This article highlights the role of obesity, sleep apnoea and raised intracranial pressure as linked pathologies in the aetiology of the spontaneous cerebrospinal fluid (sCSF) leak. The authors link sCSF leak with obesity and comment on sCSF leak incidence increasing globally with increasing rates of obesity and regionally in areas with higher obesity rates. However, this article provides an evidence-based argument that the thinning of the calvarial bone in sCSF patients is not caused by obesity itself, but by a triad of causality of obesity, obstructive sleep apnoea (OSA) and raised intracranial pressure. OSA is linked to transient increases in intracranial pressure which, they suggest, leads to reduced calvarial thickness without impact on non-calvarial skull bones (facial zygoma). Calvaria in patients with an apnoea-hypopnoea index (AHI) <5 is reported as significantly thicker than in sCSF patients or patients with an AHI>25, between whom there is no significant difference in calvarial thickness. However, whilst this is an interesting observation, further work appears to be needed to establish the effect of OSA treatment on calvarial thickness/sCSF leak rates. Although I have selected this article, it actually forms part of a series of informative articles in the October issue on the diagnosis, investigation and management of the CSF leak in ENT practice; a series worth reading in its entirety for those with an interest in gaining an overview or update on the subject.