We report a 39-year-old male who had generalized tonic-clonic seizure with loss of awareness. Investigations led to a diagnosis of a left temporal lobe tumor. He underwent resection of the mass with consequent loss of brain tissue in the temporal lobe and was found to have a complete right homonymous hemianopia in the immediate postoperative period. Macular ganglion cell analysis on optical coherence tomography (OCT) showed homonymous thinning affecting the inferonasal sector in the right eye and inferotemporal sector in the left eye. This case demonstrates transsynaptic retrograde degeneration through the interruption of the inferior optic radiation, and its corresponding effect on the structure and function of the affected retinal field. Temporal lobe lesions may cause not only a homonymous visual f ield defect contralateral to the side of the lesion but also result to homonymous sectoral thinning of the macular ganglion cell complexes in both eyes located ipsilateral to the side of the lesion.

Human ; Male ; Adult: 25-44 Yrs Old ; Retinal Ganglion Cells ; Hemianopsia ; Temporal Lobe

OBJECTIVE

This study described the etiology and clinical profile of non-glaucomatous optic neuropathy (NGON) cases in a tertiary government hospital in Quezon City, Philippines.

METHOD

This was a retrospective, cross-sectional study of patients seen at a neuro-ophthalmology clinic of a tertiary referral center in Quezon City, Philippines from January 01, 2008 to December 31, 2020. The patients’ medical records were reviewed and the following data were extracted and analyzed: demographic data, mechanism of NGON, and clinical profile.

RESULTS

A total of 911 patient records were reviewed. Most patients were males (61.3%) within the economically productive age group (72.7%). Overall, the top three mechanisms that contributed to NGON were (1) trauma-related (25.9%), (2) ischemic (19.8%), and (3) inflammatory causes (18.0%). When patients were stratified by age, the most common causes in the pediatric group were traumatic (33.9%), inflammatory (28.6%), and papilledema-related (11.3%) optic neuropathies. In the middle age group, traumatic (29.1%), inflammatory (18.5%), and ischemic (17.8%) etiologies predominated. Among the elderly, ischemic (44.0%), drug-induced (26.1%), and compressive (17.9%) causes were most frequently identified.

CONCLUSION

Traumatic optic neuropathy emerged as the leading cause of vision loss from NGON in both pediatric and middle aged groups. In the absence of trauma, further investigations should focus on inflammatory and papilledema-related etiologies in the pediatric and middle aged groups. Among the elderly, ischemia and drug-induced toxic optic neuropathies were the most prevalent, with thorough history-taking being crucial for identifying medication-related causes.

Human ; Trauma ; Optic Atrophy

We report a 39-year-old male who had generalized tonic-clonic seizure with loss of awareness. Investigations led to a diagnosis of a left temporal lobe tumor. He underwent resection of the mass with consequent loss of brain tissue in the temporal lobe and was found to have a complete right homonymous hemianopia in the immediate postoperative period. Macular ganglion cell analysis on optical coherence tomography (OCT) showed homonymous thinning affecting the inferonasal sector in the right eye and inferotemporal sector in the left eye. This case demonstrates transsynaptic retrograde degeneration through the interruption of the inferior optic radiation, and its corresponding effect on the structure and function of the affected retinal field. Temporal lobe lesions may cause not only a homonymous visual f ield defect contralateral to the side of the lesion but also result to homonymous sectoral thinning of the macular ganglion cell complexes in both eyes located ipsilateral to the side of the lesion.
Human ; retinal ganglion cells ; hemianopsia ; temporal lobe