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

Autor: Jan Hoffmann, Katharina Maria Kreutz, Christoph Csapó-Schmidt, Nils Becker, Hagen Kunte, Lucius Samo Fekonja, Anas Jadan, Edzard Wiener
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Zdroj: The Journal of Headache and Pain, Vol 20, Iss 1, Pp 1-10 (2019)
Druh dokumentu: article
ISSN: 1129-2369
1129-2377
DOI: 10.1186/s10194-019-1004-1
Popis: 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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