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Optic pathway gliomas (OPGs) manifest with neuro-ophthalmic symptoms and signs; however, presentation can vary as their location and growth patterns are highly variable. An exophytic expansion of an OPG within the intracranial cavity can cause compression on neurological structures, warranting intervention. However, management guidelines are limited and the treatment itself may also cause neuro-ophthalmic complications. Therefore, clinical decision-making must include input from a multidisciplinary team that includes ophthalmology, neurosurgery, radiation oncology and neuroradiology.

Retinal excitotoxicity is associated with retinal ischemia, and with glaucomatous and traumatic optic neuropathy. The present study investigates the role of c-Jun N-terminal kinase (JNK) activation in NMDA-mediated retinal excitotoxicity and determines whether neuroprotection can be obtained with the JNK pathway inhibitor, D-form of JNK-inhibitor 1 (D-JNKI-1). Young adult rats received intravitreal injections of 20 nmol NMDA, which caused extensive neuronal death in the inner nuclear and ganglion cell layers. This excitotoxicity was associated with strong activation of calpain, as revealed by fodrin cleavage, and of JNK. The cell-permeable peptide D-JNKI-1 was used to inhibit JNK. Within 40 min of its intravitreal injection, FITC-labeled D-JNKI-1 spread through the retinal ganglion cell layer into the inner nuclear layer and interfered with the NMDA-induced phosphorylation of JNK. Injections of unlabeled D-JNKI-1 gave unprecedentedly strong neuroprotection against cell death in both layers, lasting for at least 10 days. The NMDA-induced calpain-specific fodrin cleavage was likewise strongly inhibited by D-JNKI-1. Moreover the electroretinogram was partially preserved by D-JNKI-1. Thus, the JNK pathway is involved in NMDA-mediated retinal excitotoxicity and JNK inhibition by D-JNKI-1 provides strong neuroprotection as shown morphologically, biochemically and physiologically.

Purpose of Review: The concept that optic nerve fiber loss might be reduced by neuroprotection arose in the mid 1990s. The subsequent research effort, focused mainly on rodent models, has not yet transformed into a successful clinical trial, but provides mechanistic understanding of retinal ganglion cell death and points to potential therapeutic strategies. This review highlights advances made over the last year., Recent Findings: In excitotoxicity and axotomy models retinal ganglion cell death has been shown to result from a complex interaction between retinal neurons and Müller glia, which release toxic molecules including tumor necrosis factor alpha. This counteracts neuroprotection by neurotrophins such as nerve growth factor, which bind to p75NTR receptors on Müller glia stimulating the toxic release. Another negative effect against neurotrophin-mediated protection involves the action of LINGO-1 at trkB brain-derived neurotrophic factor (BDNF) receptors, and BDNF neuroprotection is enhanced by an antagonist to LINGO-1. As an alternative to pharmacotherapy, retinal defences can be stimulated by exposure to infrared radiation., Summary: The mechanisms involved in glaucoma and other optic nerve disorders are being clarified in rodent models, focusing on retrograde degeneration following axonal damage, excitotoxicity and inflammatory/autoimmune mechanisms. Neuroprotective strategies are being refined in the light of the mechanistic understanding.

Background: Euphorbia plants grow in many gardens. Their milky latex is, however, a strong irritant which may induce various ocular lesions from keratoconjunctivitis to severe uveitis., History and Signs: A 86-year-old woman developed a unilateral severe anterior chamber inflammation associated with descemtic folds after direct contact with sap of Euphorbia. Visual acuity was limited to counting fingers. Her eye was operated from filtering surgery ten years previously. The patient was closely followed to rule out the diagnosis of bacterial endophthalmitis., Therapy and Outcome: Symptoms progressively resolved after topical administration of 3 mg/mL ofloxacine and 1 % prednisolone acetate., Conclusions: Euphorbia sap toxicity may take different forms from keratoconjunctivitis to severe uveitis. Euphorbia sap-induced uveitis should be kept in mind when the patient has seen in contact with freshly cut plants.

Introduction: Disulfiram has been used since the late 1940s to treat chronic alcoholism. This drug interferes with alcohol metabolism resulting in an acetaldehyde increase. This causes painful symptoms, encouraging abstinence. Side effects include rare cases of bilateral optic neuropathies. Visual recovery occurs frequently upon cessation of therapy., Method and Observation: We retrospectively studied patients referred for visual loss while treated with disulfiram between 1987 and 2005. Fourteen patients (three females, 11 males; aged 35-62 years) complained of visual loss, but a toxic, disulfiram-related, optic neuropathy was diagnosed in only five patients. Following cessation of disulfiram therapy, visual acuity and field improved in all five patients., Discussion: and conclusion: When disulfiram toxicity is suspected with optic neuropathy, cessation of treatment is mandatory. Visual prognosis is good in the majority of cases, as illustrated by our series. Disulfiram toxicity can be diagnosed only after excluding all other possible causes of visual loss.

Introduction: The Leiden mutation of the factor V gene and the subsequent resistance of factor V to inactivation by activated protein C are associated with a procoagulant state, especially in the venous bed. However, its association with arterial thrombotic disease remains unclear., Observations: We report four patients with visual field defects secondary to arterial occlusions and in whom we found a factor V Leiden mutation. These patients, three females and one male, aged 32-58 years, presented with various visual field defects: bilateral arciform scotomas due to multiple infarcts of the nerve fiber layer (one case), superior defect due to anterior ischemic optic neuropathy (one case), homonymous hemianopia due to stroke (two cases). An abnormal resistance to activated protein C and a heterozygous state for factor V Leiden mutation were found in all four cases. The two patients who suffered from a stroke also showed elevated antiphospholipid antibodies (one case) and a patent foramen ovale (one case)., Comments and Conclusion: Conflicting reports on the effective role of factor V Leiden mutation in arterial thrombotic events are present in the literature. We report four cases of arterial occlusion in whom a thrombophilic predisposition was present with a heterozygous state for factor V Leiden mutation. In two cases, no other risk factor was found. We hypothesize that factor V Leiden mutation, even in a heterozygous state, might predispose to arterial occlusion in some patients.