Optic Nerve Impairment Research Articles

Current Strategies for Optic Nerve Protection and Repair

Damage to the optic nerve and its functioning is referred to as optic neuropathy, unlike the peripheral nervous system (PNS), the optic nerve is part of the central nervous system (CNS), which presents limitations in its regenerative abilities. Both intrinsic and extrinsic factors contribute to these limitations. Strategies for neuroprotection and neuroregeneration have been studied and implemented to address these challenges. While there is no definite treatment in the past two decades there have been many advances in the modulation of inflammation, apoptosis, neurotrophic factors and stem cell replacement strategies. The advances in these areas could transform our approach to optic nerve impairment in the future.

A study of nonglaucomatous optic neuropathies in a teaching hospital in Western Maharashtra

Background: Nonglaucomatous optic neuropathy (NGON) is defined as clinical evidence of optic nerve impairment without glaucomatous field/disc changes. Etiology is diverse and elusive in many patients. Causes of NGON include traumatic, compressive, inflammatory, demyelinating, toxic, nutritional, hereditary, vascular, infiltrative, and idiopathic. NGON disorders can be misdiagnosed as glaucoma and can be preventable or life-threatening. In some, fellow eye involvement is common. This can lead to inadequate management and influence prognosis which can be prevented by multispecialty approach. Physicians and ophthalmologists must be vigilant against threatening NGON forms. It is essential to track burden as most literature focused on particular NGON subtype. Aim: The aim was to study the clinical presentation of NGON in a teaching hospital. Setting and Design: This was a prospective, hospital-based, cross-sectional, observational study. Materials and Methods: A total of 86 eyes of 61 NGON patients were studied from January 2021 to June 2022 in a tertiary care hospital. Detailed history and comprehensive ophthalmic examination were performed in ambulatory patients. Nonambulatory patients were examined using torchlight. Ancillary investigations were performed, to confirm the clinical diagnosis wherever applicable. Statistical Analysis: Microsoft Excel was used for statistical analysis. Results: The mean age of study patients was 44.87 ± 16.05 years with a male: female ratio of 2.8:1. Unilateral eye involvement was seen in 36 (59.02%). Best-corrected visual acuity = 3/60–1/60 was noted in 41 (47.67%) patients. Red-green defect and contrast sensitivity were reduced by 59.30% and 66.28%, respectively. Relative afferent pupillary defect (RAPD) was noted in 52.46% of patients with Grade 5 RAPD in 40.63%. The most common visually evoked potential type and visual field defect noted were axonal and central scotoma (n = 31 [36.05%] and n = 26 [30.23%]), respectively. Traumatic optic neuropathy was diagnosed in 15 (24.59%) followed by inflammatory optic neuritis in 11 (18.04%) patients. Conclusion: Diagnosing cause of NGON in clinical practice is challenging, but emerging burden cannot be neglected. Knowledge of various NGON types helps narrow differential diagnoses and execute efficient, targeted workup. Timely recognition alters visual, neurological prognosis and saves the lives of patients sometimes.

Bi-allelic variants in SNF8 cause a disease spectrum ranging from severe developmental and epileptic encephalopathy to syndromic optic atrophy

The endosomal sorting complex required for transport (ESCRT) machinery is essential for membrane remodeling and autophagy and it comprises three multi-subunit complexes (ESCRT I-III). We report nine individuals from six families presenting with a spectrum of neurodevelopmental/neurodegenerative features caused by bi-allelic variants in SNF8 (GenBank: NM_007241.4), encoding the ESCRT-II subunit SNF8. The phenotypic spectrum included four individuals with severe developmental and epileptic encephalopathy, massive reduction of white matter, hypo-/aplasia of the corpus callosum, neurodevelopmental arrest, and early death. A second cohort shows a milder phenotype with intellectual disability, childhood-onset optic atrophy, or ataxia. All mildly affected individuals shared the same hypomorphic variant, c.304G>A (p.Val102Ile). In patient-derived fibroblasts, bi-allelic SNF8 variants cause loss of ESCRT-II subunits. Snf8 loss of function in zebrafish results in global developmental delay and altered embryo morphology, impaired optic nerve development, and reduced forebrain size. Invivo experiments corroborated the pathogenicity of the tested SNF8 variants and their variable impact on embryo development, validating the observed clinical heterogeneity. Taken together, we conclude that loss of ESCRT-II due to bi-allelic SNF8 variants is associated with a spectrum of neurodevelopmental/neurodegenerative phenotypes mediated likely via impairment of the autophagic flux.

Primary Open-Angle Glaucoma Patients in the Ophthalmology Outpatient Clinic Dr. Soetomo General Academic Hospital, Surabaya, in 2013–2015

Highlights: POAG is a common type of glaucoma. POAG patients were predominantly >60 years old, with males being more dominant than females. Abstract Introduction: Primary open-angle glaucoma (POAG) is a progressive, chronic optic neuropathy characterized by distinct optic nerve atrophy and impairment of the visual field. The purpose of this study was to describe the characteristics of primary open-angle glaucoma patients in the ophthalmology outpatient clinic of Dr. Soetomo General Academic Hospital, Surabaya, in 2013–2015. Methods: This was a descriptive-retrospective study. Samples were patients with a primary open-angle glaucoma (POAG) diagnosis in the ophthalmology outpatient clinic at Dr. Soetomo General Academic Hospital, Surabaya, in 2013–2015. Results: There were 88 samples of POAG patients in the ophthalmology outpatient clinic at Dr. Soetomo General Academic Hospital, Surabaya, in 2013–2015. POAG was dominated in the age group 60–69 years old, with a percentage of 37.50%. Males were more dominant than females, with a percentage of 55.70%. Many POAG patients were unemployed, with a percentage of 56.82%. Most patients with POAG did not have a history of hypertension or diabetes mellitus, with a percentage of 73.86%. Patients who had a history of hypertension were 11.36%, those with diabetes mellitus were 9.09%, and those who had a history of both hypertension and diabetes mellitus were 5.68%. Conclusion: POAG was a higher risk in older adults, with males being more dominant than females. Most patients did not have a history of either hypertension or diabetes mellitus.

Rhinogenic Optic Neuropathy with No Light Perception Secondary to Onodi Cell Mucocele with Visual Recovery after Optic Nerve Decompression.

Rhinogenic optic neuropathy (RON) results from ethmoid or sphenoid sinus inflammation or infection causing optic nerve impairment.1 Treatment often requires endoscopic surgery and vision restoration occurs in select cases. There is no clear evidence for the benefit of optic nerve decompression (OND) in these situations. We present a unique case of RON caused by an Onodi cell mucocele for which isolated endoscopic mucocele drainage was not enough and further OND was needed to improve vision.

Factors affecting the severity and prognosis of visual damage in inhalational methanol poisoning.

Inhalational methanol poisoning could cause severe damage to visual function. This study analyzed the prognosis of the correlation between the visual function and the relevant risk factors. In this retrospective study, 14 patients had confirmed inhalational methanol poisoning, resulting in visual impairment in both eyes. The following tests were performed: laboratory tests, best corrected visual acuity (BCVA), intraocular pressure, slit lamp, fundus photography, visual field (VF), pattern visual evoked potential (P-VEP), flash electroretinogram (F-ERG), optical coherence tomography (OCT), and orbital or cranial magnetic resonance imaging (MRI). With active treatment, visual function improved to varying degrees in all 14 cases (28 eyes) in this study. The BCVA of 21 eyes declined to no light perception at the onset; 16 eyes showed different degrees of improvement after treatment, with the final BCVA (LogMar) mainly ranging from 2 to 3, and vision acuity stabilized after the 5th month. The VF pattern in the acute phase was mostly blind. Other VF patterns included the central visual island, large paracentral scotomas, hemipleural VF defects, and the temporal visual island. Retinal nerve fiber layer (RNFL) thickening was observed commonly in the acute phase (146.8 ± 33.2 μm), which subsided in the 1st month, showed dramatic thinning at the 3rd month, and then stabilized in the 5th month after onset. MRI showed that the main sites involved were optic nerve impairment, the optic disk, and retrobulbar segments. The basal ganglia region was the site most involved in the central nervous system (CNS). Inhalational methanol poisoning could lead to severe impairment of visual function, and the prognosis of visual acuity (VA) was highly relevant to the risk factors of duration of toxic exposure, delayed admission, and degree of acidosis.

Prostaglandin-based rAAV-mediated glaucoma gene therapy in Brown Norway rats

Prostaglandin analogs are first-line treatments for open angle glaucoma and while effective at lowering intraocular pressure, they are undermined by patient non-compliance, causing atrophy of the optic nerve and severe visual impairment. Herein, we evaluate the safety and efficacy of a recombinant adeno-associated viral vector-mediated gene therapy aimed at permanently lowering intraocular pressure through de novo biosynthesis of prostaglandin F2α within the anterior chamber. This study demonstrated a dose dependent reduction in intraocular pressure in normotensive Brown Norway rats maintained over 12-months. Crucially, therapy could be temporarily halted through off-type riboswitch activation, reverting intraocular pressure to normal. Longitudinal multimodal imaging, electrophysiology, and post-mortem histology revealed the therapy was well tolerated at low and medium doses, with no major adverse effects to anterior chamber health, offering a promising alternative to current treatment strategies leading to clinically relevant reductions in intraocular pressure without the need for adherence to a daily treatment regimen.

Fractional anisotropy helps to differentiate the optic nerve impairment between neuromyelitis optica spectrum disorders and multiple sclerosis.

To assess the characteristics of optic nerve impairment between neuromyelitis optica spectrum disorders (NMOSD) and multiple sclerosis (MS) patients by fractional anisotropy (FA). Thirty-one NMOSD patients, 25 MS patients, and 17 heathy controls (HC) who underwent optic nerve DTI were included. The optic nerves of the NMOSD and MS patients were divided into vision-impaired (VI) subgroups and normal-appearing (NA) subgroups according to visual status, respectively. FA values were measured in the anterior, middle, and posterior segments of each intraorbital optic nerve. FA values in VI NMOSD were significantly decreased in the whole optic nerve, especially the posterior segment of the optic nerve (p < 0.001). FA values measured in the anterior and middle segments of the optic nerve in VI MS were significantly decreased as compared to those in the HC (p < 0.05). Between NMOSD and MS, FA values in the posterior segment of the optic nerve showed significant differences (VI NMOSD vs. VI MS, 0.458 ± 0.097 vs. 0.568 ± 0.098, p < 0.001; NA NMOSD vs. NA MS, 0.568 ± 0.098 vs. 0.600 ± 0.085, p = 0.041, respectively). The signal intensity ratio (SIR) in the posterior segment of the optic nerve was significantly increased in VI NMOSD as compared with VI MS (p = 0.002). The combination of SIR and FA for distinguishing VI NMOSD from VI MS resulted in sensitivity, specificity, and positive and negative predictive values of 86.49%, 80.00%, 88.9%, and 76.2%, respectively. FA could quantify the characteristics of NMOSD- and MS-related optic nerve impairment. DTI was a simple and effective imaging tool to differentiate between the two. • NMOSD-related optic nerve impairment is extensive, often greater than half of the optic nerve, with the most significant involvement of the posterior segment of the optic nerve. • MS-related optic nerve impairment is more limited than NMOSD, and anterior and middle optic nerve involvement is common. • Optic nerve DTI is a convenient and effective imaging tool that can help characterize NMOSD and MS.

Optic Nerve Head Vessel Density Changes from Graves' Disease without TED to TED Dysthyroid Optic Neuropathy: Does Optic Nerve Head Ischemia Play a Role?

To compare the retinal peripapillary capillary (RPC) vessel density (VD) between 5 groups of patients on the spectrum of thyroid eye disease (TED). This is a prospective comparative study looking at 5 groups of patients who were consecutively included from January 2018 to March 2021. They were composed of: Healthy volunteers (39 eyes and 20 subjects), patients with Graves' disease without TED (26 eyes and 13 patients), mild TED (28 eyes and 14 patients), moderate-severe TED (30 eyes and 17 patients), and TED with dysthyroid optic neuropathy (DON) (21 eyes and 12 patients). Ocular and periocular examination, visual field indices, RPC-VD (with optical coherence tomography angiography), and retinal nerve fiber layer, and macular ganglion cell complex thickness were recorded. An initial insignificant (0.5 < p < 0.9) rise in the peripapillary-VD (pp-VD) and whole image-VD (wi-VD) from the healthy subject to the Graves' disease without TED was followed by a significant (p = 0.001) fall in RPC-VD in different severity grades of the TED. Paired comparison between the 5 groups showed that the statistically significant fall from the Graves' disease group occurred in the moderate-severe and DON groups (0.001 ≤ p ≤ 0.04). No variable significantly affected the VD (0.08 ≤ p ≤ 0.9). A lower wi-VD and pp-VD were significantly (0.001 ≤ p ≤ 0.009) correlated with the impaired optic nerve functional and structural tests. The sensitivity and specificity of wi-VD (81% and 76%) and pp-VD (69% and 71%) for detecting the DON were statistically significant (p < 0.001). Despite an insignificant rise in the wi- and pp-VD from the healthy volunteers to the patients with Graves' disease without TED, VD showed a declining trend in the course of patients with TED, which was statistically significant in the moderate-severe TED and DON groups.

The Clinical Utility of Inpatient Brain Magnetic Resonance Imaging in Children.

The clinical applicability and yield of brain magnetic resonance imaging (MRI) in the setting of an inpatient pediatric department has not been investigated. The authors performed a retrospective chart review of nontraumatic/nonneurosurgical children who underwent brain MRI during their hospitalization in a general pediatric department over a 5-year period. Of the 331 children who underwent brain MRI, 148 (45%) had abnormal findings. High-risk headaches and focal seizures were significantly correlated with findings on brain MRI. Diagnostic and therapeutic yields were most significant in acute demyelinating events, acute cerebrovascular disorders, high-risk headaches when supported by neurologic and ophthalmologic findings, focal seizures with evidence of multifocal epileptic activity on an electroencephalogram and ophthalmic complaints when accompanied by cranial nerve palsy and optic nerve impairment. Since the contributions of a brain MRI in hospitalized children is pivotal in specific clinical situations, a judicious decision-making process should be done before its scheduling, in order to optimize clinical care.

Optic neuritis at disease onset predicts poor visual outcome in neuromyelitis optica spectrum disorders

IntroductionOptic neuritis (ON) in neuromyelitis optica spectrum disorders (NMOSD) may occur at the onset of the disease, during relapse attacks, or both. It is well known that ON in NMOSD may cause permanent visual disability, but the influence of the time of its occurrence has not been investigated. ObjectiveWe evaluated the effect of the time of ON occurrence on visual outcome in a cohort of NMOSD patients. MethodsWe retrospectively analyzed the medical records of NMOSD patients with ON who met the 2015 International consensus criteria for NMOSD diagnosis. We assessed demographic and clinical data, the Expanded Disability Status Scale (EDSS), and visual disability according to the scores of the Kurtzke Visual Function Scale (KVS) and Wingerchuk's Optic Nerve Impairment Scale (WONIS). We divided patients into three groups according to the time of ON occurrence: (1) ON at disease onset; (2) ON exclusively in relapse attacks; and (3) ON at both disease onset and in relapse attacks. ResultsOut of 187 patients with suspected NMOSD, 85 (42.4%) met the inclusion criteria. ON occurred exclusively at the disease onset in 16 (18.8%) patients, exclusively in relapse attacks in 43 (50.6%) patients, and at both the onset and in relapse attacks in 26 (30.6%) patients. There was no significant difference in the EDSS scores of the groups. In comparison with patients with ON exclusively occurring during relapse attacks, patients with ON at disease onset had higher KVS scores (p = 0.009) and WONIS scores (p = 0.005). Patients with ON at both onset and in relapses had a larger number of ON attacks and NMOSD relapses, as well as the poorest visual outcome. ConclusionsON at disease onset is a predictive factor for poor visual outcome in NMOSD patients.

Systemic and ocular determinants of mean ocular perfusion pressure in a population-based sample.

To investigate the associations between mean ocular perfusion pressure (MOPP) and several variables including body mass index (BMI), comorbid medical conditions and various ocular parameters in a population-based sample. Cross-sectional. Data of 2091 healthy participants from a previous population based cross-sectional study were reviewed. Inclusion criteria were adults ≥40 years of age who were screened on-site for glaucoma. Data on medical history, height, weight, systolic and diastolic blood pressures (SBP and DBP, respectively) were obtained. A basic ocular examination was performed which included intraocular pressure (Tono-Pen XL, Reichert Technologies) and central corneal thickness (Pacline pachymetry;) measurement, slit-lamp examination and non-mydriatic optic disc photography (nonmydα fundus camera, Kowa). MOPP was calculated using the formula [2/3 x (DBP + 1/3(SBP-DBP)]-IOP and low MOPP was defined as MOPP ≤45 mmHg. Mean age of the subjects was 63.04 ± 9.7 years (range: 44 and 99 years) and the majority were women (74.1%, n = 1549). Mean MOPP values in normal weight (BMI < 25), overweight (BMI = 25-29.9) and in obese individuals were 46.9 ± 9.0 mmHg, 48.6 ± 9.2 mmHg and 50.7 ± 10.0 mmHg, respectively (p < 0.001, in all pairwise comparisons). In the multivariable logistic regression analysis, migraine and IOP elevation (per 1 mmHg increment) were significantly associated with a low MOPP (OR: 2.10 and 1.22, p = 0.008 and < 0.001, respectively). On the other hand, risk of low MOPP was reduced in subjects with hypertension, and with increasing age (per 1-year increment) and BMI (per 1-unit increment) (OR: 0.15, 0.97, and 0.95, respectively, and p < 0.001 for all). Migraine and elevated IOP increase the risk of low MOPP and this may have a causal relationship with impaired optic nerve head blood flow.

Secondary Neuroprotection in Glaucoma from Change in Lifestyle

Glaucoma therapy usually includes lowering IOP, but a healthy lifestyle may also be recommended. We discuss how this can be defined and the underlying secondary neuroprotective mechanisms. One neuroprotective measure is to avoid common neurotoxic pollution like cigarette smoking, ethanol, methanol or lead. Nutrition should be rich in variety and prevent vitamin B12 and folate deficiency. Supernutrition may lead to the metabolic syndrome and increase IOP, arterial hypertension and serum steroid levels. The metabolic syndrome can also lead to decreased renal function, which can cause accumulation of neurotoxic substances in the blood. Enhanced physical activities is useful, as this burns calories and reduces caloric intake. In contrast to supernutrition, during starvation ketone bodies like acetone, acetoacetate and β-hydroxybutyrate are synthesised. These are thought to have neuroprotective effects, due to the additional power supply to the mitochondria. Ketosis can also occur after increased intake of fatty acids - which is generally not recommended, due to the cardiovascular risks involved. In addition to burning calories, endurance sports can reduce fear and depression, and neurotrophins with neuroprotective effects are released. Genetically determined or acquired mitochondrial dysfunction can both play a role in glaucomatous optic nerve impairment. Therefore, knowledge of secondary neuroprotective mechanisms can help in giving patient professional advice to minimise risks and to restore homeostasis in optic nerve metabolism.

P1-07-04. Multifocal motor neuropathy presenting as the optic nerve impairment: A study with VEP

P1-07-04. Multifocal motor neuropathy presenting as the optic nerve impairment: A study with VEP

MRI Histogram Texture Feature Analysis of the Optic Nerve in the Patients with Optic Neuritis.

Objective To evaluate the optic nerve impairment using MRI histogram texture analysis in the patients with optic neuritis.Methods The study included 60 patients with optic neuritis and 20 normal controls. The coronal T2 weighted imaging (T2WI) with fat saturation and enhanced T1 weighted imaging (T1WI) were performed to evaluate the optic nerve. MRI histogram texture features of the involved optic nerve were measured on the corresponding coronal T2WI images. The normal optic nerve (NON) was measured in the posterior 1/3 parts of the optic nerve. Kruskal-Wallis one-way ANOVA was used to compare the difference of texture features and receiver operating characteristic (ROC) curve were performed to evaluate the diagnostic value of texture features for the optic nerve impairment among the affected optic nerve with enhancement (ONwEN), affected optic nerve without enhancement (ONwoEN), contralateral normal appearing optic nerve (NAON) and NON.Results The histogram texture Energy and Entropy presented significant differences for ONwEN vs. ONwoEN (both P=0.000), ONwEN vs. NON (both P=0.000) and NAON vs. NON (both P<0.05). ROC analysis demonstrated that the area under the curve (AUC) of histogram texture Energy were 0.758, 0.795 and 0.701 for ONwEN vs. ONwoEN, ONwEN vs. NON and NAON vs. NON, AUC of Entropy were 0.758, 0.795 and 0.707 for ONwEN vs. ONwoEN, ONwEN vs. NON and NAON vs. NON.Conclusions The altered MRI histogram texture Energy and Entropy could be considered as a surrogate for MRI enhancement to evaluate the involved optic nerve and normal-appearing optic nerve in optic neuritis.

Pluripotent Stem Cell-Based Approaches to Explore and Treat Optic Neuropathies.

Sight is a major sense for human and visual impairment profoundly affects quality of life, especially retinal degenerative diseases which are the leading cause of irreversible blindness worldwide. As for other neurodegenerative disorders, almost all retinal dystrophies are characterized by the specific loss of one or two cell types, such as retinal ganglion cells, photoreceptor cells, or retinal pigmented epithelial cells. This feature is a critical point when dealing with cell replacement strategies considering that the preservation of other cell types and retinal circuitry is a prerequisite. Retinal ganglion cells are particularly vulnerable to degenerative process and glaucoma, the most common optic neuropathy, is a frequent retinal dystrophy. Cell replacement has been proposed as a potential approach to take on the challenge of visual restoration, but its application to optic neuropathies is particularly challenging. Many obstacles need to be overcome before any clinical application. Beyond their survival and differentiation, engrafted cells have to reconnect with both upstream synaptic retinal cell partners and specific targets in the brain. To date, reconnection of retinal ganglion cells with distal central targets appears unrealistic since central nervous system is refractory to regenerative processes. Significant progress on the understanding of molecular mechanisms that prevent central nervous system regeneration offer hope to overcome this obstacle in the future. At the same time, emergence of reprogramming of human somatic cells into pluripotent stem cells has facilitated both the generation of new source of cells with therapeutic potential and the development of innovative methods for the generation of transplantable cells. In this review, we discuss the feasibility of stem cell-based strategies applied to retinal ganglion cells and optic nerve impairment. We present the different strategies for the generation, characterization and the delivery of transplantable retinal ganglion cells derived from pluripotent stem cells. The relevance of pluripotent stem cell-derived retinal organoid and retinal ganglion cells for disease modeling or drug screening will be also introduced in the context of optic neuropathies.

AhR-deficiency as a cause of demyelinating disease and inflammation

The Aryl hydrocarbon Receptor(AhR) is among the most important receptors which bind pollutants; however it also regulates signaling pathways independently of such exposure. We previously demonstrated that AhR is expressed during development of the central nervous system(CNS) and that its deletion leads to the occurrence of a congenital nystagmus. Objectives of the present study are to decipher the origin of these deficits, and to identify the role of the AhR in the development of the CNS. We show that the AhR-knockout phenotype develops during early infancy together with deficits in visual-information-processing which are associated with an altered optic nerve myelin sheath, which exhibits modifications in its lipid composition and in the expression of myelin-associated-glycoprotein(MAG), a cell adhesion molecule involved in myelin-maintenance and glia-axon interaction. In addition, we show that the expression of pro-inflammatory cytokines is increased in the impaired optic nerve and confirm that inflammation is causally related with an AhR-dependent decreased expression of MAG. Overall, our findings demonstrate the role of the AhR as a physiological regulator of myelination and inflammatory processes in the developing CNS. It identifies a mechanism by which environmental pollutants might influence CNS myelination and suggest AhR as a relevant drug target for demyelinating diseases.

The Role of Transbasal Approach for Anterior Skull Base Tumors with Acute Visual Impairment

Introduction: As visual impairment is a common presentation of the parasellar tumors, the tumors located in the anterior skull base and craniofacial structures invading the optic canals (OCs) occasionally result in acute visual impairment from optic nerve compression. Our surgical policies in the management of these kinds of tumors extending into OCs are (1) avoiding disfiguring facial bone and skin incisions cosmetically, (2) selecting the appropriate surgical approaches to achieve the maximum safe resection of the tumor around the impaired optic nerve, and (3) employing the additional approach under making it difficult to achieve the enough resection by single surgical approach. We review our treatment experience with the above surgical strategy for the skull base tumors invading OCs with acute visual impairment, and discuss surgical approaches and patient outcomes.

Orbital apex disorders: a case series

Orbital apex syndrome is an uncommon disorder characterized by ophthalmoplegia, proptosis, ptosis, hypoesthesia of the forehead, and vision loss. It may be classified as part of a group of orbital apex disorders that includes superior orbital fissure syndrome and cavernous sinus syndrome. Superior orbital fissure syndrome presents similarly to orbital apex syndrome without optic nerve impairment. Cavernous sinus syndrome includes hypoesthesia of the cheek and lower eyelid in addition to the signs seen in orbital apex syndrome. While historically described separately, these three disorders share similar causes, diagnostic course, and management strategies. The purpose of this study was to report three cases of orbital apex disorders treated recently and to review the literature related to these conditions. Inflammatory and vascular disorders, neoplasm, infection, and trauma are potential causes of orbital apex disorders. Management is directed at the causative process. The cases described represent a rare but important group of conditions seen by the maxillofacial surgeon. A review of the clinical presentation, etiology, and management of these conditions may prompt timely recognition and treatment.

Effects of albendazole combined with TSII-A (a Chinese herb compound) on optic neuritis caused by Angiostrongylus cantonensis in BALB/c mice.

BackgroundAngiostrongylus cantonensis (A. cantonensis) infection can lead to optic neuritis, retinal inflammation, damage to ganglion cells, demyelination of optic nerve and visual impairment. Combined therapy of albendazole and dexamethasone is a common treatment for the disease in the clinic, but it plays no role in vision recovery. Therefore, it has been necessary to explore alternative therapies to treat this disease. Previous studies reported the neuro-productive effects of two constituents of Danshen (a Chinese herb)-tanshinone II-A (TSII-A) and cryptotanshinone (CPT), and this study aims to evaluate the impacts of TSII-A or CPT combined with albendazole on optic neuritis caused by A. cantonensis infection in a murine model.MethodsTo assess the effects of TSII-A or CPT combined with albendazole on optic neuritis due to the infection, mice were divided into six groups, including the normal control group, infection group and four treatment groups (albendazole group, albendazole combined with dexamethasone group, albendazole combined with CPT group and albendazole combined with TSII-A group). The infection group and treatment groups were infected with A. cantonensisand the treatment groups received interventions from 14 dpi (days post infection), respectively. At 21 dpi, the visual acuity of mice in each group was examined by visual evoked potential (VEP). The pathologic alteration of the retina and optic nerve were observed by hematoxylin and eosin (H&E) staining and transmission electronic microscopy (TEM).ResultsInfection of A. cantonensis caused prolonged VEP latency, obvious inflammatory cell infiltration in the retina, damaged retinal ganglions and retinal swelling, followed by optic nerve fibre demyelination and a decreasing number of axons at 21 dpi. In treatment groups, albendazole could not alleviate the above symptoms; albendazole combined with dexamethasone lessened the inflammation of the retina, but was futile for the other changes; however, albendazole combined with CPT and albendazole combined with TSII-A showed obvious effects on the recovery of prolonged VEP latency, destruction and reduction of ganglion cells, optic nerve demyelination and axon loss. Compared with albendazole-CPT compound, albendazole combined with TSII-A was more effective.ConclusionsThe current study demonstrates that albendazole combined with TSII-A plays a more effective role in treating optic neuritis caused by A. cantonensis in mice than with dexamethasone, as applied in conventional treatment, indicating that albendazole combined with TSII-A might be an alternate therapy for this parasitic disease in the clinic.