Optic nerve disorders or optic neuropathies stand among the most common causes for vision loss [1, 2]. Cases with optic neuropathies can get through a disconnection syndrome since once the optic nerve has been damaged, the visual inputs can no longer be tranfered from the eye to the brain to be interpretated [1, 2]. Optic neuropathies can happen suddenly or gradually. Moreover, insult to optic nerve results in progressive retrograde and anterograde degeneration, leading to transsynaptic degeneration in addition to thinning for the visual pathway [1, 3].
The main symptoms are decreased visual acuity and decrease of color vision, with colors appearing washed out in the affected eye. On clinical examination, the optic nerve head may appear edematous in early stages or may have normal appearance. A pale optic disc is a characteristic of long standing optic neuropathy . Full clinical examination is important to rule in optic neuropathy diagnosis. Other tests including visual field testing, electrophysiological testing and neuroimaging are very useful in the overall evaluation .
Optic nerve damage can be due to various causes such as inflammation, ischemia, demyelination, infiltration, hereditary, toxic/nutritional causes, compression, glaucoma, neoplasm and other neurological disorders such as stroke and demyelinating disorders [5–7]. Treatment for such issues mainly addresses the underlying etiology but whatever is the cause, as soon as optic nerve atrophy occurs; there is currently no available treatment that is able to reverse this atrophy or the corresponding loss of vision [5, 8].
Most of the ocular approaches for treating optic neuropathies use intravitreal drugs, viral vectors, or cells. This is in near proximity for the retinal ganglion cells not the optic nerve which represents the initial site of injury and is not treating the axons . Updated data showed that myelination and axonal conduction enhancement  and oligodendrocyte progenitors transplantation  are promising approaches in the treatment of CNS injuries such as optic neuropathies.
Since the discovery of the neurotrophic cytokine erythropoietin (EPO) human gene in 1985 , several efforts showed its vital ability in maintaining integrity and functions for various tissues [13, 14]. It is mainly produced from renal cells and to a lesser extent from CNS tissues. It was usually used in hematology to enhance hematopoiesis and used in neurology as neuroprotective cytokine for acute lesions such as traumatic brain injury and stroke to prevent apoptosis [14, 15]. Similarly, it was used in chronic neurodegenerative conditions such as chronic schizophrenia and chronic progressive multiple sclerosis as a neuroregenerative agent to enhance both structural and functional healing [14, 15]. Likewise, EPO have had its access to ophthalmology field after growing evidence for being produced in retinal cells, especially Muller cells [12, 16]. Studies on its safety for the protection of ganglion cell paved the way for trials of using EPO in glaucomas, optic neuritis, diabetic retinopathies, and neuropathies [16–18]. EPO intravenous injection was additionally described for the treatment of methanol induced and traumatic optic neuropathy with relative success [19, 20]. Although intravenous EPO is relatively effective to treat optic neuropathy, severe side effects such as cardiovascular complications, thrombosis, hypertension, and acute pulmonary embolism have been reported [21, 22]. Therefore, this study aimed to assess the safety and efficacy of subcutaneous EPO in the treatment of late stage optic neuropathy (LSON) due to different causes.