| With the rapid development of socio-economic and transportation, the frequency oftraumatic brain injury (TBI) increases every year, which threats to human life and healthseriously. The majority of patients of TBI are young adults which affect social laborseriously, and bring a heavy financial and mental burden to the society and family.With the raising level of traumatic brain injury treatment, there is growing emphasison traumatic brain injury with injury treatment, to reduce mortality and morbidity, andimprove patients’ quality of lives. Traumatic optic neuropathy (TON) is uncommon in theclinic, occurring in0.5–5%of head injuries. Optic nerve as part of the central nervoussystem (central nervous system, CNS), is an important cause of traumatic brain injurydisability higher, because of the sensitive to damage, the shortage of Schwann cells, andpoor self-repair capacity. Patients with TON usually have vision loss even blindness, whichseriously affect on the patient’s lives, work, study and so on. There are currently noeffective and uniform treatments available for TON，which is still the hotspots anddifficulties of medical research. The subject regarding the TON as a research object, focuson studying the pathophysiology changes of acute optic nerve injury and mesenchymalstem cells (MSCs) in nerve repair function, and mainly divided into three parts,respectively, to conduct basic research and clinical observationsObjective: Successfully establish an animal model of optic nerve crush injury, andstudy the relationship between the apoptosis of retinal ganglion cells (RGCs) and opticnerve pathological changes, to provide the experimental basis for clinical treatment andprognosis of traumatic optic neuropathy.Methods: By the surgical microscope, we fully exposed to the optic nerve through theeye approach and used aneurysm clip of20g to injury adult SD rat optic nerve9s, a total of40, injured side as experimental injury group, the contralateral as control group for theirown.40adult SD rats were randomly divided into4groups, normal group, damaged1wgroup, damaged2w group and damaged4w group. Every experimental rat was performedthe pupil diameter and light reflex testing and Flash visual evoked potential (F-VEP)before and after operation, to observe wave amplitude and latency period. When each removed to examine through the number of RGCs, HE staining andimmunohistochemistry.Results:1、The pupil diameter of damaged group is3.05±0.32mm, with direct lightreflection absent and indirect light reflection prompt; the control group is0.73±0.12mm,with direct light reflection prompt and indirect light reflection absent.2、HE staining shows damaged1w only to see a small amount of inflammatory cells,the2w with a large number of inflammatory cells and a small amount of vascularproliferation, and4w with a large number of inflammatory cells and blood vessels.3、3days after injury, there is no significant change in the number of RGCs.3d,1,2,4w after injury, the number of RGCs decreased significantly, respectively by about5.13%,27.88%,43.91%,60.58%.4、After injury, GFAP of the damaged area gradually decline; the surrounding of thedamage increased after injury,2w reached a peak and then decreased gradually.Conclusion: Optic nerve crush injury model with stability, easy operation, and goodreproducibility,can be completed in the laboratory; This model can effectively simulatetraumatic optic neuropathy in the clinical pathophysiological changes and clinicalsymptoms. Objective: Isolate, purify, culture and identify mesenchymal stem cells; And buildmesenchymal stem cells implanted stent.Methods:1、We flush out the bone marrow from the rat femur with PBS, separate andpurify bone marrow mesenchymal stem cells through centrifugation and adherencescreening, and subculture. The flow cytometry detection of bone marrow mesenchymalstem cells use positive sign of CD44, CD105, and negative signs CD45, for CD34, toidentify the purity of mesenchymal stem cell.2、Synthetic collagen as the raw materialproduced optic nerve sheath tube with porosity150μm. the optic nerve sheath tube was putinto the cell suspension for24h, then checked through laser scanning confocal observation.Results:1、Mesenchymal stem cells are easy to subculture, and the results of flowcytometry show that CD44and CD105, CD45and CD34were91.23±2.1%、85.77±3.1%、1.25±1.1%、0.78±0.3%.2、Confocal laser found optic nerve sheath covered withmesenchymal stem cells.Conclusion: It is easy to obtain mesenchymal stem cells through rat bone marrow cavity which is high purity; A large number of mesenchymal stem cells can grow into opticnerve sheath. Objective: Investigate the influence of mesenchymal stem cells on the retinalganglion cells after the optic nerve injuried, as well as the dynamic changes of RGCsMethods: Optic nerve crush injuried rats model is the experimental subject, andanimals were randomly divided into the bone marrow mesenchymal stem cell therapygroup, phosphate buffered saline (PBS) treatment control group and blank control group(untreated),20in every group. Bone marrow mesenchymal stem cells were implanted intothe optic nerve injuried site3days after optic nerve injury.3d,1w,2w,4w after treatment,checked the NO. of RGCs and compared the differences among the three groups.Results:1、In bone marrow mesenchymal stem cell therapy group, respectively,3d,1w,2w,4w after treatment (four subgroups), the NO. of RGCs were242±9,225±6,208±11,138±12; phosphate buffered saline (PBS) treatment group, four subgroups the NO. ofRGCs were238±12,198±11,166±9,131±12; blank control group were225±12,201±10,176±6,121±6.2、The NO. of RGCs were no significant differences between the two phosphatebuffer group and blank control group.3、Mesenchymal stem cell therapy group and the phosphate buffer treatment group ora blank control group at the3d and4w treatment after injury, there were no significantdifference in RGCs count;1w and2w treatment, there were differences in RGCs count,P<0.05.Conclusion: Mesenchymal stem cell transplantation can step down the apoptosis ofretinal ganglion cells, and has a certain the RGCs protection role, and is resistant toapoptosis. Objective: Investigate the influence of bone marrow mesenchymal stem cells on thepathological structure after the optic nerve injuried, and its related factors.Methods: We successfully established optic nerve crush injury model and bonemarrow mesenchymal stem cells stent. SD rats were randomly divided into the bonemarrow mesenchymal stem cell therapy group, phosphate buffered saline (PBS) treatment optic nerve injuried the optic nerve sheath were implanted into in the injury site, which wasrich in bone marrow mesenchymal stem cells. We drawn the immune staining (GFAP),transmission electron microscopy to detect and compare the three groups3d,1w,2w,4wafter treatment. Immunohistochemical detections of the PTEN, P-EGFR, respectively,weredrawn in the norrmal, injuried, treated rats.Results:1、GFAP expression gradually increased at and around damaged areas,reached the peak2w after treatment, disappeared4w after treatment; GFAP expression wasnot significantly different between phosphate buffer treatment and control group.Immunohistochemistry showed that the damaged area without expression, GFAP graduallyincreased over time, and reached a peak in2w, disappeared in4w around damage aera。2、PTEN: the optic nerve and retinal ganglion cells can have low expression in thenormal group; high expression of injuried group, low expression of the treatment group;P-EGFR: normal negative; after injury, the damaged area had low expression, the damagedarea highly expressed after treatment.3、Transmission electron microscopy showed that the number of normal axonsgradually reduced, and the medullary plate was even more loose.Conclusion: Bone marrow mesenchymal stem cell transplantation has aneuroprotective effect, delays the demyelination, and is conducive to the optic nervemyelin repair. Objective: analysis the effiicacy of the surgery and conservative treatment, discussthe clinical treatment, and then discuss the surgical technique and prognosis of traumaticoptic neuropathy.Methods: We retrospectively analyzed data of four cases (5eyes) with traumaticoptic neuropathy with an average follow-up of6months (3months to2years), when Iworked in department of neurosurgery, Changzheng Hospital.Results: Case1: Male,52years old, a car accident, head trauma, left eye only lightperception, orbital CT (plain) showed bilateral optic canal fracture, which compressedoptic nerve. On the5thday, the patient was received decompression surgery. Left eye visualacuity recovered to40/200at the sixth month;Case2: Male,23-year old, a car accident, head injury, GCS8(E1V2M5). The rightpupil dilated, the direct light reflex was absent, and indirect light reflex exists. Orbital CTshowed that the right optic canal and superior orbital fissure had no fracture. We considered the optic nerve edema. The patient was received decompression surgery. Eyesrecovered the little direct light reflex at the first postoperative day, and visual acuityreturned to normal after two weeks;Case3: Male,22-year old, a car accident to head trauma, GCS13(E3V4M6).Physical examination showed that the left pupil was5mm with the direct light reflex absentand the direct light reflex prompt. Orbital computed tomography (plain+three-dimensional reconstruction) showed that the left side of the optic canal had fracturewithout obvious oppression. The patient received conservative treatment of steroid andneurotrophic drugs. Visual acuity gradually recovered to normal in the first month.Case4: Female,48years old, a car accident, head injury, GCS15. Physicalexamination showed that both eyes had no light perception, pupil dilation, direct andindirect light reflex absent. Orbital CT showed that the optic canal had no fracture with nocompression. The patient received the optic canal decompression through bilateralsupraorbital keyhole approach; Both eyes had light perception after1month.Conclusion: Imaging should not be used as the sole indication of the optic canaldecompression surgery; Different patients depending on the circumstances take a differentsurgical approach; The range of decompression should be not less than2/5of thecircumference of the bony optic canal, and as long as the optic canal. |
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