- Department of Neurosurgery, Ronald Reagan UCLA Medical Center, 757 Westwood Plaza, Los Angeles, CA 90095, USA
- Department of Clinical Neurophysiology, Ronald Reagan UCLA Medical Center, 757 Westwood Plaza, Los Angeles, CA 90095, USA
Jorge A. Lazareff
Department of Neurosurgery, Ronald Reagan UCLA Medical Center, 757 Westwood Plaza, Los Angeles, CA 90095, USA
DOI:10.4103/2152-7806.105277Copyright: © 2012 Chen JA This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How to cite this article: Chen JA, Coutin-Churchman PE, Nuwer MR, Lazareff JA. Suboccipital craniotomy for Chiari I results in evoked potential conduction changes. Surg Neurol Int 31-Dec-2012;3:165
How to cite this URL: Chen JA, Coutin-Churchman PE, Nuwer MR, Lazareff JA. Suboccipital craniotomy for Chiari I results in evoked potential conduction changes. Surg Neurol Int 31-Dec-2012;3:165. Available from: http://sni.wpengine.com/surgicalint_articles/suboccipital-craniotomy-for-chiari-i-results-in-evoked-potential-conduction-changes/
Background:Management of Chiari I is controversial, in part because there is no widely used quantitative measurement of decompression. It has been demonstrated that brainstem auditory evoked responses (BAER) and somatosensory evoked potentials (SSEP) have decreased conduction latencies after wide craniectomy. We analyzed these parameters in a suboccipital craniectomy/craniotomy procedure.
Methods:Thirteen consecutive patients underwent suboccipital decompression for treatment of symptomatic Chiari I. Craniectomy was restricted to the inferior aspect of the nuchal line, and in most cases the bone flap was replaced. Neuronal conduction was monitored continuously with median nerve somatosensory evoked potentials (M-SEP), posterior tibial nerve somatosensory evoked potentials (T-SEP), BAER, or a combination. The M-SEP N20, T-SEP P37, and BAER V latencies were recorded at four milestones – preoperatively, following craniotomy, following durotomy, and following closure.
Results:Five males and eight females, with average age of 9 years, were studied. Clinical improvement was noted in all 13 patients. M-SEP N20 latency decreased from a mean of 18.55 at baseline to 17.75 ms after craniotomy (P = 0.01); to 17.06 ms after durotomy (P = 0.01); and to 16.68 ms after closing (P = 0.02). T-SEP P37 latency did not change significantly. BAER V latency decreased from a mean of 6.25 ms at baseline to 6.14 ms after craniotomy (P = 0.04); to 5.98 ms after durotomy (P = 0.01); and to 5.95 ms after closing (P = 0.45).
Conclusion:Significant improvements in conduction followed both craniectomy and durotomy. Bone replacement did not affect these results.
Keywords: Chari malformation, craniotomy, intraoperative neurophysiological monitoring
A great deal of uncertainty exists regarding the Chiari type I malformation. Its pathophysiology is poorly understood, its natural history is unpredictable, and its response to various treatment methods has not been supported with robust evidence. This uncertainty manifests itself in myriad ways, but the most pressing issue for surgeons is the practice variation of the management of Chiari type I malformations.
Currently there are two major approaches to patients with Chiari type I malformation. One is the sectioning of the filum terminale that is based on the principle that the Chiari malformation can result from caudal traction or craniocervical growth collision.[
A large number of variations of posterior fossa decompression have been used, further increasing the heterogeneity of surgical intervention. Some surgeons perform a large occipital craniectomy,[
It is our practice to perform craniectomy of a defined size bounded superiorly by the nuchal line.[
Between March 2011 and April 2012, 13 consecutive children presenting with symptomatic Chiari type I malformation were treated with suboccipital craniotomy [
Suboccipital craniotomy was performed in all patients by one surgeon (JAL), as previously described, with the additional use of SSEP and BAER monitoring.[
Intraoperatively, M-SEPs, T-SEPs, and BAERs were continuously recorded to functionally assess the neural tissue at risk during the surgery, as well as for the purposes of this study. Needle electrodes were inserted after anesthesia induction at Fz, C3’, Cz’, C4’, A1, A2, and at the level of C5 spine (C5s) for recording. Amplifier gain was 10 μV/div. Bandpass filters were 30-1500 Hz for SEPs and 100-3000 Hz for BAERs. The following channels were used: Ci’-Fz, Cc’- Ci’, and C5s-Fz for M-SEPs; Cz’- Fz, Ci’- Cc’c, and C5s-Fz for T-SEPs; Ai-Cz and Ac-Cz for BAERs (i = ipsilateral, c = contralateral to the stimulated side). Continuous electroencephalography (EEG) from the same channels was continuously recorded and displayed as control. Monitoring was continued until the end of the surgery, typically 40-60 minutes after replacement of the bone flap.
Electrical pulses of 200 ms duration and with intensity of 20 mA were delivered to each nerve with a rate of 4.19 Hz through needle electrode twisted pairs applied over the median nerve at the wrist and the posterior tibial nerve behind the medial malleolus. Monoaural clicks with an intensity of 80 dB nHL delivered through insert tube earphones at a rate of 11.1 Hz were used for acoustic stimulation for BAERs.
Between 500 and 750 responses were averaged for SEPs and 2000 for BAERs. Timebase was 15 ms for BAERs, 50 ms for M-SEPs, and 100 ms for T-SEPs. Responses were collected in the following sequential cycle: M-SEPs (bilateral alternating)/T-SEPs (bilateral alternating)/Left BAER/Right BAER. The time span for collecting each full set of responses was between 5 and 8 minutes, except for intervals of intense electrocautery when updates took longer due to artifact rejection. Cortical M-SEP N20 latency, cortical T-SEP P37 latency, and BAER wave V latency were followed through the case. The spinal component (N13 for M-SEP, N30 for T-SEP) was also used as reference.
The stage of surgery at which the measurement was taken - before craniotomy (baseline, BL), immediately after bony decompression (BN), immediately after opening the dura (DUR), and immediately after replacement of the bone (END) – was used as the independent variable. Latency measurements taken at each stage (average of right and left sides) were considered the dependent variable. Data was analyzed using a repeated measures design two-way analysis of variance (ANOVA), with rejection threshold α of 0.05. Statistical analysis was performed using MATLAB 7.0 R14 (The MathWorks Inc., Natick, MA).
Somatosensory evoked potentials
M-SEP N20 latency improved in all 12 patients (100%), while T-SEP P37 latency improved in 7 of the 9 patients (78%) for which this procedure was performed [
Progression of neurophysiologic parameters at each stage of decompressive craniotomy. (a) Median nerve SSEP N20 latency, (b) Posterior tibial nerve SSEP P37 latency, (c) BAER wave V latency. BL – preoperative baseline, BN – removal of the bone flap, DUR – opening of the dura, END - replacement of the bone flap at the end of the procedure. Values are reported as mean ± SEM. Significance: *-P<0.05 level, **-P<0.01
Similarly, the T-SEP P37 latency decreased from 35.65 ± 0.78 ms at preoperative baseline to 34.61 ± 0.91 ms after removal of the bone flap (P = 0.14); slightly decreasing to 33.91 ± 0.80 ms after opening of the dura (P = 0.30); and slightly decreasing to 33.07 ± 0.89 ms after closing (P = 0.18). However, none of these changes were statistically significant. Interaction terms of the ANOVA were demonstrated insignificant at the α = 0.05 level.
Brainstem auditory evoked responses
An analogous pattern of improvement in BAERs following the surgical procedure was seen in eight of nine patients (89%) [
Craniotomy versus craniectomy
In three cases the bone flap was not replaced (craniectomy), and in nine cases it was (craniotomy). A similar general trend in decreasing latencies was observed in the M-SEP, T-SEP, and BAER measurements for craniotomy compared with craniectomy [
None of the patients experienced postoperative complications or required additional decompression, and all improved clinically following surgery [
Since Penfield performed an occipital craniotomy on a “bookkeeper who could not wink”, who he initially diagnosed with bilateral cerebellopontine angle tumor,[
Evoked potentials present one possible avenue to address these questions; their correlation with impulse conduction in sensory pathways forms a putative basis for changes seen in Chiari decompression. Any process compromising these tracts (e.g., demyelination, compression, or ischemia) will affect axonal function, decrease the conduction velocity, and consequently increase evoked potential latencies.[
Determining latency improvements for each step of the surgical treatment of Chiari malformation gives us a further understanding of the decompressive effects of certain procedures. Our craniotomy demonstrated clinically notable improvements in overall latency times in both M-SEP N20 (by 1.87 ms) and BAER wave V latency (by 0.30 ms). The T-SEP pattern of decrease lacked statistical significance, likely due to the smaller sample size and greater inherent variability in the P37 latencies within the patient population. Anderson et al.[
Our procedure furthermore incorporated an additional step that was not used in previous studies, namely replacement of the bone flap. The improvements in M-SEP and BAER were retained following this step, suggesting that the technique we have devised does not compromise the decompressive effect of the surgery. The dorsoventral space created in this manner seems to be sufficient for decompression, while the lateral extent of the craniectomy is mostly preserved. Replacement of the bone flap was not feasible in three patients, providing an opportunity to compare craniotomy against craniectomy directly. The craniotomy procedure did not reverse the latency improvements seen in M-SEPs, T-SEPs, or BAERs, and a similar trend of improvements was observed in craniotomy versus craniectomy. Although this analysis lacks statistical power, it reflects our belief that replacement of the bone does not negate the objectives of decompression.
Taken together these findings suggest that our approximately 3 × 4 cm craniectomy restricted to the nuchal line can achieve a similar extent of decompression as a more extensive one, implying that sufficient space can be created with a less drastic approach. Our series also demonstrates improvements in M-SEPs and BAERs following both craniectomy and duroplasty, suggesting that in those instances duroplasty indeed had a decompressive effect. This finding could potentially explain the superior symptomatic improvements seen with duroplasty in the literature.[
Interestingly, Caldarelli et al.[
Although our results are highly suggestive, some caution must be exercised in their interpretation. The use of SSEP and BAER as a real-time, intraoperative surrogate for surgical outcome or extent of decompression in Chiari type I malformation has been proposed, but not proven. The purpose of suboccipital craniectomy itself remains debatable, with various authors asserting relief of direct compression on neural structures,[
The practice variation in the management of Chiari type I malformation suggests the need for a widely accepted quantitative measurement of decompression. While our data was analyzed in a retrospective manner, there have been previous reports of intraoperative diagnostic measurements used to guide surgical management of the Chiari type I malformation. In the recent past the use of intraoperative ultrasound imaging has been advocated to gauge the extent of the decompression.[
Essentially, the crux of the debate regarding the surgical treatment for Chiari malformation is the tradeoff between the extent of decompression and adverse effects.[
The authors thank Ms. Vanessa Marrero for administrative support. JAC is a student in the University of California, Los Angeles Medical Scientist Training Program and was supported in part by NIH NIGMS Training Grant GM08042.
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