Bilateral Disc Edema

priciple pathophysiologic finding in optic disc edema?

blockage of axonal transport

what 2 factors cause axonal flow blockage?
where does the blockage usually occur?

1. mechanical

2. vascular

occurs at the level of the lamina & results in intr-axonal swelling

what causes optic disc edema (2 possible things)

any event that:

• increases venous pressure at or near the lamina cribrosa

• anything that mechanically or physically blocks axoplasmic flow

what are the 3 bilateral optic disc edemas

• malignant papilledema

• idiopathic intracranial hypertension

• neuromyelitis optica

papilledema is referred exclusively for ____

when the optic disc edema is secondary to elevated intracranial pressure

increased intracranial pressure can be caused by what 5 mechanisms?

1. when the skull is too small for brain (craniostynoses - birth)

2. brain volume too large for skull (space occupying lesion or brain edema)

3. obstruction of CSF flow

4. increased production of CSF

5. reduced absorption of CSF

optic disc appearance changes in papilledema (3)?

1. changes at ONH - RNFL opacification, elevation of the margins, hyperemia, obliteration of the cup

2. vascular congestion - venous dilation, vascular tortuosity, hemorrhages, cws, exudates

3. mechanical features - retinal folds (paton’s lines), choroidal folds due to posterior globe deformation

what do spontaneous venous pulsations (SVPs) tell you

if present, ICP not high —> nerves are not elevated bc of high IP
if absent, ICP is high —> but not necessarily causing elevated disc

stages of ODE

stage 0 - normal ON with blurred margin

stage 1 (very early) - nasal border of disc obscured, no elevation of borders, radial NFL arrangement disrupted, gray opacity accentuating NFL bundles, normal temporal disc margin

stage 2 (early) - obscuration of all borders, elevation of nasal border, complete peripapillary halo

stage 3 (moderate) - obscuration of all borders, increased diameter of ONH, obscuration, peripapillary halo-irregular outer fringe with finer-like extensions.

stage 4 (marked) - obscuration of all borders, elevation of the entire nerve head, total obscuration on the disc of a segment of a major vessel.

stage 5 (severe) - dome-shaped protrusions (represents anterior expansion of the ONH), peripapillary halo is narrow & smoothly demarcated, total obscuration of a segment of a major BV may or may not be present. Obliteration of the optic cup.

symptoms of papilledema

• may be asymptomatic

• may have systemic symptoms (nausea, vomiting, headaches, pulsatile tinnitus)

• may have visual symptoms (transient visual obscuration, peripheral VF loss that can progress to central, double vision from 6th nerve palsy)

signs

• normal VA

• enlarged blind spot on VF

• 6th nerve palsy

RNFL thickness map would show what?

thick NFL layer

what neuro imaging would you do?

• immediate and urgent CT scan to rule out space occupying lesion

• lumbar puncture to confirm elevated CSF & analyze its composition

• MRI & MRV (less urgent) to confirme elevated CSF

management

manage underlying cause of elevated IP

medication to lower IP

chronic edema leads to ____

axon loss with the development of secondary optic nerve atrophy

what is the primary ocular finding in idiopathic intracranial hypertension

papilledema

idiopathic intracranial hypertension more likely among?

women of childbearing ages with HIGHER BMIs

risk factors for idiopathic intracranial hypertension

• systemic conditions: obstructive sleep apnea, hypothyroidism, anemia, addison disease, SLE, behcet’s, polycystic ovary syndrome, coagulation disorders

• certain medications: tetracyclins, oral contraceptives, vitamin A, lithium, anabolic steroids

idiopathic intracranial hypertension symptoms

• headache- MOST COMMON symptom

• transient vision loss

• pulsatile tinnitis (whooshing sound)

• visual disturbance

• horizontal diplopia (if 6th cranial nerve palsy)

idiopathic intracranial hypertension diagnostic criteria

1. signs/sx of ICP (headaches, nausea, vomiting, transient visual obscurations, papilledema)

2. no localizing neurologic signs, except unilateral or bilateral 6th cranial nerve palsy

3. CSF opening pressure >25 cm

4. no evidence of hydrocephalus, mass, structural, or vascular lesion on imaging

5. no other cause of ICP identified

MRI and MRV findings consistent with elevated ICP

idiopathic intracranial hypertension management

• lower ICP

• weight loss if higher BMI

• surgical intervention (CSF shunt or venous sinus shunting)

prognosis of idiopathic intracranial hypertension

• permanent vision loss is possible depending on severity of papilledema

• recurrence may occur in 3-8% of ppl within weeks-years of initial presentation