We read with great interest the article by Miller and associates titled “Long-term Follow-up and Outcomes in Traumatic Macular Holes.” In their study, the authors have very clearly mentioned regarding the timing for vitrectomy and the visual outcomes comparing between spontaneous closure and surgical intervention in patients with traumatic macular holes. However, we have a few comments to make.

According to Yamashita and associates, pathogenetically there are 2 distinct types of traumatic macular hole formation: 1 type due to primary dehiscence of the fovea, and the other type due to dehiscence of the fovea secondary to persistent vitreofoveal adhesion. The role of the internal limiting membrane in the formation of the traumatic macular hole has not been clearly understood. Further analysis of cases with vitrectomy with and without internal limiting membrane peeling would have helped in understanding the role of internal limiting membrane in the pathogenesis of formation and spontaneous closure of traumatic macular holes.

One of the mechanisms for traumatic macular hole closure, as described by Lewis and associates, was the appearance of the epiretinal membrane around the hole. In the current study, 10 of the 11 cases that underwent vitrectomy for macular hole closure had an associated epiretinal membrane. Thus one would interpret that the presence of the epiretinal membrane in traumatic macular holes actually reduced the chances of spontaneous closure of traumatic macular holes.

Patients with traumatic macular holes have associated comorbidities. This would have an impact on the initial and final visual outcome before and after closure of the macular hole. However, no mention has been made regarding the same.

In conclusion, more research is needed in understanding the exact pathogenesis of traumatic macular hole formation and its spontaneous closure.