Papilledema pathophysiology
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Papilledema |
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Papilledema pathophysiology On the Web |
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Risk calculators and risk factors for Papilledema pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]
Overview
Papilledema is in general the result of transmission of increased intracranial pressure[1] to the anterior end of optic nerve through optic nerve sheath.
Pathophysiology
- The optic nerve sheath is contiguous with the subarachnoid space of the brain and is regarded as an extension of the central nervous system.
- The cranium and the vertebral body, along with the relatively inelastic dura, form a rigid container, such that an increase in any of the contents of the dura (brain, blood and cerebrospinal fluid) can cause increased intracranial pressure.
- The increased intracranial pressure is transmitted through to the optic nerve via the optic nerve sheath.
- The anterior end of the optic nerve stops abruptly at the eye. Hence the pressure is asymmetrical and this causes a pinching and protrusion of the optic nerve at its head.
- The fibers of the retinal ganglion cells of the optic disc become engorged and bulge anteriorly.
- Persistent and extensive optic nerve head swelling, or optic disc edema, can lead to loss of these fibers and permanent visual impairment.
- Papilledema may be absent in cases of prior optic atrophy. In these cases, the absence of papilledema is most likely secondary to a decrease in the number of physiologically active nerve fibers.