Relationship between Pachymeningeal Enhancement on Brain MRI and CSF leakage on Radioisotope Cisternography in Patients with Orthostatic Headache

BACKGROUND: In orthostatic headache (OH) associated with low cerebrospinal fluid (CSF) pressure, loss of CSF vol-ume reflected by pachymeningeal enhancement (PCE) on brain magnetic resonance image (MRI) has been suggested as a pathogenenesis according to Monro-Kellie rule. We attempted to test the following hypotheses; 1) OH is caused by loss of CSF volume, 2) CSF volume loss in OH is caused by hyperabsorption of CSF or 3) by decreased production of CSF. METHODS: Nineteen patients with OH were recruited. Lumbar puncture, brain MRI and radioisotope cisternogra-phy (RIC) were performed in all of them. We evaluated duration of headache from onset to first evaluation, presence of PCE on MRI and CSF leakage (CSFL) on RIC. Firstly, we compared duration of headache between patients with and without PCE. Secondly, between those with and without PCE, we analyzed presence of CSF fistula and demonstration of CSFL on RIC. RESULTS: Mean duration (16.1 +/-19.6) of headache in 13 patients with PCE (66.7%) was significantly longer than in those without PCE (P=0.036). Among 19 patients, CSF fistula was detected in 13 patients (72%) and CSFL in 16 patients (88.9%). There was no significant difference in CSF fistula presence (P=0.114) and in demonstra-tion of CSFL between those with and without PCE. In 16 patients, delayed appearance of radioisotope along cerebral interhemispheric and sylvian regions was shown on RIC. CONCLUSIONS: Pain in OH may be caused by CSF volume loss, however, whether CSF volume loss is caused by CSF hyperabsorption or decreased production remains to be clarified.

Changes of Gas Values in the CSF and Blood during Sustained Hypoventilation / 대한마취과학회지

To evaluate the regulation of and in the CSF during respiratory acidosis, the changes in cisternal CSF and arterial plasma acid-base status were asaessed in anesthetized, paralyzed, mechanically ventilated dogs rendered hypercapneic (PaCO2 of 60~70 mmHg) by hypoventilation. The electrochemical potential difference (u) between the CSF and blood for H+ and HCO2- was calculated from values for and in CSF and arterial plasma, and CSF/plasma DC potential difference was calculated. Simultaneously arterial blood and the CSF samples were drawn at 0, 1, 2, 3, 4, 6, 8 hours after hypercapnia. After 8 hours of respiratory acidosis, the arterial pH declined 0.09 units to 7.26 whereas the CSF pH fell by 0.07 units to 7.29. The CSF rose to 34 mEq/L whereas arterial plasma increased to 29 mEq/L. Therefore, increase of the CSF was almost 11 mEq/L, while the arterial plasma HCO, had increased 7 mE/L. So, much increase in CSF bicarbonate maintained the spinal fluid significantly less acidic than the blood during sustained hypercapnia. CSF/plasma PD was not only increased during acute respiratory acidosis, but also remained high as long as the plasma pH was acid. Values of p for H+ and HCO at 8 hours had returned to +1.1 and -0.1 mV of the control value. The attainment of steady-state values for u close to the control value may be compatible with passive distribution of these ions between the CSF and blood. But active mechanism can not be ruled out, because CSF/plasma PD remained high during the study.