2025 AMA Research Challenge – Member Premier Access

October 22, 2025

Virtual only, United States

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Abstract Title

Low CSF-Pressure Diagnostic Criterion in Spontaneous Intracranial Hypotension is Potentially Misleading in Clinical Practice

Background

Low CSF pressure (Pcsf) has classically been considered a defining feature in the pathogenesis of spontaneous intracranial hypotension (SIH) and is part of the International Headache Society (IHS) diagnostic criteria for SIH. However, normal or elevated Pcsf is commonly measured in SIH during myelography. This suggests that the low Pcsf criterion may be potentially misleading in clinical practice. We report on Pcsf and its correlations in patients with SIH due to CSF-venous fistula (CVF).

Methods Following IRB approval, consecutive SIH patients undergoing myelography between 2021 and 2025 at a single quaternary care center were retrospectively analyzed. Pcsf was defined as opening pressure (OP) during myelography, with patient in decubitus positioning with mild hip elevation. In line with IHS, Low OP was defined as < 6 cm H2O. Elevated OP was defined as > 20 cm H2O.

Results Of the 86 SIH patients analyzed, 35 (41%) had a CVF average age 59±13; 12/35 (34%) male; 23/35 (66%) female. Of the 35, OP was reported for 32 patients. The mean ± SD OP was 13.97 ± 3.91 cm H2O (range: 6-25 cm H2O). None (0%) of the patients had a low OP. 29/32 (91%) had OP in the normal range, and 3/32 (9%) had elevated OP. Pcsf was positively correlated with BMI (p = 0.045); but not correlated with age, sex, prior epidural blood patching, symptom duration, or mean arterial pressure. High variability in Pcsf values was not fully accounted for by predictors included in our model (pseudo-R^2 = 0.188).

Conclusions

First, an absence of low Pcsf should not be used to rule out SIH, as our analysis of patients with CVF shows normal/elevated Pcsf in all included patients. As such, the current IHS criteria for SIH need to be reappraised. Second, such Pcsf readings in patients with active CSF leaks suggest that the development of CVF and incidence of post-treatment rebound headaches might be due to a pre-existing intracranial hypertension. Further research is needed to establish this link, as it has implications both for close post-treatment management of rebound hypertension to prevent potential recurrence of CVF, and also for management of patients with idiopathic intracranial hypertension, to monitor for potential incidence of CVF. Third, our findings support the more appropriate recharacterization of the syndrome of ‘spontaneous intracranial hypotension’ as ‘CSF hypovolemia’. Finally, while BMI is positively correlated with Pcsf, low explanatory power of our model suggests influence of other factors not considered in our analysis.

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