Superior orbital fissure syndrome caused by aspergillus infection from maxillary sinusitis

Abstract

A 62-year-old woman who was prescribed prednisolone and cyclosporine for uveitis developed right blepharoptosis, diplopia and hypesthesia of superficial sensation of the trigeminal nerve V1 domain. Preserved right visual acuity led to a diagnosis of superior orbital fissure syndrome. We could not find any abnormalities on computed tomography except for right maxillary sinusitis associated with calcification. No infectious agents were detected in the blood or cerebrospinal fluid. We concluded that maxillary aspergillus, which was proven histopathologically after surgery, caused superior orbital fissure syndrome through the ophthalmic veins. Surgical excision of the lesion and voriconazole administration resulted in complete remission. To the best of our knowledge, there have been no other reports of superior orbital fissure syndrome caused by maxillary aspergillus sinusitis. The calcified sinusitis suggested fungal infections, which allowed us to avoid using corticosteroids.

Fungal Infections of the Central Nervous System

“…113 Fungal etiologies more commonly associated with superior orbital fissure and orbital apex syndrome include aspergillosis and mucormycosis species from extension of sinus disease. 114,115 Pathogens associated with cavernous sinus syndrome are associated most commonly with development of cavernous sinus thrombosis, with aspergillus infection being the most frequent fungal etiology described in the literature. 116 Overall, fungal pathogens are a much rarer cause of infection than bacteria.…”

Traumatic superior orbital fissure syndrome: a rare case report

“…Numerous etiological factors including carotid-cavernous sinus fistula [1], maxillofacial traumas [1,[3][4][5], pseudoaneurysm of the internal carotid artery [6], orbital metastatic hepatocellular carcinoma [7], aspergillus sinusitis [8], etc., were noted as the possible causes of the SOFS. Regardless of the underlying etiological factors, the clinical symptoms of the syndrome are primarily the results of the inflammation and the compression of the neurovascular structures in the superior orbital fissure [4].…”