## 4 Discussion
The anterior chamber and the vitreous body lost their physiological water-like appearance and became hyperintense on T1-weighted images. The appearance on T2-weighted images may vary depending on the severity and the age of bleeding, and sometimes a fluid-fluid level with a relatively low signal intensity of the dependent portion can be seen. The T2-weighted FLAIR sequence of the brain study may also be of help in detecting vitreous hemorrhage, easily demonstrating the loss of the physiological water-like hypointensity of the vitreous body. [PERSON] et al. reported a series of three patients in which secondary enucleation was performed because of proton beam radiotherapy-related complications. In the patient with the longest time interval between irradiation and enucleation (11 months), the authors found optic nerve atrophy under light microscopy, although the tumor involved the ciliary body and choroid without covering the optic disc [24]. [PERSON] et al. reported a series of five patients with uveal melanoma treated with proton beam radiotherapy, in which secondary enucleation was performed because of clinical complications and tumor growth. In two patients the authors described optic nerve atrophy; moreover, in these cases the tumor was away from the optic disc [25]. In our series, three patients showed optic nerve degeneration at the histologic examination and corresponding optic nerve thinning with T2 hyperintensity under MRI; in these cases, the tumor involved the optic disc. Whether optic nerve degeneration represents the result of the location of the lesion covering the optic nerve head, the consequence of the radiotherapy, or both, is debatable. The slightly hyperintense signal of the optic nerve we observed on T2-weighted images resembles the appearance of the subacute and chronic phases of Wallerian degeneration--a progressive anterograde disintegration of axons associated with demyelination following an injury to the cell body or the proximal portion of the axon [39]. In our case the optic nerve, formed by the axons of the ganglion cells of the retina, represents the first neuron of the visual pathway, extending from the ganglion cell layer of the retina to the lateral geniculate body of the thalamus. Ganglion cell injury--caused by tumor invasion, by radiation, or by both--determined, in turn, the degeneration of the axons constituting the optic nerve. These changes were displayed under MRI in the form of hyperintensity on T2-weighted images, volume loss (nerve thinning), and atrophy. Neovascular glaucoma is one of the most serious complications of radiotherapy, as well as a leading indication for secondary enucleation [25]. [PERSON] et al. found iris neovascularization in 39% of the irradiated eyes undergoing secondary enucleation after plaque brachytherapy, and postulated that this alteration could be the result of radiation-induced ischemia [19]. In the case reported by [PERSON] et al. of a ciliary body melanoma enucleated after proton beam radiotherapy, the patient exhibited rubeosis iridis--iris neovascularization involving both the treated and the untreated areas [22]. [PERSON] et al. investigated the pathogenesis of iris neovascularization, and its link with irradiation, in 11 patients who underwent secondary enucleation after proton beam radiotherapy. Differently from the previous author, they found that neovascularization more often affected the nonirradiated side of the iris, and when it was observable on both sides of the iris, it was more conspicuous on the untreated side [21]. The pathogenesis of iris neovascularization and neovascular glaucoma has been clarified in the last few decades. It has been postulated that the detached retina, the tumor, and even the residual scar resulting from irradiation of the neoplasm, synthesize angiogenic factors that, in turn, would be responsible for iris neovascularization [21; 37].