Objective: Determine if patients with increased opening pressure (OP) on lumbar puncture (LP) have thinner calvaria and skull bases. Study Design: Retrospective cohort study. Setting: Tertiary referral center. Patients: Patients (≥18 yr of age) who had a recorded OP on LP and high-resolution computed tomography imaging of the head. Patient age, sex, body mass index were calculated. Intracranial hypertension (IH) was defined with an OP≥25 cm-H2O and low intracranial pressure with an OP<15 cm-H2O. Intervention: Measurement of calvarial, zygoma, and skull base thickness when blinded to OP with three-dimensional slicer and radiologic calipers. Main Outcome Measures: Association of calvarial, skull base, and zygoma thickness with OP and age. Results: Fifty-eight patients were included with a mean (SD) age of 53.1 (16.2) years and average (SD) body mass index of 30.1 (9.1) kg/m2. Patients with IH had thinner mean (SD) calvaria (3.01 [0.81] versus 2.70 [0.58] mm; p = 0.036) and skull bases (5.17 [1.22] versus 4.60 [1.42] mm; p = 0.043) when compared with patients without IH. The mean (SD) extracranial zygoma thickness was similar between the two groups (5.09 [0.76] versus 5.00 [0.73] mm; p = 0.56). General linear model regression demonstrated advancing age was associated with increasing calvarial thickness in patients without IH and calvarial thinning in patients with IH (p = 0.038). Conclusion: IH is independently associated with intracranial bone (calvaria and skull base) thinning and not extracranial (zygoma) thinning. Skull thinning occurs with IH and advancing age. These findings support a possible role of increased ICP in the pathophysiologic development of spontaneous cerebrospinal fluid leaks.

Obstructive sleep apnea was independently associated with intracranial bone (calvaria and skull base) thinning and not with extracranial (zygoma) thinning. These findings support a possible role of OSA in the pathophysiologic development of sCSF-L.

OSA is highly prevalent among patients with sCSF leaks. All patients with sCSF leaks should undergo formal PSG testing. Future studies are needed to determine the role of OSA in the development of sCSF leaks.

Despite increasing interest in the treatment of phantosmia and reports of successful therapies, there remains a paucity of data and lack of consensus regarding optimal management of this difficult condition.

Purpose of review Spontaneous cerebrospinal fluid (sCSF) leaks often occurs in middle age, obese females. Here we investigate the role of obesity, idiopathic intracranial hypertension (IIH), and obstructive sleep apnea (OSA) in the pathophysiology of sCSF leaks. Recent findings The association of obesity and sCSF leaks has been well established in many studies. It has now been revealed that sCSF leak patients have thinner calvariums along with the skull base. An intracranial process likely leads to calvarium and skull base thinning in sCSF leaks patients since this occurs independent of extracranial bone thinning and independent of obesity. OSA, which is known to cause spikes in intracranial pressure (ICP), has been found to be significantly prevalent in the sCSF population and has been shown to lead to both calvarial and skull base thinning. Chronically elevated ICP (IIH) has also been shown to impact calvarial and skull base thicknesses. Summary The incidence of sCSF leaks has increased in recent decades along with an increasing rate of obesity. OSA and IIH, which are obesity-related factors and cause transient and chronic elevations in ICP, have now been implicated as critical factors leading to calvarial and skull base thinning and resultant sCSF leaks.