Purpose of Review
Development of safe targeted therapies for idiopathic intracranial hypertension requires a thorough understanding of recent evidence discovering the pathophysiology of the condition. The aim is to provide a review of studies that inform on the underpinning mechanisms that have been associated with idiopathic intracranial hypertension.
Recent Findings
People living with active idiopathic intracranial hypertension and obesity have been found to have with insulin resistance, hyperleptinaemia, and adverse cardiovascular outcomes. Clinically their adipose tissue is predominantly located in the truncal region and on detailed laboratory analysis the cells are primed for weight gain. There is evidence of androgen excess, altered glucocorticoid regulation and changes in pro-inflammatory cytokines. There are distinct alterations in metabolic pathways found in serum, urine and cerebrospinal fluid, that resolve following disease remission. These findings are associated with raised intracranial pressure and are likely secondary to cerebrospinal fluid hypersecretion.
Summary
Idiopathic intracranial hypertension has a profile of systemic metabolic changes, endocrine dysfunction and cardiovascular risk profile distinct from that associated with obesity alone. These systemic metabolic changes are likely to contribute to dysregulation of cerebrospinal fluid dynamics, primarily hypersecretion but with a possible additional effect of reduced clearance resulting in the core feature of raised intracranial pressure.
