Hemodynamic Impairment Measured by Positron-Emission Tomography Is Regionally Associated with Decreased Cortical Thickness in Moyamoya Phenomenon.

BACKGROUND AND PURPOSE: Impaired cerebrovascular reactivity has been associated with decreased cortical thickness in patients with arterial occlusive diseases. This study tests the hypothesis that severe hemodynamic impairment, indicated by increased oxygen extraction fraction ratios on positron-emission tomography with 15O tracers, is associated with decreased cortical thickness in patients with Moyamoya phenomenon. MATERIALS AND METHODS: Patients with unilateral or bilateral idiopathic Moyamoya phenomenon were recruited. Oxygen extraction fraction ratio maps were generated from cerebral images of O[15O] counts divided by H2[15O] counts with normalization by corresponding cerebellar counts. The normal range of the oxygen extraction fraction ratio was estimated from historically available healthy control subjects. Cortical thickness was estimated from T1-weighted MR imaging and FreeSurfer. Regional samples of oxygen extraction fraction ratios and cortical thicknesses were drawn using FreeSurfer parcellations, retaining only parcellations from the vascular territory of the middle cerebral artery. RESULTS: Complete MR imaging and PET datasets were available in 35 subjects, including 23 women; the mean age at scanning was 44 years. Patients with Moyamoya phenomenon had a significantly increased regional oxygen extraction fraction ratio compared with 15 healthy control subjects (P < .001). Regional oxygen extraction fraction ratio and age were significant predictors of cortical thickness (P < .001 for each) in a generalized linear mixed-effects model. Using hemisphere averages and patient averages, we found that only age was a significant predictor of cortical thickness (P < .001). CONCLUSIONS: Chronic hemodynamic impairment, as indicated by a higher regional oxygen extraction fraction ratio, was significantly predictive of reduced cortical thickness in mixed-effects analysis of FreeSurfer regions. This phenomenon may be related to reversible metabolic down-regulation.

The current surgical management of intracranial aneurysms.

For more than two decades, surgical clipping of ruptured intracranial aneurysms was considered the stan-dard of care. However, as technology improved, a new treatment option was developed, endovascular emoblization. The treatment of cerebral aneurysms, is now in an era where deciding when to clip versus coil can be difficult. Today's cerebrovascular specialist must consider a multitude of factors when developing the best treatment strategy for an individual patient. Optimal management requires a thorough understanding of the natural history of aneurysms as well as risks and benefits related to the different treatment modalities. The purpose of this article is not to proclaim one treatment better than the other, but rather to provide the reader with an up-to-date, comprehensive insight into the management of cerebral aneurysms. We will review data regarding the natural history of aneurysms along with the effectiveness of both surgical clipping and endovascular embolization. We will further discuss our current management strategy for some of the most common aneurysms encountered. The successful treatment of intracranial aneurysms requires a multidisciplinary approach, where surgery and endovascular therapies are viewed as complimentary instead of competing.

Effect of antiplatelet therapy on thromboembolic complications of elective coil embolization of cerebral aneurysms.

BACKGROUND AND PURPOSE: Thromboembolic events are the most common complications of elective coil embolization of cerebral aneurysms. Administration of oral clopidogrel and/or aspirin could lower the thromboembolic complication rate. MATERIALS AND METHODS: Records over a 10-year period were reviewed in a retrospective cohort study. For 369 consecutive elective coil embolization procedures, 25 patients received no antiplatelet drugs, 86 received antiplatelet drugs only after embolization, and 258 received antiplatelet drugs before and after embolization. RESULTS: Symptomatic thromboembolic complications (transient ischemic attack or stroke within 60 days) occurred in 4 (16%) of 25 when no antiplatelet drugs were given, in 2 (2.3%) of 86 when antiplatelet drugs were administered only after embolization, and in 5 (1.9%) of 258 when antiplatelet drugs were administered before and after embolization. The lower symptomatic thromboembolic complication rate in the patients who received any antiplatelet therapy was statistically significant (P = .004). Clots were visible intraprocedurally in 5 (4.5%) of 111 when no antiplatelet drugs were administered before procedures and in 4 (1.6%) of 258 when they were (P value not significant). None of the 9 was symptomatic postprocedurally, but 7 were lysed or mechanically disrupted. Extracerebral hemorrhagic complications occurred in 0 (0%) of 25 when no antiplatelet drugs were given and in 11 (3.2%) of 344 when they were (P value not significant). CONCLUSION: Oral clopidogrel and/or aspirin significantly lowered the symptomatic thromboembolic complication rate of elective coil embolization of unruptured cerebral aneurysms. There were trends toward a lower rate of intraprocedural clot formation in patients given antiplatelet drugs before procedures and a higher hemorrhagic complication rate in patients given antiplatelet drugs. Benefits of antiplatelet therapy appear to outweigh risks.

Rapid enlargement of a posterior communicating artery aneurysm after Guglielmi detachable coil treatment of ipsilateral carotid artery aneurysms.

This case illustrates rapid aneurysm enlargement, presumably due to altered hemodynamics resulting from endovascular treatment of aneurysms on the same artery. We postulate that increased hemodynamic force directed to the inflow zone of the posterior communicating artery aneurysm was caused by the treatment of the two ophthalmic artery aneurysms. Originally, many of the flow vectors may have been directed into the larger ophthalmic segment aneurysm, located on the outside of the curve of the internal carotid artery. After treatment, flow may have been directed more smoothly around the carotid siphon and into the posterior communicating artery aneurysm.

Vasodilatory effect of basic fibroblast growth factor in isolated rat cerebral arterioles: mechanisms involving nitric oxide and membrane hyperpolarization.

Basic fibroblast growth factor (bFGF), a potent mitogen, acutely dilates cerebral blood vessels and may be effective in reducing cerebral infarction. However, the vasodilatory mechanism, which may involve nitric oxide (NO), is not completely understood. This study investigated whether membrane hyperpolarization is also involved in this mechanism. Membrane potential (MP) of smooth muscle cells and vessel diameter of isolated intracerebral arterioles were simultaneously measured following extraluminal application of bFGF in rats. The involvement of NO and adenosine triphosphate-sensitive potassium (KATP) channels in bFGF-induced vasodilation and membrane hyperpolarization was evaluated using specific inhibitors, NG-monomethyl-L-arginine (L-NMMA, 10(-4) M) and glibenclamide (GB, 10(-5) M), respectively. The resting MP was recorded at a mean value of -31.9 +/- 4.5 mV. bFGF (1 to 1000 ng/ml) produced significant vasodilation and hyperpolarization. Treatment with L-NMMA caused vasoconstriction and significantly attenuated bFGF-induced vasodilation without affecting membrane hyperpolarization. In the presence of GB, the membrane potential was significantly depolarized but the vessel diameter was only marginally reduced, so bFGF-induced membrane hyperpolarization was inhibited while arteriolar dilation was attenuated. These results suggest that bFGF-induced vasodilation is mediated by a mechanism involving both NO and membrane hyperpolarization, and that membrane hyperpolarization is caused by the activation of KATP channels.

Analysis of purine- and pyrimidine-induced vascular responses in the isolated rat cerebral arteriole.

Effects of extraluminal UTP were studied and compared with vascular responses to ATP and its analogs in rat cerebral-penetrating arterioles. UTP, UDP, 2-methylthio-ATP, and alpha,beta-methylene-ATP dilated arterioles at the lowest concentration and constricted them at high concentrations. Low concentrations of ATP dilated the vessels; high concentrations caused a biphasic response, with transient constriction followed by dilation. Endothelial impairment inhibited ATP- and UTP-mediated dilation and potentiated constriction to UTP but not to ATP. ATP- and 2-methylthio-ATP- but not UTP-mediated constrictions were inhibited by desensitization with 10(-6) M alpha,beta-methylene-ATP or 3 x 10(-6) M pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS). PPADS at 10(-4) M abolished the UTP-mediated constriction and induced vasodilation in a dose-dependent manner but did not affect the dilation to ATP. These results suggest that in rat cerebral microvessels 1) ATP and 2-methylthio-ATP induce transient constriction via smooth muscle P(2X1) receptors in the cerebral arteriole, 2) UTP stimulates two different classes of P(2Y) receptors, resulting in constriction (smooth muscle P(2Y4)) and dilation (possibly endothelial P(2Y2)), and 3) ATP and UTP produce dilation by stimulation of a single receptor (P(2Y2)).

Reversal of focal misery perfusion after intracranial angioplasty: case report.

OBJECTIVE AND IMPORTANCE: The presence of reduced blood flow and increased oxygen extraction fraction (OEF) (misery perfusion) in the hemisphere distal to an occluded carotid artery is a proven risk factor for subsequent stroke. Whether angioplasty of intracranial stenosis is sufficient to reverse this condition has not been documented. CLINICAL PRESENTATION: A 67-year-old man exhibited progressive right hemispheric ischemic symptoms despite maximal antiplatelet and antithrombotic therapy. Angiography demonstrated focal 80% stenosis of the supraclinoid segment of the ipsilateral internal carotid artery. TECHNIQUE: 15O positron emission tomographic measurements of cerebral blood flow and OEF were made before and after transfemoral percutaneous angioplasty. OEF values measured before angioplasty were elevated in the middle cerebral artery distal to the stenosis. Angioplasty reduced the degree of luminal stenosis to 40% (linear diameter). OEF values measured 36 hours after angioplasty were normal. CONCLUSION: Angioplasty of intracranial stenosis can restore normal cerebral blood flow and oxygen extraction, despite mild residual stenosis after the procedure. Hemodynamic measurements may be useful for the identification of patients with the greatest potential to benefit from angioplasty.

Role of potassium channels in regulation of brain arteriolar tone: comparison of cerebrum versus brain stem.

BACKGROUND AND PURPOSE: Potassium channels are important regulators of resting tone in large cerebral arteries, but their activity and distribution may vary according to vessel location and species studied. In the cerebral microcirculation in vivo, however, these channels appear to be silent at rest. Our goal was to determine the activity of potassium channels of brain arterioles from 2 origins under basal conditions in vitro. METHODS: Penetrating cerebral (40. 9+/-2.2 microm control diameter) and brain stem (36.2+/-1.2 microm) arterioles of rats were prepared from middle cerebral and basilar arteries, respectively. The internal diameter of cannulated and pressurized vessel was monitored with the inverted microscope before and after administration of potassium channel inhibitors. In addition, we studied the effect of nitric oxide synthase inhibition on potassium channel activity. RESULTS: Cerebral and brain stem arterioles were significantly constricted by 4-aminopyridine and low concentration of BaCl(2) but not by glibenclamide. The addition of N:(omega)-nitro-L-arginine to 4-aminopyridine further decreased diameters of both arterioles. Tetraethylammonium ion caused a significant constriction of brain stem but not cerebral arteriole. The brain stem arteriole was further constricted by additional N:(omega)-nitro-L-arginine. CONCLUSIONS: Voltage-dependent and inward-rectifier, but not ATP-sensitive, potassium channels are active under basal conditions of rat cerebral and brain stem arterioles. There is a regional difference in the activity of calcium-activated potassium channels, which, at rest, are open in brain stem but silent in cerebral arterioles. In addition, basal endogenous nitric oxide may not contribute to the activation of voltage-dependent and calcium-activated potassium channels.

Experimental study of the magnetic stereotaxis system for catheter manipulation within the brain.

OBJECT: The magnetic stereotaxis system (MSS) is a device designed to direct catheter tips through magnetic forces. In this study the authors tested the safety and performance of the MSS in directing catheters through a nonlinear path to obtain biopsy specimens in pig brains. METHODS: Sixteen pigs underwent biopsy of the frontal brain region with the aid of an MSS (11 pigs) or a standard stereotactic biopsy tool (five pigs). Surgical preparation consisted of placement of six fiducial markers in the skull and the creation of a burr hole for attachment of a cranial bolt and passage of the biopsy catheter. The pigs underwent magnetic resonance (MR) imaging of the head to define a biopsy target and to plan a nonlinear path. Guided by the MSS, which used nearly real-time fluoroscopic imaging fused to the preoperative MR image, the authors advanced a catheter to the biopsy target. A biopsy tool was passed through the catheter and a tissue sample was obtained. The animals were observed for 3 to 5 days postoperatively, when they were assessed for neurological abnormalities or other signs of morbidity. Actual catheter placement was within 1.5 mm of the planned path to the biopsy site, using a minimum path radius of 30 mm. The registration error associated with the use of the MSS x-ray fluoroscopy and MR imaging averaged 1.7 mm. Tissue disruption caused by the MSS was similar to that of standard stereotactic procedures. CONCLUSIONS: The MSS affords accurate and safe guidance of brain catheters in animals. The application tested here, brain biopsy, is one of a number of potential catheter-guided procedures.

Red blood cell regulation of microvascular tone through adenosine triphosphate.

The matching of blood flow with metabolic need requires a mechanism for sensing the needs of the tissue and communicating that need to the arterioles, the ultimate controllers of tissue perfusion. Despite significant strides in our understanding of blood flow regulation, the identity of the O(2) sensor has remained elusive. Recently, the red blood cell, the Hb-containing O(2) carrier, has been implicated as a potential O(2) sensor and contributor to this vascular control by virtue of its concomitant carriage of millimolar amounts of ATP, which it is able to release when exposed to a low-O(2) environment. To evaluate this possibility, we exposed perfused cerebral arterioles to low extraluminal O(2) in the absence and presence of red blood cells or 6% dextran and determined both vessel diameter and ATP in the vessel effluent. Only when the vessels were perfused with red blood cells did the vessels dilate in response to low extraluminal O(2). In addition, this response was accompanied by a significant increase in vessel effluent ATP. These findings support the hypothesis that the red blood cell itself serves a role in determining O(2) supply to tissue.

Molecular keys to the problems of cerebral vasospasm.

The mechanisms responsible for subarachnoid hemorrhage (SAH)-induced vasospasm are under intense investigation but remain incompletely understood. A consequence of SAH-induced vasospasm, cerebral infarction, produces a nonrecoverable ischemic tissue core surrounded by a potentially amenable penumbra. However, successful treatment has been inconsistent. In this review, we summarize the basic molecular biology of cerebrovascular regulation, describe recent developments in molecular biology to elucidate the mechanisms of SAH-induced vasospasm, and discuss the potential contribution of cerebral microcirculation regulation to the control of ischemia. Our understanding of the pathogenesis of SAH-induced vasospasm remains a major scientific challenge; however, molecular biological techniques are beginning to uncover the intracellular mechanisms involved in vascular regulation and its failure. Recent findings of microvascular regulatory mechanisms and their failure after SAH suggest a role in the development and size of the ischemia. Progress is being made in identifying the various components in the blood that cause SAH-induced vasospasm. Thus, our evolving understanding of the underlying molecular mechanism may provide the basis for improved treatment after SAH-induced vasospasm, especially at the level of the microcirculation.

No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury.

OBJECT: Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). METHODS: Nine patients were studied a mean of 11.2+/-1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6+/-1.8 and their mean age 27+/-9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30+/-2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59+/-0.44 ml/100 g/minute [p < 0.01] and 0.31+/-0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5+/-8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8+/-0.56 ml/100 g (p < 0.001), OEF rose to 0.45+/-0.13 (p < 0.02), and CvO2 fell to 8.3+/-3 vol% (p < 0.02); CMRO2 remained unchanged. CONCLUSIONS: The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

Sagittal sinus occlusion by intraluminal dural cysts. Report of two cases.

Lesions involving the sagittal sinus typically present as masses compressing the sinus externally. The authors describe two cases of lesions entirely within the lumen of the sagittal sinus. In one of the cases, syncope was the presenting symptom and surgical resection of the cyst was performed. An entirely intraluminal cyst, consistent with a dural cyst, was resected, followed by reconstruction of the sinus and resolution of symptoms. Entirely intraluminal lesions of the sagittal sinus have rarely been reported as incidental findings. This represents the first report of symptomatic occlusion of a venous sinus by an intraluminal cyst.

Intracranial pressure monitoring during intraarterial papaverine infusion for cerebral vasospasm.

PURPOSE: Intraarterial papaverine infusions are performed to reverse cerebral arterial vasospasm resulting from subarachnoid hemorrhage, but such infusions may lead to increases in intracranial pressure (ICP). This study was undertaken to determine when ICP monitoring is indicated during papaverine treatment. METHODS: Seventy-eight vessels were treated in 51 sessions in 28 patients with symptomatic vasospasm. ICP, papaverine doses, and infusion rates were recorded during treatment sessions. The procedural data, Hunt and Hess scores, Fisher grades, Glasgow Coma Scale scores, and ages for all subjects were reviewed and analyzed retrospectively. RESULTS: Baseline ICP ranged from 0 to 34 mm Hg. With typical papaverine doses of 300 mg per territory and infusion times ranging from 5 to 60 minutes per vessel, ICP increases above baseline during papaverine infusion ranged from 0 to 60 mm Hg. Significant (> or = 20 mm Hg) ICP increases during therapy were observed even in patients with low baseline ICP and with papaverine infused at the slowest rate. Patients with a baseline ICP of more than 15 mm Hg were much more likely to have significant ICP increases than were patients with a baseline ICP of 0 to 15 mm Hg. Hunt and Hess scores, Fisher grades, age, and Glasgow Coma Scale scores on admission and immediately before treatment did not correlate with ICP increases during papaverine infusion. Patients with ICP increases of more than 10 mm Hg during therapy were more likely to experience adverse clinical events than were patients with ICP increases of < or = 10 mm Hg. Reduction in the rate of papaverine infusion, or termination of infusion, resulted in reversal of drug-induced ICP elevation. CONCLUSION: ICP monitoring during intraarterial papaverine infusions for cerebral vasospasm is recommended for all patients and is particularly important for patients with elevated baseline ICP. Continuous ICP monitoring facilitates safe and time-efficient drug delivery.

Posterior ventricular catheter burr-hole localizer. Technical note.

Proper ventricular catheter placements are associated with improved shunt performance. When placing ventricular catheters via the posterior approach, the surgeon must determine an optimum trajectory and then pass a catheter along that trajectory. The incidence of optimal posterior catheter placements is increased by using a posterior catheter guide (PCG); however, errors may still occur because of poor selection of a posterior burr-hole site. In this report an easy-to-use posterior burr-hole localizer (Localizer) is described that defines the optimum burr-hole location based on geometric relationships involving the ear and supraorbital rims. The basic design principle of the Localizer was formulated and tested by using neuronavigational imaging tools to examine normal adult ventricular anatomy in relation to surface landmarks and by reviewing imaging studies obtained in 50 adult patients with hydrocephalus. Subsequently, the Localizer was used in 28 consecutive patients scheduled to undergo shunt surgery performed by using the PCG. In all cases the catheter entered the ventricle on the first pass and postoperative imaging studies demonstrated successful placement in the ipsilateral anterior horn. There were no catheter-related complications. These early results indicate that the Localizer and PCG devices may be safe and effective when used in combination for placement of posterior ventricular catheters.

Possible role of nitric oxide in autoregulatory response in rat intracerebral arterioles.

OBJECTIVE: Cerebral autoregulation is an important regulatory mechanism that maintains a constant cerebral blood flow over a wide range of perfusion pressures. The goal of this study was to determine whether nitric oxide contributes to the autoregulatory response of cerebral arterioles to altered transmural pressure (TMP). METHODS: Seventy-nine intraparenchymal arterioles (53.6 +/- 3.5 microm mean diameter) isolated from rats were cannulated with micropipettes and pressurized at a TMP of 60 mm Hg (control pressure). Vessel diameters were monitored continuously using a video dimensional analyzer. The autoregulatory diameter responses to varying intraluminal pressures were observed in the presence and absence of a nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA). The effect of L-NMMA-induced constriction on autoregulatory response also was compared with responses after prostaglandin F2alpha and alkalosis-induced constrictions. RESULTS: Autoregulatory responses were observed over a range from 10 to 90 mm Hg of TMP. Treatment with 10(-4) mol/L L-NMMA constricted arterioles and inhibited the autoregulatory vasodilation to TMP reductions from 60 mm Hg to 10 or 30 mm Hg. In L-NMMA-treated arterioles, elevation in TMP from 60 to 90 mm Hg caused an autoregulatory vasoconstriction. Treatment with alkaline pH 7.65 constricted arterioles to a similar degree as that induced by L-NMMA at 60 mm Hg, and under these conditions, the autoregulatory response remained intact. Arterioles severely constricted with prostaglandin F2alpha showed no significant autoregulatory response. CONCLUSION: These results suggest that 1) vascular nitric oxide release increases in response to a decrease in TMP from 60 mm Hg, thereby contributing to the autoregulatory vasodilation intrinsic to the vessel during hypotension, 2) arteriolar nitric oxide appears not to be involved in the autoregulatory vasoconstriction induced by elevating TMP from 60 to 90 mm Hg, and 3) a marked increase in vascular tone may affect autoregulatory response.

Increased functional vascular response in the region of a glioma.

Functional imaging of a language task using positron emission tomography was performed as part of the preoperative assessment of a patient with a left supplementary motor area (SMA) tumor. Positron emission tomography scans were obtained during language tasks (verb generation and word reading of visually presented nouns) that normally lead to increased blood flow in the SMA relative to a control condition (visual fixation). In the patient, the normal SMA response was an order of magnitude larger in the region of the tumor. Other regions, such as left inferior frontal cortex and right cerebellum, showed equivalent activation in the patient and normal subjects. Histopathologic study revealed an anaplastic astrocytoma. Thus, this exaggerated vascular response to local neuronal activation occurred in the setting of a proliferation of glial cells. This is consistent with models of coupling of regional CBF and neuronal activity that implicate glia as the mediator between neurons and vasculature. The concept that tumoral disruption of normal vascular responses could, in some cases, potentially enhance rather than dampen the response is proposed.

Increase in diameters of vasospastic intracranial arteries by intraarterial papaverine administration.

OBJECT: This study was conducted to determine if there is a change in intracranial arterial diameters after papaverine infusion for vasospasm and to determine whether the change occurs in proximal, intermediate, and distal arteries. METHODS: The authors measured arterial diameters retrospectively in all patients who received intraarterial papaverine for treatment of vasospasm between November 1992 and August 1995. Patients who received papaverine in the same session with or following angioplasty were excluded. Measurements were made in a blinded manner with the aid of a magnification loupe at 12 predetermined sites on each angiogram before and after papaverine infusion. Eighty-one treatments in 34 patients were included. Angiograms obtained at the time of presentation with subarachnoid hemorrhage (SAH) were examined in 26 of the 34 patients. Nine carotid territories visualized by repeated angiography on the day after infusion were examined to determine the duration of the papaverine effect. CONCLUSIONS: In all treatment groups an increase was found in the average arterial diameters ranging from 2.8 to 73.9%, with a mean increase of 26.5%. Increases in diameter were observed in proximal, intermediate, and distal arteries. The timing of treatments ranged from Day 3 to Day 19 post-SAH, and there was no relationship between timing and arterial responsiveness (r = -0.06). There was a moderately good correlation between the degree of vasospasm in an artery and its responsiveness to papaverine (r = -0.54, -0.66, and -0.66, for proximal, intermediate, and distal arteries, respectively). The effect of papaverine did not persist until the following day in patients in whom repeated angiography was performed.

Intracranial aneurysm: anatomic factors that predict the usefulness of intraoperative angiography.

PURPOSE: To correlate the size and location of intracranial aneurysm with the need to reposition the aneurysm clip after intraoperative angiography. MATERIALS AND METHODS: In 199 consecutive patients with 234 clipped intracranial aneurysms, 273 intraoperative angiographic studies were retrospectively reviewed. Aneurysm size and location, determined with preoperative angiographic and surgical reports, were correlated with the frequency of clip repositioning because of parent- or branch-vessel compromise or unexpected residual aneurysm. RESULTS: Findings from intraoperative angiograms resulted in clip repositioning in 46 of 273 (16.8%) studies. Clip repositioning was statistically significantly less frequent with aneurysms of the posterior communicating (three of 52 [5.7%] studies) and anterior choroidal (none of 12 studies) arteries. High rates of clip repositioning were found in aneurysms of the superior hypophyseal artery (seven of 18 [38.9%] studies), superior cerebellar artery (three of five [60.0%] studies), and bifurcation of the internal carotid artery (three of nine [33.3%] aneurysms). In 98 conventional follow-up angiographic studies, seven (7%) false-negative cases with unsuspected aneurysm neck remnant were found. CONCLUSION: The rate of clip repositioning in aneurysms of the posterior communicating or anterior choroidal arteries was less than that at other locations (P < .05). Intraoperative angiography may not be necessary when aneurysms are at these two locations.

Convection versus conduction cooling for induction of mild hypothermia during neurovascular procedures in adults.

Hypothermia for cerebral protection is usually achieved by administration of intravenous fluids at room temperature, cooling ambient air, ice packs, and a temperature-adjustable circulating water mattress. We compared cooling by conduction by using a water mattress to cool by convection by using a forced-air cooling device. Twenty patients were prospectively randomized to two groups: 10 patients cooled by convection (CC) and 10 patients cooled by traditional methods (TC). Two patients in the CC group were withdrawn from the study and excluded from the analysis; one patient for failure to cool despite the use of both techniques, and the other for the abrupt onset of arrhythmias and myocardial depression during hypothermia. Temperature was measured at the tympanic membrane, pulmonary artery, and esophageal probe sites and recorded every 15 min. The time required to reach the target temperature range of 33-34 degrees C was recorded. We found no differences in the temperatures measured at the three sites during cooling and rewarming. Baseline temperatures recorded from the pulmonary artery catheter before beginning "active cooling" were similar in both groups (TC, 35.0 +/- 0.2 degrees C vs. CC, 35.3 +/- 0.1 degrees C). We found no difference in the time to target temperature between TC and CC (TC, 178 +/- 25 min vs. CC, 142 +/- 21 min). One patient had some arrhythmias on cooling in the convective group, but her preoperative condition may have been responsible. In conclusion, cooling by convection appears to be a safe alternative to conduction cooling.