The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension
- PMID: 31122204
- PMCID: PMC6734439
- DOI: 10.1186/s10194-019-1004-1
The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension
Abstract
Background: Elevation of intracranial pressure in idiopathic intracranial hypertension induces an edema of the prelaminar section of the optic nerve (papilledema). Beside the commonly observed optic nerve sheath distention, information on a potential pathology of the retrolaminar section of the optic nerve and the short-term effect of normalization of intracranial pressure on these abnormalities remains scarce.
Methods: In this exploratory study 8 patients diagnosed with idiopathic intracranial hypertension underwent a MRI scan (T2 mapping) as well as a diffusion tensor imaging analysis (fractional anisotropy and mean diffusivity). In addition, the clinical presentation of headache and its accompanying symptoms were assessed. Intracranial pressure was then normalized by lumbar puncture and the initial parameters (MRI and clinical features) were re-assessed within 26 h.
Results: After normalization of CSF pressure, the morphometric MRI scans of the optic nerve and optic nerve sheath remained unchanged. In the diffusion tensor imaging, the fractional anisotropy value was reduced suggesting a tissue decompression of the optic nerve after lumbar puncture. In line with these finding, headache and most of the accompanying symptoms also improved or remitted within that short time frame.
Conclusion: The findings support the hypothesis that the elevation of intracranial pressure induces a microstructural compression of the optic nerve impairing axoplasmic flow and thereby causing the prelaminar papilledema. The microstructural compression of the optic nerve as well as the clinical symptoms improve within hours of normalization of intracranial pressure.
Keywords: DTI; Idiopathic intracranial hypertension; Intracranial pressure; Lumbar puncture; MRI; Optic nerve.
Conflict of interest statement
Jan Hoffmann has consulted for and/or serves on advisory boards for Allergan, Autonomic Technologies Inc. (ATI), Chordate Medical AB, Eli Lilly, Hormosan Pharma, Novartis and Teva. He received honoraria for speaking from Allergan, Autonomic Technologies Inc. (ATI), Chordate Medical AB, Novartis and Teva. These activities are unrelated to the content of this manuscript.
Katharina Maria Kreutz reports no conflict of interest.
Christoph Csapó-Schmidt reports no conflict of interest.
Nils Becker reports no conflict of interest.
Hagen Kunte received personal compensation for speaking from Biogen-Idec, Norvartis, Genzyme, Teva, Merck, Mylan, and Bayer. He also received honoraria for participation in advisory boards from Norvartis, Roche, Genzyme, and Teva as well as travel support to congresses by Norvartis, Genzyme, Teva.
Lucius Samo Fekonja reports no conflict of interest.
Anas Jadan reports no conflict of interest.
Edzard Wiener reports no conflict of interest.
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