Idiopathic intracranial hypertension: can studies of obesity provide the key to understanding pathogenesis?
The pathogenesis of idiopathic intracranial hypertension (IIH) is poorly understood. Several mechanisms have been suggested, but no one mechanism has been able to account for all manifestations of the disease. Although IIH predominantly affects obese, premenopausal women, little is known about whether or how the obesity contributes to the IIH. Obesity is a heterogeneous condition, consisting of different phenotypes that are influenced by the regional distribution of adipose tissue. This review explores the literature to integrate current knowledge on the relationships between obesity and IIH. The review evaluates the hypotheses that dysregulation of insulin, glucose metabolism, sex hormones, adipokines, glucocorticoids, lipids and free fatty acids in obesity could predispose to IIH. One potential common pathway linking metabolic disorders to the pathogenesis of IHH is a thrombotic tendency due to dysregulation of haemostatic risk factors. This could cause either occult cerebral sinus thrombosis or partial thrombosis of the parasagittal venous lacunae, with subsequent impaired resorption of cerebrospinal fluid and venous hypertension. Investigations that evaluate obesity, fat metabolism, endocrinological dysregulation and thrombotic tendency in patients with IIH are required so that pathogenic mechanisms can be clarified and management strategies in IIH can be improved.
Ooi
L-Y
LY
Department of Clinical Neurosciences, Western General Hospital and Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Walker
B R
BR
Bodkin
P A
PA
Whittle
I R
IR
D000273:Adipose Tissue / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism*; D015170:Cerebrospinal Fluid Pressure; D005260:Female; D006801:Humans; D020738:Leptin / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000150:complications*; D010641:Phenotype; D011559:Pseudotumor Cerebri / Q000209:etiology* / Q000378:metabolism; D012307:Risk Factors; D012737:Sex Factors
D001786:Blood Glucose; D020738:Leptin