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The effect of CSF drain on the optic nerve in idiopathic intracranial hypertension

Research output: Contribution to journalArticle

Jan Hoffmann, Katharina Maria Kreutz, Christoph Csapó-schmidt, Nils Becker, Hagen Kunte, Lucius Samo Fekonja, Anas Jadan, Edzard Wiener

Original languageEnglish
Article number59
JournalJournal of Headache and Pain
Volume20
Issue number1
Early online date23 May 2019
DOIs
Accepted/In press22 Apr 2019
E-pub ahead of print23 May 2019
Published23 May 2019

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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.

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