Gypenosides attenuate lipopolysaccharide-induced optic neuritis in rats.

PURPOSE: To evaluate the effect of gypenosides (GPs) on lipopolysaccharide (LPS)-induced optic neuritis rats. METHODS: Optic neuritis was induced by a single microinjection of LPS into the optic nerve of Sprague Dawley rats. GPs (400 mg/kg) was administrated by gavage for 21 days. The optic nerve structure changes and demyelination were observed after hematoxylin & eosin and Luxol-fast blue staining. Apoptosis of retinal ganglion cells (RGCs) was evaluated using Brn3a-TUNEL double staining. Expression of CD68 and glial fibrillary acidic protein (GFAP) were detected using immunofluorescence staining. The mRNA levels of inflammatory factors were measured using quantitative real-time PCR. The protein expression levels in the signal transducer and activator of transcription (STAT) and nuclear factor-κB (NF-κB) pathways were detected using Western blot. RESULTS: GPs treatment prevented the optic nerve structure changes and demyelination in the rats with optic neuritis. GPs treatment downregulated LPS-induced overexpressions of CD68, GFAP and pro-inflammatory factors. GPs treatment inhibited STAT1 and 3 phosphorylation and NF-κB nuclear translocation in the optic nerve and retina of rats with optic neuritis. CONCLUSION: GPs attenuate LPS-induced inflammation, demyelination and optic nerve damage which may be associated with the inhibition of the NF-κB and STAT pathways.

Elevated serum anti-phosphatidylcholine IgG antibodies in patients with influenza vaccination-associated optic neuritis.

INTRODUCTION: Because the optic nerve is mainly comprised from phospholipids such as phosphatidylcholine, the association between optic neuritis, anti-phospholipids antibodies and vaccination was examined. SUBJECTS: Two female pediatric patients suddenly presented bilateral optic neuritis after administration of trivalent inactivated influenza vaccine. METHODS: These two patients and another 11 patients with central nervous system demyelinating diseases were examined these anti-phospholipids antibodies. And immune histopathology was examined using serum derived from a patient with optic neuritis. RESULTS: High serum titer of anti-phosphatidylcholine antibody levels were detected during acute phase in patients with optic neuritis. The patient's serum IgG antibodies were found to have stained the capillary endotheliums in the preserved autopsied optic nerve. Patients with optic neuritis had significantly elevated serum levels of anti-phosphatidylcholine antibody in comparison to the other patients without optic neuritis. CONCLUSION: Anti-phosphatidylcholine antibodies may be one of the causes of optic neuritis.

Toxic optic neuropathy following ingestion of homeopathic medication Arnica-30.

We report a case of acute, bilateral and severe vision loss after inadvertent consumption of a large quantity of the homoeopathic medication Arnica-30. Severe vomiting which required hospitalization preceded visual symptoms. In the acute stage, pupillary responses to light were absent and fundus examination was normal. Vision loss followed a fluctuating course, with profound loss noted after 6 weeks along with bilateral optic disc pallor. Neuro-ophthalmic examination and detailed investigations were performed, including magnetic resonance imaging, electroretinography (ERG) and visual evoked potentials (VEP). Ocular coherence tomography (OCT) showed gross thinning of the retinal nerve fiber layer. While a differential diagnosis of posterior ischemic optic neuropathy was kept in mind, these findings supported a diagnosis of bilateral toxic optic neuropathy. Arnica-30 is popularly used to accelerate wound healing, including after oculoplastic surgery. While homeopathic medicines are generally considered safe due to the very low concentrations involved, Arnica-30 may be neurotoxic if consumed internally in large quantities.

Optic neuritis with visual field defect--possible Ibuprofen-related toxicity.

OBJECTIVE: To report a case of optic neuritis with visual field defect associated with ibuprofen. CASE SUMMARY: A 41-year-old white man developed blurred vision in his right eye and pain with eye and head movements that lasted 2 days after use of ibuprofen 400 mg 3 times daily during the preceding 3 weeks. Medical and family histories were negative for significant related disease. Ophthalmologic examination revealed a marked decrease in visual acuity to 20/200 in the right eye with quadrant visual field loss and absent responses in visual evoked potential (VEP). After discontinuation of the drug and treatment with high-dose intravenous methylprednisolone and subcutaneous low-molecular-weight heparin, the patient's vision improved to 20/70, the visual field defect vanished, and the VEP returned to almost normal values during a 1 year follow-up period. An objective causality assessment revealed that the adverse reaction was possibly related to ibuprofen. DISCUSSION: Ocular toxicity with blurred vision and centrocecal visual field defects have been rarely associated with long-term ibuprofen intake. We report a case of retrobulbar optic neuritis with quadrant visual field defect following short-term but regular ibuprofen intake. Although idiopathic optic neuritis cannot be completely ruled out, the absence of other risk factors and additional findings plus the improvement after discontinuation of the drug speak for isolated toxic optic neuritis of the right eye. CONCLUSIONS: Drug toxicity is an important differential diagnosis in retrobulbar optic neuritis. Clinicians should be aware of the potential optic toxicity, even with short-term use of a drug, and perform a thorough medication history in every patient with visual disturbances without a clear cause.

Methylprednisolone increases neuronal apoptosis during autoimmune CNS inflammation by inhibition of an endogenous neuroprotective pathway.

Optic neuritis is one of the most common clinical manifestations of multiple sclerosis (MS), a chronic inflammatory disease of the CNS. High-dosage methylprednisolone treatment has been established as the standard therapy of acute inflammation of the optic nerve (ON). The rationale for corticosteroid treatment lies in the antiinflammatory and immunosuppressive properties of these drugs, as shown in experimental autoimmune encephalomyelitis (EAE), the animal model of MS. To investigate the influence of methylprednisolone therapy on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the ON, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Optic neuritis was diagnosed by recording visual evoked potentials, and RGC function was monitored by measuring electroretinograms. Methylprednisolone treatment significantly increased RGC apoptosis during MOG-EAE. By Western blot analysis, we identified the underlying molecular mechanism: a suppression of mitogen-activated protein kinase (MAPK) phosphorylation, which is a key event in an endogenous neuroprotective pathway. The methylprednisolone-induced inhibition of MAPK phosphorylation was calcium dependent. Hence, we provide evidence for negative effects of steroid treatment on neuronal survival during chronic inflammatory autoimmune disease of the CNS, which should result in a reevaluation of the current therapy regimen.