Fredric B. Meyer
Fredric B. Meyer
Focal cerebral ischemia
Fredric B. Meyer
Fredric B. Meyer and Jeffrey N. Bruce
This edition of the Video Supplement entitled “Microsurgery of the Third Ventricle, Pineal Region, and Tentorial Incisura” highlights approaches to accessing the third ventricle for surgical resection of a variety of pathologies. The third ventricle has critical neurovascular anatomy that must always be respected to prevent patient harm. Visualization of critical anatomy in three dimensions from a surgeon' line of sight is important when planning the optimum surgical approach. Some of the keys to safely operating in this region include thoughtful head positioning, limitation of brain retraction, and the use of trajectories which capitalize on CSF cisterns and fissures. Some of the videos included in this volume illustrate standard operations while others depict more unique and innovative approaches that take advantage of these surgical windows. We hope you enjoy the videos included in this supplement.
Michelle J. Clarke and Fredric B. Meyer
✓The mathematical modeling of hydrocephalus is a relatively young field. The discipline evolved from Hakim's initial description of the brain as a water-filled sponge. Nagashima and colleagues subsequently translated this description into a computer-driven model by defining five important system rules. A number of researchers have since criticized and refined the method, providing additional system constraints or alternative approaches. Such efforts have led to an increased understanding of ventricular shape change and the development of periventricular lucency on imaging studies. However, severe limitations exist, precluding the use of the mathematical model to influence the operative decisions of practicing surgeons. In this paper, the authors explore the history, limitations, and future of the mathematical model of hydrocephalus.
Fredric B. Meyer and Donald A. Muzzi
✓ A strategy for intraoperative cerebral protection is described in which intraoperative electroencephalography is used to titrate the level of inspired isoflurane given for anesthesia to obtain isoelectricity prior to temporary vessel occlusion during repair of difficult aneurysms. During temporary vessel occlusion, arterial blood pressure is maintained or increased with an inotropic or vasopressor agent. After clipping of the aneurysm, the concentration of isoflurane is reduced to allow the patient to awaken in the operating room for early postoperative neurological examination. The combination of a high concentration of isoflurane, temporary vessel occlusion, and maintenance of arterial blood pressure may be a useful protective regimen during neurovascular procedures.
Fredric B. Meyer and Wanda L. Windschitl
Saphenous vein patch closure of carotid endarterectomies may decrease the risk of acute postoperative occlusion and recurrent stenosis. However, the disadvantages of a vein patch include postoperative rupture and pseudoaneurysm formation.
Object. The authors sought to assess the effectiveness of collagen-impregnated fabric grafts as substitutes for saphenous vein grafts.
Methods. In this report the authors prospectively analyzed 290 consecutive carotid endarterectomies in which a secondary closure was accomplished using a knitted double-velour graft. The 30-day major neurological morbidity and mortality rate was 1.7%. There were no postoperative occlusions or wound hematomas. The rate of recurrent carotid artery stenosis was less than 1%, and the graft site in one patient became infected.
Conclusions. For surgeons who prefer a secondary closure of carotid endarterectomies, the synthetic graft may prove to be a viable alternative to a saphenous vein.
Bernard A. Coert, Robert E. Anderson and Fredric B. Meyer
Object. A nitric oxide (NO) donor that has been successfully used in the treatment of myocardial infarction, 3-morpholinosydnonimine (SIN-1), may be a potential neuroprotective agent. Production of NO in brain microsomes is dependent on the pH. The purpose of this study was to determine the efficacy of SIN-1 and its dependence on pH in vivo during periods of focal cerebral ischemia.
Methods. At 0.1 or 1 mg/kg, SIN-1 was administered to 54 Wistar rats 30 minutes before a 2-hour period of focal cerebral ischemia under moderate hypo-, normo-, and hyperglycemic conditions. Measurements of brain intracellular pH (pHi); regional cortical blood flow, and the redox state of nicotinamide adenine dinucleotide were obtained in three additional animals to confirm the effects of the serum glucose manipulations. The animals were killed at 72 hours after the ischemic period to obtain infarction volumes. Administration of SIN-1 significantly reduced infarction in normoglycemic animals and, to a lesser extent, in hyperglycemic animals, indicating that SIN-1 was less effective under hyperglycemic conditions. At either dose SIN-1 had no significant effect on infarction volume in moderately hypoglycemic animals because moderate hypoglycemia in itself significantly (p < 0.005) reduced infarction volume.
Conclusions. The NO donor SIN-1 may be a useful intraoperative cerebral protective agent. Furthermore, it is hypothesized that a mechanism that could explain the published discrepancies regarding the effects of NO donors in vivo may be affected by differences in ischemic brain acidosis.
Bert A. Coert, Robert E. Anderson and Fredric B. Meyer
Object. A critical review of the literature indicates that the effects of nitric oxide synthase (NOS) inhibitors on focal cerebral ischemia are contradictory. In this experiment the authors methodically examined the dose-dependent effects of two NOS inhibitors and two NO donors on cortical infarction volume in an animal model of temporary focal cerebral ischemia simulating potential ischemia during neurovascular interventions.
Methods. Ninety-two Wistar rats underwent 3 hours of combined left middle cerebral artery and bilateral common carotid artery occlusion after having been anesthetized with 1% halothane. A nonselective NOS inhibitor, NG-nitro-l-arginine-methyl-ester (l-NAME), and two NO donors, 3-morpholinosydnonimine hydrochloride and NOC-18, DETA/NO, (Z)-1-[2(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate, were administered intravenously 30 minutes before ischemia was induced. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), was administered intraperitoneally in dimethyl sulfoxide (DMSO) 60 minutes before ischemia was induced. Two ischemic control groups, to which either saline or DMSO was administered, were also included in this study. Seventy-two hours after flow restoration, the animals were perfused with tetrazolium chloride for histological evaluation.
Cortical infarction volume was significantly reduced by 71% in the group treated with 1 mg/kg l-NAME when compared with the saline-treated ischemic control group (27.1 ± 37 mm3 compared with 92.5 ± 26 mm3, p < 0.05). The NOS inhibitor 7-NI significantly reduced cortical infarction volume by 70% and by 92% at doses of 10 and 100 mg/kg: 35.2 ± 32 mm3 (p < 0.05) and 9 ± 13 mm3 (p < 0.005), respectively, when compared with the DMSO-treated ischemic control group (119 ± 43 mm3). There was no significant difference between the saline-treated and DMSO-treated ischemic control groups. Treatment with NO donors did not significantly alter cortical infarction volume.
Conclusions. These results support an important role for NO in ischemic neurotoxicity and indicate that neuronal NOS inhibition may be valuable in reducing cortical injury in patients suffering temporary focal cerebral ischemia during neurovascular procedures.