Beyond idiopathic intracranial hypertension: optic nerve decompression for vision preservation in cerebrospinal fluid flow disorders. A mechanism-based approach.
Papilledema resolved in most eyes after optic nerve decompression for CSF flow disorders
Beyond idiopathic intracranial hypertension: optic nerve decompression for vision preservation in cerebrospinal fluid flow disorders. A mechanism-based approach.
The aim of this study was to evaluate the long-term visual outcomes following optic nerve decompression in patients with CSF flow disturbances and to propose a mechanistic framework for surgical qualification based on infusion testing and orbital MRI, independent of idiopathic intracranial hypertension (intracranial hypertension) diagnostic criteria.
This retrospective study analyzed 30 eyes in 26 patients with progressive visual impairment and evidence of CSF flow abnormalities.
Mean deviation of the visual field improved by a median of +1.89 dB (p < 0.05), and P100 latency (i.e., the time between a visual stimulus and the visual cortex's response) decreased by -5 msec at 24 months.
Retinal nerve fiber layer thickness remained stable or modestly increased across the cohort, with a trend toward greater thickening following endoscopic optic nerve sheath decompression (+9 µm at both 6 and 24 months) compared with optic nerve sheath fenestration (minimal change at 6 months [+1 µm] and slight thinning at 24 months [-2 µm]), although the differences were not statistically significant.
The authors found that optic nerve decompression guided by CSF infusion testing and orbital MRI effectively stabilizes or improves visual function in patients with CSF-related optic neuropathy, including those without elevated intracranial pressure.
A mechanism-based classification into three surgical phenotypes enables individualized treatment beyond syndromic definitions.
This approach may redefine surgical eligibility and expand access to vision-preserving interventions in CSF-mediated optic nerve dysfunction.