[Endarterectomy and carotid angioplasty: surgical perspective]. / La endarterectomía y la angioplastia carotídea: perspectiva quirúrgica.

INTRODUCTION: Carotid endarterectomy (CE) is a well-established operation, although recently it has been challenged by newer, less invasive procedures such as carotid angioplasty with or without insertion of a stent. DEVELOPMENT: In this article the author gives his views on the use of CE in patients with carotid stenosis, both those with and those without symptoms, and also those in whom no definite indication has yet been established. In symptomatic carotid stenosis it had been clearly shown that CE is an effective procedure for the prevention of strokes and death from strokes in patients with carotid stenosis of over 70%, provided that the patients have reasonable general health and life expectation. There is only minor benefit from surgery in patients with asymptomatic disease of the carotid arteries and much less than in those with symptomatic carotid disease. Therefore endarterectomy is recommended when there is obvious progression of the degree of stenosis, especially when the stenosis has reached 70% or the patient begins to complain of symptoms. One of the most serious complications of CE is acute myocardial infarction. CONCLUSION: It is a good time to design careful randomised studies to compare endarterectomy with angioplasty, probably with stenting, in a selected group of patients at greater risk than those accepted for endarterectomy.

Stroke: indications for emergent surgical intervention.

As the brain attack message is disseminated throughout our medical community and the awareness of the public increases, neurosurgeons will have the opportunity to treat patients with stroke at a much earlier time in the evolution of the process than we have been accustomed. Are the relatively unimpressive results of acute surgical intervention in patients operated on later in the course of the disease applicable to those who seek medical attention early, within the first few hours of ictus? There is little firm data. However, there is an overwhelming amount of anecdotal and experimental evidence supporting the potential for ultra-early intervention, which frequently should be surgical. New surgical techniques may improve safety and feasibility of emergent operations. In the coming years, diagnostic techniques such as perfusion/diffusion magnetic resonance imaging will allow the clinician to determine who may benefit from intervention. These determinations will be made on physiological data, addressing the issues of tissue viability and degree of compromise of the blood-brain barrier. In the future, the window of opportunity for intervention will not be solely a function of time from ictus or a qualitative impression based on collateral circulation as extrapolated from angiography, transcranial Doppler, or magnetic resonance angiography. These new magnetic resonance imaging techniques, which are beginning to be tested clinically or are still in the developmental stages, will provide the functional data now provided by positron emission tomography and xenon computed tomography, but with improved sensitivity, specificity, and logistical ease. Neurosurgeons have been leaders in stroke care and have provided some of the most important experimental rationale for the brain attack concept. These contributions include demonstration of the ischemic penumbra, the importance of time and potential collateral circulation as factors determining viability of ischemic tissue, and the value of early revascularization and many neuroprotective maneuvers in preserving brain tissue after arterial occlusion. There is every reason to preserve and to enhance the role of the neurosurgeon as a "stroke expert" and as a leading member of the brain attack team. Early access to patients with stroke will offer us the opportunity to test clinically, in a rigorous fashion, the value of surgical revascularization procedures (open or endovascular) and medical maneuvers that we have developed clinically and tested in the laboratory. We have shown, as we did with the bypass study, that neurosurgeons know how to perform these trials and abide by their results, even when they are not to our liking.

Microsurgical treatment of infratentorial malformations.

The brain stem has long lost the designation of "no-man's land." Armed with a detailed knowledge of skull base and parenchymal neuroanatomy, coupled with the advances in intraoperative mapping and monitoring, most intrinsic brain stem cavernous malformations can be resected microsurgically. Success continues to depend on proper patient selection, optimal timing, thorough planning, meticulous technique, and completeness of the resection.

Surgical treatment of internal carotid and posterior communicating artery aneurysms.

Saccular aneurysms of the subarachnoid segment of the internal carotid artery (ICA) are very common. Although some of the aneurysms arising from the subarachnoid ICA have earned the reputation of easy to treat surgically, aneurysms in this region may be complex and quite difficult to repair. Even a simple aneurysm associated with the posterior communicating artery may harbor surprises for the unwary or inexperienced surgeon. This article details the pertinent anatomy of the subarachnoid internal carotid artery and associated saccular aneurysms, provides a guide to their diagnosis and surgical treatment, and briefly reviews some of the published surgical results. Pitfalls and technique tips are highlighted.

The pathogenesis of arteriovenous malformations: insights provided by a case of multiple arteriovenous malformations developing in relation to a developmental venous anomaly.

OBJECTIVE AND IMPORTANCE: Developmental venous anomalies (DVAs) are common anomalies of intracranial venous drainage that may occur in conjunction with other cerebral vascular malformations. The present case raises important questions regarding the association between anomalous venous drainage patterns and the development of arteriovenous malformations (AVMs). CLINICAL PRESENTATION: We present the case of a 24-year-old man with small AVMs fed by the superior cerebellar artery that drained directly into a large DVA of the cerebellum. INTERVENTION: The patient was managed conservatively and returned 10 years later with recurrent symptoms. A repeat angiogram demonstrated spontaneous thrombosis of the previously documented AVMs; however, new AVMs at a different site that was also fed by the superior cerebellar artery and drained into the same DVA had appeared. The AVMs were completely embolized, and the DVA was left intact. CONCLUSION: Recently, increasing attention has focused on the possible importance of venous outflow disturbance and venous hypertension in the pathogenesis and pathophysiology of AVMs. The potential mechanisms for this association and the implications of the present case are discussed, and the pertinent literature is reviewed.

Exophytic malignant brainstem mixed glioma in an adult: a case report.

Anaplastic mixed gliomas are rare tumors that occur mostly in the cerebral hemispheres. They have a distinctive histological appearance characterized by the presence of two or more glial cellular constituents. The incidence of malignant mixed glioma of the brainstem and posterior fossa is extremely low. The authors report an unusual case of an exophytic malignant mixed glioma. Following subtotal resection, the patient received conventional radiotherapy, but continued to deteriorate, and died five months after surgery. The extensive literature review focuses on histopathology, clinical features, natural history, and possible treatment modalities of this unusual neoplasm.

Brain attack. Introduction.

In today's medical community, the term "brain attack" is used in two ways. It is used as a synonym for stroke, and also as a reference to an educational and logistic campaign aimed at earlier recognition and treatment of stroke. This article presents an introduction to both uses of the phrase "brain attack," and focuses on the need for a brain attack campaign.

Neuronal protection from cerebral ischemia by synthetic fibronectin peptides to leukocyte adhesion molecules.

Leukocytes play an important role in the development of ischemia/reperfusion injury. Recent work in our laboratory has demonstrated that a mixture of synthetic fibronectin peptides to leukocyte adhesion molecules reduces ischemic brain damage after transient focal cerebral ischemia. The purpose of this study was to evaluate the efficacy of the individual peptides on leukocyte accumulation, infarct size, and neurological outcome in rats subjected to 1 h of cerebral ischemia and 48 h of reperfusion. Thirty-five animals were divided into five groups: transient ischemia without treatment (Group I), treatment with arginyl-glycyl-aspartic acid (RGD) peptide (Group II), connecting segment (CS)-1 peptide (Group III), fibronectin (FN)-C/H-V peptide (Group IV), and scrambled FN-C/H-V peptide (Group V). Groups III and IV showed a significant decrease in the degree of leukocyte infiltration in the lesion and in the infarct size (p < 0.05) when compared to Groups I, II, and V. The neurological grade of Groups III and IV was significantly better than in Groups I, II, and V at 48 h after reperfusion (p < 0.01). Thus, in addition to demonstrating the potential efficacy of synthetic peptides as therapeutic agents for ischemia-reperfusion, these results also offer new insights into the mechanisms of leukocyte arrest and recruitment in ischemia/reperfusion injury.

Synthetic fibronectin peptides and ischemic brain injury after transient middle cerebral artery occlusion in rats.

Leukocytes play an important role in the development of ischemia-reperfusion injury. This study was conducted to ascertain whether synthetic peptides corresponding to the cell- and heparin-binding sequences of fibronectin that disturb leukocyte adhesion molecules were effective in neuronal protection after transient focal cerebral ischemia in rats. The authors evaluated the efficacy of peptides on infarction size, leukocyte infiltration in the ischemic tissue, and neurological outcome in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion. Twenty-one animals were divided into three groups: transient ischemia without treatment (Group I), transient ischemia with administration of vehicle (Group II), and transient ischemia with administration of fibronectin peptides (Group III). The mean myeloperoxidase activity (U/g wet wt) in the ischemic area was as follows: Group I, 0.19% +/- 0.05; Group II, 0.21% +/- 0.03; and Group III, 0.08% +/- 0.02. The mean size of the infarction as a percentage of the total hemispheric volume was as follows: Group I, 38.35% +/- 1.34%; Group II, 39.21% +/- 2.42%; and Group III, 25.81% +/- 4.87%. Group III showed a significant decrease in myeloperoxidase activity in the lesion and the infarction size was smaller when compared to Groups I and II (p < 0.05). The neurological grade in Group III was significantly better than in Groups I and II at 48 hours after reperfusion (p < 0.01). This study is the first to explore the therapeutic potential of synthetic fibronectin peptides in brain protection after transient focal ischemia, and the results also serve as a basis for studies of important cellular and molecular events that contribute to tissue damage.

Optimal timing of hemodilution for brain protection in a canine model of focal cerebral ischemia.

BACKGROUND AND PURPOSE: Hemodilution is known to ameliorate the effects of focal ischemia when used shortly after cerebral arterial occlusion; however, it remains to be proved whether hemodilution will be effective when used at more clinically relevant times, ie, with some delay between the onset of ischemia and initiation of therapy. METHODS: Thirty-two dogs were selected for inclusion in this study. Cerebral infarction was induced by permanent occlusion of the middle cerebral and the azygos anterior cerebral arteries. The animals were allocated to 1 of 4 groups of eight animals each: arterial occlusion without hemodilution (group 1); hemodilution immediately after occlusion (group 2); hemodilution 3 hours after occlusion (group 3); and hemodilution 6 hours after occlusion (group 4). Isovolemic hemodilution to a hematocrit of 30% was performed. The animals were killed 6 days after induction of ischemia, and the infarct size was determined. RESULTS: Groups 2 and 3 showed significant reduction of infarct size (P < .0001) when compared with group 1. The neurological grade of group 3 on postoperative days 4, 5, and 6 was significantly better than those of groups 1 and 4 (P < .01). Group 4 showed a significant increase in the incidence of hemorrhagic infarction when compared with groups 1 and 2 (P < .01). CONCLUSIONS: The current study indicates that hemodilution administered as much as 3 hours after ischemia is effective in reducing infarct size and improving neurological status. When administered 6 hours after ischemia, hemodilution is not helpful and may be harmful.

Therapeutic time window for the 21-aminosteroid, U-74389G, in global cerebral ischemia.

A novel 21-aminosteroid (U-74389G), a new potent antioxidant, was evaluated for its protective effect on transient global cerebral ischemia. Ischemia was induced by 20 minutes of four-vessel occlusion in adult male Wistar rats. Injection of 21-aminosteroid (U-74389G, 5 mg/kg intraperitoneally injected) was repeated three times. The second injection was performed 30 minutes after the first injection, and the third injection was performed 210 minutes after that. Experimental animals were divided into five groups according to the time drug administration was initiated. Group I (n = 8) began vehicle administration 30 minutes before occlusion. Group II (n = 9) started 21-aminosteroid administration 30 minutes before occlusion. Drug administration in Group III (n = 9) began at the time of reperfusion, in Group IV (n = 8), 30 minutes after reperfusion, and in Group V (n = 6), 60 minutes after reperfusion. Animals in the control group (n = 5) underwent sham operations. One week after ischemia, the number of viable pyramidal neurons was counted in the hippocampal CA1 subfield. The results were as follows: the number of living neurons in Group I was 18.8 +/- 8.7; in Group II, was 44.7 +/- 9.5; in Group III, was 46.4 +/- 9.4; in Group IV, was 40.3 +/- 6.6; in Group V, was 10.2 +/- 2.5; and in the control group was 131 +/- 3.3. Groups II, III, and IV demonstrated significantly higher numbers of living neurons compared with Group I (P < 0.05). The present study revealed that U-74389G attenuated delayed neuronal death in global cerebral ischemia when it was administered before or soon after the ischemic episode.

Cost-effectiveness of carotid endarterectomy.

Carotid endarterectomy (CEA) reduces the risk of stroke in symptomatic patients with high-grade carotid stenosis. In this study, we evaluated the long-term, societal cost-benefit ratio of endarterectomy using a decision analysis model. We reviewed the results of 150 CEAs performed at an academic center and established a Markov model comparing cohorts of patients who experienced transient ischemic attacks and then underwent observation, aspirin therapy, or CEA. The cost-effectiveness of CEA was estimated using perioperative complication rates from our review and from the North American Symptomatic Carotid Endarterectomy Trial. Stroke and mortality rates were estimated from the literature. Cost estimates were based on medicare reimbursement data. Among the 150 CEAs reviewed, complications included major stroke (0.67%), minor stroke (1.33%), myocardial infarction (1.33%), pulmonary edema (0.67%), and wound hematoma (3.33%). There were no deaths or intracerebral hemorrhages. Using complication rates from our review, CEA produced cost savings of $5730.62 over the cost of observation and $3264.66 over the cost of aspirin treatment. CEA extended the average quality-adjusted life expectancy 15.8 months over that of observation and 13.2 months over that of aspirin. Substituting the North American Symptomatic Carotid Endarterectomy Trial results, CEA yielded savings of $2997.50 over the cost of observation and $531.54 over the cost of aspirin. Quality-adjusted life expectancy was extended 13.8 months compared with observation and 11.2 months compared with aspirin therapy. This analysis demonstrates that when performed with low perioperative morbidity and mortality rates, CEA is a highly cost-effective therapy for symptomatic carotid stenosis and results in substantial societal cost and life savings.

Functional magnetic resonance imaging as a management tool for cerebral arteriovenous malformations.

The location of eloquent cortex, such as the motor strip, the visual cortex, or Broca's area, may be difficult to predict even with multiprojectional magnetic resonance imaging (MRI). Distortion and displacement of this cortex may occur with a congenital lesion, such as an arteriovenous malformation, or by an acquired disease, such as a neoplasm. A desire to avoid damaging these eloquent areas by conventional surgery, radiosurgery, or endovascular surgery makes their accurate identification an important part of the pretherapeutic planning process. Blood oxygen level dependent functional MRI is a technique that uses the local increase of oxyhemoglobin concentration in the patient that occurs as a result of the increase in flow rate and blood volume in eloquent cortex undergoing stimulation from, for example, flashing lights, hand movements, or speech. We have used the blood oxygen level dependent technique to localize eloquent cortex relative to arteriovenous malformations and tumors. Using a 4.0-T magnetic resonance (MR) system, there is a sufficiently high degree of spatial resolution of the MR signal intensity changes during stimulation to allow the identification of eloquent cortex. Alternative, non-MR, invasive techniques for functional localization include electrocorticography and stimulation from subdural grids and strips. Noninvasive, non-MR technologies, such as positron emission tomography and magnetoencephalography, can also provide functional localization of eloquent cortex. However, the perfection of functional MRI at the 1.5-T field strength and the large number of such MR systems in operation mean that a highly accurate cerebral cortical localization technique can be available to most neuroscientists without the need to purchase alternative expensive technology.

Intra-aortic balloon counterpulsation augments cerebral blood flow in a canine model of subarachnoid hemorrhage-induced cerebral vasospasm.

We tested the effect of intra-aortic balloon counterpulsation (IABC) on cerebral blood flow (CBF) in a canine model of cerebral vasospasm. Cerebral vasospasm was induced in ten adult mongrel dogs using a "two-hemorrhage" model. CBF was then measured using radiolabeled microspheres, before and after activation of an intra-aortic balloon pump. Physiologic parameters including pCO2 and cardiac filling pressures were maintained constant during the experiment. Cardiac output was monitored in each animal. CBF increased with IABC in all ten animals. The mean CBF was 78.5 milliliters per 100 grams per minute (ml/100g/min) before versus 93.3ml/100g/min after IABC (P = 0.0001). Increases in CBF were associated in most, but not all, cases with increases in cardiac output. This study supports the ability of IABC to raise CBF in the setting of cerebral vasospasm. IABC may represent an important clinical option in cases of refractory vasospasm following aneurysmal subarachnoid hemorrhage.