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Object: Fenestration of the lamina terminalis (FLT) during aneurysm surgery for subarachnoid hemorrhage can, in theory, improve CSF circulation from the lateral and third ventricles to the cortical subarachnoid space, which may, in turn, decrease the incidence of hydrocephalus and vasospasm. However, the actual effects of FLT on CSF circulation have been difficult to determine, due to confounding factors. In addition, it is unclear whether the lamina terminalis remains functionally patent when the brain resumes its normal position. The goal of this study was to assess the functional patency of the fenestrated lamina terminalis in patients who underwent surgery for ruptured aneurysms., Methods: This prospective study included 15 patients who underwent surgical clipping of ruptured anterior circulation aneurysms, with FLT performed during surgery. On postoperative Day 1, the external ventricular drain of each patient was closed, and 1 ml of Omnipaque 300, an iodine based contrast agent, was injected intraventricularly, accompanied by cranial maneuvering designed to position the contrast agent adjacent to the lamina terminalis. Three to 5 minutes after cranial maneuvering, the flow of contrast agent into the basal cisterns was assessed with CT imaging. Flow was verified by an increase in Hounsfield units in a prespecified "region of interest" within the basal cisterns on the CT scan. This procedure was performed using a standardized protocol designed in consultation with the Department of Radiology and approved by the institutional review board. One patient who underwent endoscopic third ventriculostomy was recruited as a positive control to validate the technique, and 1 patient who underwent aneurysm clipping but not FLT was recruited as a negative control., Results: Seventeen patients consented to study participation. In the 15 patients who underwent aneurysm clipping and FLT, and the negative control patient who underwent aneurysm clipping but not FLT, the contrast agent followed the normal ventricular pathway from the lateral ventricles into the fourth ventricle, and did not appear in the basal cisterns. In the positive control patient, the contrast agent robustly and immediately filled the basal cisterns., Conclusions: Fenestration of the lamina terminalis did not result in functional patency of the lamina terminalis when performed as part of surgical clipping for ruptured aneurysms.

Object: The goal of this study was to explore whether the levels of soluble adhesion molecules were elevated in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). This association was suggested by the known inflammatory response in vasospasm and the role of vascular adhesion molecules in regulating leukocytic adhesion to, and migration across, vascular endothelium., Methods: A prospective analysis was performed on CSF samples obtained in 17 patients who had suffered a recent aneurysmal SAH and in 16 control patients by using quantitative enzyme-linked immunosorbent assays for E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and L-selectin. Levels of soluble forms of E-selectin (p=0.0013), ICAM-1 (p=0.0001), and VCAM-1 (p=0.048) were found to be elevated in the CSF of patients after SAH compared with levels in the CSF of norminal controls, patients with unruptured aneurysms, and patients tested months after SAH occurred. In addition, individual patients tested at the time of their initial ictus demonstrated a fall in adhesion molecule levels over time. Levels of E-selectin (p=0.044) were highest in patients who later developed moderate or severe vasospasm., Conclusions: Adhesion molecules are known to be involved in white cell adherence to the endothelium and subsequent diapedesis and migration in which a role in initiation of tissue damage is postulated. The authors have demonstrated the elevation of three adhesion molecules, with severely elevated levels of E-selectin seen in patients who later develop vasospasm. A correlation with a role of vascular adhesion molecules in the pathogenesis of cerebral vasospasm is suggested.

Object: The present study was conducted to estimate the frequency and timing of rebleeding after initial subarachnoid hemorrhage (SAH) from ruptured giant aneurysms., Methods: The authors reviewed records of 109 patients who suffered an initial SAH from a giant aneurysm and were treated at the Mayo Clinic between 1973 and 1996. They represented 25% of patients with giant intracranial aneurysms seen at this institution during that 23-year period. Seven of the patients were residents of Rochester, Minnesota, and the rest were referred from other institutions. The aneurysms ranged from 25 to 60 mm in diameter, and 74% were located on arteries of the anterior intracranial circulation. The cumulative frequency of rebleeding at 14 days after admission was 18.4%. Cerebrospinal fluid drainage, cerebral angiography, and delayed aneurysm recurrence were implicated in rebleeding in some of the patients. Rebleeding was not precluded by intraaneurysm thrombosis. Among those who suffered recurrent SAH at the Mayo Clinic, 33% died in the hospital., Conclusions: Rebleeding from giant aneurysms occurs at a rate comparable to that associated with smaller aneurysms, a finding that should be considered in management strategies.

Vasoconstrictor activity was examined in serial samples of cerebrospinal fluid (CSF) obtained from 10 patients undergoing aneurysm clipping within 48 hours after subarachnoid hemorrhage (SAH). There was no close relationship between vasoconstrictor activity in postoperative CSF samples and the patient's clinical condition or angiographic vasospasm. The identity of the vasoconstrictor substance(s) in CSF was not established, but serotonin, histamine, norepinephrine, epinephrine, acetylcholine, or angiotensin II were eliminated as prime vasoconstrictor agents inducing cerebral vasospasm. Differences in the temporal profile of the responses of isolated tissues to CSF from patients with early and late surgery suggested that differing substances were involved in the production of spasm. A correlation between CSF potassium concentrations and vasoactive substances was found, but potassium could not account for vasoconstrictor activity of CSF. A log:linear correlation between total vasoconstrictor activity and total CSF collected could not be explained. Also, because of possible differences in the identity of vasoactive substances in CSF in this study compared to earlier studies, clinical comparisons based on apparent differences in pharmacological potency of CSF were not warranted. Nevertheless, removal of subarachnoid blood by cisternal rinsing seemed to be a useful surgical adjunct.

Cerebrospinal fluid (CSF) was collected preoperatively (by lumbar puncture) or perioperatively (by lumbar or ventricular drain) from 32 patients with subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms. Samples were also obtained from six control patients without evidence of subarachnoid blood. Smooth-muscle constrictor activity in the CSF was measured by bioassay using the isolated rat stomach fundus preparation. Concentrations of unidentified smooth-muscle constrictor substances were considerably greater in CSF from a group of seven patients with evidence of severe angiographic vasospasm and/or delayed ischemic deficits who died (73.8 +/- 39.7 nmol/liter prostaglandin E2 (PGE2) equivalents), as compared to 25 other SAH patients who survived (6.5 +/- 1.4 nmol/liter PGE2 equivalents), and six control patients (1.17 +/- 0.34 nmol/liter PGE2 equivalents). The data suggest that there is a relationship between smooth-muscle constrictor substances in the CSF after SAH and both the degree of angiographic vasospasm and the outcome. It is possible that this relationship might be exploited clinically.

The fibrinolytic activity in cerebrospinal fluid has been monitored by determination of levels of fibrin split products (FSP) in 23 patients with ruptured intracranial aneurysms. In 20 of these 23, FSP was found in the cerebrospinal fluid (CSF), with levels ranging from 10 to 80 micrograms/ml. Eleven of the 23 patients were treated with 2 gm tranexamic acid daily. In these patients FSP was found in only two cases during the 2nd week, while in 12 untreated patients it was found in 10 cases. These results suggest that there exists a localized fibrinolytic activity, and monitoring the FSP levels in the CSF may be a simple and accurate method for controlling the efficiency of antifibrinolytic therapy. Thus, treatment could be begun with a lower dose, which could be increased later as deemed necessary from the results of careful monitoring.

Intracranial pressure (ICP) was continuously recorded, isotope cisternography was performed, and the ventricular system size was evaluated on serial computerized tomography scans in 39 patients. All of these patients had communicating hydrocephalus after subarachnoid hemorrhage (SAH) from rupture of an intracranial aneurysm. The studies were carried out in both the acute stage (within 7 days after SAH) and the communicating hydrocephalus stage. In patients in the acute stage who had no ventricular dilatation, but who later developed communicating hydrocephalus, the resting ICP was high, and an ICP pattern of B-wave activity was seen; there was no delay in cerebrospinal fluid (CSF) absorption on isotope cisternography. Patients with communicating hydrocephalus in whom ICP recordings were started within 63 days after SAH had a pattern of plateau waves in conjunction with B-waves, and there was a marked delay in CSF circulation. In general, patients with higher resting ICP's had more frequent ICP irregularities. Patients with communicating hydrocephalus in whom recordings were begun more than 6 months after SAH had a low and flat ICP pattern, and there was no delay in CSF absorption in spite of bilateral convexity blocks on isotope cisternography. The results suggest that the ICP pattern of plateau waves in conjunction with B-waves can be regarded as a sign of delayed CSF absorption; hence, shunting procedures may be indicated in patients with plateau waves in conjunction with B-waves visualized on continuous ICP recordings.

In small human cerebral arteries preincubated with indomethacin, contractions induced by cerebrospinal fluid (CSF), from patients with subarachnoid hemorrhage were markedly increased. Also contractions induced by noradrenaline, but not 5-hydroxytryptamine, were augmented. Prostacyclin and its metabolite 6-keto-prostaglandin (PG)E1 reversed the contractions induced by CSF, as well as by noradrenaline, 5-hydroxytryptamine, and PGF2 alpha. The findings suggest that these substances are able to counteract the influence of vasoconstrictor material in hemorrhagic CSF. If the capacity to synthesize these "protective" arachidonic acid metabolites is reduced, the resulting imbalance between contractile and relaxant forces acting on the vessel wall may lead to sustained cerebral vasoconstriction.

Intraventricular pressure (IVP) was measured continuously by the method of Lundberg for an average period of 8 days in 52 patients with recent rupture of an intracranial saccular aneurysm. The patients were graded as follows according to the system of Hunt and Hess: 13 patients were Grades I-II, 19 patients Grades II-III, and 20 patients Grades III-V. The degree of cerebral arterial spasm was measured on angiograms taken on admission and approximately 7 days later. Drainage of ventricular cerebrospinal fluid was performed intermittently when IVP exceeded 25 mm Hg. The results showed a close correlation between changes in clinical grade and in mean IVP. Drainage improved the condition in uncomplicated cases, but was less effective or ineffective when severe vasospasm or rebleeding occurred. Lowering the IVP by drainage did not appear to increase the risk of rebleeding. In contrast to patients with no or slight spasm, patients with severe spasm had a permanently elevated IVP, even before spasm was demonstrable angiographically. A mean IVP exceeding 25 mm Hg for the whole period of monitoring was associated with a poor prognosis. Finally, indications for continuous monitoring of IVP and ventricular drainage in aneurysm patients are suggested.