Optic nerve sheath diameters in nontraumatic brain injury:A scoping review and role in the intensive care unit

BACKGROUND Neuromonitoring in medical intensive care units is challenging as most patients are unfit for invasive intracranial pressure(ICP)modalities or unstable to transport for imaging.Ultrasonography-based optic nerve sheath diameter(ONSD)is an attractive option as it is reliable,repeatable and easily performed at the bedside.It has been sufficiently validated in traumatic brain injury(TBI)to be incorporated into the guidelines.However,currently the data for non-TBI patients is inconsistent for a scientific recommendation to be made.AIM To compile the existing evidence for understanding the scope of ONSD in measuring ICP in adult non-traumatic neuro-critical patients.METHODS PubMed,Google Scholar and research citation analysis databases were searched for studies in adult patients with non-traumatic causes of raised ICP.Studies from 2010 to 2024 in English languages were included.RESULTS We found 37 articles relevant to our search.The cutoff for ONSD in predicting ICP varied from 4.1 to 6.3 mm.Most of the articles used cerebrospinal fluid opening pressure followed by raised ICP on computed tomography/magnetic resonance imaging as the comparator parameter.ONSD was also found to be a reliable outcome measure in cases of acute ischaemic stroke,intracerebral bleeding and intracranial infection.However,ONSD is of doubtful utility in septic metabolic encephalopathy,dysnatremias and aneurysmal subarachnoid haemorrhage.CONCLUSION ONSD is a useful tool for the diagnosis of raised ICP in non-traumatic neuro-critically ill patients and may also have a role in the prognostication of a subset of patients.

Intranasal nerve growth factor for prevention and recovery of the outcomes of traumatic brain injury

Traumatic brain injury is one of the main causes of mortality and disability worldwide.Traumatic brain injury is characterized by a primary injury directly induced by the impact,which progresses into a secondary injury that leads to cellular and metabolic damages,starting in the first few hours and days after primary mechanical injury.To date,traumatic brain injury is not targetable by therapies aimed at preventing and/or limiting the outcomes of secondary damage but only by palliative therapies.Nerve growth factor is a neurotrophin targeting neuronal and non-neuronal cells,potentially useful in preventing/limiting the outcomes of secondary damage in traumatic brain injury.This potential has further increased in the last two decades since the possibility of reaching neurotrophin targets in the brain through its intranasal delivery has been exploited.Indeed,molecules intranasally delivered to the brain parenchyma may easily bypass the blood-brain barrier and reach their therapeutic targets in the brain,with favorable kinetics,dynamics,and safety profile.In the first part of this review,we aimed to report the traumatic brain injury-induced dysfunctional mechanisms that may benefit from nerve growth factor treatment.In the second part,we then exposed the experimental evidence relating to the action of nerve growth factor(both in vitro and in vivo,after administration routes other than intranasal)on some of these mechanisms.In the last part of the work,we,therefore,discussed the few manuscripts that analyze the effects of treatment with nerve growth factor,intranasally delivered to the brain parenchyma,on the outcomes of traumatic brain injury.

Indirect traumatic optic neuropathy:modeling optic nerve injury in the context of closed head trauma

Traumatic optic neuropathy:Traumatic brain injury is one of the leading causes of disability and mortality in the United States.It impacts people of all ages and demographics,particularly younger males and members of the military.Vision loss is commonly associated with traumatic brain injuries of all severities and can leave patients permanently disabled.This vision loss can be caused by injury to the visual system at multiple levels,including the eyes,optic nerves,and many different sites in the brain and brainstem(Sen,2017).Despite the far-reaching effects of visual impairment after traumatic brain injury,its incidence after traumatic brain injury is not well measured,and few successful treatments have been identified or implemented.

The role of monocytes in optic nerve injury

Monocytes,including monocyte-derived macrophages and resident microglia,mediate many phases of optic nerve injury pathogenesis.Resident microglia respond first,followed by infiltrating macrophages which regulate neuronal inflammation,cell proliferation and differentiation,scar formation and tissue remodeling following optic nerve injury.However,microglia and macrophages have distinct functions which can be either beneficial or detrimental to the optic nerve depending on the spatial context and temporal sequence of their activity.These divergent effects are attributed to pro-and anti-inflammatory cytokines expressed by monocytes,crosstalk between monocyte and glial cells and even microglia-macrophage communication.In this review,we describe the dynamics and functions of microglia and macrophages in neuronal inflammation and regeneration following optic nerve injury,and their possible role as therapeutic targets for axonal regeneration.

Selective deletion of zinc transporter 3 in amacrine cells promotes retinal ganglion cell survival and optic nerve regeneration after injury

Vision depends on accurate signal conduction from the retina to the brain through the optic nerve,an important part of the central nervous system that consists of bundles of axons originating from retinal ganglion cells.The mammalian optic nerve,an important part of the central nervous system,cannot regenerate once it is injured,leading to permanent vision loss.To date,there is no clinical treatment that can regenerate the optic nerve and restore vision.Our previous study found that the mobile zinc(Zn^(2+))level increased rapidly after optic nerve injury in the retina,specifically in the vesicles of the inner plexiform layer.Furthermore,chelating Zn^(2+)significantly promoted axonal regeneration with a long-term effect.In this study,we conditionally knocked out zinc transporter 3(ZnT3)in amacrine cells or retinal ganglion cells to construct two transgenic mouse lines(VGAT^(Cre)ZnT3^(fl/fl)and VGLUT2^(Cre)ZnT3^(fl/fl),respectively).We obtained direct evidence that the rapidly increased mobile Zn^(2+)in response to injury was from amacrine cells.We also found that selective deletion of ZnT3 in amacrine cells promoted retinal ganglion cell survival and axonal regeneration after optic nerve crush injury,improved retinal ganglion cell function,and promoted vision recovery.Sequencing analysis of reginal ganglion cells revealed that inhibiting the release of presynaptic Zn^(2+)affected the transcription of key genes related to the survival of retinal ganglion cells in postsynaptic neurons,regulated the synaptic connection between amacrine cells and retinal ganglion cells,and affected the fate of retinal ganglion cells.These results suggest that amacrine cells release Zn^(2+)to trigger transcriptomic changes related to neuronal growth and survival in reginal ganglion cells,thereby influencing the synaptic plasticity of retinal networks.These results make the theory of zinc-dependent retinal ganglion cell death more accurate and complete and provide new insights into the complex interactions between retinal cell networks.

Resuscitation therapy for traumatic brain injuryinduced coma in rats:mechanisms of median nerve electrical stimulation

In this study, rats were put into traumatic brain injury-induced coma and treated with median nerve electrical stimulation. We explored the wake-promoting effect, and possible mechanisms, of median nerve electrical stimulation. Electrical stimulation upregulated the expression levels of orexin-A and its receptor OX1R in the rat prefrontal cortex. Orexin-A expression gradually in-creased with increasing stimulation, while OX1R expression reached a peak at 12 hours and then decreased. In addition, after the OX1R antagonist, SB334867, was injected into the brain of rats after traumatic brain injury, fewer rats were restored to consciousness, and orexin-A and OXIR expression in the prefrontal cortex was downregulated. Our ifndings indicate that median nerve electrical stimulation induced an up-regulation of orexin-A and OX1R expression in the pre-frontal cortex of traumatic brain injury-induced coma rats, which may be a potential mechanism involved in the wake-promoting effects of median nerve electrical stimulation.

Wake-promoting effects of vagus nerve stimulation after traumatic brain injury: upregulation of orexin-A and orexin receptor type 1 expression in the prefrontal cortex

Orexins, produced in the lateral hypothalamus, are important neuropeptides that participate in the sleep/wake cycle, and their expres- sion coincides with the projection area of the vagus nerve in the brain. Vagus nerve stimulation has been shown to decrease the amounts of daytime sleep and rapid eye movement in epilepsy patients with traumatic brain injury. In the present study, we investigated whether vagus nerve stimulation promotes wakefulness and affects orexin expression. A rat model of traumatic brain injury was established using the free fall drop method. In the stimulated group, rats with traumatic brain injury received vagus nerve stimulation （frequency, 30 Hz, current, 1.0 mA; pulse width, 0.5 ms; total stimulation time, 15 minutes）. In the antagonist group, rats with traumatic brain injury were intracerebroventricularly injected with the orexin receptor type 1 （OXIR） antagonist SB334867 and received vagus nerve stimulation. Changes in consciousness were observed after stimulation in each group. Enzyme-linked immunosorbent assay, western blot assay and immunohistochemistry were used to assess the levels of orexin-A and OX1R expression in the prefrontal cortex. In the stimulated group, consciousness was substantially improved, orexin-A protein expression gradually increased within 24 hours after injury and OX1R expres- sion reached a peak at 12 hours, compared with rats subjected to traumatic brain injury only. In the antagonist group, the wake-promoting effect of vagus nerve stimulation was diminished, and orexin-A and OX1R expression were decreased, compared with that of the stim- ulated group. Taken together, our findings suggest that vagus nerve stimulation promotes the recovery of consciousness in comatose rats after traumatic brain injury. The upregulation of orexin-A and OXIR expression in the prefrontal cortex might be involved in the wake-promoting effects of vagus nerve stimulation.

Self-assembling peptide nanofibrous hydrogel as a promising strategy in nerve repair after traumatic injury in the nervous system

Following injury in central nervous system（CNS）,there are pathological changes in the injured region,which include neuronal death,axonal damage and demyelination,inflammatory response and activation of glial cells.The proliferation of a large number of astrocytes results in the formation of glial scar.

Biomechanical analysis of optic nerve injury treated by compound light granules and ciliary neurotrophic factor

In this study, rabbit models of optic nerve injury were reproduced by the clamp method. After modeling, rabbit models were given one injection of 50 ng recombinant human ciliary neurotrophic factor into the vitreous body and/or intragastric injection of 4 g/kg compound light granules containing Radix Angelicae Sinensis and Raidix Paeoniae Alba at 4 days after modeling, once per day for 30 consecutive days. After administration, the animals were sacrificed and the intraorbital optic nerve was harvested. Hematoxylin-eosin staining revealed that the injured optic nerve was thinner and optic nerve fibers were irregular. After treatment with recombinant human ciliary neurotrophic factor, the arrangement of optic nerve fibers was disordered but they were not markedly thinner. After treatment with compound light granules, the arrangement of optic nerve fibers was slightly disordered and their structure was intact. After combined treatment with recombinant human ciliary neurotrophic factor and compound light granules, the arrangement of optic nerve fibers was slightly disordered and the degree of injury was less than after either treatment alone. Results of tensile mechanical testing of the optic nerve showed that the tensile elastic limit strain, elastic limit stress, maximum stress and maximum strain of the injured optic nerve were significantly lower than the normal optic nerve. After treatment with recombinant human ciliary neurotrophic factor and/or compound light granules, the tensile elastic limit strain, elastic limit stress, maximum stress and maximum strain of the injured optic nerve were significantly increased, especially after the combined treatment. These experimental findings indicate that compound light granules and ciliary neurotrophic factor can alleviate optic nerve injury at the histological and biochemical levels, and the combined treatment is more effective than either treatment alone.

Ultrastructural changes in the optic nerve and capillary vessels during early stages of optic nerve injury

BACKGROUND： Capillaries are the only blood supply for optic nerves, which makes the system more vulnerable to impaired blood circulation. OBJECTIVE： To observe the ultrastructural changes in the optic nerves and capillaries in rabbits following intracanalicular segment injury to the optic nerve. DESIGN, TIME AND SETTING： Comparative, observational, pathological morphology was performed at the Department of Anatomy, Weifang Medical College from September to November 2007. MATERIALS： Models of intracanalicular segment injury to the optic nerve were induced in the right eye of thirty healthy, adult rabbits by a free-falling metal cylinder. The H-7500 transmission electron microscope was provided by Hitachi, Japan. METHODS： All rabbits were randomly assigned into experimental （n = 25） and control （n = 5） groups. Optic nerve specimens were obtained from the experimental group at 0.5, 6, 12, 48, and 96 hours, respectively, following injury. Ultrastructural changes to the optic nerves and their capillaries were observed by electron microscopy. Optic nerve injury was not established in the control group, but optic nerve specimens were collected similarly to the experimental group. MAIN OUTCOME MEASURES： Ultrastructural changes in the injured optic nerves and their capillaries. RESULTS： Thirty rabbits were included in the final analysis. In the control group, cross-sections of the optic nerves exhibited varied thicknesses with regularly arranged fibers. The axons appeared to be smooth with condensed myelin sheaths and oval mitochondria. The microtubules and microfilaments were clearly seen. The lumens of the capillaries were regular with densely arranged endothelial cells and visible mitochondria. In the experimental group, 30 minutes after injury to the optic nerves, swollen axons, sparse myelin sheath, disordered microtubules and microfilaments, swollen mitochondria, and a decreased number of pinocytosis vesicles and microfilaments in endothelial cells of the capillaries were observed. At 6 hours, medullary and vacuolar degeneration in the mitochondria, and swollen endothelial cells in the capillary, were visible. At 12 hours, these changes were more obvious. At 48 hours, granular dissolution of microtubules, microfilaments, and mitochondria, as well as diffuse degeneration of mitochondria in the endothelial cells, were observed. At 96 hours, axonal disintegration, vacuolar degeneration, and dilated capillaries were observed. CONCLUSION： During early stages, the injured intracanalicular optic nerve exhibited swollen axons with vacuolar degeneration, swollen and degenerated mitochondria, decreased number of microtubules and microfilaments, and dilated capillaries with increased permeability.

Research progress of stem cells on glaucomatous optic nerve injury

Glaucoma, the second leading cause of blindness, is an irreversible optic neuropathy. The mechanism of optic nerve injury caused by glaucoma is undefined at present. There is no effective treatment method for the injury. Stem cells have the capacity of self-renewal and differentiation. These two features have made them become the research focus on improving the injury at present. This paper reviews the application progress on different types of stem cells therapy for optic nerve injury caused by glaucoma.

Human umbilical cord blood stem cells and brainderived neurotrophic factor for optic nerve injury: a biomechanical evaluation

Treatment for optic nerve injury by brain-derived neurotrophic factor or the transplantation of human umbilical cord blood stem cells has gained progress, but analysis by biomechanical indicators is rare. Rabbit models of optic nerve injury were established by a clamp. At 7 days after injury, the vitreous body received a one-time injection of 50 μg brain-derived neurotrophic factor or 1 × 10^6 human umbilical cord blood stem cells. After 30 days, the maximum load, maximum stress, maximum strain, elastic limit load, elastic limit stress, and elastic limit strain had clearly improved in rabbit models of optical nerve injury after treatment with brain-derived neurotrophic factor or human umbilical cord blood stem cells. The damage to the ultrastructure of the optic nerve had also been reduced. These findings suggest that human umbilical cord blood stem cells and brain-derived neurotrophic factor effectively repair the injured optical nerve, improve biomechanical properties, and contribute to the recovery after injury.

Neuronal apoptosis and neurofilament protein expression in the lateral geniculate body of cats following acute optic nerve injuries

The visual pathway have 6 parts, involving optic nerve, optic chiasm, optic tract, lateral geniculate body, optic radiation and cortical striatum area. Corresponding changes may be found in these 6 parts following optic nerve injury. At present, studies mainly focus on optic nerve and retina, but studies on lateral geniculate body are few. OBJECTIVE： To prepare models of acute optic nerve injury for observing the changes of neurons in lateral geniculate body, expression of neurofilament protein at different time after injury and cell apoptosis under the optical microscope, and for investigating the changes of neurons in lateral geniculate body following acute optic nerve injury. DESIGN： Completely randomized grouping design, controlled animal experiment. SETTING： Department of Neurosurgery, General Hospital of Ji＇nan Military Area Command of Chinese PLA. MATERIALS： Twenty-eight adult healthy cats of either gender and common grade, weighing from 2.0 to 3.5 kg, were provided by the Animal Experimental Center of Fudan University. The involved cats were divided into 2 groups according to table of random digit： normal control group （n=3） and model group （n=25）. Injury 6 hours, l, 3, 7 and 14 days five time points were set in model group for later observation, 5 cats at each time point. TUNEL kit （Bohringer-Mannheim company ）and NF200＆ Mr 68 000 mouse monoclonal antibody （NeoMarkers Company） were used in this experiment. METHODS： This experiment was carded out in the Department of Neurosurgery, General Hospital of Ji＇nan Military Area Command of Chinese PLA between June 2004 and June 2005.① The cats of model group were developed into cat models of acute intracranial optic nerve injury as follows： The anesthetized cats were placed in lateral position. By imitating operation to human, pterion approach was used. An incision was made at the joint line between outer canthus and tragus, and deepened along cranial base until white optic nerve via optic nerve pore and further to brain tissue. Optic nerve about 3 mm was liberated and occluded by noninvasive vascular clamp for 20 s. After removal of noninvasive vascular clamp, the area compressed by optic nerve was hollowed and narrowed, but non-fractured. Skull was closed when haemorrhage was not found. Bilateral pupillary size, direct and indirect light reflect were observed. Operative side pupil was enlarged as compared with opposite side, direct light reflect disappeared and indirect light reflect existed, which indicated that the models were successful. Animals of control group were not modeled .② The animals in the control group and model group were sacrificed before and 6 hours, 1, 3, 7 and 14 days after modeling respectively. Lateral geniculate body sample was taken and performed haematoxylin ＆ eosin staining. Immunohistochemical staining showed lateral geniculate body neurofilament protein expression, and a comparison of immunohistochemial staining results was made between experimental group and control group. Terminal deoxynucleo-tidyl transferase （TdT）-mediated dUTP-biotin nick end labeling （TUNEL） was used to label apoptotic cells in lateral geniculate body. MAIN OUTCOME MEASURES： Neuronal morphological change, neurofilament protein expression and cell apoptosis in lateral geniculate body following acute optic nerve injury. RESULTS： Twenty-eight involved cats entered the final analysis. ① Histological observation results： In the control group, cell processes were obviously found, which were few or shortening in the model group. ② Neuronal neurofilament protein expression： Cells in lateral geniculate body in the control group and at 6 hours after injury presented clear strip-shaped staining, and those at 7 and 14 days presented irregular distribution without layers and obviously decreasing staining intensity. The positive rate of neurofilament protein in lateral geniculate body in control group and 6 hours, l, 3, 7 and 14 days after injury was （ 10.22±0.42） %, （10.03±0.24） %, （9.94±0.14） %, （9.98±0.22） %, （8.18±0.34） % and （6.37±0.18）%, respectively. Positive rate of neurofilament protein in control group, at 6 hours, 1 or 3 days after injury was significantly different from that at 7 days after injury （P 〈 0.05）; Positive rate of neurofilament protein in control group, at 6 hours, 1, 3 or 7 days after injury was significantly different from that at 14 days after injury （P 〈 0.05）. It indicated that neuronal injury in lateral geniculate body was not obvious within short term after optic nerve injury, but obvious at 7 days after injury and progressively aggravated until at 14 days after injury.③ Neuronal apoptosis： TUNEL staining showed that neuronal apoptosis in lateral geniculate body appeared at 7 days after injury, and a Lot of neuronal apoptosis in lateral geniculate body was found at 14 days after injury. It indicated that neuronal injury in lateral geniculate body was related to apoptosis. CONCLUSION： In short term after optic nerve injury （within 7 days）, nerve injury of lateral geniculate body is not obvious, then, it will aggravate with the elongation of injury time. The occurrence of neuronal iniury of lateral geniculate body is related to the apoptosis of nerve cells.

Establishing a cat model of acute optic nerve injury

BACKGROUND： In order to investigate the progress in optic nerve injury and the following regeneration and repair, many kinds of animal models of optic nerve injury have been established, such as models of acute and chronic ocular hypertension, compression, amputating wound, ischemia reperfusion or hypoxia, intravitreal injection of excitatory amino acids, etc. However, most of these models are established by squeezing intraorbital optic nerve, and suitable for ophthalmology, and there are fewer models suitable for the acute cranial contusion in neurosurgery. OBJECTIVE： To observe the changes of optic nerve after acute injury, and the characteristics of methods for establishing model of acute optic nerve injury in cats. DESIGN： A complete randomized grouping and controlled animal trial. SETTING： Department of Neurosurgery, General Hospital of Ji＇nan Military Area Command of Chinese PLA. MATERIALS： Twenty-eight healthy adult cats, common degree, either sex, weighing 2.0-3.5 kg, were provided by the animal experimental center of Fudan University. The cats were randomly divided into control group （n =3） and model group （n =25）, and 5 cats in the model group were observed at 6 hours and 1, 3, 7 and 14 days after injury respectively. JX-2000 biological signal processing system （Department of Physiology, Second Military Medical University of Chinese PLA, Shanghai）; Inverted phase contrast microscope （Olympus）; Axioplan 2 imaging microgram analytical system （Labsystems）. METHODS： The experiments were carried out in the Department of Neurosurgery, General Hospital of Jinan Military Area Command of Chinese PLA from June 2004 to June 2005. The cats in the model groups were made into models of acute optic nerve injury： The cats were anesthetized, then the limbs were fixed in a lateral recumbent position. Pterion approach in human was imitated, the operative incision was made along the line between lateral canthus and tragus, and it could be seen deep along the skull base that white optic nerve （about 3 mm） went through optic foramen and entered into brain tissue. It was squeezed with noninvasive vascular clip for 20 seconds, then the clip was removed, and then the skull was closed after it was examined to be no bleeding. The size of bilateral pupils, direct and indirect light reflexes were observed postoperatively. Successfully established models were judged by larger operated pupil than controlateral one, disappearance of direct light reflex and the existence of indirect light reflex. No model establishment was performed in the control group. Each cat was tested with flash visual evoked potential （F-VEP） to observe the electrophysiological changes before and after experiment. All the cats in the control group and model groups were killed under anesthesia before model establishment and at 6 hours, 1, 3, 7 and 14 days after model establishment respectively, and the pathological changes of the optic nerve after injury were observed under electron microscope and light microscope. MAIN OUTCOME MEASURES： VEP and the ultrastructural changes of optic nerve after acute optic nerve injury in both groups. RESULTS： All the 28 cats were involved in the analysis of results. ① VEP results： The VEP latencies were obviously different between the control group and model group at each time point （P 〈 0.05）, whereas there were no obvious differences among different time points in the model group （P 〉 0.05）. The VEP amplitudes were obviously different between the control group and model group at each time point （P 〈 0.05）, whereas there were no obvious differences among different time points in the model group （P 〉 0.05）. ② Ultrastructural changes of the optic nerve： Under electron microscope, normal optic nerve myelin sheath had complete structure, tramal plates were clear and arranged tightly, axolemma was complete, whereas the structures of endoneurium, myelin sheath, tramal plates, axolemma and axon were in disorders after optic nerve injury. CONCLUSION： Models of acute optic nerve injury established by squeezing intracranial optic nerve with noninvasive vascular clip can be applied in studying intracranial acute optic nerve injury.

Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist inhibits apoptosis of retinal ganglion cells in a rabbit model of optic nerve injury

A rabbit model of traumatic optic nerve injury, established by occlusion of the optic nerve using a vascular clamp, was used to investigate the effects of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist GYKI 52466 on apoptosis of retinal ganglion cells following nerve injury. Hematoxylin-eosin staining and a terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that retinal ganglion cells gradually decreased with increasing time of optic nerve injury, while GYKI 52466 could inhibit this process. The results demonstrate that following acute optic nerve injury, apoptosis of retinal ganglion cells is a programmed process, which can be inhibited by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist.

Neurolin expression in the optic nerve and immunoreactivity of Pax6-positive niches in the brain of rainbow trout(Oncorhynchus mykiss) after unilateral eye injury

In contrast to astrocytes in mammals, fish astrocytes promote axon regeneration after brain injury and actively participate in the regeneration process. Neurolin, a regeneration-associated, Zn8-1abeled protein, is involved in the repair of damaged optic nerve in goldfish. At 1 week after unilateral eye injury, the ex- pression of neurolin in the optic nerve and chiasm, and the expression of Pax6 that influences nervous system development in various brain regions in the rainbow trout （Oncorhynchus mykiss） were detected. Immunohistochemical staining revealed that the number of Zn8~ cells in the optic nerve head and intraor- bital segment was obviously increased, and the increase in Zn8~ cells was also observed in the proximal and distal parts of injured optic nerve. This suggests that Zn8＊ astrocytes participate in optic nerve regeneration. ELISA results revealed that Pax6 protein increased obviously at 1 week post-injury. Immunohistochemi- cal staining revealed the appearance of Pax6＋ neurogenic niches and a larger number of neural precursor cells, which are mainly from Pax6＋ radial glia cells, in the nuclei of the diencephalon and optic tectum of rainbow trout （Oncorhynchus mykiss）. Taken together, unilateral eye injury can cause optic nerve reaction, and the formation of neurogenic niches is likely a compensation phenomenon during the repair process of optic nerve injury in rainbow trout （Oncorhynchus mykiss）.

The clinical value of dynamic ultrasound measurement of optic nerve sheath diameter in the treatment of patients with moderate and severe craniocerebral injury

Objective:To explore the clinical value of dynamic ultrasound monitoring of optic nerve sheath diameter(ONSD)in the treatment of patients with moderate and severe head injury(CI).Methods:A total of 160 patients with moderate and severe CI admitted to the First Affiliated Hospital of Hainan Medical University from January 2018 to January 2020 were selected and divided into observation group(80 cases)and control group(80 cases)a Januaryccording to the random number table.Patients in control group and observation group were dehydrated to reduce intracranial pressure(ICP)according to clinical symptoms/brain CT and ONSD monitoring guidance.National Institutes of Health Stroke Scale(NIHSS),Acute Physiology and Chronic Health EvaluationⅡ(APACHEⅡ),Glasgow Coma Scale(GCS),complications,prognosis,ICU stay time and mechanical ventilation time were compared between the two groups.Results:NIHSS score[control group:(19.58±3.19)points vs(37.98±5.75)points,observation group:(10.33±2.42)points vs(38.05±5.83)points]and APACHE II score[control group:(14.55±2.17)points vs(19.87±3.50)points,observation group:(8.71±2.03)points vs(20.12±3.56)points]of the two groups at 1 month after injury were significantly lower than those at admission(P<0.05),GCS score[control group:(10.78±1.66)points vs(8.03±1.34)points,observation group:(13.10±1.72)points vs(7.99±1.32)points]were significantly higher than that at admission(P<0.05).At 1 month after injury,NIHSS score[(10.33±2.42)points vs(19.58±3.19)points],APACHE II score[(8.71±2.03)points vs(14.55±2.17)points]in the observation group were significantly lower than those in the control group(P<0.05),and GCS score[(13.10±1.72)points vs(10.78±1.66)points]in the observation group was significantly higher than that in the control group(P<0.05).The proportion of hydrocephalus(2.50%vs 12.50%),total complication rate(5.00%vs 21.25%),proportion of severe disability(5.00%vs 17.50%),proportion of survival in plant man(3.75%vs 15.00%),mortality rate(2.50%vs 12.50%),ICU stay time[(5.01±1.25)d vs(8.38±2.29)D],mechanical ventilation time[(2.18±0.75)D]in observation group were lower than those in the control group,and the good rate(56.25%vs 32.50%)and the total effective rate(93.75%vs 72.50%)in the control group were significantly higher than those in the control group(P<0.05).Conclusion:Dynamic ultrasound monitoring ONSD is effective in guiding dehydration treatment of patients with moderate and severe CI,it can significantly reduce ICP and complications,improve prognosis,which is worthy of promotion and application.

Analysis of the Activation of the Nrf2-ARE Pathway Following Optic Nerve Injury in Mice

Purpose:The Nrf2-ARE pathway plays a cytoprotective role in many tissues,but its protective function in the optic nerve is unclear. The purpose of the study is to investigate the changes in activation of the Nrf2-ARE pathway following optic nerve injury (ONI) in mice. Methods:Using ONI mice models,the expression levels of Nrf2 in optic nerves were determined by real-time PCR at various time points. Results:The expression of Nrf2mRNA was significantly up-regulated at 1 d after ONI, peaking at 30 min after ONI. Conclusion:The Nrf2-ARE pathway was activated after ONI, providing evidence for the study of the protection and underlying mechanism of Nrf2-ARE pathway on optic nerves.

Establishing a cat model of chronic optic nerve compression injury

BACKGROUND： An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved. OBJECTIVE： To establish a stabilized, chronic, optic nerve crush model, which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury. DESIGN, TIME AND SETTING： A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004, MATERIALS： A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT, France; JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA, China; inverted phase contrast microscopy by Olympus, Japan. METHODS： A total of twenty normal adult cats were randomly assigned to control （n = 5） and model （n = 15） groups, according to different doses of contrast agent injected through balloons as follows： 0.2 mL injection, 0.25 mL injection, and 0.35 mL injection, with each group containing 5 animals. Imitating the clinical pterion approach, the optic nerves were exposed using micro-surgical methods. An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter. Balloon size was controlled with a contrast agent injection （0.1 mL/10 min） to form an occupying lesion model similar to sellar tumors. MAIN OUTCOME MEASURES： The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury. Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy. RESULTS： During the early period （day 11 after modeling）, visually evoked potential demonstrated no significant changes. In the late period （day 51 after modeling）, recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced. Following injury, the endoneurium, myelin sheath, lamella, axolemma, and axon appeared disordered. CONCLUSION： Results demonstrated that the chronic, intracranial, optical nerve crush model was stable and could simulate optic nerve lesions induced by sellar tumors. Under the condition of chronic optical nerve crush, visually evoked potentials were aggravated.

Delayed Visual Recovery from Optic Nerve Injury Following a Procedure of Orbital Wall Reconstruction

The acute onset of the vision loss by optic never injury following orbital wall reconstruction, has been reported in 0.5% - 5.0% of the cases. Visual impairment can be recovered within an early period after injury. Delayed visual recovery from optic nerve injury during a procedure of orbital wall reconstruction has not been reported. We report a case of delayed recovery from optic nerve injury which occurred following orbital wall reconstruction. A 78-year-old man underwent orbital wall reconstruction for medial wall fracture and resulting enophthalmos in the right eye, one week after a traffic accident. Immediate after surgery, postoperative visual acuity in the right eye decreased to light perception, and relative afferent pupillary defect (RAPD) was detected. In spite of mega-dose steroid treatment, the visual acuity did not improve. However, 8 months after surgery, visual acuity began to recover to 0.1, and the degree of RAPD decreased. Twelve months after surgery, visual acuity in the right eye was 0.4, and pupillary light reflex was normal. Our report suggests that patients with optic neuropathy by surgery or trauma require long-term follow-up, regardless of early response to mega-dose steroid treatment.