Idiopathic Intracranial hypertension IIH

Caveats-- occurrence in a man, child, older woman, or non-obese female. Mimics include venous sinus occlusion. 21 % may have permanent vision loss (Corbett) hence removal of "benign intracranial hypertension" term. Visual field testing is important since loss of fields preceded loss of acuity. Visual field loss can be identified in 92 % (with automated field) or 96 % (with Goldmann fields) often presenting with arcuate scotoma or nasal step. Contrast sensitivity and color vision are more sensitive than acuity testing.

Identifying the subset of patients who have progressive visual loss is difficult. Consider treating aggressively those with high grade papilledema, frequent TOV's (transient obscurations of vision) and significant visual loss at presentation.

Medicine treatments are problematic. Diamox is used, 500 mg Sequels are best with a starting dose of one bid, with furosamide 40 mg per day an alternative, along with therapy of associated problems such as anemia or hypoxia.

Lumbar shunting works, but requires an average of five revisions per patient. Optic nerve sheath fenestration (ONSF) works, to save vision, but may not fix diplopia or headache.

THE MOST COMMON REASON FOR POOR VISUAL OUTCOME IN IIH IS NOT THE CHOICE OF PROCEDURE BUT THE FAILURE TO MONITOR OPTIC NERVE FUNCTION ADEQUATELY AND BEING SLOW TO RESPOND TO CHANGES IN THE CLINICAL PICTURE.

CAVEATS Patients with malignant clinical course are the minority but need a stepped up plan of treatment. Hypertensive optic neuropathy due to accelerated or malignant hypertension can mimic IIH, but recall that treatment is NOT designed to restore normal BP but to prevent end organ damage through minor or slow adjustments of the blood pressure. Avoid sublingual drugs such as nitroglycerin. Among men, consider sleep apnea syndrome which can cause vision changes indistinguishable from IIH.