In this issue

In this issue

Available online at www.sciencedirect.com Surgical Neurology 72 (2009) 441 – 442 www.surgicalneurology-online.com Editorial In this issue... Chien ...

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Available online at www.sciencedirect.com

Surgical Neurology 72 (2009) 441 – 442 www.surgicalneurology-online.com

Editorial

In this issue... Chien et al from the United States have written a critically important article that advances our knowledge of which aneurysms to select for surgery. This decision process is not based upon aneurysm size but on individual aneurysm hemodynamic parameters. (This work is another example of how treatments in the 21st century will be totally individualized to each patient rather than being developed from a group or randomized study.) The authors were able to determine wall shear stress (WSS) at several points from the neck to the dome of the aneurysm. They compared ruptured and unruptured internal carotid ophthalmic aneurysms. They found that WSS in unruptured aneurysms was low, whereas it was almost as high as parent artery WSS in ruptured aneurysms. Also, ruptured aneurysms had multiple jets (vortices) of flow compared with the single jet found in an unruptured aneurysm. The real question here is what comes first—pathologic change in the aneurysm, or flow and WSS changes that produce the pathologic alterations leading to aneurysm formation and rupture. We do not know this answer. So, that means that patients with known unruptured aneurysms would have to be studied for WSS changes and imaged regularly. Still, if WSS changes were high in a single study on a patient, the evidence presented in this article would be very persuasive to direct the clinician to take action because the aneurysm would be at risk of rupture from this evidence. This study is superb, innovative, and will change our approach to the treatment of cerebral aneurysms. Yes, more data need to be reported, but this study is powerful enough to strongly suggest a relationship between WSS and aneurysm rupture. Kadkhodayan et al from the United States report on their experience with angioplasty and stenting of the origin of the common carotid artery. The origins of the common carotid arteries are often ignored by angiographers, but as the authors show, up to 10% of patients with cerebral ischemia have stenosis at the common carotid origin. The authors report that angioplasty and stenting were successful in their 7 patients. Their stroke rate was 0. In my opinion, this approach has far less risk than the surgical option at the The views and opinions expressed in this editorial are those of the Editor-in-Chief, and the views expressed herein are not necessarily those of the Publisher. 0090-3019/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.surneu.2009.08.055

common carotid origin. The real key is the restenosis rate. The authors had a 30-month follow-up period, and not all patients were reangiogrammed. This is a good approach to these lesions that are uncommon. More long-term follow-up data would be helpful, but for now, this treatment is the preferred one for lesions of this kind, in my opinion. Ebner et al from Germany report on their study of the distance between the carotid arteries at the level of the sella in acromegalic patients. They found that the distance between the inner walls of the carotids was statistically smaller compared with controls. Hypertension also reduced this distance between the carotid arteries. The internal carotids were also larger in diameter at this sellar level in acromegalics compared with controls. Carotid artery laceration is a serious complication in pituitary surgery. This article provides a means of knowing the position of the carotids in these patients and of avoiding that complication. The authors suggest a preoperative computed tomography with bone windows to determine the location of the bony carotid canal. Vascular imaging would also be helpful. If this problem occurs 1 time in your career, is that enough to take this preventative measure? Read Post's comments at the end. de Lacy et al from the United Kingdom analyzed their population of 30 patients with microprolactinomas. Fourteen percent developed a CSF leak after dopamine therapy for high prolactin levels. Two other complications were seen using this drug therapy for a 20% complication rate. If the tumors invaded the sphenoid sinus, the chance of CSF leak increased. To me, I am seeing and reading about too many CSF leak complications from transsphenoidal and skull-based surgery. What bothers me is the acceptance by the neurosurgical community that this complication is to be expected. Work should be done to eliminate this complication. Yen et al from Taiwan have done an interesting study trying to determine if white matter tracts are edematous, displaced, invaded, or disrupted by tumor by using diffusion tensor imaging on magnetic resonance. Noriko Salamon makes some excellent comments at the end, suggesting that animal models or autopsied specimens could be used to verify the findings of the authors. This research would not be easy to do. The authors' logic in this article seems reasonable but must be subjected to confirmation by other methods. This

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Editorial / Surgical Neurology 72 (2009) 441–442

study should stimulate other investigators to look at this problem. The article has potential value in the resection of tumors based on this information. Ito et al from Japan describe their experience with an ultrasonic bone curette for performing a minimally invasive laminoplastic laminotomy. Read the Abstract and look at Figure 3 for a quick understanding of what the authors are doing. Read the comments at the end for other opinions. Is this instrument essential or unnecessary? For the developing world, this is not a priority purchase, in my opinion. Fujimura et al from Japan investigated the serum levels of matrix metalloproteinase-9 (MMP-9) and MMP-2 in patients with moyamoya disease. The matrix metalloproteinases are proteins acting as enzymes that come from a gene template. The MMPs degrade the components of the extracellular matrix in normal and pathologic conditions. By digesting the basal lamina of endothelial cells in a blood vessel, these enzymes can alter blood-brain barrier permeability. The action of these enzymes is also related to the formation of aneurysms and cerebral hemorrhage. Apparently, there is a genetically-determined balance between the MMPs and the TIMP enzymes on the extracellular matrix that may be disturbed in moyamoya. TIMPs are tissue inhibitors of metalloproteinases. The authors found that MMP-9 levels in the serum of patients with moyamoya disease were elevated. This work is the beginning of a molecular understanding of why moyamoya disease occurs, looking at the extracellular matrix. The article is short and easy to read. The Discussion is useful. Huang et al from China describe their study in which they related the serum and CSF levels of microparticles (MPs) to the outcome of patients with ICH. Microparticles are the fragments of a cell membrane that enter the plasma and the CSF after the death of cells. These fragments contain phospholipids, as do all cell membranes, which promote coagulation. It is unclear how these particles reach the CSF or serum unless through large tissue spaces that allow their

transfer. Yet, the authors found that high serum and CSF levels of MPs compared with controls were related to the low GCS scores, high ICH volumes, presence of IVH, and survival. So, can we use the serum MPs as a marker of survival after ICH? We are not sure yet. So, what do we do with this information? First, it would seem reasonable to track each ICH patient and to repeat these observations. Next, are certain levels associated with bad outcomes? If so, will we evolve into using MP serum levels as the only test for survival or mortality with ICH? Before we reach that point, we must be certain what we are measuring. Gürses et al from Turkey studied raloxifene, a drug originally used to prevent osteoporosis and breast cancer, for the treatment of vasospasm. Raloxifene has estrogenpromoting effects in some tissues and antiestrogen effects in others. The drug seemed to cause vasodilatation of the cerebral vessels. Read the Abstract and then the comments of Macdonald and Tamargo at the end for their ideas on how this molecule may work. Jalloh et al from Canada report on a patient in whom activation of the latent herpes simplex virus occurred after acoustic neuroma resection. The patient developed herpes simplex encephalitis that responded to acyclovir. At a time when imaging has taken the place of a neurologic examination of patients, Vilela and Goodkin report on the preservation of hand function in a patient with C7-T1 complete cord injury. Cole adds his comments at the end about the anatomical variability to explain this occurrence. The Abstracts of the 2009 Belgian Neurosurgical Society meeting are included in this issue. This is the next to last issue of Surgical Neurology. Read my note about the end of Surgical Neurology. I have written an editorial entitled “What is the truth?” James I. Ausman, MD, PhD (Editor) E-mail address: [email protected]