0925hrs Clinical approach to idiopathic intracranial hypertension - Kimberley Cockerham, MD

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A pressure dependent optic neuropathy

Range of pressures just like glaucoma, from 10-20

Crucial point: these patients can go blind. Just like glaucoma as well.

Defined: awake, alert patient

- normal neuro exam, occ. double vision, no other cause (ie Flu, Tb, etc)

- content of CSF therefore important to r/o cause

- not all classic woman of child bearing age who is overweight

- always confusing when patient thin

Specifically ask about drugs including supplements. eg. natural estrogens can be in these

Classic assocn: Vit A, steroid withdrawal, tetracylcine, naladixic acid (cipro etc)

Headache follows whole glaucoma thing, ie worse in AM just like glaucoma's IOP

Nausea, dizzines without syncope, transient visual obscurations (very brief!), intracranial noises/buzzing (like listening to sea shell), double vision horiz persistent at distance

Atypical: other neuro findings

Afferent fcn

- VA, color, VF

Motility

- ductions, versions, saccades, cross-cover

Disc Appearance

- NFL, spontaneous venous pulsations (very important tool)

Pathophysiology:

- axoplasmic stasis, disc edema, compression of vessels, ischemia

- these things take time

Why 6th nerve injured: its the non-specific nerve, related to relationship to petrous temporal ridge

Pursuits not enough; patient could be asymptomatic; need cross cover in primary and side gazes

If disc drusen and raised ICP, won't detect disc swelling

B-scan, FA can help identify drusen if not obvious

Other fundus findings: CRVO, choroidal folds, subret neovasc, ION

Beware of cotton wool spots: could be malignant hypertension; also beware of vasculitis or severe abrupt elevated ICP

The work-up

- r/o ext causes

- image: CT or MRI/MRV

- lumbar puncture

- image before tapping so don't herniate the brain if big tumor; looking for massive and venous thrombosis

- structural associations: small ventricles, Chiari malformation, sinus thrombosis

Looking for cause:

- remember to get opening pressure when doing LP, get cells, protein, and save sample too eg if need to culture

- time of day matters for opening pressure too, patient position, too stressed out doing valsalva, if ICP >200mm doesn't make sense

Corbett looked at opening pressure in patients with different body weights and showed no correlation between weight and opening pressure.

Opening pressure not enough:

- infection, inflammation, neoplasia to be considered

Diag confirmed, now what?

- don't be the one to manage the headache; get neurologist or pain specialist

- our job prevent visual loss

Poor prognostic factors discussed (see talk once posted)

VF are key to management, again just like glaucoma

- if normal, observe

- nasal step: diamox 500mg BID,

Management also includes encouraging weight loss, diamox, finding cause, surgery (if diamox not working or not compliant, or VF loss at presentation)

Diamox decreases CSF production; can't be just glaucoma like doses; must be big

Annoying side effects but probably OK if sulfa allergies

Emergent mgmt:

- post-trauma, inflammation, post-infection, etc

- may need steroids

If severe visual loss: nerve sheath fenestration or shunt

Gastric bypass if obese

Admit to hospital if emergent

- consult neurology and neurosurgery

Disk at risk: very ischemic with advanced VF loss

Bad things that can happen with fenestration

- failure to correct neuropathy, conj scarring, diplopia, etc

Shunts

- meningitis, peritonitis, subdural hematoma, shunt failure, visual loss, death

Conclusion:

- glaucoma of the brain

- ICP dependent optic neuropathy

- VF key to mgmt

TALK OVER 1019hrs

Session 1