The death of idiopathic intracranial hypertension?

Intracranial hypertension is often of known etiology but may be primary or idiopathic. Elevated intracranial pressure has been attributed to cerebral venous sinus occlusion, radical neck dissection (with removal of the jugular vein), hypoparathyroidism, vitamin A intoxication, systemic lupus erythematosus, renal disease, and drug side effects.1 In idiopathic intracranial hypertension (IIH), the typical patient is a young, obese woman with chronic daily headaches, a normal neurologic examination (except for papilledema), and normal laboratory studies (except for an empty sella).1 Other symptoms include transient visual obscurations, pulsatile tinnitus, diplopia, and visual loss.2 Signs include papilledema and VI nerve palsy. However, IIH can also occur without papilledema.3 Friedman and Jacobson have recently published diagnostic criteria for IIH.4 The criteria, in essence, limit diagnosis to patients with elevated CSF pressure not attributed to another specific cause. Is the term IIH a misnomer? Perhaps an etiology can be found if one performs the correct investigations? Is conventional wisdom wrong? Are all cases of IIH really secondary (attributable to another cause)? Intracranial hypertension can be secondary to changes in cranial venous outflow due to venous obstruction or elevated central venous pressures (e.g., cardiac failure or pulmonary failure). Cerebral venous thrombosis, one cause, is frequently underdiagnosed. Headache, present in 80 to 90% of cases, is often associated with papilledema and can mimic IIH; it accounted for 40% of 160 patients in one series.5 IIH has been proposed to result from decreased CSF reabsorption, leading to elevated CSF pressures, or from increased venous sagittal sinus pressure secondary to extracellular edema.6 Both these scenarios would lead to relative venous outflow obstruction by external compressive effects on the …