Spontaneous intracranial hypotension is caused by a spinal cerebrospinal fluid leak. It is typically associated with orthostatic headache and a broad range of additional neurological symptoms. Brain MRI features include pachymeningeal enhancement, subdural collections, pituitary enlargement, venous sinus engorgement and downward displacement of the brain. Ocular involvement has been described as optic neuropathy and changes in the optic nerve sheath fluid, but signal changes in the optic tracts have not been systematically reported. We retrospectively reviewed our patients with spontaneous intracranial hypotension and MRI confirmed sagging brain and identified six patients with T2 hyperintense signal consistent with edema in the optic tracts. In all six patients the optic tracts and the chiasm were displaced. The edema was observed in the optic tracts in all six patients and in the chiasm in four of them. In one patient the edema was primarily in the chiasm. Edema was best visualized on coronal T2-weighted fast spin echo sequences with fat saturation through the orbits and could also be appreciated on three-dimensional fluid attenuated inversion recovery sequences. None of the patients reported overt visual symptoms and detailed neuro ophthalmological examination were not been performed. Five out of six patients received non-targeted (blood patch) or targeted (fibrin patch) treatment for the spinal cerebrospinal fluid leak or surgery, while one had spontaneous recovery. In all cases, follow-up MRI after successful treatment showed normalization of optic tract position and resolution of T2 hyperintensity. Optic tract edema appears to be a new and reversible imaging sign of spontaneous intracranial hypotension and may serve as a marker of treatment response.
Smilkov et al. (Thu,) studied this question.