Up until 1 year ago, I had read some scientific reports discussing the use of cell phones and their association with brain tumors. At that time, to me, the reports were not convincing. Ron Pawl contacted me a few months ago and alerted me to new information that he believed was convincing—that cell phone use is associated with the development of brain tumors. He researched the topic more thoroughly, and his report is published in this issue. The data now strongly support the development of brain tumors ipsilateral to the side of cell phone use. Read his report. It and the information it contains will be widely reported.
Tateshima et al from the United States studied wall shear stress in a model of a large MCA aneurysm containing an atherosclerotic plaque. In an elegant series of experiments, the authors demonstrated low shear stress values at the plaque compared to higher shear stress values in the aneurysm where there was no plaque. What significance does this information have to a neurosurgeon? In an introductory editorial, Tateshima et al describe, in simple terms, why this concept is important in the development of cerebral aneurysms and atherosclerotic plaques. The authors suggest that there is some evidence to support the concept that aneurysms with high wall shear stress values are prone to rupture. Citing other studies, the authors state that high wall shear stress induces molecular and genetic factors leading to vessel remodeling and possibly aneurysm formation. They cite an experiment in which aneurysms were formed related to high wall shear stress values. The editorial is packed with interesting information that is logically presented to give the reader the basic understanding necessary to comprehend the article that follows. It should be mentioned that low shear stress can induce inflammation in the vessel wall by altering molecular endothelial factors. There is abundant evidence that atherosclerotic plaques are an end result of an inflammatory process in the vessel wall. It is possible from the work reported by the authors and others that the low wall shear stress can induce the initial changes that lead to atherosclerotic plaque development. As we all know, these plaques form at carotid bifurcations and other specific areas in arteries. The formation at these sites may be governed by changes in wall shear stress. At the bifurcations, where there is turbulent blood flow, low wall shear stress occurs. This low wall shear stress may produce the environment for inflammatory change leading to atherosclerotic plaque development. Kern Guppy, who is a fluid mechanics engineer and a neurosurgeon, provides excellent comments at the end of the article, which follows the editorial. Obviously, this is a new and exciting area of investigation, and much more has to be learned. The authors have produced a superb explanation of these new concepts in their editorial with an excellent article that follows. This is 21st century, first-class research and science. It is worth the extra time it takes to read these 2 articles. Read the introductory editorial article first. (Note the case report that follows both on the remodeling of the vertebral artery after occlusion of the opposite vertebral for dissection.)
Russell et al from the United States tested patients with moderate (<70%) or severe carotid stenosis (>70%) with acetazolamide (a potent vasodilator) to determine if each group of patients had vascular reserve to dilate their vessels further. All patients had 3-vessel cerebral angiography. The authors found that those patients who demonstrated an increase in MCA velocity after the acetazolamide treatment had the capacity to dilate their cerebral vessels, further leading to greater blood flow. Those who were not able to dilate their vessels further after the acetazolamide challenge had less increase in their MCA velocities. Less of an increase in MCA velocity could indicate that the vessels in the MCA territory being examined were already dilated or that there was such abundant collateral circulation that little change in MCA velocity occurred. This difference must be determined by knowledge of the patient's angiographic anatomy—which the authors evaluated. Christopher Loftus has made some excellent comments at the end with which I totally agree. What can be done with these data will require other publications. Its use in determining whether to use a shunt at carotid endarterectomy is better determined at surgery as Loftus notes.
Simis et al from Brazil report on a study of 61 patients with meningiomas. They looked at the association of peritumoral edema in relation to tumor size, irregular tumor borders, seizures, and recurrence, among other factors. They found that the aforementioned 4 factors were highly associated with peritumoral edema. To me, this report is interesting from all 4 associations they found. Next time I see a large meningioma with peritumoral edema, I will suspect that the tumor may be more invasive. I will look for the irregular borders and check for seizures in the history. Likely, all of these factors will point to a finding of a more aggressive meningioma at surgery.
Shi et al from China and the United States report on 3 patients with meningiomas who were embolized with the liquid agent Onyx. The results are impressive in tumor vasculature obliteration, tumor necrosis, and shrinkage of the tumor evaluated 10 days after embolization. There was no recurrence at a 12-month follow-up—which may be a short period to see recurrence. The authors make an interesting point in suggesting Onyx embolization as the only treatment for these tumors. This is the first report to observe the tumor for 10 days after embolization and to record the imaging changes for this period. Is this report another example of a surgical lesion that will be treated endovascularly? Read my editorial on this subject.
Dusick et al from the United States report some useful data on the postoperative recovery of endocrine function after endonasal removal of Rathke's cleft cysts (RCC), tuberculum sella meningiomas, and craniopharyngiomas. The authors found that only in the RCC did a recovery of pituitary function occur in more than 50% of their patients. In one-third of the craniopharyngiomas and 10% of the meningioma and RCC patients, worse pituitary function was found postoperatively.
Li et al from the United States discuss whether the peritoneal end of a VP shunt should be exteriorized in abdominal or urological surgery. Before I read this article, I would have recommended externalization in all cases because I would be sure if the abdominal procedure was contaminated or not. The authors found that externalization was not necessary unless gross contamination was present.
Okutan et al from Turkey performed a very simple but excellent experiment, demonstrating the protective value of erythropoietin (EPO)—which is known to have neuroprotective properties—in experimentally induced brain edema in rats. Erythropoietin was as effective as dexamethasone (DSP). Not only did the EPO and DSP limit edema formation measured by brain water content, but also both agents limited molecular damage leading to cell death. Ultrastructural alterations were also reduced in the animals receiving EPO or DSP treatment. So, the authors have shown that EPO has neuroprotective effects in experimentally induced brain injury.
Most of us have had difficulty puncturing the frontal horn from a pterional exposure. Park et al from Korea have done an excellent study to demonstrate in a simple manner how a ventricular puncture can be performed from a pterional exposure successfully. Read the article and look at the video. This is a very useful article.
There are some interesting case reports that follow these articles.
Mel Cheatham, who edits our section on Profiles in Volunteerism, has written an inspiring story about William Rambo, a neurosurgeon who has volunteered his life and skills to help the people of Kenya. This is a terrific story.
Read my editorial on the article by Shi et al in this issue about a new treatment for meningiomas and its implications to physicians, neurosurgeons, and medicine.
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