Effect of a cervical collar on optic nerve sheath diameter in trauma patients

BACKGROUND:As advocated in advanced trauma life support and prehospital trauma life support protocols,cervical immobilization is applied until cervical spine injury is excluded.This study aimed to show the difference in optic nerve sheath diameter(ONSD)between patients with and without a cervical collar using computed tomography(CT).METHODS:This was a single-center,retrospective study examining trauma patients who presented to the emergency department between January 1,2021,and December 31,2021.The ONSD on brain CT of the trauma patients was measured and analyzed to determine whether there was a difference between the ONSD with and without the cervical collar.RESULTS:The study population consisted of 169 patients.On CT imaging of patients with(n=66)and without(n=103)cervical collars,the mean ONSD in the axial plane were 5.43±0.50 mm and 5.04±0.46 mm respectively for the right eye and 5.50±0.52 mm and 5.11±0.46 mm respectively for the left eye.The results revealed an association between the presence of a cervical collar and the mean ONSD,which was statistically significant(P<0.001)for both the right and left eyes.CONCLUSION:A cervical collar may be associated with increased ONSD.The effect of this increase in the ONSD on clinical outcomes needs to be investigated,and the actual need for cervical collar in the emergency department should be evaluated on a case-by-case basis.

Mesenchymal stem cell therapy in retinal and optic nerve diseases: An update of clinical trials

Retinal and optic nerve diseases are degenerative ocular pathologies which lead to irreversible visual loss. Since the advanced therapies availability, cell-based therapies offer a new all-encompassing approach. Advances in the knowledge of neuroprotection, immunomodulation and regenerative properties of mesenchymal stem cells(MSCs) have been obtained by several preclinical studies of various neurodegenerative diseases. It has provided the opportunity to perform the translation of this knowledge to prospective treatment approaches for clinical practice. Since 2008, several first steps projecting new treatment approaches, have been taken regarding the use of cell therapy in patients with neurodegenerative pathologies of optic nerve and retina. Most of the clinical trials using MSCs are in Ⅰ/Ⅱ phase, recruiting patients or ongoing, and they have as main objective the safety assessment of MSCs using various routes of administration. However, it is important to recognize that, there is still a long way to go to reach clinical trials phase Ⅲ-Ⅳ. Hence, it is necessary to continue preclinical and clinical studies to improve this new therapeutic tool. This paper reviews the latest progress of MSCs in human clinical trials for retinal and optic nerve diseases.

PTEN knockdown with the Y444F mutant AAV2 vector promotes axonal regeneration in the adult optic nerve

The lack of axonal regeneration is the major cause of vision loss after optic nerve injury in adult mammals. Activating the PI3K/AKT/mTOR signaling pathway has been shown to enhance the intrinsic growth capacity of neurons and to facilitate axonal regeneration in the central nervous system after injury. The deletion of the mTOR negative regulator phosphatase and tensin homolog （PTEN） enhances regeneration of adult corticospinal neurons and ganglion cells. In the present study, we used a tyrosine-mutated （Y444F） AAV2 vector to efficiently express a short hairpin RNA （shRNA） for silencing PTEN expression in retinal ganglion cells. We evaluated cell survival and axonal regeneration in a rat model of optic nerve axotomy. The rats received an intravitreal injection of wildtype AAV2 or Y444F mutant AAV2 （both carrying shRNA to PTEN） 4 weeks before optic nerve axotomy. Compared with the wildtype AAV2 vector, the Y444F mutant AAV2 vector enhanced retinal ganglia cell survival and stimulated axonal regeneration to a greater extent 6 weeks after axotomy. Moreover,post-axotomy injection of the Y444F AAV2 vector expressing the shRNA to PTEN rescued ～19% of retinal ganglion cells and induced axons to regenerate near to the optic chiasm. Taken together, our results demonstrate that PTEN knockdown with the Y444F AAV2 vector promotes retinal ganglion cell survival and stimulates long-distance axonal regeneration after optic nerve axotomy. Therefore, the Y444F AAV2 vector might be a promising gene therapy tool for treating optic nerve injury.

Pathological changes in the retina and growth associated protein-43 expression following treatment of intracanalicular optic nerve injury via optic canal decompression,dexamethasone or their combination

BACKGROUND： The main clinical treatments for optic nerve injury are optic canal decompression and systemic administration of hormones, but both treatments have disadvantages. OBJECTIVE： To observe the pathological changes in the retina and growth associated protein-43 （GAP-43） expression, to compare the treatment of optic canal decompression, hormones, and their combination with the intracanalicular optic nerve injury.DESIGN, TIME AND SETTING： A randomized, controlled animal study was performed at the Department of Anatomy, Weifang Medical University, China, from September 2007 to November 2008.MATERIALS： Dexamethasone （Shandong Huaxin Pharmaceutical, China） and rabbit anti-GAP-43 polyclonal antibody （Boster, China） were used.METHODS： All 36 healthy adult rabbits were randomly assigned to control group （n = 4）, simple injury group （n = 20）, and treatment group （n = 12）. Intracanalicular optic nerve injury models were established using the metal cylinder free-fall impact method. The control group was left intact. The treatment group （four rabbits in each subgroup） was treated by optic nerve decompression, dexamethasone treatment （1 mg/kg daily via two intravenous infusions, 1/5 total dose reduction every 3 days, for 14 days）, and simultaneously giving surgery and hormone treatment.MAIN OUTCOME MEASURES： Pathological changes in the retina were determined using hematoxylin-eosin staining. GAP-43 expression was detected using immunohistochemistry in the retina.RESULTS： Retina injury induced obvious pathological changes in the retina. With prolonged time after optic nerve injury, the number of retinal ganglion cells was gradually decreased, and reached the minimum on day 14 （P〈0.01）. All three treatments increased the number of retinal ganglion cells （P〈0.01）, but surgery ＋ hormone treatment was most effective. No GAP-43 cells were present in the normal retinal, but they appeared 3 days after injury, peaked 7 days after injury, and then began to decline.CONCLUSION： Intracanalicular optic nerve injury induced obvious pathological changes in the retina, including increased GAP-43 expression. Optic canal decompression and hormones improved nerve repair after injury, and their combination produced better outcomes.

Phosphorylated S6K1 and 4E-BP1 play different roles in constitutively active Rheb-mediated retinal ganglion cell survival and axon regeneration after optic nerve injury

Ras homolog enriched in brain(Rheb) is a small GTPase that activates mammalian target of rapamycin complex 1(mTORC1).Previous studies have shown that constitutively active Rheb can enhance the regeneration of sensory axons after spinal cord injury by activating downstream effectors of mTOR.S6K1 and4E-BP1 are important downstream effectors of mTORC1.In this study,we investigated the role of Rheb/mTOR and its downstream effectors S6K1 and 4E-BP1in the protection of retinal ganglion cells.We transfected an optic nerve crush mouse model with adeno-associated viral 2-mediated constitutively active Rheb and observed the effects on retinal ganglion cell survival and axon regeneration.We found that overexpression of constitutively active Rheb promoted survival of retinal ganglion cells in the acute(14 days) and chronic(21 and 42 days) stages of injury.We also found that either co-expression of the dominant-negative S6K1mutant or the constitutively active 4E-BP1 mutant together with constitutively active Rheb markedly inhibited axon regeneration of retinal ganglion cells.This suggests that mTORC1-mediated S6K1 activation and 4E-BP1 inhibition were necessary components for constitutively active Rheb-induced axon regeneration.However,only S6K1 activation,but not 4E-BP1 knockdown,induced axon regeneration when applied alone.Furthermore,S6K1 activation promoted the survival of retinal ganglion cells at 14 days post-injury,whereas 4E-BP1 knockdown unexpectedly slightly decreased the survival of retinal ganglion cells at 14 days postinjury.Ove rexpression of constitutively active 4E-BP1 increased the survival of retinal ganglion cells at 14 days post-injury.Likewise,co-expressing constitutively active Rheb and constitutively active 4E-BP1 markedly increased the survival of retinal ganglion cells compared with overexpression of constitutively active Rheb alone at 14 days post-injury.These findings indicate that functional 4E-BP1 and S6K1 are neuroprotective and that 4E-BP1 may exert protective effects through a pathway at least partially independent of Rhe b/mTOR.Together,our results show that constitutively active Rheb promotes the survival of retinal ganglion cells and axon regeneration through modulating S6K1 and 4E-BP1 activity.Phosphorylated S6K1 and 4E-BP1 promote axon regeneration but play an antagonistic role in the survival of retinal ganglion cells.

Optic Nerve Metastasis from Breast Carcinoma after Treatment with Taxanes

Introduction: The incidence of ocular metastasis from Breast Carcinoma is only between 5% - 30%, mainly located in choroid, but the location in optic nerve is even more infrequent. We present a rare case that combined both locations sequentially in the same eye. Methods: Case report. Results: A 58-year-old woman with advanced breast cancer was referred with a choroidal metastasis in her right eye which responded well to systemic Taxol and Avastin. Afterwards, she developed an optic nerve metastasis in the same eye when she was under the treatment, so it was changed to Docetaxel. Unfortunately the patient didn’t respond to this treatment and died. Conclusions: Choroidal metastasis secondary to breast cancer generally responds well to radiotherapy. Even so, in cases that a great deterioration of visual acuity is expected after radiation, chemotherapy like taxanes is an alternative to preserve vision with complete tumor regression. Nevertheless, the presentation of a second metastasis in optic nerve can be indicative of inadequate treatment of metastatic disease or complication of the treatment, or both.

Indirect traumatic optic neuropathy

Indirect traumatic optic neuropathy(ITON) refers to optic nerve injury resulting from impact remote to the optic nerve. The mechanism of injury is not understood, and there are no confirmed protocols for prevention, mitigation or treatment. Most data concerning this condition comes from case series of civilian patients suffering blunt injury, such as from sports- or motor vehicle-related concussion, rather than military-related ballistic or blast damage. Research in this field will likely require the development of robust databases to identify patients with ITON and follow related outcomes, in addition to both in-vivo animal and virtual human models to study the mechanisms of damage and potential therapies.

The concept of gene therapy for glaucoma:the dream that has not come true yet

Gene therapies,despite of being a relatively new therapeutic approach,have a potential to become an important alternative to current treatment strategies in glaucoma.Since glaucoma is not considered a single gene disease,the identified goals of gene therapy would be rather to provide neuroprotection of retinal ganglion cells,especially,in intraocular-pressure-independent manner.The most commonly reported type of vector for gene delivery in glaucoma studies is adeno-associated virus serotype 2 that has a high tro pism to retinal ganglion cells,res ulting in long-term expression and low immunogenic profile.The gene thera py studies recruit inducible and genetic animal models of optic neuropathy,like DBA/2J mice model of high-tension glaucoma and the optic nerve crush-model.Reported gene therapy-based neuroprotection of retinal ganglion cells is targeting specific genes translating to growth factors(i.e.,brain derived neurotrophic factor,and its receptor TrkB),regulation of apoptosis and neurodegeneration(i.e.,Bcl-xl,Xiap,FAS system,nicotinamide mononucleotide adenylyl transferase 2,Digit3 and Sarm1),immunomodulation(i.e.,Crry,C3 complement),modulation of neuroinflammation(i.e.,e rythropoietin),reduction of excitotoxicity(i.e.,Com KIlα)and transcription regulation(i.e.,Max,Nrf2).On the other hand,some of gene therapy studies focus on lowering intra ocular pressure,by impacting genes involved in both,decreasing aqueous humor production(i.e.,aquaporin 1),and increasing outflow facility(i.e.,COX2,prostaglandin F2a receptor,RhoA/RhoA kinase signaling pathway,MMP1,Myocilin).The goal of this review is to summarize the current stateof-art and the direction of development of gene therapy strategies for glaucomatous neuropathy.

HOW TO TREAT OPTIC ATROPHY WITH ACUPUNCTURE ?

Optic atrophy results mostly from affection by exopathic wind pathogen, insufficiency of Qi and Xue(blood) or hyperactivity of the liver-yang. We choose Qiuhou(EX-HN 7), Jingming(BL1 ), Taiyang(EX-HN 5 ) and Fengchi(GB 20) as the main acupoints and combine other auxiliary points according to different syndromes. For example, Hegu(LI 4) and Waiguan(TE 5 ) are supplemented for affection by exopathic wind pathogen, Qihai(CV 6), Zusanli(ST 36), Xuehai(SP 10) and Guang-ming(GB 37) for insufficiency of Qi and Xue, and Guanshu(BL 18), Baihui(GV 20), Taixi(KI 3),Sanyinjiao(SP 6) and Guangming(GB 37) for hyperactivity of the liveryang. When Qiuhou(EX-HN 7), Jingming(BL 1 ) and Fenchi(GB 20) punctured, the need1ing direction, angle and depth should be controlled very appropriate for achieving good therapeutic effect.

Primary retinal ganglion cells for neuron replacement therapy

Optic nerve damage as a result of trauma, ischemia, glaucoma or other forms of optic neuropathy disease, leads to disconnection between the eye and brain and death of retinal ganglion cells(RGCs), causing permanent loss of vision. Therapeutic options for treating optic neuropathy are limited and represent a significant unmet medical need. Development of a regenerative strategy for replacement of lost RGCs lies at the core of the future cell-based therapy for these conditions. Successful long-term restoration of visual function depends on the type of cells for transplantation. Primary RGCs of neonatal mice are now reported to have the potential for serving such a purpose.

超声测量视神经鞘直径在颅脑外伤患者中的应用价值

目的探讨超声测量视神经鞘直径(ONSD)在颅脑外伤患者中的应用价值。方法选取100例颅脑外伤患者作为研究对象,随机分为对照组和研究组,每组50例。对照组患者接受有创颅内压(ICP)监测,研究组患者接受有创ICP监测联合ONSD超声测量,且2组患者均根据实际情况接受治疗。观察2组患者的一般资料、治疗情况。比较研究组不同ICP患者的一般资料、ICP监测结果和ONSD超声测量结果,分析颅脑外伤患者ONSD与ICP的相关性,并分析ONSD对颅脑外伤患者ICP升高的诊断效能。结果治疗后28 d时,研究组患者的平均动脉压高于对照组,心率、呼吸频率低于对照组,差异有统计学意义(P<0.05);研究组患者机械通气时间、入住ICU时间短于对照组,甘露醇使用量少于对照组,治疗后ICP、28 d病死率低于对照组,差异有统计学意义(P<0.05)。ICP≥22 mmHg患者的ICP高于ICP<22 mmHg患者,不同体位、甘露醇使用前后的ONSD大于ICP<22 mmHg组,差异有统计学意义(P<0.05)。颅脑外伤患者ONSD与ICP呈显著正相关(r=0.723,P<0.001);受试者工作特征曲线分析结果显示,ONSD诊断ICP升高的最佳临界值为5.25 mm,曲线下面积为0.879。结论将ICP监测联合超声测量ONSD应用于颅脑外伤患者的治疗中,可有效改善患者体征,缩短机械通气时间、入住ICU时间,减少甘露醇使用量,降低28 d病死率。颅脑外伤患者ONSD与ICP呈显著正相关,且ONSD对ICP升高具有较高的诊断效能。

通窍活血汤对颅脑外伤手术患者的治疗效果研究

目的探究通窍活血汤对颅脑外伤手术患者的治疗效果。方法选取2022年1月—2023年1月于徐州市贾汪区人民医院进行手术治疗的78例颅脑外伤患者,根据随机数表法分成针刺组与中药组,每组39例。所有患者均接受手术治疗与术后康复训练(包括常规肢体功能与认知功能训练),在此基础上,针刺组接受针刺治疗,中药组接受通窍活血汤治疗。比较两组治疗总有效率、神经功能、运动功能、日常生活能力改善情况。结果中药组的治疗总有效率(92.31%)明显高于针刺组(71.79%),差异有统计学意义(χ^(2)=5.571,P<0.05)。经治疗,中药组神经功能评分低于针刺组,肢体运动功能及日常生活能力评分均高于针刺组,差异有统计学意义(P均<0.05)。结论颅脑外伤手术患者术后采用通窍活血汤治疗,疗效显著,可改善其神经功能、运动功能,加强其日常生活自理能力。

皮质类固醇治疗急性外伤性视神经病变疗效评价

目的 评价皮质激素对外伤性视神经病变的治疗作用及影响疗效的相关因素。方法 外伤性视神经病变61例,50例应用大剂量皮质激素(甲基强的松龙500～1000 mg/d)治疗;11例应用低剂量皮质激素(地塞米松10 mg/d)治疗。根据末次随访视力及治疗后视力的变化,评价治疗效果,并通过多因素分析筛选影响疗效的相关因素。结果 50例大剂量甲基强的松龙治疗组,显效12例,有效10例,无效28例,有效率44.0％;11例低剂量地塞米松治疗组,显效1例,有效3例,无效7例,有效率36.4％。两组间有效率无显著性差异(P=0.745)。Logistic回归分析显示有效率与伤后视力(P<0.001)及伤后开始治疗的时间(P=0.024)密切相关。结论 皮质激素对外伤性视神经病变有一定的治疗作用。伤后视力情况及伤后开始治疗的时间是影响疗效的重要因素。

外伤性视神经病变复方樟柳碱治疗效果分析

目的 观察复方樟柳碱治疗外伤性视神经病变的效果 ,旨在寻找治疗外伤性视神经病变的有效手段。方法 外伤性视神经病变患者59例 (65眼 ) ,随机分成复方樟柳碱组 2 7例 (30眼 ) ,其他药物治疗对照组32例 (35眼 )。复方樟柳碱组 ,采用其 2ml患侧颞浅动脉旁皮下注射或球后注射 ,每日 1次 ,每疗程 1 4天 ,3～ 4疗程。其他药物治疗对照组 ,采用血管扩张剂 ,营养视神经药物 45～ 60天。全部患者早期同时均给予大剂量皮质类固醇、甘露醇。结果 疗效的主要观察指标是视力。两组比较结果显示 :复方樟柳碱组疗效明显优于对照组 ,差异有显著性。结论 复方樟柳碱治疗外伤性视神经病变是一种可供选择的、且无明显全身毒副作用的、有效的治疗手段。

外伤性视神经病变的甲基强的松龙冲击疗法

目的 评估大剂量甲基强的松龙冲击疗法治疗外伤性视神经病变的效果。方法 甲基强的松龙 10 0 0mg( 15～ 30mg/kg)加于 5 %葡萄糖溶液 5 0 0ml静脉滴注 3～ 5天 ,每天 1次 ,治疗 15例外伤性视神经病变。结果 15例中 ,6例显效 ,3例有效 ,6例无效。总有效率达 60 %。结论 大剂量甲基强的松龙冲击疗法治疗外伤性视神经病变患者有肯定疗效 ,值得推广应用。

外伤性视神经病变视力预后的相关因素分析

目的探讨外伤性视神经病变视力预后的影响因素。方法回顾性分析1999年8月—2008年1月中南大学湘雅三医院眼科收治的88例外伤性视神经病变患者临床资料。88例患者以性别、年龄、眼别、伤后有无光感、有无骨折、昏迷史、受伤原因、治疗方式8个临床观察因素作为自变量(X),疗效作为因变量,进行非条件Logistic回归分析,观察视力预后的影响因素。所有治疗均在患者及家属签署知情同意书后进行。结果单因素分析显示伤后有无光感X4(P=0.010)、昏迷史X6(P=0.010)和治疗方式X8(P=0.006)是视力预后的影响因素。多因素分析显示伤后无光感(OR=3.392,P=0.010)、有昏迷史(OR=3.162,P=0.010)是影响预后的危险因素(χ2=20.333,P=0.000),手术治疗是保护视力的有力措施(OR=1.459,P=0.006)。Logistic回归方程为:LogistP=-1.674+1.222X4+1.151X6+1.459X8(χ2=20.333,P=0.000)。结论伤后无光感、有昏迷史是影响眼视力预后的危险因素,手术治疗是保护视力的有力措施。

经鼻内镜视神经管减压术治疗外伤性视神经病疗效分析

目的探讨鼻内镜下视神经管减压术对外伤性视神经病的临床疗效、手术技巧和适应证的选择。方法通过对210例(212侧)外伤性视神经病患者经鼻内镜进行神经管减压,提高患者视力级别作为判断临床疗效。结果本组患者在大量激素冲击治疗后,采用经鼻内镜视神经管减压手术,术后定期随访6个月以上,观察患者视力恢复情况,其中显效72侧(33.96%),有效29侧(13.68%),总有效101例(47.64%)。其中残留光感以上视力的患眼135侧,术后显效71侧(52.59%),有效20侧(14.81%),总有效91例(67.4%)。无光感患者77侧,术后显效1侧(1.3%),有效9侧(11.7%),总有效10(12.99%)。残余有光感以上视力和完全无光感的患眼,手术治疗后的有效率有明显的差异(P<0.01)。结论采用经鼻内镜进行减压手术是治疗外伤性视神经病重要措施之一,手术时机的选择和手术操作技巧至关重要。

间接视神经损伤的CT表现及临床意义

目的 评价CT对间接视神经损伤的诊断价值。方法 对临床诊断为间接视神经损伤的 10 6例 112只眼CT检查结果进行研究。结果 112只眼中发生眶壁骨折 84只眼 ,占 75 % ,其中以内壁骨折最为常见。 49只眼有明确视神经管骨折 ,占 43 .8% ,2 4只眼既无明显视神经管骨折 ,又无眶壁骨折及窦腔积液 ,占 2 1.4%。视神经增粗者 16只眼 ,占 14 .3 %。结论 CT可较好地显示眶壁骨及眶内视神经形态 ,对间接视神经损伤的诊断及选择治疗方案具有重要的价值。

视神经损伤常见合并症及诊疗策略

目的探讨视神经损伤患者出现的合并症及其产生的原因、症状、诊断及治疗。方法选择478例视神经损伤患者,入院后经过头颅CT、MRI及全脑DSA检查,通过手术及非手术方法进行治疗。手术包括开颅视神经减压术、经鼻镜下视神经减压术;非手术治疗包括使用脱水药物、糖皮质激素、钙离子拮抗剂、神经营养药物以及高压氧治疗。结果视神经损伤常见合并症按产生部位可分为:颅脑损伤、血管源性、神经源性、肌源性、骨源性及其他。其中以颅脑损伤(93.1%)、神经源性(43.9%)及骨源性(78.5%)合并症为主。视神经损伤常见合并症中,颅脑损伤发病率较高;创伤性动脉瘤(1.5%)、颈内动脉海绵窦瘘(2.5%)等血管源性损伤虽然发病率低,但后果严重。结论视神经损伤常见合并症亦关系到患者的生命安全及生存质量,在治疗视神经损伤同时应予以重视并及时处理。

颅脑外伤合并视神经损伤的临床分析

目的探讨颅脑外伤合并视神经损伤的诊断与治疗方法以及疗效。方法回顾分析30例颅脑损伤合并视神经损伤病例的临床资料,总结其治疗方法及治疗后视力的恢复情况。结果19例进行视神经管减压手术,12例视力提高。无光感3例,1例恢复至0.06,2例无恢复;视神经损伤保守治疗11例中,7例视力不同程度提高,无光感6例,其中4例恢复至数指,2例无改变。结论视神经损伤一经确诊就应当立即进行治疗,有手术指证的应尽早手术治疗。