SEP 15, 2010
This case study reports magnetic resonance imaging (MRI) results that may improve the understanding of Terson's syndrome and help clarify the mechanism responsible for vitreous hemorrhage. The pathogenesis of vitreous hemorrhage in Terson's syndrome patients remains controversial in several respects.
Earlier studies assumed that blood from the subarachnoid hemorrhage enters the vitreous space directly through the intervaginal space around the optic nerve, an extension of the subarachnoid space, by penetrating the lamina cribrosa of the sclera. Another proposed mechanism, which is now generally accepted, is that the subarachnoid hemorrhage induces sudden intracranial hypertension. Transmitted to the optic nerve head, it induces swelling of the optic disc and occlusion of the retinochoroidal anastmosis. The venous return from the eye eventually decreases, resulting in stasis of the retinal veins and causing the intraocular hemorrhage.
The current study presents the case of a 49-year-old male Terson's syndrome patient, Fisher Grade 3, whose MRIs showed a dilated subarachnoid space around the optic nerve. The source image obtained by 3-D magnetic resonance angiography demonstrated an area with high intensity, a finding suggestive of hemorrhage along the central portion of optic nerve. This high-intensity area is the perivascular space around the central retinal vessels which was dilated and filled with blood.
The MRIs of this patient indicate that the vitreous hemorrhage may be caused by a large amount of blood, originally formed by Terson's syndrome, entering the subarachnoid space around the optic nerve and from there infiltrating the intraocular space through the perivascular space around the central retinal vessels within the optic nerve.