Spontaneous disappearance and recurrence of impending macular hole: a case report
There have been several reports of spontaneous closure and reopening of a macular hole, however, in most of those cases, it was observed in eyes post vitrectomy. Here, we report a case of multiple episodes of spontaneous disappearance and recurrence of impending macular hole (stage 1B macular hole) with no history of previous surgery.
A 76-year-old Japanese man presented with a primary complaint of reduced visual acuity in his right eye. On initial examination, the visual acuity in his right and left eye was 0.4 and 0.01, respectively. He had previously been diagnosed as having macular degeneration of unknown origin in his left eye. Optical coherence tomography imaging confirmed vitreomacular traction and impending macular hole in his right eye. After a 1-week follow-up period, posterior vitreous detachment was detected, and the impending macular hole appeared to be resolved. Two months later, the impending macular hole had completely disappeared and his visual acuity had improved to 0.9. Six months later, he again noticed decreased vision in his right eye. An examination revealed that his visual acuity had dropped to 0.4, and there was a recurrence of impending macular hole. An optical coherence tomography examination showed no definitive findings of vitreous traction, and, 1 month later, spontaneous disappearance was observed again and his visual acuity improved to 0.7.
In this case, both the initial onset and the recurrence involved impending macular hole, however, the optical coherence tomography findings differed at each examination. These findings suggest that some causes other than vitreous traction were responsible for both the spontaneous disappearance and recurrence of the impending macular hole in this present case.
KeywordsImpending macular hole Spontaneous disappearance Recurrence Optical coherence tomography (OCT)
There have been several reports of spontaneous closures in cases of both idiopathic and traumatic macular holes (MHs) [1, 2]. Some possible mechanisms for the spontaneous closure of an MH are the release of vitreous traction or the proliferation of glial cells. However, the reopening of a MH after a spontaneous closure is rare, and, in most of the previous reports, it occurred following a vitrectomy [3, 4, 5, 6, 7]. Many investigators have speculated that the pathogenesis for multiple episodes of spontaneous closure and reopening of a MH is due to tangential traction by the epiretinal membrane (ERM), macular edema, and glial cell proliferation. Here, we report a rare case of an impending MH (IMH) with multiple episodes of spontaneous disappearance and recurrence.
It should be noted that this case is very unusual due to the fact that our patient had no history of previous surgery.
In this case report, we describe a very unusual and rare case of an IMH with spontaneous closure and reopening with no history of previous surgery. As previously reported by Gass , the main cause of MH is thought to be vitreous traction in the fovea centralis. Due to advancements in OCT, ophthalmologists are now able to achieve clearer images of the progression of an MH [9, 10, 11, 12]. Kishi et al.  suggested that due to contraction of the posterior wall of the posterior precortical vitreous pocket, tractional force is applied to the fovea centralis of the retina, which can lead to retinal detachment and fovea centralis cyst formation. Hence, if the traction on the fovea centralis of the precortical vitreous can be relieved, the fovea centralis will repeatedly return to its normal shape.
Similar to the findings above, it has been reported that if the MH has reached stage 2, the completion of posterior vitreous detachment can lead to spontaneous closure in approximately 50% of the cases . In this present case also, we found traction on the fovea centralis during the initial examination, yet, 1 week later, the traction was found to have released and spontaneous remission occurred.
Although the rate of reopening after spontaneous closure in cases of MH is thought to be very low, there have been several previous reports of repeated spontaneous closures and reopenings [3, 4, 5, 6, 7]. In the majority of those cases, it reportedly occurred post vitrectomy, and many of those cases involved traction of the ERM over the macula following surgery. Moreover, the primary diseases included rhegmatogenous retinal detachment and diabetic macular edema, which affect the fragility of the macular area.
To date, and to the best of our knowledge, there has only been one previous report of a case of spontaneous closure and reopening of an MH with no history of previous surgery . In that study, the authors reported a case of high myopia with no history of previous surgery in which the spontaneous closure and reopening of the MH occurred three times. In that study, the authors pointed out the involvement of glial cell proliferation as the primary mechanism. The case in this present study has many points in common with that previous case, with the one difference being that our case involved a patient with emmetropia. Although differential diagnoses such as macular edema and serous retinal detachment caused by some other eye disease should be considered, no particular clinical findings were detected in our patient.
It should be noted that it is difficult to attribute the improvement in VA and the restoration of the lamella structure of the fovea centralis simply to glial cell proliferation. In previous studies, we speculated the presence of neural stem cell-like cells with regenerative ability in the fovea centralis [15, 16], and reported the possible involvement of serine proteases such as chymase and tryptase in the vitreous body in the development of MH and ERM [17, 18, 19]. Since chymase has an apoptotic effect and tryptase induces tissue fibrosis, we theorized that such serine proteases might be involved in the pathogenesis of MH and ERM. The OCT findings in this present case clearly showed differences in the IMH between the initial occurrence and the subsequent recurrence, thus indicating that different pathogenic mechanisms may be involved. Unfortunately, we were unable to measure the serine proteases in the vitreous body of the case in this present study. However, our assumption is that biochemical factors, in addition to physical factors such as traction, are involved in the spontaneous disappearance and recurrence of the IMH. Further studies are needed to elucidate the pathogenesis of spontaneous disappearance and recurrence of an IMH.
In this present case, the OCT results revealed an IMH that differed at each examination, that is, at the initial onset and the recurrence, and our findings suggest that some causes other than vitreous traction were responsible for both the spontaneous disappearance and recurrence of the IMH in this patient.
The authors wish to thank John Bush for reviewing the manuscript.
TI and MM have made substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data. KS, YS, BK, NM, and HW have given final approval of the version to be published. All authors read and approved the final manuscript.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
The authors declare that they have no competing interests.
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