Spontaneous Evolution of Lamellar Macular Hole into Full Thickness Macular Hole, and Resolution of the Same, Followed by Optical Coherence Tomography

Aim: Aim of this study is to, with the aid of optical coherence tomography, follow and evaluate spontaneous evolution of lamellar macular hole into full thickness macular hole, and vice versa. Methods: A 70-year-old female with metamorphopsia and decreased central vision was examined and followed both clinically and with the aid of high-resolution optical coherence tomography. Idiopathic lamellar macular hole on the right eye and epiretinal membrane on the left eye were noted. Both, evolution of lamellar macular hole and epiretinal membrane were followed over a 2 year period. Results: Over a period of 6 months lamellar macular hole had progressed into full thickness macular hole only to later ‘close’ and resolve into lamellar macular hole. High-definition optical coherence tomography confirmed that one of the mechanisms responsible for lamellar macular hole was opening of cystic spaces on the edges of lamellar macular hole. Loss of IS/OS juncture, or in other words, defects in the photoreceptor layer could be responsible for poor visual outcome. During the course of follow-up examinations of the left eye, there was partial separation of the Case Report Paović and Paović; OR, 5(4): 1-7, 2016; Article no.OR.25581 2 epiretinal membrane without subsequent development of macular hole. Conclusion: Lamellar macular hole slowly progresses and rarely evolves into a full thickness macular hole, and vice versa.


INTRODUCTION
Disruption of vitreomacular interface (VMI) consists of a group of macular disorders including pseudohole; lamellar hole; full thickness macular hole; pseudocyst; and myopic maculoschisis. There exists considerable overlap between these lesions and it is sometimes very difficult to distinguish between pseudocyst; pseudohole; and lamellar hole [1]. Upon funduscopic examination these changes seem like isolated, well-defined, lesions in the macula. While lamellar macular hole (LMH) and macular pseudohole (MPH) may result in a slight decrease of visual acuity (VA), full thickness macular hole (FTMH) may result in significantly decreased VA.
Data obtained in this way can aid in explaining various mechanisms of occurrence and in monitoring individual states that belong to this group of disorders thus making it easier to form a decision regarding surgical intervention [7,8]. On the other hand, besides an OCT, histological examination of epiretinal membranes (ERM) obtained through vitrectomy may also aid in detecting certain VMI disorders.
Mechanisms of VMI occurrence, which have been obtained via an OCT, indicate that MPH occurs as consequence of ERMs centripetal traction [9]. In 1975 Gass described LMH as opening of the cystic roof (abortive process) of persistent cystoid macular edema (CME) [9]. There are several possible ways of development of LMH however such as progressive contraction of ERM; disruption of foveal cysts; and front-rear traction [10,11].
LMH slowly progresses and can be one of the evolutive stages of development of FTMH. On an OCT, LMH appears as an intraretinal split (cleft) with layered inner retinal layers; where there exists irregular retinal contour and thinning. On the other hand outer retinal layers cover retinal pigment epithelium (RPE) and there are no defects in the photoreceptor layer [11][12][13][14][15][16].
FTMH is full thickness macular tissue defect described for the first time by both Hee and Takahashi [17,18] Besides FTMH, HD-OCT also shows defects of the inner/outer segment (IS/OS) with persistent foveal detachment.
Patients that have FTMH generally present with considerably decreased visual acuity.
Tears in the photoreceptor layer and/ persistent foveal detachment may be the reason for significant visual decrease. Spontaneous closure of LMH and FTMH is relatively rare, and that of LMH can result in visual recovery whereas spontaneous closure of FTMH generally has poor visual outcome [19][20][21][22].
Results obtained via an OCT indicate that Müller cells and astrocytes participate in spontaneous closing of FTMH [23][24][25].
Aim of this study is to show both evolution of LMH into FTMH and resolution of FTMH into LMH.

MATERIALS AND METHODS
Patient was followed over a period of two years, and before and during each follow-up examination patients' VA and intraocular pressure (IOP) was taken. Biomicroscopic and high-definition spectral domain OCT (SOCT Copernicus) performed.
During research, principles outlined in the Declaration of Helsinki (2008) were followed. Patient provided informed consent. Neither the patient nor researchers received any financial compensation.

Initial Examination, September 2013
An ophthalmologist assessed a 70-year-old female as she experienced decreased visual acuity on the right eye, together with associated distortion of horizontal and vertical lines around the central fixation point that worsened over the course of the preceding three months. Patient stated that, to the best of her knowledge, she had no additional ophthalmic diseases or illnesses, and that she was not on any medication. Upon examination, best-corrected visual acuity (BCVA) was 0.4 on the right and 0.7 on the left eye. Intraocular pressure (IOP) was 15mmHg on the right and 16mmHg on the left eye. Examination of the posterior segment of the right eye revealed reduced macular reflex; cystic change; as well as macular ERM, and discrete macular ERM on the left eye. OCT was performed in order to provide complete, in-depth, precise, diagnostic assessment of various macular changes ( Fig. 1A; 2A).
In conjunction with oral antioxidants and vitamins, topical non-steroidal anti-inflammatory drug (NSAID) was administered to the right eye.

Second Examination, November 2013
At a three month follow-up examination patient stated that her vision on the right eye had worsened considerably and it was noted that her BCVA had decreased from 0.4 to 5/60 (Snellen chart). Left eye BCVA remained unchanged i.e. there were no significant changes ( Fig. 1B; 2B). Clinical assessment and right eye OCT revealed presence of FTMH and macular ERM. There were no bilateral variations of IOP.

Third Examination, August 2014
Follow-up examination performed less than a year later revealed that right eye BCVA increased, whilst left eye BCVA decreased (0.3 and 0.1, Snellen chart; respectively). On the other hand, there was no change of IOP on either eye. Clinical examination of the posterior segment of the right eye revealed that there was spontaneous resolution of FTMH into LMH and progression of ERM on the left eye, findings which were then confirmed via an OCT (Fig. 1C,  2C). Left eye OCT examination revealed nasally detached ERM and retinal layering in the central region.

Fourth and Final Examination, October 2015
Final examination revealed bilateral improvement (0.5 and 0.3, Snellen chart; right and left eye respectively). Clinical examination via an OCT showed that there exists right eye LMH as well as persistent ERM on the left eye ( Fig. 1D; 2D). Previously mentioned findings were confirmed via an OCT, which also revealed decreased retinal layering. There was no bilateral change of IOP.

DISCUSSION
MHs belong to a group of disorders characterised by vitreoretinal surface changes that occurred due to incomplete or abnormal separation of vitreous and the retina from one another. HD-OCT allows for objective analysis of various mechanisms through which abnormal or incomplete separation occurs. Presence of ERM, its' contraction and opening of cystic spaces in the retina, are deemed to be one of the possible mechanisms of disease progression [26].
As consequence of tractional ERM both the inner retinal layers and the photoreceptor layer have been preserved and centrally elevated.
Evolution of LMH into FTMH; deepening of defects due to micro-cystic layering; disruption of photoreceptors; weakening of IS/OS junctures; all lead to decreased visual acuity [27,28].
A 70-year-old female patient was examined by an ophthalmologist and diagnosed with right eye LMH that had evolved into FTMH; loss of outer retinal layers; disruption of photoreceptor layer; and RPE layer that remained unchanged but of varying reflectivity.
Resolution of FTMH into LMH is extremely rare [23,22], and there exist various mechanisms, such as reduction of pre-existing VMT; ERM contraction followed by retinal folding and development of retinal tissue bridges, that may participate in this process [11]. Seeing that LMH may be seen as an abortive form of FTMH, it is possible that same mechanisms that participate in closing of LMH also participate in closing of FTMH [14]. Results obtained as part of this study suggest that closing of LMH occurs as consequence of separation of ERM from the edges of the hole and complete posterior vitreous detachment (PVD), or in other words, as consequence of released retinal surface tension.  It is possible that tissue that covers base of the LMH, formed as a result of spontaneous closure of FTMH, originates from Müller cells which spread and proliferate from the external limiting membrane (ELM) to the internal limiting membrane (ILM). Anatomical recovery that follows leads to functional visual recovery [27,28].
Patient who was presented as part of this study had LMH resolve into FTMH on the right eye, which did not occur due to ERM contraction. HD-OCT shows thickened edges of MH; fewer cystic spaces; and presence of subretinal fluid.
For these reasons there was displacement of liquid from retinal to subretinal space thus separating edges of the hole and thus closing the previously separated layers. There appear to be no tissue bridges.
As seen via an OCT, improved visual acuity could be explained through the fact that the IS/OS line appears to be preserved and there exists only elevated photoreceptor layer.

CONCLUSION
Formation of certain forms of LMH and FTMH is multifactorial and depends on which one of the existing factors prevails in the particular phase of their formation. HD-OCT has proven to be useful and precise tool used to diagnose and monitor previously mentioned states.
LMH slowly progresses and can be seen as abortive form of FTMH while on the other hand opening of cystic spaces may be one of the mechanisms responsible for formation of FTMH.
Loss of full thickness retinal tissue and disruption of photoreceptor layer are responsible for considerable visual decrease.
So, decreased tractional ERM; formation of tissue bridges; and Müller cells can, through decrease of cystic spaces; fluid displacement into subretinal space; and convergence of edges, be responsible for a rare closing of FTMH and its' evolution towards LMH.

ETHICAL APPROVAL
Authors have obtained all necessary ethical approvals and patients informed consent has been granted. All authors hereby declare that all data has been examined and approved by the appropriate ethics committee and performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki.