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Background
The most widely accepted pathophysiological mechanism for idiopathic intracranial hypertension (IIH) is obstruction of the intracranial venous drainage. 1 However, there exists debate over whether venous sinus obstruction is the primary mechanism or secondary to intracranial hypertension. Some studies have suggested that the appearance of transverse sinus stenosis may improve after cerebrospinal fluid (CSF) diversion (ie, serial LPs and VP shunts); lending credence to the theory that elevated CSF pressures may cause transverse sinuses to appear stenotic even when they are not. Contrastingly, other studies have suggested that transverse sinus stenosis persisted even after normalisation of ICP. 1 In our patient's case of IIH, the MRI revealed not only transverse sinus stenosis but also a dilated network of venous channels suggesting a long-standing defect in cerebral venous drainage. The finding of dilated venous collaterals supports the notion that this patient has long-standing transverse sinus stenosis, unlikely to be artefactual, that is likely responsible for his intracranial hypertension. This case provides further insight into the debate over the pathophysiology of IIH with regard to transverse sinus stenosis and could contribute in changing the surgical treatment paradigm for this disease process.