We read the interesting idiopathic intracranial hypertension (IIH) pathogenetic Medical Hypothesis by Lenck et al.1 We agree that the lymphatic interstitial fluid (ISF)/CSF outflow is increased by intracranial hypertension and may explain part of IIH symptoms. However, the asymptomatic primary impairment of ISF/CSF outflow proposed by the authors—mediated by a putative aquaporin 4 (AQP4) dysfunction at the vascular arachnoid granulation (VAG) interface with the dural sinuses, followed by the secondary sinus stenosis with symptomatic shift—is exceedingly weak and possibly misleading. In fact, the AQP4 glymphatic existence as a convective vs diffusive ISF/CSF outflow route has been very recently questioned.2 ISF/CSF containing intraventricular administered tracers do not drain through venous sinus, as proposed, but through the nasal lymphatics.3 The VAGs are very common in subjects without intracranial vascular pathology,4 whereas IIH is rare. The sinus wall should bear CSF pressure much higher than that possibly associated with an asymptomatic stage of lymphatic dysfunction.5 Finally, after sinus stenting, the intracranial pressure returns to fully physiologic values in responders.6 Therefore, the hypothesis of an asymptomatic primary CSF hypertension by glymphatic impairment leading to a secondary symptomatic sinus stenosis is highly unlikely.

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