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Cations of Cisternal Cerebrospinal Fluid in Humans and the Effect of Different Doses of Nimodipine on CSF Calcium after Stroke

Bereczki, Dániel*; Fekete, István*; Loof, Ingo; Köbberling, Werner; Valikovics, Attila*; Németh, György*; Fülesdi, Béla*; Csiba, László*

Original Articles
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Cisternal samples of cerebrospinal fluid (CSF) were analyzed for protein, albumin, sodium (Na), potassium (K), and calcium (Ca) content in 21 control subjects and 64 patients who had experienced acute stroke. A second cisternal CSF sample was taken in 37 of the stroke patients after 2–3 weeks treatment with the calcium antagonist nimodipine. Increased permeability of the blood-brain barrier was reflected by the significantly higher CSF/serum ratio of albumin in stroke patients than in control subjects (0.0046 vs. 0.0028, p = 0.0012). Serum and CSF concentrations of Na, K, and Ca did not differ between control subjects and stroke patients. In control subjects and in stroke patients, concentration of calcium in cisternal CSF ([Ca]) was smaller than values reported by others in lumbar samples. In stroke patients, the pH of CSF was lower than that of simultaneously taken blood (7.38 vs. 7.44, p < 0.001). No differences between stroke patients and control subjects were found for the cisternal CSF/serum ratios of Na (1.0 and 0.99), K (0.61 and 0.63), and Ca (0.25 and 0.24). When patients and controls were pooled together, CSF total [Ca] correlated weakly with serum total [Ca] (Spearman r = 0.28, p = 0.014) and with serum ionized [Ca] (Spearman r = 0.27, p = 0.016). After 2–3 weeks of nimodipine treatment, CSF [Ca] was significantly lower in the subgroup treated with 60 mg nimodipine four times daily (240 mg/d) than with 30 mg four times daily. A nimodipine dosage of 30 mg four times daily (120 mg/d) did not affect CSF [Ca]. A 240 mg daily dosage, but not a 120 mg daily dosage, of nimodipine may affect the Ca transport system in humans at the choroid plexus.

*Department of Neurology, University of Debrecen Medical School, Debrecen, Hungary and †Department of Toxicology, Clinical Chemical Laboratory, Bayer AG, Wuppertal, Germany

Address correspondence to László Csiba, Department of Neurology, University of Debrecen Medical School, Debrecen, Nagyerdei krt. 98, H-4012 Hungary.

© 2000 Lippincott Williams & Wilkins, Inc.