New paradigms of immune regulation in glaucoma during the whole clinical process / 中华实验眼科杂志

Glaucoma is an irreversible blinding eye disease caused by the structural and functional damage of optic nerve induced by pathological increase of intraocular pressure (IOP), characterized by multiple causes and strong heterogeneity.The control of IOP to reduce the risk of optic damage has been the main therapeutic strategy of glaucoma for many years.However, in clinical experience, some patients show progress of optic nerve damage despite the effectively controlled IOP, the mechanism of non-IOP-dependent secondary damage is still an urgent problem to be solved and a research hotspot in the pathogenesis of glaucoma.With the continuous innovation of molecular biological technology, breakthroughs have been made in the field of basic research.Partial visual recovery can be boosted by alleviating local immune and inflammatory responses.Due to a lack of symbolic clinical application results, it has become an immediate priority to attach importance to the combination of basic clinical research and facilitate the transformation of results.Starting from the theory of glaucoma-immune inflammation, understanding the importance of the immune homeostasis of eyes, paying close attention to the linkage of eyes and brain in physiopathological process and the progression of diseases in the whole visual pathway, and fully understanding and effectively making good use of the opportunities and implications brought by new techniques will have significant effect in formulating clinical diagnosis and treatment plans.

Identificação da velocidade anormal da dilatação de pupila como biomarcador de lesão cerebral em pacientes neurocríticos / Identification of abnormal pupil dilation velocity as a biomarker of cerebral injury in neurocritically ill patients

RESUMO Objetivo: Calcular as velocidades médias da dilatação de pupila para classificar a gravidade da lesão derivada da escala de coma de Glasgow, estratificada por variáveis de confusão. Métodos: Neste estudo, analisaram-se 68.813 exames das pupilas para determinar a velocidade normal de dilatação em 3.595 pacientes com lesão cerebral leve (13 - 15), moderada (9 - 12) ou grave (3 - 8), segundo a escala de coma de Glasgow. As variáveis idade, sexo, raça, tamanho da pupila, tempo de permanência na unidade de terapia intensiva, pressão intracraniana, uso de narcóticos, classificação pela escala de coma de Glasgow e diagnóstico foram consideradas confundidoras e controladas para análise estatística. Empregou-se regressão logística com base em algoritmo de classificação com aprendizado de máquina para identificar os pontos de corte da velocidade de dilatação para as categorias segundo a escala de coma de Glasgow. Resultados: As razões de chance e os intervalos de confiança desses fatores se mostraram estatisticamente significantes em sua influência sobre a velocidade de dilatação. A classificação com base na área sob a curva mostrou que, para o grau leve, na escala de coma de Glasgow, o limite da velocidade de dilatação foi de 1,2mm/s, com taxas de falsa probabilidade de 0,1602 e 0,1902 e áreas sob a curva de 0,8380 e 0,8080, respectivamente, para os olhos esquerdo e direito. Para grau moderado na escala de coma de Glasgow, a velocidade de dilatação foi de 1,1mm/s com taxas de falsa probabilidade de 0,1880 e 0,1940 e áreas sob a curva de 0,8120 e 0,8060, respectivamente, nos olhos esquerdo e direito. Mais ainda, para o grau grave na escala de coma de Glasgow, a velocidade de dilatação foi de 0,9mm/s, com taxas de falsa probabilidade de 0,1980 e 0,2060 e áreas sob a curva de 0,8020 e 0,7940, respectivamente, nos olhos esquerdo e direito. Esses valores foram diferentes dos métodos prévios de descrição subjetiva e das velocidades de dilatação previamente estimadas. Conclusão: Observaram-se velocidades mais lentas de dilatação pupilar em pacientes com escores mais baixos na escala de coma de Glasgow, indicando que diminuição da velocidade pode indicar grau mais grave de lesão neuronal.

ABSTRACT Objective: To calculate mean dilation velocities for Glasgow coma scale-derived injury severity classifications stratified by multiple confounding variables. Methods: In this study, we examined 68,813 pupil readings from 3,595 patients to determine normal dilation velocity with brain injury categorized based upon a Glasgow coma scale as mild (13 - 15), moderate (9 - 12), or severe (3 - 8). The variables age, sex, race, pupil size, intensive care unit length of stay, intracranial pressure, use of narcotics, Glasgow coma scale, and diagnosis were considered as confounding and controlled for in statistical analysis. Machine learning classification algorithm-based logistic regression was employed to identify dilation velocity cutoffs for Glasgow coma scale categories. Results: The odds ratios and confidence intervals of these factors were shown to be statistically significant in their influence on dilation velocity. Classification based on the area under the curve showed that for the mild Glasgow coma scale, the dilation velocity threshold value was 1.2mm/s, with false probability rates of 0.1602 and 0.1902 and areas under the curve of 0.8380 and 0.8080 in the left and right eyes, respectively. For the moderate Glasgow coma scale, the dilation velocity was 1.1mm/s, with false probability rates of 0.1880 and 0.1940 and areas under the curve of 0.8120 and 0.8060 in the left and right eyes, respectively. Furthermore, for the severe Glasgow coma scale, the dilation velocity was 0.9mm/s, with false probability rates of 0.1980 and 0.2060 and areas under the curve of 0.8020 and 0.7940 in the left and right eyes, respectively. These values were different from the previous method of subjective description and from previously estimated normal dilation velocities. Conclusion: Slower dilation velocities were observed in patients with lower Glasgow coma scores, indicating that decreasing velocities may indicate a higher degree of neuronal injury.

Survival rate change of retinal ganglion cells following optic nerve injuries in mice / 中华创伤杂志

Objective:To investigate the survival rate change of retinal ganglion cells（RGCs）in a mouse of optic nerve crush（ONC）.Methods:Ninety-seven male C57BL/6J mice（6 to 8 weeks）were selected and divided into normal group（ n=5）, sham-operation group（ n=5）and ONC group（ n=5）according to the random number table. In normal group, both eyes of the mice did not receive any intervention. In sham-operation group, the right eye of the mice received sham operation, while the left eye reveived no intervention. In ONC group, the left eye received ONC, and the right eye received sham operation. In normal group, the density of RGCs in both eyes was quantified and compared. In sham-operatioin group, the density of RGCs in the sham operation eye was calculated and then compared to the average density of RGCs in normal group. In ONC group, the survival rate of RGCs was set as the ratio between the left eye（ONC eye）and the right eye（sham-operation eye）. The survival rate of RGCs in ONC group was compared after crush injury for 5, 10, 20, 30 seconds）（the sacrifice time was set at day 7）, and was compared after sampling on days 3, 4, 5, 7, 14, 30, 60, 90, 180（the duration of crush injury was set as 20 seconds）. Results:In normal group, the density of RGCs in the right eye was（5, 167.3±55.6）cell/mm 2, with no statistical difference from that in the left eye［（5, 199.6±44.8）cell/mm 2］（ P>0.05）. The density of RGCs in normal group and sham-operation group was（5, 183.5±33.4）cell/mm 2 and（5, 151.5±87.6）cell/mm 2, showing no statistical difference（ P>0.05）. The survival rate of RGCs in ONC group after crush injury for 5, 10, 20, 30 seconds was（37.6±1.1）%,（34.0±0.9）%,（33.6±1.6）% and（30.3±0.6）%（ P<0.01）. In comparison, there was statistical difference in the survival rate of RGCs between crush injury for 5 seconds and for 30 seconds（ P<0.01）, but not among other duration of crush injury（ P>0.05）. The survival rate of RGCs in ONC group after sampling on days 3, 4, 5, 7, 14, 30, 60, 90, 180 was（85.4±2.0）%,（67.6±3.1）%,（43.0±1.0）%,（33.6±1.6）%,（22.7±2.0）%,（12.8±0.6）%,（10.4±0.8）%,（8.6±0.5）% and（6.7±0.2）%（ P<0.01）, showing the most obvious drop from day 3 to day 5. Additionally, the curve became flattened after 30 days. Conclusions:In a mouse model of ONC, varying durations of crushing will lead to different damage to RGCs in a progressive mode, indicating that following the primary injury（ONC）, the RGCs suffer secondary injury as well. Therefore, effectively controlling the secondary injury may be the key point of treating optic nerve injuries.

Importância do raciocínio etiológico e topográfico de lesões: relato de neuropatia óptica traumática conduzida como acidente vascular cerebral / Importance of etiological and topographic injury reactions: report of a traumatic optic neuropathy conducted as a cerebrovascular accident

Introdução: O trauma ocular ou periocular pode afetar o nervo óptico e causar baixa acuidade visual ou alteração de campo visual. Essa lesão, denominada neuropatia óptica, quando de etiologia traumática, pode ser classificada como direta, através da compressão, perfuração ou laceração do nervo óptico por ação de corpos estranhos, fraturas do assoalho da órbita ou hemorragias, e indireta, quando a partir de um trauma externo ao globo ocular há lesão por transmissão da onda de choque ou desaceleração, levando à lesão do nervo óptico pelo estiramento de suas fibras ou edema comprometendo sua vascularização, comum nos acidentes automobilísticos e nas quedas. Descrição do Caso: O presente estudo objetiva relatar um caso de neuropatia óptica traumática conduzida erroneamente como acidente vascular cerebral em uma paciente do sexo feminino de 29 anos, com história de queda da própria altura. Discussão: A investigação feita pela história clínica, evolução do quadro e novos achados fundoscópicos permitiu o diagnóstico correto e melhor orientação da paciente. Conclusão: O conhecimento da neuropatia óptica traumática e da anatomia da via óptica têm extrema importância no raciocínio topográfico e etiológico das lesões traumáticas que cursam com comprometimento visual, poupando o paciente de possíveis intervenções invasivas e desnecessárias (AU)

Introduction: Eye or periocular trauma can affect the optic nerve and cause low visual acuity or visual field alteration. This lesion, called optic neuropathy, when of traumatic etiology, can be classified as direct, through compression, perforation or laceration of the optic nerve by action of foreign bodies, fractures of the orbit floor or hemorrhages, and indirect, when from an external trauma to the eyeball there is injury by transmission of the shock wave or deceleration, leading to optic nerve injury by stretching its fibers or edema compromising its vascularization, common in automobile accidents and falls. Case Report: The present study aims to describe a case of traumatic optic neuropathy mistakenly conducted as a stroke in a 29-yearold female patient with a history of falling from his own height. Discussion: The investigation was possible because of the clinical history, evolution of the condition and new fundoscopic findings that allowed the correct diagnosis and better orientation of the patient. Conclusion: Knowledge of traumatic optic neuropathy and anatomy of the optical pathway have extreme importance in the topographic and etiological reasoning of traumatic lesions that present with visual impairment, saving the patient from possible interventions invasive and unnecessary. (AU)

Research progress in treatment of traumatic optic nerve injury / 中华创伤杂志

Traumatic optic nerve injury is common in patients with traumatic brain injury,mainly in young adults.The optic nerve has no regenerative function,leaving problems of visual field defect and loss of vision and causing high disability rate among patients with traumatic brain injury.The current clinical treatments of traumatic optic nerve injury are hormonotherapy and decompression of optic nerve canal,lacking definite clinical efficacy and treatment norm.In recent years,a series of brand new treatments,such as neuroprotective drugs,neurotrophic factor therapy,nerve transplantation,stem cell therapy and gene therapy,have offered new perspectives for solving the problem of high disability rate of traumatic optic nerve injury clinically.This article attempts to summarize the status quo and latest progress in clinical treatment of traumatic optic nerve injury based on relevant literature in recent years,which can serve as reference for clinicians in choosing the optimal therapeutic regimen.

Optic Nerve Crush Induces Changes of Hydrogen Sulfide Synthases Expression in the Rat Retina / 法医学杂志

Objective To investigate the expression changes of the hydrogen sulfide synthases cystathionineγ-lyase (CSE), cystathionineβ-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST), after optic nerve crush (ONC) in rat the retina.Methods The rat model of ONC was established.Rats were divided into normal control, ONC, and sham control groups.Histopathologic changes in retina, the number of retinal ganglion cells (RGC) and retinal thickness of inner part (RTIP) were measured.The changes of CSE, CBS and 3-MST mRNA expression were detected with quantitative real-time PCR.Results The retinal histostructure was normal in normal controls and with minor changes in sham controls, respectively.Compared with sham group, significant retina damages were found in the ONC group:a time-dependent reduction of RGC number and RTIP.Expressions of CSE, CBS and 3-MST mRNA in rat retina were detected in normal control.Compared with normal controls, the expressions of CSE, CBS and 3-MST mRNA did not show any significant changes in the sham controls.Compared with sham controls, CBS mRNA expressions showed a time-dependent increase at 3 d, 7 d and 14 d after crush in the ONC group;CSE mRNA expressions increased to the peak at 3 d and then slightly reduced at 14 d after crush;3-MST mRNA expressions showed the trend of increase at 3 d and 7 d and then enhanced remarkably at 14 d after crush.Conclusion Hydrogen sulfide synthases CSE, CBS and3-MST expressions were up-regulated in rat retina following ONC, which may cause an increase in local endogenous hydrogen sulfide production in the retina and a compensatory protective effect.

Surgical Treatment for Traumatic Optic Neuropathy / 대한신경손상학회지

Traumatic optic neuropathy (TON) is an important cause of severe visual loss after blunt or penetrating head and facial trauma. High-dose steroids and surgical interventions have been applied in the indirect TON. However, there is no convincing evidence that results of the treatment have any strong benefits in terms of improvement of visual acuity. Nevertheless, surgical decompression should be considered in the case of a direct bony compression to the optic nerve and a progressive visual loss in indirect TON. Neurosurgeon should be aware the surgical indication, optimal timing and relevant technique for the optic canal (OC) decompression. In this review article, we will focus on the surgical approaches to the OC and how to decompress it.

Evolution of optic nerve and retina alterations in a child with indirect traumatic neuropathy as assessed by optical coherence tomography / Evolução das alterações no nervo óptico e na retina em criança com neuropatia traumática indireta avaliadas com tomografia de coerência óptica

ABSTRACT Herein, we describe the case of a 4-year-old child with indirect traumatic optic neuropathy and serial changes of the optic nerve head and retinal nerve fiber layer (RNFL) documented using optical coherence tomography (OCT). Visual acuity improved despite progressive RNFL thinning and optic disc pallor. We concluded that OCT may be useful for monitoring axonal loss but may not predict the final visual outcome.

RESUMO Descrição do caso de uma criança de 4 anos de idade com neuropatia óptica traumática indireta, cujas alterações no nervo óptico e na camada de fibras nervosas da retina foram documentadas com tomografia de coerência óptica seriadas. A acuidade visual apresentou melhora apesar da diminuição progressiva da camada de fibras nervosas e da palidez do disco óptico. Em conclusão, a tomografia de coerência óptica pode ser útil para monitorar a perda axonal na neuropatia óptica traumática indireta, sem no entanto, predizer o desfecho visual.

The current status and progress of the pathological changes and related molecular mechanisms of neuroretinal injury in diabetic retinopathy / 中华眼底病杂志

The neuroretinal injuries of diabetic retinopathy (DR) include retinal neuronal damage and reactive gliosis,both of which are induced by hyperglycemia and presented as early features of DR.They promote to develop mutually and accelerate the progression of DR.The molecular mechanisms study of neuronal damage mainly focuses on the alterations of extracellular environment and related signaling pathways,include inflammation,oxidative stress,endoplasmic reticulum stress,the formation of advanced glycation end products,glutamate toxicity and so on.These alterations mainly result in neuronal apoptosis and autophagy.The damaged neurons activate the glial cells with apparent changes in morphology,cell counts and the level of intracellular protein expression.In non-proliferative DR,glial cells are moderately hypertrophic and slightly increased in numbers.In proliferative DR,there is a significant rise in glial cell number with enhanced level of inflammatory factors and vascular active substances which lead a further neuronal damage.Signaling pathways of extracellular signal-regulated kinase 1/2,c-Fos and p38 mitogen-activated protein kinase are associated with their activation.Researches on the molecular mechanisms and signaling pathways of the DR will promote controlling the DR progression at the cellular level.

Good Anatomical Outcome of Orbital Plasmacytoma Following Chemo-Radiotherapy

Extramedullary plasmacytoma is a rare complication from multiple myeloma. We report a 56-year-old lady with underlying multiple myeloma who developed swelling over the left eye. It caused a non-axial proptosis, exposure keratopathy and visual acuity of counting fingers. A tissue biopsy revealed infiltration of tissue fragments with neoplastic plasma cells positive for CD138 and Kappa light chain restrictions consistent with plasmacytoma. Following radio-chemotherapy, the mass shrunk tremendously but her visual outcome remained poor.

Clinical features of traumatic optic neuropathy in 265 cases / 中华耳鼻咽喉头颈外科杂志

Objective@#To analyze the clinical features and the pathogenetic law of traumatic optic neuropathy through epidemiologic study.@*Methods@#265 cases (275 eyes) with TON treated in Department of Otorhinolaryngology Head and Neck Surgery, the Affiliated Hospital of Qingdao University from April 1999 to August 2015 were retrospectively analyzed. Multiple Logistic regression analyses were used to evaluate potential prognostic factors on visual acuity.@*Results@#TON occured mostly in young (194/265, 73.21%) man (235/265, 88.68%), the majority of patients came from villages and towns (209/265, 78.87%). Traffic accident (197/265, 74.34%) remained the main etiology, with strike (36/265, 13.58%) and fall (17/265, 6.42%) as the common etiology. Most patients had head injuries. The effective rate of vision improvement was 53.45%(147/275). Multiple logistic regression analyses identified that initial visual acuity with light perception or better vision, optic canal fracture and orbital wall fracture were visual acuity key factors of TON (χ2 value was 24.674, 19.755, 9.175, respectively, all P<0.01), initial visual acuity with light perception or better vision was the protective factor on visual acuity recovery (OR=5.008, P<0.001), the presence of optic canal fracture and orbital wall fracture were the risk factors on visual acuity recovery (OR value was 0.110, 0.329, respectively, all P<0.01).@*Conclusions@#Ton occurs mostly in young man because of traffic accident. Visual impairment of TON is severe. The suitable preventive measures should be carried out according to its epidemiological features.

Endoscopic salvage treatment for optic neuropathy caused by sinonasal fibro-osseous lesions / 中华耳鼻咽喉头颈外科杂志

Objective@#To summarize the surgical techniques, benefits and limitations of transnasal endoscopic resection and optic nerve decompression for patients with optic neuropathy caused by fibro-osseous lesions.@*Methods@#Eight patients with optic neuropathy caused by fibro-osseous lesions who accepted endoscopic surgery of either resection of the lesion or decompression of optic nerve in Otorhinolaryngology Hospital, First Affiliated Hospital of Sun Yat-sen University from 2007 to 2016 were retrospectively reviewed and followed until April, 2017. Analyses were performed on the pathology type, disease extent and disease duration, especially on the visual acuity and visual field changes before and after surgery.@*Results@#Eight patients (5 male and 3 female) were included in this study, with a median age of 12 years old (8-19 years old). The median disease duration was 12 months (1-72 months). The visual acuity (VA) of five patients (40 cm/FC, 0.2, 0.1, 0.2, 10 cm/FC, respectively) improved after surgery (0.1, 0.3, 1.2, 0.1, 0.6, respectively), and one patient had no change of VA after the surgery. Two patients (0.02, hand movement, before surgery) became deprived of light perception (VA=0) immediately after surgery. One patient complicated with intra orbital hemorrhage because of anterior artery injury. No complications of cerebral spinal fluid leak, intra-ocular muscle injury, intra-cranial hemorrhage or brain tissue injury occurred.@*Conclusion@#For the treatment of optic neuropathy caused by fibro-osseous lesions, transnasal endoscopic surgery might have a good outcome.

Diagnosis and treatment of traumatic optic neuropathy with internal carotid artery trauma / 中华耳鼻咽喉头颈外科杂志

Objective@#To summarize our experience in the diagnosis of internal carotid artery trauma in patients with traumatic optic neuropathy, and to make recommendations for the treatment.@*Methods@#The clinic data of 6 cases who had traumatic optic neuropathy with internal carotid artery trauma and who were admited in Department of Otorhinolaryngology, the Second Affiliated Hospital and Yuying Children′s Hospital of Wenzhou Medical University from Jan. 2013 to Dec. 2015 were analyzed retrospectively.@*Results@#All 6 cases were monocular blindness. Four cases did not undergo nasal endoscopic optic nerve decompression because of the diagnoses of internal carotid artery trauma. One case was diagnosed after nasal endoscopic optic nerve decompression because of fatal bleeding during the operation. One case was diagnosed because of late-onset recurrent epistaxis. Among the 6 cases with internal carotid artery trauma, 3 cases were successfully treated with endovascular interventional treatment (stent embolization was used in one case, Coil embolization was used in two cases), and 3 patients refused treatment.@*Conclusions@#The patients with traumatic optic neuropathy have the possibility of severe carotid artery trauma. Endoscopic optic nerve decompression is not suitable for these cases. It should pay more attention to patients with traumatic optic neuropathy. For suspected cases, vascular-enhanced computed tomography screening and digital subtraction angiography should be recommended and patients should be treated by endovascular intervention in a timely manner.

Near-complete optic nerve transection by high-pressure air

The use of high-pressure air instruments has become more common. Consequently, there have been a number of cases of orbital emphysema caused by contact with high-pressure air. In this case, a 62-year-old male patient visited an emergency medical center after his left eye was shot by an air compressor gun that was used to wash cars. Lacerations were observed in the upper and lower eyelids of his left eye. Radiological examinations revealed orbital emphysema, optic nerve transection, pneumocephalus, and subcutaneous emphysema in the face, neck, shoulder, and mediastinum. Canalicular injury repair was performed, and the emphysema resolved. However, there was near-complete vision loss in the patient's left eye. Because most optic nerve transections occur after a severe disruption in bone structure, pure optic nerve transections without any injury of the bone structure, as in the present case, is extremely rare.

The efficacy of transnasal optic nerve decompression for traumatic optic neuropathy in different ;surgery time：Meta analysis / 中国医师进修杂志

Objective To evaluate the effect of transnasal optic nerve decompression for traumatic optic neuropathy in different surgery time. Methods The databases of the Cochrane library, Embase, PubMed, Wanfang Database, China Journal Full-text Database (CNKI), Weipu Database(VIP) were searched for retrospective studies and clinical controlled trials. The search words included traumatic optic neuropathy, TON, eye traumas, transnasal endoscopicoptic decompression, TEOND, decompression of optic canal and endoscopy. According to the inclusion and exclusion criteria, the data were extracted. The RevMan 5.3 was used to analyze the data. Results All of 1 087 studies were detected. Sixteen eligible studies were enrolled, including 803 eyes. Meta analysis showed that the recovery degree of visual acuity, curative effect in operation group within 7 d of trauma was obviously superior to the operation group 7 d after trauma (OR=2.78;95%CI:2.02-3.82;P<0.01). Conclusions Transnasal endoscopic optic nerve decompression in treatment of traumatic optic neuropathy should be operated as soon as possible, and it is better to operate within 7 d.

Lesões traumáticas do nervo óptico / Optic nerve traumatic lesions

Documentar a incidência de lesões traumáticas da via óptica, assim como a etiologia traumática; correlacionar as lesões do nervo óptico com achados radiológicos (lesões cranianas e intracranianas); e estudar lesões múltiplas de nervos cranianos. Métodos: Dezoito pacientes admitidos no Serviço de Emergência da Santa Casa de Misericórdia de São Paulo com lesão traumática da via óptica foram incluídos. Os pacientes foram divididos em três grupos de acordo com o escore da Escalade Coma de Glasgow (ECG) em: trauma leve (ECG de 13 a 15), moderado(ECG de 9 a 12) e grave (ECG de 3 a 8), distribuição quanto a gênero, presença de fraturas, lesões intracranianas, fístulas liquóricas emecanismo de trauma. Resultados: Dos 18 casos, 17 lesões ocorreram em conjunto com outros nervos cranianos e em 1 caso houve lesão exclusiva do nervo óptico. Atropelamentos, acidentes automobilísticos, motociclísticos e ferimento por projétil de arma de fogo constituíram as causas mais frequentes de lesão do nervo óptico, de forma isolada, assim como nas lesões de múltiplos nervos. Hematomas extradurais e contusões cerebrais foram as lesões intracranianas mais frequentes e, quando presentes, as fraturas cranianas localizavam-se no teto orbitário ou na região frontal. Conclusão: Neuropatia traumática do óptico deve ser pesquisada à admissão do paciente (quando possível), pois é passívelde tratamento clínico (corticoides) ou cirúrgico. Achados sugestivos de neuropatia óptica traumática incluem fraturas do assoalho ou teto orbitário e traumas de alta energia cinética...

To register the incidence of the traumatic lesions to the optic nerve and its etiology; to correlate these lesions to the radiological findings (cranial and intracranial) and study multiple cranial nerve lesions.Methods: Eighteen patients admitted to the Emergency Service of Santa Casa de Misericórdia de São Paulo Hospital have been studied and lesions to the optic nerves were described. The patients were divided into 3 groups according to the Glasgow Coma Scale (GCS) in: mild trauma (GCS: 13 to 15), moderate (GCS: 9 to 12) and severe (GCS: 3 to 8), gender, fractures, intracranial lesions, CSF fistulas and type of trauma. Results: Posttraumatic single nerve lesion was observed in 1 patient and in 17patients multiple nerve lesions associated with the optic nerve lesion were documented. Running over, vehicle and motorcycle accidents and gunshot wounds were the main causes of these lesions (single nerve and multiple nerves). Extradural hematomas and cerebral contusions were the most frequent intracranial lesions. Whenever present, the cranial fractures involved the orbital roof or the frontal region. Conclusion: Traumatic optic neuropathy occurs must be searched on the patient admission (wheneverit is possible), because medical or surgical treatment can be proposed. Finding signs of traumatic optic neuropathy include fractures of the roof or floor of the orbit and traumas with high kinetic energy...

Using ImageJ to Evaluate Optic Disc Pallor in Traumatic Optic Neuropathy

PURPOSE: To evaluate optic disc pallor using ImageJ in traumatic optic neuropathy (TON). METHODS: This study examined unilateral TON patients. The optic disc was divided into 4 quadrants (temporal, superior, nasal, and inferior), consistent with the quadrants on optical coherence tomography (OCT) retinal nerve fiber layer (RNFL) thickness maps. Optic disc photography was performed and disc pallor was quantified using gray scale photographic images imported into ImageJ software. The correlation between optic disc pallor and RNFL thickness was examined in each quadrant. RESULTS: A total of 35 patients (31 male, 4 female) were enrolled in the study. The mean participant age was 34.8 +/- 15.0 years (range, 5 to 63 years). Overall RNFL thickness decreased in 6 patients, with thinning most often occurring in the inferior quadrant (28 of 35 eyes). There was a significant correlation between optic disc pallor and RNFL thickness (superior, rho = -0.358, p = 0.04; inferior, rho = -0.345, p = 0.04; nasal, rho = -0.417, p = 0.01; temporal, rho = -0.390, p = 0.02). The highest level of correspondence between disc pallor and RNFL thickness values outside of the normative 95th percentiles was 39.3% and occurred in the inferior quadrant. CONCLUSIONS: Optic disc pallor in TON was quantified with ImageJ and was significantly correlated with RNFL thickness abnormalities. Thus, ImageJ evaluations of disc pallor may be useful for evaluating RNFL thinning, as verified by OCT RNFL analyses.

MR diffusion tensor imaging of optic nerve in anterior ischemic optic neuropathy at 3.0 T and correlation between diffusion tensor imaging and pattern visual evoked potential / 中华放射学杂志

Objective To study the value of MR diffusion tensor imaging (MR-DTI)using a 3.0 T scanner in anterior ischemic optic neuropathy(AION).Methods A total of 26 patients suffering from unilateral subacute AION were examined using DTI and pattern visual evoked potential(P-VEP).The parameters values of optic nerves including fractional anisotropy (FA),ADC,vertical diffusivity (λ⊥),paralleldiffusion (λ//),P100 value and amplitude were obtained.Paired t-tests were used for comparing the FA,ADC,λ⊥,and λ// values of the two groups.Correlations of DTI parameters and P-VEP parameters were analysed by using the Pearson rank correlation analysis.Results The values of FA,ADC,λ//,and λ_ in the affected nerve were 0.28±0.07,(1.43±0.20) ×103 mm2/s,(1.79±0.16) ×10-3 mm2/s,and (1.25±0.17) ×10-3 mm2/s respectively,and the corresponding values of unaffected nerve were 0.57±0.05,(1.04±0.17) ×10-3 mm2/s,(1.71 ±0.19) × 10-3 mm2/s,and (0.75±0.08) × 10-3 mm2/s respectively.Compared to unaffected contralateral nerves,the mean FA was reduced,the mean ADC,λ⊥ were increased in the affected nerves(t=-19.269,10.537,15.301,P＜0.01).However,there were no significant difference of the λ//(t=l.632,P＞0.05).There was significant negative correlation between ADC and P-VEP amplitude in affected optic nerves (r=-0.722,P＜0.01).There was moderate negative correlation between λ⊥ and P-VEP amplitude in affected optic nerves (r=-0.634,P＜0.01).There was moderate correlation between FA and P-VEP amplitude (r=0.539,P＜0.01).There was no correlation between λ// and P-VEP amplitude.There was moderate negative correlation between FA and P-VEP P100 latency(r =-0.619,P＜0.01).Conclusions DTI can sensitively detect diffusional abnormality of anterior ischemic optic neuropathy.DTI could be used as a supplemental way in the assessment of AION.

Lesões traumáticas de nervos cranianos / Traumatic lesions to the cranial nerves

Objetivo: Documentar a incidência de lesões traumáticas de nervos cranianos, assim como a etiologia traumática, correlacionar as lesões dos nervos cranianos com achados radiológicos (lesões cranianas e intracranianas) e estudar lesões múltiplas de nervos cranianos. Métodos: Cinquenta e quatro pacientes admitidos no Serviço de Emergência da Santa Casa de Misericórdia de São Paulo com lesões traumáticas nos diferentes nervos cranianos foram incluídos. Todos os pacientes foram submetidos à radiografia simples de crânio, tomografia computadorizada e, quando indicada, ressonância magnética de encéfalo. Os pacientes foram divididos em três grupos de acordo com o escore da Escala de Coma de Glasgow (ECG) em: trauma leve (ECG de 13 a 15), moderado (ECG de 9 a 12) e grave (ECG de 3 a 8). Resultados: Os nervos cranianos mais afetados de forma isolada foram olfatório, facial e oculomotor. O atropelamento foi a causa mais comum de lesão de nervos cranianos de forma isolada, assim como nas lesões de múltiplos nervos. Contusões e hematomas extradurais foram as lesões intracranianas mais frequentes. Conclusão: Neuropatia craniana de etiologia traumática ocorre frequentemente e deve ser pesquisada à admissão do paciente, pois pode exigir descompressão de estruturas nervosas importantes como nervo óptico e facial.

Objective: To register the incidence of the traumatic lesions to the cranial nerves and its etiology; to correlate the lesions to the radiological findings (cranial and intracranial) and study multiple cranial nerve lesions. Methods: Fifty-four patients admitted to the Emergency Service of Santa Casa de Misericórdia de São Paulo Hospital have been studied and lesions to the different cranial nerves were described. All patients were submitted do radiographic exams, computed tomography, and, when necessary, magnetic resonance imaging. The patients were divided into 3 groups according to the Glasgow Coma Scale (GCS) in: mild trauma (GCS: 13 to 15), moderate (GCS: 9 to 12) and severe (GCS: 3 to 8). Results: Posttraumatic single nerve lesion was more frequent seen on olfactory, facial and oculomotor nerves. Running over was the main cause of these lesions (single nerve and multiple nerves). Contusions and extradural hematomas were the most frequent intracranial lesions. Conclusion: Traumatic cranial neuropathy occurs frequently and must be searched on the patient admission, because it can surgical decompression may necessary, such as decompression of the optic or facial nerves.

Noninvasive evaluation of intracranial hypertension? Is there a gold standard? / Avaliação não invasiva da hipertensão intracraniana? Existe um padrão-ouro?

Computed tomography is essential in head injuried patients for the detection of structural damage to the brain. However, the ability of CT scanning to predict the presence or absence of intracranial hypertension has been debated in the literature. Since the optic nerve is part of the central nervous system and in case of raised pressure in the cerebrospinal fluid its sheath inflates. Based in this hypothesis the authors reviewed the role of the optic nerve sheat diameter in diagnosis intracranial hypertension after traumatic brain injury. This non-invasive method is useful to predict the risk of intracranial hypertension and select patients to ICP monitoring, especially in those with normal CT scans.

A tomografia de crânio é um exame fundamental para avaliação estrutural dos pacientes com traumatismo craniano. Entretanto, a capacidade da tomografia em predizer a ausência ou presença de hipertensão intracraniana é controversa. Como o nervo óptico é parte do sistema nervoso central, em situações de hipertensão intracraniana há aumento da bainha neural. Com base nessas hipóteses, os autores revisaram o papel da análise do diâmetro da bainha do nervo óptico no diagnóstico de hipertensão intracraniana pós-traumatismo. Esse método não invasivo é útil para predizer os riscos de hipertensão intracraniana e selecionar os pacientes para monitorização da pressão intracraniana, principalmente naqueles com tomografia de crânio normal.