地发挥了各自的优势 ,同时避免了其缺点。     

黄芪注射液加纳洛酮治疗急性脑出血53例

目的初步探讨黄芪注射液加纳洛酮治疗急性脑出血的临床疗效。方法分别采用黄芪注射液治疗方案(A组:51例)、纳洛酮治疗方案(B组:49例)、黄芪注射液加纳洛酮治疗方案(C组:53例),对153例急性脑出血患者进行治疗,并于入院后第7、14、28天分别进行血肿体积、水肿容积测量和临床神经功能缺损程度评分。结果入院后第7天三组血肿体积、水肿容积、临床神经功能缺损程度评分比较差异均无统计学意义(P>0.05);入院后第14天C组分别与A、B组比较,血肿体积、水肿容积均显著减小(P<0.05),但A与B比较差异无统计学意义(P>0.05),三组临床神经功能缺损程度评分比较差异无统计学意义(P>0.05);入院后第28天C组分别与A、B组比较,血肿体积、水肿容积、临床神经功能缺损程度评分均有显著减少(P<0.05)。结论黄芪注射液加纳洛酮治疗方案是一种治疗急性脑出血更有效、更安全的方法。     

新生儿视网膜出血的相关因素分析

[目的]对新生儿视网膜出血的相关因素进行临床分析,为临床干预提供理论依据.[方法]间接检眼镜检查276例新生儿,随访5年.[结果]新生儿视网膜出血的发生率在初产妇128.53%高于经产妇（5.56%）;阴道产（29.3%）高于剖腹产（6.26%）.视网膜出血累及黄斑者,视功能发育受到影响.[结论]新生儿视网膜出血主要与产妇的分娩方式有关,累及黄斑区的视网膜出血将有碍于患儿的视力发育.     

Severe pulmonary hemorrhage in a 3‐week‐old neonate with COVID‐19 infection: A case report

Our patient is a 3‐week‐old female neonate, presented with complaints of low‐grade fever and a congested nose for one day. Eventually, she developed progressive desaturation, hypotension, and poor perfusion due to severe pulmonary hemorrhage. Then, she developed cardiac arrest and was declared dead.     

转运早期早产儿对其脑室内出血的影响及其对策探讨

目的探讨搬运早期早产儿对其脑室内出血(IVH)的影响,并研究其对策。方法以1998年1月到2007年10月我院收治的206例早期早产儿为研究对象。设为三组:A组,无搬运组;B组,有搬运组,且搬运前未预防性使用苯巴比妥;C组,有搬运组,但搬运前半小时预防性地使用了苯巴比妥。再比较三组早产儿IVH的发生率。结果三组早产儿IVH发生率明显不同,A组、B组、C组分别为36.4%(24/66)、82.8%(72/87),56.6%(30/53),经统计学处理有非常显著性意义。结论搬运早期早产儿易使其IVH发生率明显增加,因此对于早期早产儿应尽量避免搬运,以减少其脑室内出血(IVH)的发生率;若必须搬运则可在搬运前半小时预防性地运用苯巴比妥,便可部分地减少其脑室内出血的发生率。     

Phenotypic Expression of CFH Rare Variants in Age-Related Macular Degeneration Patients in the Coimbra Eye Study

PurposeTo determine the association between rare genetic variants in complement factor H (CFH) and phenotypic features in age-related macular degeneration (AMD) patients from the Coimbra Eye Study (CES).MethodsAMD patients from the Incidence CES ({"type":"clinical-trial","attrs":{"text":"NCT02748824","term_id":"NCT02748824"}}NCT02748824) underwent ophthalmologic examination and color fundus photography, spectral-domain optical coherence tomography (SD-OCT), fundus autofluorescence, and near-infrared imaging. Multimodal phenotypic characterization was carried out in a centralized reading center. The coding and splice-site regions of the CFH gene were sequenced through single-molecule molecular inversion probe–based next-generation sequencing in association with the EYE-RISK consortium. Variants with minor allele frequency <0.05 resulting in splice-site or protein change were selected. Differences in phenotypic features between carriers and noncarriers were analyzed using generalized estimated equations logistic regression models, considering intereye correlations.ResultsWe included 39 eyes of 23 patients carrying rare CFH variants and 284 eyes of 188 noncarriers. Carrier status was associated with having higher drusen burden in the macula in the inner Early Treatment Diabetic Retinopathy Study circle (odds ratio [OR], 5.44 [95% confidence interval {CI}, 1.61–18.37]; P = 0.006), outer circle (OR, 4.37 [95% CI, 1.07–17.77]; P = 0.04), and full grid (OR, 4.82 [95% CI, 1.13–20.52]; P = 0.033). In SD-OCT, a lower total macular volume and lower inner retinal layers’ volume (OR, 0.449 [95% CI, 0.226–0.894]; P = 0.023; OR, 0.496 [95% CI, 0.252–0.979]; P = 0.043) and pigment epithelial detachments (PEDs) (OR, 5.24 [95% CI, 1.08–25.44]; P = 0.04) were associated with carrying a rare CFH variant. Carriers with subretinal drusenoid deposits (SDD) had the rare variant P258L in all cases except one.ConclusionsWe identified in our cohort phenotypic differences between carriers and noncarriers of rare variants in the CFH gene. Carriers had more severe disease, namely superior drusen burden, PEDs, and thinner retinas. The rare variant P258L may be associated with SDD. Carriers are probably at increased risk of progression.     

Onyx embolization of a spinal epidural hemorrhage caused by thoracic spinal epidural arteriovenous fistula: A case report and literature review

Spinal epidural hemorrhages (SEDH) caused by spinal epidural arteriovenous fistulas (SEAVFs) are rare; thus, their specific pathogenesis has not been explained. Furthermore, the standard treatment for SEAVFs has not yet been defined. Here we report the case of a 36-year-old Chinese man who experienced acute onset chest pain and tightness. His symptoms rapidly aggravated until the lower limbs were unable to support him. Spinal magnetic resonance angiography (MRA) revealed a localized SEAVF and a secondary spinal cord lesion at the T4 level. Digital subtraction angiography (DSA) confirmed the presence of the SEDH/SEAVF at the T3–4 level with the left radicular artery feeding the fistula. Based on DSA and MRA findings, SEDH, local spinal cord infarction, and spinal venous reflux disorder were conditionally diagnosed. Using the arterial route, Onyx-34 was injected into the fistula to embolize the feeding arteries and the venous system. Angiography was performed after the microcatheter was withdrawn, and no residual fistula or anterior spinal artery was observed. The six-week follow-up MRI showed acceptable healing of the SEAVF, and the patient improved neurologically. This case suggests that endovascular treatment with Onyx-34 embolization should be considered a promising treatment strategy for this type of complicated SEAVF.     

Simultaneous occurrence of subarachnoid hemorrhage and cerebral venous sinus thrombosis: A systematic review of cases

Although the leading causes of subarachnoid hemorrhage (SAH) are aneurysm rupture and arteriovenous malformations, cerebral venous sinus thrombosis (CVST) can, in rare cases, be associated with SAH. This phenomenon is an uncommon presentation, with less than a hundred cases reported based on our review of the literature. The purpose of this review is to highlight what is known regarding these cases, how they are managed and to highlight the need for further studies that will serve as a basis for the development of a standard management guideline across board. The following databases were searched: PubMed and Ovid Embase. A complementary search of Google Scholar and AJOL was done. Gray literature search was also conducted on the Google search engine for any additional relevant papers. We were able to extract data regarding 33 cases from 29 identified studies. The mean age was 46.6 ± 14.08. 17 (51.5%) of the cases were female, and the female‐to‐male ratio is 1.1:1. Headache was by far the commonest symptom, occurring in 82% of cases followed by seizures in 42% of cases. Four patients (12%) had loss of consciousness while 5 patients (15%) had some form of focal neurologic deficit. Twenty patients had cerebral venous sinus thrombosis in at least two different sinuses. The superior sagittal sinus was the most common location for CVSTs (79%), followed by the transverse sinus (57.5%). Twenty‐nine cases (89%) were managed with anticoagulation alone and one case had a mechanical thrombectomy. We have performed a comprehensive review of cases that had the simultaneous occurrence of SAH and CVST and have identified their peculiarities and the challenges to management. Further research is needed in order to identify a causal relationship and to serve as a basis for the development of a standard management guideline across the board.