We report a 34-year-old male with a previously uninvestigated lifelong blindness of the right eye from compressive optic neuropathy secondary to congenital herniation of the gyrus rectus (HGR). His past medical history was otherwise unremarkable, with no history of prior head or ocular trauma. On examination, he had no light perception in the right eye, right relative afferent pupillary defect (RAPD), and primary optic atrophy. His left eye had normal visual acuity, color vision, and a healthy optic disc. There was a sensory exotropia in the right eye; however, extraocular movements were intact and the remainder of his neurological exam was normal. MRI revealed compression of the prechiasmatic right optic nerve from HGR and atrophy of the right optic nerve and optic chiasm (Figures 1 and 2), without any parenchymal mass lesions. There were no signal abnormalities in the optic nerves or the chiasm.

An 80-year-old man was seen in urgent neuro-ophthalmology consultation for bilateral vision loss. He had a past medical history of hypertension and metastatic stage IV colorectal adenocarcinoma. Four months prior to presentation, he developed gradual onset, painless blurred vision in his right eye. He underwent cataract surgery in that eye, but his vision continued to decline to the point of no light perception. He developed new onset, painless, blurred vision in his left eye 3 weeks prior to presentation and woke up with no light perception in his left eye one day prior to presentation.

Two cases of ischaemic optic neuropathy, which occurred as a complication of oncological neck surgery, are reported. These cases are submitted because of the apparent scarcity in the literature of this complication after head and neck surgery. They are also unusual because they presented with different clinical manifestations of ischaemic optic neuropathy after separate forms of bilateral neck dissection. A literature review identifies a small number of similar cases and risk factors and preventative measures are discussed.

Pregnant female mice were divided on day 12 post coitum into a control and an experimental group. The experimental group was given a single intraperitoneal dose of 0.015 ml/g body weight of 25% solution of alcohol in distilled water while the control group was exposed to a similar weight related dose of normal saline. The optic nerves were isolated from the offspring of both control and experimental groups at wk 2, 3 and 5 (i.e. during the juvenile period of postnatal development) and analysed by light and electron microscopy. Although in both groups the optic nerve grew in size rapidly during the period studied, the rate of growth in the experimental groups lagged behind that of the controls. The difference was initially significant but tailed off, so that by wk 5 it was no longer significant. The time of initial onset and progression of myelinogenesis in the optic nerve of alcohol exposed mice also lagged behind that of controls. In both groups the size distribution of the myelinated nerve fibres in the optic nerve was unimodal with a positive skewing for all ages. The spectrum of size distribution of the nerve fibres was, however, broader in controls than in the corresponding experimental groups. With increasing age the proportion of small and medium size fibres was greater in the experimental group than in the controls, while for the large diameter fibres the reverse was observed. It is suggested that this study may shed light on the teratogenic effect of ‘binge’ drinking during pregnancy and that it is the critical period when exposure occurs that is more important than the duration of administration.