From the Northern Neurosciences, Inc., Dearborn, MI (Dr. Borsody); Northwestern Memorial Hospital, Neurology, Chicago, IL (Drs. Semenov, Carroll, Kessler, Dubow, Olson, Stern, Barion, Hammond, and Raizer); Department of Neurology, The Detroit Medical Center, Detroit, MI (Dr.Van Stavern); and Heart Institute, The University of Ottawa, Ottawa, Canada (Ms. White and Dr. Leenen).
The Relation of Brain Ouabain-Like Compounds and Idiopathic Intracranial Hypertension
Article first published online: 12 JUL 2006
Headache: The Journal of Head and Face Pain
Volume 46, Issue 8, pages 1255–1260, September 2006
How to Cite
Borsody, M., Semenov, I., Carroll, K., Kessler, A., Dubow, J., Olson, E., Stern, J., Barion, A., Hammond, C., Van Stavern, G., Raizer, J., White, R. and Leenen, F. (2006), The Relation of Brain Ouabain-Like Compounds and Idiopathic Intracranial Hypertension. Headache: The Journal of Head and Face Pain, 46: 1255–1260. doi: 10.1111/j.1526-4610.2006.00527.x
- Issue published online: 12 JUL 2006
- Article first published online: 12 JUL 2006
- Accepted for publication March 20, 2006.
- pseudotumor cerebri;
- intracranial pressure
Objectives.—To determine the relationship between levels of ouabain-like compounds (OLC) in the cerebrospinal fluid (CSF) and the occurence of idiopathic intracranial hypertension (IIH).
Background.—OLC are naturally occurring inhibitors of the sodium-potassium ATPase that are found in the CSF of mammals. Since the production of CSF is dependent upon sodium-potassium ATPase activity, and since there is evidence that the increased intracranial pressure found in the condition of IIH may be the result of increased CSF production, we hypothesized that the level of endogenous OLC would be reduced in the CSF of patients with IIH.
Methods.—CSF samples were obtained from n = 7 patients with IIH and n = 31 patients with neurological disorders other than IIH (“control” patients) who had lumbar puncture as part of their routine evaluation or treatment. The concentration of OLC in the CSF samples was measured using an established ELISA.
Results.—Patients with IIH exhibited a concentration of OLC in the CSF of 0.11 ± 0.03 ng/mL. In comparison, the concentration of OLC in CSF samples from non-IIH control patients was 0.12 ± 0.01 ng/mL. These values were not statistically different when compared with a t-test (P= 0.31). However, the concentration of OLC did negatively correlate to the opening pressure on lumbar puncture, but only in the IIH group (r=−0.80, P= .03). Furthermore, IIH patients who were newly diagnosed or who were unsuccessfully treated (n = 5 of 7 IIH patients) exhibited OLC concentrations of 0.06 ± 0.1 ng/mL, which is nearly lower than that of the control group (P= .06).
Conclusions.—The average concentration of OLC in IIH patients (treated and untreated) is unlikely to be distinguishable from that in non-IIH control patients with other neurological conditions. However, the concentration of OLC may be inversely related to the intracranial pressure in patients with IIH, and it may prove to be lower in the subgroup of untreated and unsuccessfully treated IIH patients.