Curious M2... I am struggling to understand why there is such a strong correlation between intracranial pressure and increasing optic nerve sheath diameter. Intuitively, I want the diameter to get SMALLER as pressure increases, not LARGER, but a quick review of medline tells me I am exactly wrong. Unfortunately, it doesn't tell me WHY I am wrong.

Is it because of a change in the central retinal vein diameter? But that doesn't make sense, because then we would expect to see the nerve get larger with simple HTN.

I can't wrap my brain around this, figured some smart person here might be able to help me. Thanks in advance!

Curious M2... I am struggling to understand why there is such a strong correlation between intracranial pressure and increasing optic nerve sheath diameter. Intuitively, I want the diameter to get SMALLER as pressure increases, not LARGER, but a quick review of medline tells me I am exactly wrong. Unfortunately, it doesn't tell me WHY I am wrong.

Is it because of a change in the central retinal vein diameter? But that doesn't make sense, because then we would expect to see the nerve get larger with simple HTN.

I can't wrap my brain around this, figured some smart person here might be able to help me. Thanks in advance!

Think about CSF.

Think about CSF.

I am for some reason still not seeing this. If there is an increase in ICP (for example, a mass) wouldn't you expect the increase of CSF to put pressure on the nerve sheath, thus the sheath would be compressed? OR is the pressure tamponading off the cavernous sinus which would prevent outflow from the ophthalmic vein.

Sorry for being a bit dense today - I am just not seeing this, and am curious. Saw a cool paper about the sensitivity of ultrasound used for detecting increased ICP, and now just want to understand how it is possible.

The optic nerve is a cranial nerve, and as such is a direct extension of the brain. CSF is inside the sheath, not outside. The sheath is being expanded, not crushed.

Correct me if I'm wrong, but I remember hearing that true "papilledema" is simply an enlarged nerve due to slowed axon-plasma flow (or whatever the terms is for slowed flow down the nerve axons) secondary to increased pressure.

The optic nerve is a cranial nerve, and as such is a direct extension of the brain. CSF is inside the sheath, not outside. The sheath is being expanded, not crushed.

Ah.. Now it makes sense.. thanks!

Correct me if I'm wrong, but I remember hearing that true "papilledema" is simply an enlarged nerve due to slowed axon-plasma flow (or whatever the terms is for slowed flow down the nerve axons) secondary to increased pressure.

Papilledema is edema of the "papilla" (i.e., optic nerve head - ONH). The term papilledema technically only refers to edema of the ONH due to increased intracranial pressure (ICP). This is the result of increased CSF pressure within the optic nerve sheath, as described above. ONH edema of other etiology (e.g., optic neuritis, ischemic optic neuropathy) is not considered true papilledema and may be due variably to decreased axoplasmic flow, as you describe, vascular engorgement & exudation, or inflammation. Of course, these causative factors may also be present in the setting of papilledema. You cannot, however, call ONH edema papilledema without a documented increase of ICP.

Papilledema is edema of the "papilla" (i.e., optic nerve head - ONH). The term papilledema technically only refers to edema of the ONH due to increased intracranial pressure (ICP). This is the result of increased CSF pressure within the optic nerve sheath, as described above. ONH edema of other etiology (e.g., optic neuritis, ischemic optic neuropathy) is not considered true papilledema and may be due variably to decreased axoplasmic flow, as you describe, vascular engorgement & exudation, or inflammation. Of course, these causative factors may also be present in the setting of papilledema. You cannot, however, call ONH edema papilledema without a documented increase of ICP.

Hmm, I'll have to look this up, but I believe that papilledema is really not "edema." Traditional edema refers to accumlation of fluid. Whereas, in papilledema the nerve is enlarged because of slowed axonal transport (basically it's a misnomer).

According to the neuro-op BCS "papilledema refers to true edema of the optic nerve head that results from increased intracranial pressure." I think Mirror Form is questioning what "true edema" means. Most histologic studies demonstrate that icreased intracranial pressure leads to disruption of slow axoplasmic transport. Thus, transported material builds up anterior to the lamina cribosa and leads to axonal swelling. This is different from a "true" accumulation of fluid within the optic nerve head.

I think the take home message for the first year residents on this forum is be very specific about what neurology and neurosurgery are asking you to evaluate. You can NOT rule in or rule out papilledema with a dilated fundus exam. Papilledema requires a documented increase in intracranial pressure.


Hmm, I'll have to look this up, but I believe that papilledema is really not "edema." Traditional edema refers to accumlation of fluid. Whereas, in papilledema the nerve is enlarged because of slowed axonal transport (basically it's a misnomer).

I think Mirror Form is questioning what "true edema" means. Most histologic studies demonstrate that icreased intracranial pressure leads to disruption of slow axoplasmic transport. Thus, transported material builds up anterior to the lamina cribosa and leads to axonal swelling. This is different from a "true" accumulation of fluid within the optic nerve head.

Agreed. I must have misinterpreted Mirror Form's post. There is no direct connection between the subarachnoid space and the sub-NFL space anterior to the lamina cribrosa. Thus, the fluid accumulation in the ONH is not CSF. I see your point that buildup of fluidic axonal transport material technically may not be "true" edema. Edema refers to fluid accumulation within the interstitial space of a tissue. I don't know if the transport material can be released from the axons during this process. Interesting thought.

As you correctly reiterated, the key point is that papilledema, in contrast to the more general term ONH edema, does not exist without documented increase of ICP.

You can NOT rule in or rule out papilledema with a dilated fundus exam. Papilledema requires a documented increase in intracranial pressure.

You can most certainly rule OUT papilledema if there is no optic disc swelling on fundus exam. A patient may have increased intracranial pressure and NOT have papilledema (yet). I think what you really mean is, you cannot rule out increased intracranial pressure with dilated fundus exam alone, right?

You can also rule IN papilledema when you have a patient with bilateral florid optic disc swelling, intact visual function (acuity, colour vision and visual fields, except enlarged blind spots), and normal blood pressure. Your diagnosis will be papilledema until proven otherwise (i.e. with normal opening pressure on repeated LP's. Keep in mind that ICP fluctuates and if you get borderline ICP on one LP it doesn't really rule out papilledema).

You can most certainly rule OUT papilledema if there is no optic disc swelling on fundus exam. A patient may have increased intracranial pressure and NOT have papilledema (yet). I think what you really mean is, you cannot rule out increased intracranial pressure with dilated fundus exam alone, right?

You can also rule IN papilledema when you have a patient with bilateral florid optic disc swelling, intact visual function (acuity, colour vision and visual fields, except enlarged blind spots), and normal blood pressure. Your diagnosis will be papilledema until proven otherwise (i.e. with normal opening pressure on repeated LP's. Keep in mind that ICP fluctuates and if you get borderline ICP on one LP it doesn't really rule out papilledema).

You guys are beating a dead horse here. But let me add a few points.
Don't forget that clinically, you can also look for spontaneous venous pulsations at the optic nerve. These are absent in the minority of the normal population and very helpful when present to rule out papilledema as a fairly reliable indicator.

There are some subtle signs of increased ICP one can look for on MR imaging including posterior scleral flattening, empty sella, perioptic csf distension, anterior protusion of the prelaminar optic nerve, and vertical totuosity of the retrobulbar optic nerve. Most radiologists do not know these subtle indicators

Sometimes imaging findings will provide for a reason for increased ICP to further hone in on a diagnosis...such as, dural venous sinus thrombosis, inctracranial hemmorage, mass, or cerebral edema from stroke, infection, trauma, etc...an LP is not always necessary but certainly helpful in many of the above.

Lastly, remember when ordering MR scans in situtations with optic disc edema, that while the T2 images are pretty good at showing the anatomy of the optic nerve, true optic nerve enhancement can only be demonstrated on the contrast enhanced T1 images with orbital fat suppression. I've seen many radiologists read an MRI as normal when a)orbital fat suppression algorithms were not applied in which case optic nerve enhancement could not be seen if present or b) the cuts imaged were too wide and did not even include much of the optic nerve and c) did not recognize subtle enhancement seen at the optic nerve head or just poterior to the globe.
So always looks at the scans yourself.