The presumed pathophysiology of ON is inflammation and demyelination of the optic nerve. Activated peripheral T cells migrate across the blood–brain barrier and release cytokines and other inflammatory mediators leading to neuronal cell death and axonal degeneration. In most cases, visual recovery will occur spontaneously but treatment with corticosteroid resulted in a more rapid rate of visual recovery and may be important in monocular patients, patients with significant bilateral visual loss, or those with occupations requiring faster recovery to normal visual acuity [8].

Considering that the patient presented with symptoms of painful vision loss accompanied by color vision disorder, and after consultation with the neurology service and brain MRI evaluation of the patient, no pathological lesion and compressive mass were observed, the most probable diagnosis for the patient was acute retrobulbar optic neuritis. This case presented an unusual manifestation of involvement following HZO, characterized by acute retrobulbar optic neuritis and sixth nerve palsy.

One of the proposed differential diagnoses for cranial nerve involvement, especially 6th nerve, in patients with vascular risk factors such as diabetes and hypertension, is vascular causes. But in this case, due to the presence of skin lesions from 2 weeks ago and also the occurrence of painful blurred vision, which was not sudden, and the patient gradually developed pain and blurred vision over the course of several days, and also because two cranial nerves (2 and 6) have been involved and also because in multiple cranial nerve palsy, involvement in the field of vascular causes is less likely, non-vascular causes were suggested for this patient.

In very rare instances, limited number of case reports have documented the simultaneous involvement of the abducens nerve and optic neuritis in patients with HZO (Table 1).

In the case reported by Ryu et al., the patient presented with ON and sixth nerve palsy simultaneously, but the patient’s vision was no light perception (NLP) and there was progressive outer retinal necrosis (PORN). In contrast, our patient experienced much milder vision loss with no evidence of retinal detachment [3].

Additionally, the patient in Ryu et al.’s report had a history of pulmonary tuberculosis, suggesting a compromised immune system, whereas our patient appears to have a favorable immune status. In Ryu et al.’s case, optic nerve involvement was bilateral, with the opposite eye showing an abnormal visual field. However, in our patient, there was no evidence of involvement of the opposite optic nerve.

In the case reported by Matsuo et al., there was no retinal involvement, and the degree of vision loss was similar to that of our patient. However, the patient in Matsuo et al.’s study exhibited optic disc swelling, which was not present in our patient [4].

The amount of vision loss of the patient was also similar to our patient. The difference between the patient in this study and our patient is optic disc swelling, which is not present in our patient. Additionally, Muhammad Abbas Abid et al. reported cases of optic neuritis and sixth nerve involvement following ocular herpes zoster. In their patient, there was no vision loss, and vision remained normal. The only indication of optic nerve involvement was the presence of a positive relative afferent pupillary defect (RAPD) [9].

The pathogenesis of ophthalmoplegia is controversial, and several mechanisms have been postulated. The first is a direct cytopathic effect of the virus on the surrounding neural tissue. The second is an immune response of the central nervous system to the virus. The third attributes it to an occlusive vasculitis induced by the virus. A fourth theory suggests that VZV activates another latent neuropathic virus within the brain [10].