Neurosurgical forum Letters to the editor

Creative use of endovascular devices in cerebral aneurysm treatment To The Editor: The “balloon bounce” technique by Wolfe et al. (Wolfe SQ, Farhat H, Moftakhar R, et al: Intraaneurysmal balloon assistance for navigation across a wide-necked aneurysm. Technical note. J Neurosurg 112:1222–1226, June 2010) is a creative solution to the problem of how to navigate a device across the neck of a wide-necked cerebral aneurysm when tortuosity of the afferent artery or a sharp angle of the efferent artery becomes a challenge to all available guidewires and microcatheters. The authors inflated a HyperForm balloon (ev3) within the aneurysm sac to provide a contact surface to “bounce” another remodeling balloon across the aneurysm neck to a stable position. The HyperForm balloon was then deflated and removed, and a microcatheter was placed in the aneurysm for embolization. Three patients had aneurysms successfully occluded using embolization with Onyx 500 (ev3), but endosaccular coiling could surely have been done instead, and the same technique could have been used as a tool for “bouncing” a stent catheter as well. Some years ago I described one technical variant of intraaneurysmal balloon assistance for endovascular coiling of a wide-necked, unruptured aneurysm of the middle cerebral artery.3 In that case, after exhausting all available technical possibilities of navigating a remodeling balloon across the aneurysm neck, I placed a HyperForm balloon into the aneurysm neck and a microcatheter into the aneurysm fundus distally for coiling. The aneurysm was occluded using platinum coils, with the balloon inflated as necessary at the neck and into the aneurysm to keep the coils inside the aneurysm sac and the balloon withdrawn as the coils were deployed. The procedure was uncomplicated, and aneurysm occlusion was satisfactory on angiographic follow-up. I would like to address two technical aspects of intraaneurysmal balloon assistance that were not mentioned by Wolfe et al.4 First, blood flow tends to move the balloon forward against the aneurysm fundus, and some length of the balloon catheter must be pulled out as the balloon is inflated to keep it in optimal position. The HyperForm balloon has a hard, 5-mm-long translucent tip that is positioned inside the aneurysm and that can be pushed against the aneurysm wall by the blood flow. Thus, the aneurysm sac must be large enough to accommodate the balloon, the balloon tip, and some length of the balloon system’s guidewire. This inconvenience can be avoided by using a rounded, guidewire-free, flow-directed balloon for intraaneurysmal assistance. Second, Wolfe et al. warned against balloon overinflation to avoid aneurysm rupture, but a dangerous situation is also theoretically possible if the HyperForm balloon occludes the aneurysm ostium partially, resulting in a siphon effect, with inflow of blood J Neurosurg / Volume 121 / November 2014

into the aneurysm during systole and outflow hindrance in diastole, which could cause aneurysm expansion with the risk of rupture. Other reports on intraaneurysmal techniques permitting the endovascular treatment of complex aneurysms when more conventional techniques have failed describe the “neck bypass technique,”1 also mentioned by Wolfe et al., in which a balloon catheter is navigated over a guidewire into the aneurysm until it makes a complete loop along the dome wall and exits into the afferent artery. Another is the “waffle cone technique”2 in which one deploys a stent into the aneurysm sac and afferent artery. These techniques have in common the fact that devices designed to bridge the aneurysm neck were instead used inside the aneurysm sac, and the procedures were successful and uncomplicated. It is important that such unconventional, “creative” techniques are subjected to peer review and description in the literature. It is also important to point out that the decision to use such a technique for the first time should be based on the operator’s skills, experience in treating the actual pathology, and extensive experience with the devices involved.

Sandro Rossitti, M.D., Ph.D. University Hospital Linköping, Sweden

Disclosure The author reports no conflict of interest.

References   1.  Cerkige SH, Yavuz K, Geyik S, Saatci I: HyperForm balloonassisted endovascular neck bypass technique to perform balloon or stent-assisted treatment of cerebral aneurysms. AJNR Am J Neuroradiol 28:1388–1390, 2007   2.  Horowitz M, Levy E, Sauvageau E, Genevro J, Guterman LR, Hanel R, et al: Intra/extra-aneurysmal stent placement for management of complex and wide-necked-bifurcation aneurysms: eight cases using the waffle cone technique. Neurosurgery 58 (4 Suppl 2):ONS-258–ONS-262, 2006   3.  Rossitti S: Intra-aneurysmal balloon inflation as an aid to endovascular wide-necked cerebral aneurysm coiling. Clin Neuroradiol 17:127–129, 2007  4. Wolfe SQ, Farhat H, Moftakhar R, Elhammady MS, AzizSultan MA: Intraaneurysmal balloon assistance for navigation across a wide-necked aneurysm. Technical note. J Neurosurg 112:1222–1226, 2010

Response: No response was received from the authors of the original article. Please include this information when citing this paper: published online August 29, 2014; DOI: 10.3171/2010.8.JNS101187. ©AANS, 2014

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Neurosurgical forum The effect of carotid endarterectomy To The Editor: I read with interest the article by Nagaki et al.1 (Nagaki T, Sato K, Yoshida T, et al: Benefit of carotid endarterectomy for symptomatic and asymptomatic severe carotid artery stenosis: a Markov model based on data from randomized controlled trials. Clinical article. J Neurosurg 111:970–977, November 2009). The purpose of this letter was to determine whether the effect of endarterectomy can be assessed only observationally or only experimentally. For patients with both symptomatic and asymptomatic carotid artery stenosis, several major randomized controlled trials of carotid endarterectomy (CEA) have previously tackled the remaining effects of CEA on the risk of stroke. Nevertheless, because the risk of stroke among patients with asymptomatic carotid artery stenosis is quite low, whether to treat their stenosis with CEA continues to be an important public health concern. The authors established a Markov model in order to assess the efficacy of CEA. There were 4 different health states modeled. The authors did consider the probability of transition from one health state to another state and calculated such a probability approximately by using data from major randomized controlled trials. With regard to their baseline analyses, they adopted 3 comorbidity index values. They stated outcomes via the use of the anticipated number of quality-adjusted life years (QALYs) for a theoretical cohort treated with CEA and another without CEA. In fact, CEA for asymptomatic stenosis had little benefit (0.07 QALY) for normal-risk CEA candidates who were older than 70 years of age, not to mention those who were even much older, according to the authors’ baseline analysis. It is understood that some ethical and practical issues may hinder randomized trials in medicine and surgery.2 Therfore, despite the fact that the authors established a Markov model in order to assess the efficacy of CEA, of importance in this context is the other fact that in order to determine whether a study is truly experimental, it will be necessary to ascertain at least some comparisons between two groups that differ on the basis of an intervention of interest. Endarterectomy, for instance, is the intervention in the context of current discussion. In fact, if the endarterectomy treatment is not properly (i.e., with randomized controls) compared to a conservative treatment or condition, the effect of endarterectomy can then be interpreted only as observational, not experimental at all. Bing Tang, M.D., M.P.H. Department of Research Danville, CA

Disclosure The author reports no conflict of interest.

rotid artery stenosis: a Markov model based on data from randomized controlled trials. Clinical article. J Neurosurg 111: 970–977, 2009   2.  Tang B: Biostatistics with neurosurgical importance. J Neurosurg 168:1256–1261, 2008 (Letter)

Response: We appreciate the author’s interest in our study. Carotid endarterectomy for asymptomatic carotid artery stenosis has been the focus of many reports and trials during the past decade. Although large randomized control trials have demonstrated a net benefit of CEA beyond that of the best medical treatment,1,4 the initial increase in events associated with perioperative mortality and morbidity required a few years for a benefit in eventfree ratio to emerge. Therefore, long-term survival after CEA for asymptomatic stenosis is an important consideration when deciding whether to perform this prophylactic procedure. However, several natural history studies of patients with carotid artery stenosis have demonstrated decreased survival rates compared with the general population.2,3 These findings caused some concern about the long-term overall benefit from CEA. Moreover, the clinical situation is more complicated than for simple stroke-risk versus treatment-risk analysis. It is undoubtedly important that CEA would be properly compared with a conservative treatment. We used a Markov model to address this problem. Although in order to construct the mathematical model, several simplifications are inevitable, Markov modeling permits an increase in complexity of the model, such as incorporating stroke rate in patients with or without CEA, surgical risk, or the long-term survival rate of “CEA candidates.” In our baseline analysis for symptomatic stenosis, surgery produced a relatively large QALY gain. Sensitivity analysis regarding symptomatic carotid artery stenosis showed a net benefit of CEA, and the results were robust for parameter variation within clinically plausible ranges. Irrespective of comorbidities limiting life expectancy, as well as advanced age, symptomatic patients were deemed to be operative candidates for CEA. Even if increased perioperative risk was observed in patients with symptomatic stenosis, CEA nonetheless might be beneficial in the long term. On the contrary, in our baseline analysis, treatment for asymptomatic carotid stenosis yielded very little QALY gain, and surgery is not likely to have a large impact upon the burden of stroke. The benefit of CEA for such patients is only marginal and is rapidly lost to be negative because of the increased rate of surgical complications, advanced age, and comorbidities. Our results suggest that only carefully selected conditions, such as very low treatment risks in relatively young patients without comorbidities, could justify CEA for asymptomatic stenosis. Yuhei Yoshimoto, M.D. Tomohito Nagaki, M.D. Koji Sato, M.D. Takaaki Yoshida, M.D. Gunma University Graduate School of Medicine Maebashi, Japan

References

References

  1.  Nagaki T, Sato K, Yoshida T, Yoshimoto Y: Benefit of carotid endarterectomy for symptomatic and asymptomatic severe ca-

  1.  Halliday A, Mansfield A, Marro J, Peto C, Potter J, Thomas D, et al: Prevention of disabling and fatal strokes by successful

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Neurosurgical forum carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet 363:1491– 1502, 2004   2.  Kragsterman B, Björck M, Lindbäck J, Bergqvist D, Pärsson H, Swedish Vascular Registry (Swedvasc): Long-term survival after carotid endarterectomy for asymptomatic stenosis. Stroke 37:2886–2891, 2006   3.  LaMuraglia GM, Brewster DC, Moncure AC, Dorer DJ, Stoner MC, Trehan SK, et al: Carotid endarterectomy at the millennium: what interventional therapy must match. Ann Surg 240:535–546, 2004   4.  Walker MD, Marler JR, Goldstein M, Grady PA, Toole JF, Baker WH, et al: Endarterectomy for asymptomatic carotid artery stenosis. JAMA 273:1421–1428, 1995 Please include this information when citing this paper: published online September 5, 2014; DOI: 10.3171/2010.5.JNS10591. ©AANS, 2014

Neuritis ossificans To The Editor: We read with great interest the paper This article contains some figures that are displayed in color on­line but in black-and-white in the print edition.

by Kemper et al.1 (Kemper CM, Rojas JC, Bauserman S: Neuritis ossificans of a cranial nerve. Case report. J Neurosurg 113:1112–1114, November 2010). We also observed a somewhat similar finding in a 56-year-old woman who presented with progressive dysphagia and dysphonia that was the result of an intradural calcified lesion of the lower cranial nerves. Our preoperative diagnosis in this case, based largely on the finding of the patient’s clinical history and imaging, was calcified meningioma (Fig. 1). Laryngoscopic examination revealed the presence of a total preoperative left vocal cord palsy. Using a left suboccipital retromastoid approach, we were able to expose the lesion, which turned out to be inseparable from the lower cranial nerves, the anterior inferior cerebellar artery, and the posterior inferior cerebellar artery, and it was inseparable from both the dura mater and the brainstem. For these reasons, we could do no more than a partial resection. When the patient recovered from anesthesia, she reported worsened dysphagia and respiratory difficulties, which prompted a tracheostomy to be performed. An MRI examination ruled out both ischemia and/or infarction, but it did reveal an increase in the edema surrounding the surgical cavity. The ensuing course of action was then further complicated by systemic sepsis, which required prolonged

Fig. 1.  Preoperative CT scans and MR images showing the right C-1 and the left jugular tubercle calcified lesions.  A: Preoperative CT scans without intravenous contrast administration.  B: Preoperative axial T2-weighted MR images.  C: Preoperative coronal T1-weighted MR image.  D: Preoperative axial T1-weighted MR image with intravenous contrast administration.

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Neurosurgical forum assistance in the intensive care unit. Histopathological examination disclosed calcified tissue fragments within a granulomatous reaction with inflammatory infiltrates, giant cells, and fibrosis. Ziehl-Neelsen staining ruled out the possibility of a specific granuloma (Fig. 2). The course of the disease we observed (progressive cranial nerve impairment) and the results of imaging seem to be strikingly similar to the report by Kemper et al. Although histological diagnosis does provide for a differentiation made possible due to the lack of nerve fibers, there does not appear to be enough evidence to rule out the possibility of a diagnosis of ossificans neuritis. We say this because, in our case, the deliberate choice of the surgeon (G.B.) was to avoid resection of cranial nerves along with the pathological mass. Our sense is that, perhaps, we may have actually found a second case of ossificans neuritis of cranial nerves. These considerations led us to ask 2 questions that in our opinion remain unanswered. The first regards the epidemiology of this disease. Is ossificans neuritis of the cranial nerves really as rare as was first reported in 2010, or is this yet another example of a misdiagnosis that goes unreported? The second consideration involves the putative etiopathogenesis of this disease. Ossificans neuritis involving the peripheral nerves is a rare entity that, given its pathological resemblance to myositis ossificans, is currently thought to be to be secondary to a traumatic event. With that said, however, it needs to be emphasized that even in cases involving the peripheral nervous system, the disease’s etiology continues to remain unclear. Although Kemper and colleagues’ idea that neuritis ossificans “is caused by a repetitive mechanical trauma or friction of the nerve near the porous hypoglossus” does seem to be quite original, we wonder why the disease should be so uncommon when it is known that the hypoglossal nerve is, indeed, quite prone to mechanical trauma or friction. Could the anatomy of their patient be significantly different from the normal anatomical pattern? If this is the case, what then are we to conclude about the findings in our

Fig. 2.  Photomicrograph showing a calcification surrounded by a gran­ulomatous reaction. H & E, original magnification ×400.

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patient? Are we to conclude that the lower cranial nerves are also prone to mechanical trauma or friction? We know that the environment surrounding the cranial nerves is quite different from that surrounding peripheral nerves. The cranial nerves are bathed in a liquid medium of CSF, whereas peripheral nerves are surrounded by a more solidified fatty tissue. Such a dramatically different kind of surrounding should be expected to affect the nature of the susceptibility of these different nerves to mechanical trauma. It certainly seems reasonable to expect that such dramatically different environments should call into question any kind of simplistic trauma hypothesis that treats peripheral and cranial nerves in the same way. On the contrary, it seems much more realistic and plausible to recognize that the etiology of this disease, at the level of cranial nerves, continues to be unknown and is probably unrelated to trauma. We invite the neurosurgical community to share the experience of such a fascinating, puzzling, and seemingly unusual disease. It should also be noted that, since the lesion in question is, in our experience, unresectable, we recommend the avoidance of any kind of aggressive surgical approach before the course of this disease is clarified. Paolo Ferroli, M.D. Angelo Franzini, M.D. Morgan Broggi, M.D. Francesco Acerbi, M.D., Ph.D. Emanuela Maderna, M.D. Bianca Pollo, M.D. Giovanni Broggi, M.D. Fondazione IRCCS Istituto Neurologico Carlo Besta Milan, Italy Disclosure The authors report no conflict of interest. Reference   1.  Kemper CM, Rojas JC, Bauserman S: Neuritis ossificans of a cranial nerve. Case report. J Neurosurg 113:1112–1114, 2010

Response: We thank Ferroli and colleagues for their interest and comments regarding our paper with the first report of neuritis ossificans of a central nerve. The definitive diagnosis was made by pathological analysis showing zonal heterotopic calcification and observation of Haversian canals confirming ossification. Positive staining for neurofilament protein, S100, and epithelial membrane by immunohistochemical analysis confirmed the presence of nerve fiber. We believe that the description of intracranial neuritis ossificans will increase with the addition of this entity to the differential diagnosis. The occurrence of neuritis ossificans is in fact a rare entity itself. The reporting of this phenomenon is uncommon even in the general literature. With the quality of current imaging we find ever-increasing ability to resolve or identify intracranial pathology radiographically. We suspect that the report by Ferroli et al. and ours will prompt neuroscientists to further investigate the incidence, natural history and response to treatment of this pathology. We J Neurosurg / Volume 121 / November 2014

Neurosurgical forum believe that this entity will be described in the future or in retrospect. The suggestion that this entity is either underreported or misdiagnosed is supported. The source of this lesion was suggested to be from localized trauma at the entrance to the hypoglossal foramen. For example, the theory of syrinx formation relies on local physiological trauma at the foramen magnum to produce deformation of its contents. Additionally, tension, as a source of local trauma, is a known factor in cranial nerve damage. We maintain that it is conceivable for localized trauma by tension of the nerve at the hypoglossal foramen to be a possible explanation for pathogenesis in central neurositis ossificans. No abnormal anatomy of this patient was observed intraoperatively or radiographically. The treatment for neurositis ossificans, as always, should be based on a risk-benefit analysis. The case presented in the original article described a patient’s fixed deficit and end organ damage as demonstrated by electromyography and allowed a total resection of this focal lesion under evoked potential monitoring with little risk to additional structures. If vital viable tissue were involved with this lesion, we would concur with Ferroli et al. that a measured surgical response would be appropriate. Based on the comments by Dr. Ferroli, as well as findings in our own patient, it appears that this lesion can result in significant neurological morbidity. Due to the uncommon incidence of this entity, further observations would be helpful in establishing its natural history. Craig M. Kemper, M.D. Julio C. Rojas, M.D., Ph.D. University of Texas at Austin Austin, TX Steven Bauserman, M.D. University of Texas Medical Branch Austin Campus Austin, TX

Please include this information when citing this paper: published online September 12, 2014; DOI: 10.3171/2010.8.JNS101289. ©AANS, 2014

Minute-by-minute monitoring of autoregulation To The Editor: We read with great interest the recently published paper by Depreitere and colleagues2 (De­ preitere B, Güiza F, Van den Berghe G, et al: Pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in patients with severe traumatic brain injury based on minute-by-minute monitoring data. Clinical article. J Neurosurg 120:1451–1457, June 2014), in which they report the use of minute-by-minute intracranial pressure (ICP) and mean arterial blood pressure (MABP) data to assess the vascular pressure reactivity of cerebral autoregulation with an algorithm called the low-frequency autoregulation index (LAx). This index is similar to the pressure reactivity index (PRx) proposed by Czosnyka et al.;1 nevertheless, PRx requires second-bysecond ICP and MABP data for its calculation. The hypothetically optimal cerebral perfusion pressure (CPPopt) J Neurosurg / Volume 121 / November 2014

can be individually assessed from the minima of the Ushaped plot of PRx values at different CPPs. The novelty of the algorithm used here lies in the “dynamic adaptive target of active cerebral autoregulation” (DATACAR), which considers historical data up to 24 hours preceding the time point of interest and allows the calculation of a dynamic CPPopt during 95% of the time. The time that the patients were close to this individualized CPPopt correlated with the outcome. These results are encouraging since many neurocritical care units around the world have the ability to obtain by-the-minute data samples, where these findings can be easily reproduced. As mentioned in the authors’ paper, in 2011, in a small study with 18 patients suffering from nontraumatic intracerebral hemorrhage, we reported the use of minute-by-minute ICP and MABP data with an index called low-frequency pressure reactivity index (LPRx) to assess autoregulation.4 In that study we found a good correlation with PRx (p = 0.846, p < 0.001) and were able to obtain CPPopt in 66.6% of the patients. Moreover, L-PRx correlated and PRx correlated comparably with the outcome as assessed using the National Institutes of Health Stroke Scale. In a later study of 29 patients with traumatic brain injury, we also monitored cerebral autoregulation using L-PRx. We found a significant negative correlation with the 6-month Glasgow Outcome Scale (r = −0.556, p = 0.002),3 giving more support to the hypothesis that the minute-by-minute data contain important autoregulation information. One of the reasons why LAx works fine in critical patients (only the first 48 hours were used in this study) may be the high variability in the MABP curves due to the use of fluids and catecholamines to reach certain MABP or CPP goals. In centers where the MABP is forced to reach higher thresholds, the variability of MABP would be artificially increased, and autoregulation would be more challenged in a wave band that can be obtained using minute-by-minute data and having fewer artifacts than those in high-frequency data. Also, the nature of the DATACAR algorithm (that is, weighted contribution of 45 time-window calculations) allows for a higher frequency of successful CPPopt calculations. The results are promising given the steadily increasing number of neurocritical care units using minute-byminute sampling with commercial monitoring devices capable of obtaining this information for direct analysis. Renan Sánchez-Porras, M.D. Edgar Santos, M.D. Humberto Silos, M.D. Oliver W. Sakowitz, M.D. Department of Neurosurgery Heidelberg University Hospital Heidelberg, Germany

Disclosure The authors report no conflict of interest. References   1.  Czosnyka M, Smielewski P, Kirkpatrick P, Laing RJ, Menon

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Neurosurgical forum D, Pickard JD: Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery 41:11–19, 1997   2.  Depreitere B, Güiza F, Van den Berghe G, Schuhmann MU, Maier G, Piper I, et al: Pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in patients with severe traumatic brain injury based on minute-by-minute monitoring data. Clinical article. J Neurosurg 120:1451–1457, 2014   3.  Sánchez-Porras R, Santos E, Czosnyka M, Zheng Z, Unterberg AW, Sakowitz OW: “Long” pressure reactivity index (LPRx) as a measure of autoregulation correlates with outcome in traumatic brain injury patients. Acta Neurochir (Wien) 154: 1575–1581, 2012   4.  Santos E, Diedler J, Sykora M, Orakcioglu B, Kentar M, Czosnyka M, et al: Low-frequency sampling for PRx calculation does not reduce prognostication and produces similar CPPopt in intracerebral haemorrhage patients. Acta Neurochir (Wien) 153:2189–2195, 2011

Response: We thank Dr. Sánchez-Porras and colleagues for their positive comments on our paper on autoregulation monitoring and CPP target recommendation based on minute-by-minute data. Sánchez-Porras et al. and Santos et al. have already reported on their expertise with the use of minute-by-minute ICP and MABP data for the monitoring of cerebrovascular pressure reactivity.2,3 Our basic methodology, as well as theirs, follows the same principles as those for the calculation of the PRx, and we are therefore indebted to Czosnyka et al.1 Our paper does not at all question the established value of PRx but instead represents a pragmatic exercise on the optimization of the information on pressure reactivity present in monitoring data with standard resolution. By dynamically widening the window of data under investigation, we significantly increased the percentage of monitoring time for which a CPPopt recommendation could be given. The wider range of blood pressures that are consequently incorporated into the calculation of CPPopt might have contributed to this, as is suggested by Dr. Sánchez-Porras. The use of routine ICP and MABP data in combination with the almost permanent CPPopt recommendation makes the method applicable in most intensive care units. The DATACAR calculation method is now being programmed and tested. We agree with the conclusions made in the Letter to the Editor and thank the authors for their support. Bart Depreitere, M.D., Ph.D. Geert Meyfroidt, M.D., Ph.D. Fabian Güiza, Ph.D. University Hospitals Leuven Leuven, Belgium

References   1.  Czosnyka M, Smielewski P, Kirkpatrick P, Laing RJ, Menon D, Pickard JD: Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery 41:11–19, 1997   2.  Sánchez-Porras R, Santos E, Czosnyka M, Zheng Z, Unterberg AW, Sakowitz OW: “Long” pressure reactivity index (LPRx) as a measure of autoregulation correlates with outcome in traumatic brain injury patients. Acta Neurochir (Wien) 154:1575–1581, 2012   3.  Santos E, Diedler J, Sykora M, Orakcioglu B, Kentar M, Czosnyka M, et al: Low-frequency sampling for PRx calculation

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does not reduce prognostication and produces similar CPPopt in intracerebral haemorrhage patients. Acta Neurochir (Wien) 153:2189–2195, 2011

Please include this information when citing this paper: published online September 19, 2014; DOI: 10.3171/2014.5.JNS141056. ©AANS, 2014

Supraorbital and transorbital minicraniotomies To The Editor: We read with interest the article by Beretta et al.1 (Beretta F, Andaluz N, Chalaala C, et al: Image-guided anatomical and morphometric study of supraorbital and transorbital minicraniotomies to the sellar and perisellar regions: comparison with standard techniques. Laboratory investigation. J Neurosurg 113:975– 981, November 2010). In this cadaveric study, to quantify and compare the surgical exposure afforded by the pterional, supraorbital keyhole, and transorbital keyhole approaches, the authors defined 3 quantitative parameters for comparison. First, a “working area,” relative to the target deep in the surgical field, was defined as a sum of 6 adjacent triangles with the anterior communicating artery (ACoA) at the center. The other 2 parameters were “depth of the surgical window” and “angle of basal view.” Using frameless stereotactic navigation, they found that the “working area” increased progressively from the pterional approach (425.73 ± 85.85 mm2) to the supraorbital keyhole approach (460.24 ± 160.19 mm2), and then to the transorbital keyhole approach (568.78 ± 70.09 mm2). When comparing the surgical exposure provided by different craniotomies, there are several useful concepts such as the working area at the level of the target, the angle of attack on different anatomical structures around the target, and the intracranial optical field in the keyhole concept.2,4,5 The intracranial optical field increases with the depth of the targeted pathology; this concept is used in the keyhole approach, by which a small craniotomy is fashioned after thorough understanding of the location of the lesion and its relationship with the surrounding normal anatomical structures. In this way even a small craniotomy can provide adequate exposure for deep-seated pathological entities. However, because of the limited angle of attack, for example, in doing a keyhole supraorbital craniotomy, the craniotomy may need to be placed slightly medially or laterally in different patients. On the other hand, all large-scale approaches in microneurosurgery can be considered to consist of a side-byside combination of several small keyhole approaches.5 Therefore, provided a keyhole craniotomy falls within the boundary of a standard craniotomy (e.g., a supraorbital keyhole approach and a pterional approach6), the surgical exposure affordable through the keyhole craniotomy will be attainable via the standard craniotomy if the center of the view of the microscope is shifted to align with that of the keyhole craniotomy (Fig. 1). However, when part of a keyhole craniotomy lies outside the boundary of a stanJ Neurosurg / Volume 121 / November 2014

Neurosurgical forum Tuen Mun Hospital Tuen Mun, Hong Kong Disclosure The authors report no conflict of interest. References

Fig. 1.  Sketch diagram showing a pterional craniotomy (dashed line), a supraorbital keyhole craniotomy (square-dotted line), and an additional orbital osteotomy (shaded area). The arrows that radiate from point A show directions in which to move a microscope to align with the view of a supraorbital keyhole craniotomy, at point B. Point C marks an additional viewing window after an orbital osteotomy.

dard craniotomy (e.g., a transorbital keyhole approach and a pterional approach), then in that particular direction the keyhole approach can provide certain surgical exposure that is not attainable by the standard craniotomy. However, there exists also a standard craniotomy encompassing the transorbital keyhole approach.3 In summary, we think by that simple deduction, the supraorbital keyhole approach should not be able to provide a greater “working area” than the pterional approach. There are certainly other characteristics of a neurosurgical approach that are difficult to quantify for comparison, relevant to this study, such as the advantage of a widely split sylvian fissure affordable via the pterional approach. We think that to fully evaluate the surgical exposure afforded by a craniotomy, the surgical window at the surface, which is related to the angle of attack, should be taken into consideration as well. One also needs to bear in mind that throughout an operation, the view of a microscope is constantly shifted and a retractor blade is repeatedly adjusted. Last, although the title of the article is about the sellar and perisellar region, the “working area” was defined as centered at the ACoA. We think the information derived from this study cannot be directly generalized to the whole region but should be limited to around the ACoA complex, as mentioned in the article (the last paragraph in Discussion): “When using the midACoA as the main target, we noted the transorbital keyhole craniotomy afforded the best visualization of the entire ACoA complex….” Sui-To Wong, M.B.B.S. Dawson Fong, M.B., B.S., F.H.K.A.M. (Surgery), F.R.C.S. (Edin)

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  1.  Beretta F, Andaluz N, Chalaala C, Bernucci C, Salud L, Zuccarello M: Image-guided anatomical and morphometric study of supraorbital and transorbital minicraniotomies to the sellar and perisellar regions: comparison with standard techniques. Laboratory investigation. J Neurosurg 113:975–981, 2010   2.  Figueiredo EG, Deshmukh V, Nakaji P, Deshmukh P, Crusius MU, Crawford N, et al: An anatomical evaluation of the minisupraorbital approach and comparison with standard craniotomies. Neurosurgery 59 (4 Suppl 2):ONS212–ONS220, 2006   3.  Jane JA, Park TS, Pobereskin LH, Winn HR, Butler AB: The supraorbital approach: technical note. Neurosurgery 11:537– 542, 1982   4.  Schwartz MS, Anderson GJ, Horgan MA, Kellogg JX, McMenomey SO, Delashaw JB Jr: Quantification of increased exposure resulting from orbital rim and orbitozygomatic osteotomy via the frontotemporal transsylvian approach. J Neurosurg 91:1020–1026, 1999   5.  van Lindert E, Perneczky A, Fries G, Pierangeli E: The supraorbital keyhole approach to supratentorial aneurysms: concept and technique. Surg Neurol 49:481–490, 1998   6.  Yaşargil MG, Reichman MV, Kubik S: Preservation of the frontotemporal branch of the facial nerve using the interfascial temporalis flap for pterional craniotomy. Technical article. J Neurosurg 67:463–466, 1987

Response: Thank you for the opportunity to respond to Drs. Wong and Fong. The authors of the letter question the clinical validity of the results of our study and state that the same results could be accomplished by changing the position of the microscope, the use of retractors, and the consistent use of a pterional craniotomy. They provide no anatomical, morphometric, radiological, or clinical data to support their claim. While we respect and value their opinion, we beg to differ with their statements based not only on our surgical experience, but also the results of nearly a decade of anatomical, morphometric, and clinically proven data in multiple peer-reviewed publications that we have produced during that period.1–4 Furthermore, our results have been confirmed by others who have used both similar and different methodologies.8–11,13–15,18–20,23–28,31,32,34,35 The authors claim that similar views can be afforded by changing the position of the microscope. Although intuitively correct, this is a limited resource; in a deep surgical field, sooner or later, the vectors of vision will be blocked by either the edges of the craniotomy (including the base of the skull), or the brain itself. We have previously proven those facts in a cadaveric study, 2 as well as in the work in question. The authors later suggest the use of retractors and their repositioning, and opening of the sylvian fissure as additional measures to improve surgical exposure. These maneuvers, while helpful, are known to 1291

Neurosurgical forum be associated with increased risk of brain damage and operating times.5–7,12,16,17,21,22,29,30,33,36 In summary, it was precisely because of the potential (and certainly avoidable) consequences associated with the use the maneuvers proposed by the authors of the Letter to the Editor that we have been conducting our studies on the topic for the last 10 years. Ever since the introduction of endovascular coiling, the bar has been raised for microvascular surgery, and outcomes that were previously irrelevant, such as cognitive function, independent living, employability, and even cosmesis have attained a more prevalent role in modern neurosurgery. We have found the techniques described in our article to be helpful toward the accomplishment of those goals, as documented throughout our clinical peerreviewed reports. We challenge the authors of the Letter to present (as we have) compelling anatomical, morphometric, radiographic, and long-term clinical data to support their statements before issuing any further judgment based on intuition, subjective observations, and “simple deduction.”

Norberto Andaluz, M.D.1,2 Mario Zuccarello, M.D.1–3 1 University of Cincinnati Neuroscience Institute University of Cincinnati College of Medicine Cincinnati, OH 2 Cincinnati Department of Veterans Affairs Medical Center Cincinnati, OH 3 Mayfield Clinic Cincinnati, OH

References   1.  Andaluz N, Romano A, Reddy LV, Zuccarello M: Eyelid approach to the anterior cranial base. J Neurosurg 109:341– 346, 2008   2.  Andaluz N, Van Loveren HR, Keller JT, Zuccarello M: Anatomic and clinical study of the orbitopterional approach to anterior communicating artery aneurysms. Neurosurgery 52: 1140–1149, 2003   3.  Andaluz N, van Loveren HR, Keller JT, Zuccarello M: The one-piece orbitopterional approach. Skull Base 13:241–245, 2003   4.  Andaluz N, Zuccarello M: Anterior communicating artery aneurysm surgery through the orbitopterional approach: longterm follow-up in a series of 75 consecutive patients. Skull Base 18:265–274, 2008  5. Andrews RJ: Intraoperative Neuroprotection. Baltimore: Williams & Wilkins, 1996, pp 471–489  6. Andrews RJ, Bringas JR: A review of brain retraction and recommendations for minimizing intraoperative brain injury. Neurosurgery 33:1052–1064, 1993   7.  Böttger S, Prosiegel M, Steiger HJ, Yassouridis A: Neurobehavioural disturbances, rehabilitation outcome, and lesion site in patients after rupture and repair of anterior communicating artery aneurysm. J Neurol Neurosurg Psy­chiatry 65: 93–102, 1998   8.  Cavalcanti DD, García-González U, Agrawal A, Crawford NR, Tavares PL, Spetzler RF, et al: Quantitative anatomic study of the transciliary supraorbital approach: benefits of additional orbital osteotomy? Neurosurgery 66 (6 Suppl Op­ era­tive):205–210, 2010   9.  Chen L, Tian X, Zhang J, Huang Y, Chen E, Lan Q: Is eyebrow approach suitable for ruptured anterior circulation aneurysms

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on early stage: a prospective study at a single institute. Acta Neurochir (Wien) 151:781–784, 2009 10.  Czirják S, Szeifert GT: The role of the superciliary approach in the surgical management of intracranial neoplasms. Neurol Res 28:131–137, 2006 11.  Dare AO, Landi MK, Lopes DK, Grand W: Eyebrow incision for combined orbital osteotomy and supraorbital mini­crani­ otomy: application to aneurysms of the anterior circulation. Technical note. J Neurosurg 95:714–718, 2001 12.  DeLuca J: Cognitive dysfunction after aneurysm of the anterior communicating artery. J Clin Exp Neuropsychol 14: 924–934, 1992 13.  Figueiredo EG, Deshmukh P, Zabramski JM, Preul MC, Crawford NR, Siwanuwatn R, et al: Quantitative anatomic study of three surgical approaches to the anterior communicating artery complex. Neurosurgery 56 (2 Suppl):397–405, 2005 14.  Filipce V, Pillai P, Makiese O, Zarzour H, Pigott M, Ammirati M: Quantitative and qualitative analysis of the working area obtained by endoscope and microscope in various approaches to the anterior communicating artery complex using computed tomography-based frameless stereotaxy: a cadaver study. Neurosurgery 65:1147–1153, 2009 15.  Gonzalez LF, Zabramski JM: Anatomic and clinical study of the orbitopterional approach to anterior communicating artery aneurysms. Neurosurgery 54:1031–1032, 2004 (Letter) 16.  Hillis AE, Anderson N, Sampath P, Rigamonti D: Cognitive impairments after surgical repair of ruptured and unruptured aneurysms. J Neurol Neurosurg Psychiatry 69:608–615, 2000 17.  Hongo K, Kobayashi S, Yokoh A, Sugita K: Monitoring re­trac­ tion pressure on the brain. An experimental and clinical study. J Neurosurg 66:270–275, 1987 18.  Jallo GI, Bognár L: Eyebrow surgery: the supraciliary cra­ni­o­ tomy: technical note. Neurosurgery 59 (1 Suppl 1):ONSE157– ONSE158, 2006 19.  Jho HD: Orbital roof craniotomy via an eyebrow incision: a sim­plified anterior skull base approach. Minim Invasive Neuro­surg 40:91–97, 1997 20.  Kabil MS, Shahinian HK: Application of the supraorbital endoscopic approach to tumors of the anterior cranial base. J Craniofac Surg 16:1070–1075, 2005 21.  Kivisaari RP, Salonen O, Ohman J: Basal brain injury in aneurysm surgery. Neurosurgery 46:1070–1076, 2000 22.  Ljunggren B, Säveland H, Brandt L: Causes of unfavorable outcome after early aneurysm operation. Neurosurgery 13: 629–633, 1983 23.  Mitchell P, Vindlacheruvu RR, Mahmood K, Ashpole RD, Grivas A, Mendelow AD: Supraorbital eyebrow mini­crani­ otomy for anterior circulation aneurysms. Surg Neurol 63: 47–51, 2005 24.  Mori K, Yamamoto T, Nakao Y, Oyama K, Esaki T, Watanabe M, et al: Lateral supraorbital keyhole approach to clip unruptured anterior communicating artery aneurysms. Minim Invasive Neurosurg 51:292–297, 2008 25.  Profeta G, De Falco R, Ambrosio G, Profeta L: Endoscope-assisted microneurosurgery for anterior circulation aneurysms using the angle-type rigid endoscope over a 3-year period. Childs Nerv Syst 20:811–815, 2004 26.  Raza SM, Garzon-Muvdi T, Boaehene K, Olivi A, Gallia G, Lim M, et al: The supraorbital craniotomy for access to the skull base and intraaxial lesions: a technique in evolution. Minim Invasive Neurosurg 53:1–8, 2010 27.  Reisch R, Perneczky A: Ten-year experience with the supraorbital subfrontal approach through an eyebrow skin incision. Neurosurgery 57 (4 Suppl):242–255, 2005 28.  Reisch R, Stadie A, Kockro R, Gawish I, Schwandt E, Hopf N: The minimally invasive supraorbital subfrontal key-hole approach for surgical treatment of temporomesial lesions of the

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Neurosurgical forum dominant hemisphere. Minim Invasive Neurosurg 52:163– 169, 2009 29.  Rosenørn J: The risk of ischaemic brain damage during the use of self-retaining brain retractors. Acta Neurol Scand Suppl 120 (Suppl 120):1–30, 1989 30.  Schaller C, Klemm E, Haun D, Schramm J, Meyer B: The transsylvian approach is “minimally invasive” but not “atraumatic.” Neurosurgery 51:971–977, 2002 31.  Shanno G, Maus M, Bilyk J, Schwartz S, Savino P, Simeone F, et al: Image-guided transorbital roof craniotomy via a suprabrow approach: a surgical series of 72 patients. Neurosurgery 48:559–568, 2001 32.  Steiger HJ, Schmid-Elsaesser R, Stummer W, Uhl E: Transorbital keyhole approach to anterior communicating artery aneurysms. Neurosurgery 48:347–352, 2001 33.  Tidswell P, Dias PS, Sagar HJ, Mayes AR, Battersby RD: Cognitive outcome after aneurysm rupture: relationship to an-

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eurysm site and perioperative complications. Neurology 45: 875–882, 1995 34.  Warren WL, Grant GA: Transciliary orbitofrontozygomatic approach to lesions of the anterior cranial fossa. Neurosurgery 64 (5 Suppl 2):324–330, 2009 35.  Wiedemayer H, Sandalcioglu IE, Wiedemayer H, Stolke D: The supraorbital keyhole approach via an eyebrow incision for resection of tumors around the sella and the anterior skull base. Minim Invasive Neurosurg 47:221–225, 2004 36.  Yundt KD, Grubb RL Jr, Diringer MN, Powers WJ: Cerebral hemodynamic and metabolic changes caused by brain retraction after aneurysmal subarachnoid hemorrhage. Neurosurgery 40:442–451, 1997 Please include this information when citing this paper: published online September 19, 2014; DOI: 10.3171/2010.10.JNS101680. ©AANS, 2014

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