Vitreomacular observations. II. Data on the pathogenesis of idiopathic macular breaks.
BACKGROUND
The pathogenesis of idiopathic macular breaks is still uncertain. Their formation has been ascribed to anteriorly oriented intravitreous traction and to shrinkage of the prefoveal cortical vitreous. The validity of both hypotheses is considered in this paper.


METHODS
In order to clarify the pathogenesis of idiopathic macular breaks 127 consecutive patients had their vitreous examined and photographed with the El Bayadi-Kajiura precorneal lens and a slit-lamp microscope.


RESULTS
A comparison with 127 matched controls demonstrated that the vitreous was significantly more often attached in eyes with a macular break than in controls (P < 0.01). In eyes with a macular break the vitreous was significantly more often attached in early cases (Gass stage 1) than in Gass stages 3 and 4 (P < 0.01). Still photographs and observation of the movements of the operculum demonstrated that, in some cases of stage 3 and also in stage 4, it moved inside the partially liquefied posterior vitreous, anteriorly to the retinal surface and frequently without evidence of posterior vitreous detachment over the macular area. The following anatomical features characterize the vitreomacular area: extremely thin hyaloid membrane (< 100 microns) and inner limiting lamina (10 nm) that adhere strongly to each other and to the underlying Mueller cells. There is no evidence that these structures can shrink selectively to cause a macular break. The premacular vitreous gel contains collagen fibers that attach posteriorly to the macula and anteriorly to the vitreous base.


CONCLUSIONS
Our working hypothesis is that when detachment of the posterior vitreous is abnormally delayed, anteroposterior traction by collagen fibers may pull a foveal operculum off the retina. Our observations make this hypothesis attractive. However, the generally accepted hypothesis of Johnson and Gass cannot be entirely dismissed. In reality, since the two hypotheses are not mutually exclusive, they may both the partially correct.
Kakehashi
A
A
Schepens Eye Research Institute, Boston, MA 02114, USA.
Schepens
C L
CL
Trempe
C L
CL
D000368:Aged; D000369:Aged, 80 and over; D005128:Eye Diseases / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology; D005260:Female; D005451:Fluorescein Angiography; D005654:Fundus Oculi; D006801:Humans; D008266:Macula Lutea / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009887:Ophthalmoscopy; D012167:Retinal Perforations / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D012189:Retrospective Studies; D014792:Visual Acuity; D014822:Vitreous Body / Q000473:pathology*