Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.
Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, Wellcome Foundation Building, Denmark Hill Campus, London, SE5 9PJ, UK.
J Headache Pain. 2019 May 23;20(1):59. doi: 10.1186/s10194-019-1004-1.
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.
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.
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.
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.
特发性颅内高压会导致颅内压升高，从而引起视盘前节的视神经水肿（视盘水肿）。除了常见的视神经鞘扩张外，关于视盘后段潜在的病理改变以及颅内压正常化对视神经这些异常的短期影响的信息仍然很少。
在这项探索性研究中，8 名被诊断为特发性颅内高压的患者接受了 MRI 扫描（T2 图谱）和扩散张量成像分析（各向异性分数和平均弥散系数）。此外，还评估了头痛的临床表现及其伴随症状。然后通过腰椎穿刺使颅内压正常化，并在 26 小时内重新评估初始参数（MRI 和临床特征）。
在 CSF 压力正常化后，视神经和视神经鞘的形态学 MRI 扫描保持不变。在扩散张量成像中，各向异性分数值降低，提示腰椎穿刺后视神经组织减压。与这些发现一致，头痛和大多数伴随症状也在短时间内得到改善或缓解。
这些发现支持颅内压升高导致视神经微观结构压缩，从而损害轴浆流，从而导致视盘前水肿的假说。视神经的微观结构压缩以及临床症状在颅内压正常化数小时内得到改善。
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