Papilledema pathophysiology
Papilledema |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief:Kalsang Dolma
Overview
Papilledema results due to transmission of increased intracranial pressure to the anterior end of optic nerve through optic nerve sheath.
Pathophysiology
Papilledema results mainly due to transmission of increased intracranial pressure to optic nerve.
- Optic nerve sheath is continuous 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 the increase in any of its contents—brain, blood and cerebrospinal fluid can cause increased intracranial pressure.
- The brain itself is relatively spared from pathological consequences of high pressure.
- Increased intracranial pressure is transmitted through to the optic nerve via this 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 does not result from raised ICP alone but in some cases by compartmentation of the subarachnoid space of the optic nerve, leading to a toxic milieu (lipocalin-like prostaglandin D synthase, a substance toxic to astrocytes) around the nerve.<ref>Killer HE, Jaggi GP, Miller NR (2009). "Papilledema revisited: is its pathophysiology really understood?". Clin. Experiment. Ophthalmol. 37 (5): 444–7. doi:10.1111/j.1442-9071.2009.02059.x. PMID 19624339. Unknown parameter |month=
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