[Lumbar meningeal enhancement after surgery in the posterior cranial fossa: a normal finding in children?]. / Lumbales meningeales Enhancement in der KM-MRT.

PURPOSE: Spinal meningeal Gd-DTPA enhancement after cranial surgery is a known observation of a not well understood underlying mechanism. This paper demonstrates that this MRI finding is a normal meningeal reaction to subarachnoid hemorrhage, which should not be mistaken for metastatic spread. MATERIAL AND METHODS: Three pediatric patients were examined by MRI for metastatic spread of malignant infratentorial tumors along the spinal canal two to nine days after the removal of the primary cerebral lesion. The findings were compared with a control group that underwent cranial surgery (cyst resection or fenestration of the posterior cranial fossa) without major bleeding into the subarachnoid space. Unenhanced and enhanced sequences were obtained to prove that the high signal within the CSF is caused by an abnormal Gd-DTPA uptake and not by methemoglobin. RESULTS: Meningeal enhancement was observed in all patients with intraoperative bleeding resembling subarachnoid masses on enhanced T 1 -weighted images. This was not present in any patient of the control group. This finding lasts for approximately two weeks. CONCLUSION: The meningeal enhancement renders immediate postoperative studies inconclusive for the detection of metastatic spread. Consequently, the obligatory tumor staging along the spinal canal should ideally be done prior to the resection of a cerebral tumor.

Is blood pressure really a trigger for the circadian rhythm of subarachnoid hemorrhage?

BACKGROUND AND PURPOSE: Circadian blood pressure changes are not infrequently cited as a trigger for the onset of subarachnoid hemorrhage (SAH). Our purpose was to determine the reliability of this chronorisk and study the variability and consequences of it as it occurs in hypertensive and normotensive individuals. METHODS: Of 273 consecutive patients with proven SAH of aneurysmal origin seen between January 1990 and December 1993, we studied 120 (44%) for whom the exact time of hemorrhage could be reliably determined. Beyond the recognition of a circadian rhythm for this collective, the patients were then sorted by blood pressure, yielding one group each of 80 normotensive (group N, 66.7%) and hypertensive (group H, 33.3%) individuals. The differential chronorisk of these two groups was studied. RESULTS: A circadian rhythm with a definitive characteristic acrophase was observed for the entire group, occurring between 9 AM and 10 AM (chi 2 test, P < .0005) with a possible secondary peak in the afternoon hours. The separation into two blood pressure groups somewhat surprisingly revealed a different curve for each group (chi 2 test, P = .01). Statistical analysis of each group's separate chronorisk revealed that this acrophase only holds true for hypertensive individuals, whereas normotensive patients not only lack a morning peak, but an apparent elevation in the afternoon is statistically irrelevant, leading to the impression that SAH in normotensive persons seems to be subject to no circadian rhythm at all. CONCLUSIONS: The incidence of SAH conforms to circadian blood pressure variation in hypertensive patients, similar to the diurnal rhythms observed with strokes and myocardial infarctions. This leads to the hypothesis that blood pressure elevation is a trigger for the onset of bleeding in this group. In clear contrast, normotensive individuals with cerebrovascular aneurysms seem to have a random 24-hour distribution of SAH onset times, thus leaving the nature of a possible trigger mechanism unresolved.