Skip to main content
Dear Editor:
We read with interest the recent article by Mark et al [1] discussing imaging findings in patients with skull base CSF leaks. The authors found that imaging signs of spontaneous intracranial hypotension (SIH) such as pachymeningeal enhancement, cisternal effacement and venous sinus engorgement were absent in most patients with skull base CSF leaks. The authors concluded that skull base and spinal CSF leaks represent different pathophysiologies. While we agree with the authors, that these patients fall into distinct cohorts, we believe that the reader should be aware of some important caveats in this take-home message.
An increasing body of evidence has emerged over the last few years linking CSF leaks, particularly spontaneous CSF leaks from the skull base to intracranial hypertension (IIH) [2]. Skull base remodeling is commonly seen in patients with IIH and predisposes them to CSF leaks in the form of CSF rhinorrhea or otorrhea [3]. In the group of patients studied by the authors, about 10% had proven IIH. More importantly however, about 40% of the patients had spontaneous CSF leaks from the skull base with no apparent cause such as surgery or trauma. Given the association between spontaneous leaks and IIH, it is likely that a significant proportion of these spontaneous cases had undiagnosed IIH; the study though provides little information about this subset of patients. It is unknown whether these 40% patients had elevated opening pressures or even other imaging signs of IIH such as empty sella and transverse sinus stenosis. Information on IIH associations, such as gender and obesity status, is also notably absent.
Given the above limitations, it is theoretically possible that as many as 50% of the patients studied by the authors had IIH as the underlying cause of CSF leak. Thus, by extension, it is also plausible that imaging signs such as pachymeningeal enhancement were not seen merely because these patients had IIH. In other words, about half of the studied patients potentially never had intracranial hypotension and so the imaging signs were naturally absent.
In summary, although we agree that the patients with spinal and skull base CSF leak have different pathophysiology, we believe that underlying IIH is a significant confounding factor and arguably the most important reason behind the difference noted by the authors between the two groups.
References:
1. Mark IT, Cutsforth-Gregory J, Luetmer P, et al. Skull base CSF leaks: Potential underlying pathophysiology and evaluation of brain MR imaging findings associated with spontaneous intracranial hypotension. AJNR Am J Neuroradiol 2024;45:1593-96, https://doi.org/10.3174/ajnr.A8333
2. Chen BS, Britton JOT. Expanding the clinical spectrum of idiopathic intracranial hypertension. Curr Opin Neurol 2023;36:43-50, https://doi.org/10.1097/WCO.0000000000001131
3. Leal PRL, Barbier C, Hermier M, et al. Association of intracranial hypertension with calvarial and skull base thinning. Otol Neurol 2019;40:e619-26, https://doi.org/0.1097/MAO.0000000000002249