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Idiopathic intracranial hypertension (IIH) is a neurological disorder that is characterized by severe headache, pulsatile tinnitus, transient visual obscurations, and elevated intracranial pressure (ICP) seen on lumbar puncture (LP) without any secondary causes such as intracranial mass or venous sinus thrombosis. Papilledema remains a key sign to determine disease severity. The pathophysiology of IIH is not clearly understood but there are theories that suggest that changes in CSF (cerebrospinal fluid) drainage may play a role. Looking for signs of increased ICP on imaging can help clinicians in diagnosing IIH. One of the main diagnostic tools often utilized is a brain MRI which can show signs of increased intracranial pressure. MR venogram can show venous sinus stenosis which is yet another important radiological finding that can suggest intracranial hypertension. The recognition of venous sinus stenosis as a radiologic finding in most patients with IIH has dramatically improved our understanding of the pathophysiology of IIH. The understanding is that with venous stenosis, there can be increased pressure buildup, leading to IIH. However, not all patients with venous sinus stenosis have signs and symptoms associated with IIH. The role of venous sinus stenosis as a cause, consequence, or amplifier of elevated intracranial pressure remains uncertain. This narrative examines the relationship between IIH and CVSS through a multilevel venous-pressure framework. Intrinsic, extrinsic, and mixed stenoses may produce distinct hemodynamic patterns, while elevated downstream venous pressure can impair cerebrospinal fluid absorption even when the focal trans-stenotic gradient is modest. High-resolution venography and venous manometry frequently identify focal venous sinus stenosis with a measurable trans-stenotic pressure gradient, informing current pathophysiologic models, although the role of stenting remains limited to carefully selected patients.
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Gowda et al. (2026) studied this question.
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