Shadi Awwad, MD

It is useful to characterize the changes in the optic nerve head that occur in papilledema as being mechanical or vascular in nature.
The five mechanical clinical signs of optic disc edema are:

1. Blurring of the optic disc margins
2. Filling-in of the optic disc cup
3. Anterior extension of the nerve head (3D = 1mm of elevation)
4. Edema of the nerve fiber layer
5. Retinal and/or choroidal folds.

The five vascular clinical signs of optic disc edema are:

1. Venous congestion of arcuate and peripapillary vessels
2. Papillary and retinal peripapillary hemorrhages
3. Nerve fiber layer infarcts (cotton-wool spots)
4. Hyperemia of the optic nerve head
5. Hard exudates of the optic disc.

These combination of these signs help characterize the papilledema as:
A. Early
B. Fully developed
C. Chronic
D. Late

Early papilledema:
Disc hyperemia
Disc swelling
Blurring of the disc margins
Blurring of the nerve fiber layer

Fully developed papilledema:
Gross elevation of the optic nerve head
Engorged and dusky veins appear
Peripapillary splinter hemorrhages and sometimes choroidal folds arise
Retina striae
In chronic papilledema:
Fewer hemorrhages occur
The optic disc cup is obliterated completely
Less disc hyperemia is seen
Hard exudates occur within the nerve head
Optociliary shunts can start showing
In late disc edema:
Secondary optic atrophy occurs
Disc swelling subsides
Retinal arterioles are narrowed or sheathed
The optic disc appears dirty gray and blurred, secondary to gliosis
Retinochoroidal vein shunts(or Optociliary) may be seen
Symptoms of increased intracranial pressure include:
Headache
Brief transient obscurations of vision.
Less commonly, the patient may describe blurred vision, constriction of visual fields, dyschromatopsia, and/or diplopia.
Cause for concern exists if the headache is particularly severe or associated with nausea and vomiting or a sense of pressure around the ears.
This concern is heightened if the headache becomes worse in a recumbent position, or is worst 
in the early morning, when the patient wakes up, but improves during the day.
Even more specific are the transient obscurations of vision, usually described as monocular or binocular blackouts, that last 3-4 seconds and most often occur as the patient arises from the recumbent position to sitting or standing.
Papilledema may produce visual blurring because of enlargement of the blind spot and adjacent retinal folds or edema; the blurring usually is reversible.
However, further injury to the optic nerve may be associated with secondary optic atrophy and 
be permanent, which results in symptoms such as constricted visual fields and poor color vision. Diplopia usually arises from nonlocalizing VIth nerve palsies, and often resolves after the 
increased intracranial pressure has been controlled.

Papilledema showing blurred disc margins and dilated tortuous vessels