Since the evaluation of effective treatments is entirely based on evidence from a limited number of case reports, there is some uncertainty surrounding the proposed efficacy of the drugs for treating RPON. Potential treatments for RPON can be divided into three main categories: preventative therapy, symptomatic treatment, and management of residual symptoms. Preventative therapy
Migraine preventive medications, including beta-blockers (e.g. propranolol), calcium channel blockers (e.g. flunarizine), anticonvulsants (e.g. valproate), and antidepressants (e.g. amitriptyline), may be given to those with RPON with the intent of preventing RPON recurrence. Although the efficacy of these preventives has been proposed in various published case studies, there is a lack of compelling evidence suggesting that these anti-migraine drugs have long-term prophylactic effect on future RPON attacks. The initiation of migraine preventive therapy in RPON is only recommended for people who have typical migraine with frequent attacks as a concurrent condition. Symptomatic treatment
Corticosteroids are the most frequently reported drugs for treating acute symptoms of RPON. The rationale behind their use in RPON treatment is to reduce ocular cranial nerve inflammation, which is indicated by the presence of nerve enhancement and is also theorized to be a pathophysiological mechanism of RPON, in affected individuals. Early implementation of corticosteroid therapy is considered beneficial to the majority (96.2%) of people with RPON because it can shorten their recovery time and reduce the severity of existing symptoms.
Cranial nerve enhancement resulted from RPON would gradually disappear as the symptoms subside after an episode, but spontaneous resolution of nerve enhancement is very unlikely to be seen in neoplastic (e.g. schwannoma), inflammatory and infectious diseases. Contrast-enhanced MRI results can also reveal the location of nerve inflammation for disease diagnosis. Although Tolosa–Hunt syndrome (THS) and RPON share many clinical features, THS can be identified by the presence of granulomatous inflammation in the cavernous sinus, superior orbital fissure, or orbit in MRI scans.Magnetic resonance angiography (MRA) or CT angiography (CTA) can be used to examine cerebral blood vessels and to rule out vascular abnormalities, such as an aneurysm. In cases where intracranial vascular lesions, for example, subarachnoid hemorrhage cannot be completely ruled out after performing MRA or CTA, physicians may consider using traditional digital subtraction angiography (DSA) for more detailed investigation. Laboratory tests
Lumbar punctures and blood tests might be performed on those with RPON to identify other possible causes of cranial neuropathy, including diabetes, inflammatory diseases, infections, tumors, and other systemic diseases that involve either the central nervous system or the peripheral nervous system. The detection of abnormalities in these tests suggests that RPON is highly unlikely to be the culprit in cranial neuropathy, and more diagnostic tests should be done to find out the underlying condition. Treatment
To date, no clinical trials or treatment guidelines for RPON have been published.