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Griffin Ernst, Fares Qeadan and Andrew P. Carlson

OBJECTIVE

Decompressive craniectomy is used for uncontrolled intracranial pressure in traumatic brain injury and malignant hemispheric stroke. Subcutaneous preservation of the autologous bone flap in the abdomen is a simple, portable technique but has largely been abandoned due to perceived concerns of resorption. The authors sought to characterize their experience with subcutaneous preservation of the bone flap and cranioplasty.

METHODS

The authors performed a retrospective single-institution review of subcutaneous preservation of the autologous bone flap after decompressive craniectomy from 2005 to 2015. The primary outcome was clinically significant bone resorption, defined as requiring a complete mesh implant at the time of cranioplasty, or delayed revision. The outcome also combined cases with any minor bone resorption to determine predictors of this outcome. Logistic regression modeling was used to determine the risk factors for predicting resorption. A cost comparison analysis was also used via the 2-sided t-test to compare the cost of cranioplasty using an autologous bone flap with standard custom implant costs.

RESULTS

A total of 193 patients with craniectomy were identified, 108 of whom received a cranioplasty. The mean time to cranioplasty was 104.31 days. Severe resorption occurred in 10 cases (9.26%): 4 were clinically significant (2 early and 2 late) and 6 demonstrated type II (severe) necrosis on CT, but did not require revision. Early resorption of any kind (mild or severe) occurred in 28 (25.93%) of 108 cases. Of the 108 patients, 26 (24.07%) required supplemental cranioplasty material. Late resorption of any kind (mild or severe) occurred in 6 (5.88%) of 102 cases. Of these, a clinically noticeable but nonoperative deformity was noted in 4 (3.92%) and minor (type I) necrosis on CT in 37 (37%) of 100. Bivariate analysis identified fragmentation of bone (OR 3.90, 95% CI 1.03–14.8), shunt-dependent hydrocephalus (OR 7.97, 95% CI 1.57–40.46), and presence of post-cranioplasty drain (OR 9.39, 95% CI 1.14–1000) to be significant risk factors for bone resorption. A binary logistic regression optimized using Fisher’s scoring determined the optimal multivariable combination of factors. Fragmentation of bone (OR 5.84, 95% CI 1.38–28.78), diabetes (OR 7.61, 95% CI 1.37–44.56), and shunt-dependent hydrocephalus (OR 9.35, 95% CI 1.64–56.21) were found to be most predictive of resorption, with a C value of 0.78. Infections occurred in the subcutaneous pocket in 5 (2.60%) of the 193 cases and after cranioplasty in 10 (9.26%) of the 108 who underwent cranioplasty. The average cost of cranioplasty with autologous bone was $2156.28 ± $1144.60 (n = 15), and of a custom implant was $35,118.60 ± $2067.51 (3 different sizes; p < 0.0001).

CONCLUSIONS

Craniectomy with autologous bone cranioplasty using subcutaneous pocket storage is safe and compares favorably to cryopreservation in terms of resorption and favorably to a custom synthetic implant in terms of cost. While randomized data are required to definitively prove the superiority of one method, subcutaneous preservation has enough practical advantages with low risk to warrant routine use for most patients.

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Muhammad Omar Chohan, Andrew P. Carlson, Blaine L. Hart and Howard Yonas

Object

Fenestration of the lamina terminalis (FLT) during aneurysm surgery for subarachnoid hemorrhage can, in theory, improve CSF circulation from the lateral and third ventricles to the cortical subarachnoid space, which may, in turn, decrease the incidence of hydrocephalus and vasospasm. However, the actual effects of FLT on CSF circulation have been difficult to determine, due to confounding factors. In addition, it is unclear whether the lamina terminalis remains functionally patent when the brain resumes its normal position. The goal of this study was to assess the functional patency of the fenestrated lamina terminalis in patients who underwent surgery for ruptured aneurysms.

Methods

This prospective study included 15 patients who underwent surgical clipping of ruptured anterior circulation aneurysms, with FLT performed during surgery. On postoperative Day 1, the external ventricular drain of each patient was closed, and 1 ml of Omnipaque 300, an iodine based contrast agent, was injected intraventricularly, accompanied by cranial maneuvering designed to position the contrast agent adjacent to the lamina terminalis. Three to 5 minutes after cranial maneuvering, the flow of contrast agent into the basal cisterns was assessed with CT imaging. Flow was verified by an increase in Hounsfield units in a prespecified “region of interest” within the basal cisterns on the CT scan. This procedure was performed using a standardized protocol designed in consultation with the Department of Radiology and approved by the institutional review board. One patient who underwent endoscopic third ventriculostomy was recruited as a positive control to validate the technique, and 1 patient who underwent aneurysm clipping but not FLT was recruited as a negative control.

Results

Seventeen patients consented to study participation. In the 15 patients who underwent aneurysm clipping and FLT, and the negative control patient who underwent aneurysm clipping but not FLT, the contrast agent followed the normal ventricular pathway from the lateral ventricles into the fourth ventricle, and did not appear in the basal cisterns. In the positive control patient, the contrast agent robustly and immediately filled the basal cisterns.

Conclusions

Fenestration of the lamina terminalis did not result in functional patency of the lamina terminalis when performed as part of surgical clipping for ruptured aneurysms.

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Laila M. Mohammad, Alexander L. Coon and Andrew P. Carlson

The authors present an unusual case of a 15-year-old boy in whom sensorineural hearing loss and disequilibrium developed in the setting of a giant basilar artery aneurysm. This patient was treated with a flow-diverting stent and had complete resolution of his clinical symptoms including hearing loss. This case demonstrates the efficacy of flow diversion in select pediatric patients with posterior circulation aneurysms. The features that are thought to result in successful treatment are discussed.

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Andrew P. Carlson, Christopher L. Taylor and Howard Yonas

Object

A dural arteriovenous fistula (DAVF) typically involves meningeal feeding arteries and can cause clinical symptoms ranging from tinnitus to rupture of draining cortical or parenchymal veins. Surgical treatment may be technically demanding. Ethylene vinyl alcohol (Onyx, ev3 Neurovascular) has several properties that make it potentially useful as a primary treatment agent for DAVF. Onyx is expected to be a permanent embolic agent. It should have a decreased risk of catheter retention when compared with other permanent embolic materials.

Methods

The authors report a series of six patients with symptomatic DAVF who were treated initially with transarterial Onyx embolization and other endovascular techniques.

Results

Five patients had complete occlusion of their DAVF noted on the follow-up angiogram obtained between 2 and 4 months. One patient had residual filling via a small arterial branch that was stable on follow-up angiography. None of the patients had worsening of neurological function. One case was complicated by a retained catheter fragment.

Conclusions

Transarterial Onyx embolization and other endovascular methods can angiographically obliterate DAVF. In some cases, embolization allowed occlusion of multiple arterial feeding arteries from a single arterial injection. Technically, the embolization was optimized when a microcatheter position immediately adjacent to the point(s) of fistulization was achieved.

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Jed A. Hartings, Laura B. Ngwenya, Christopher P. Carroll and Brandon Foreman

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Andrew P. Carlson, C. William Shuttleworth, Brittany Mead, Brittany Burlbaw, Mark Krasberg and Howard Yonas

OBJECTIVE

Cortical spreading depression (CSD) has been observed with relatively high frequency in the period following human brain injury, including traumatic brain injury and ischemic/hemorrhagic stroke. These events are characterized by loss of ionic gradients through massive cellular depolarization, neuronal dysfunction (depression of electrocorticographic [ECoG] activity) and slow spread (2–5 mm/min) across the cortical surface. Previous data obtained in animals have suggested that even in the absence of underlying injury, neurosurgical manipulation can induce CSD and could potentially be a modifiable factor in neurosurgical injury. The authors report their initial experience with direct intraoperative ECoG monitoring for CSD.

METHODS

The authors prospectively enrolled patients undergoing elective craniotomy for supratentorial lesions in cases in which the surgical procedure was expected to last > 2 hours. These patients were monitored for CSD from the time of dural opening through the time of dural closure, using a standard 1 × 6 platinum electrode coupled with an AC or full-spectrum DC amplifier. The data were processed using standard techniques to evaluate for slow potential changes coupled with suppression of high-frequency ECoG propagating across the electrodes. Data were compared with CSD validated in previous intensive care unit (ICU) studies, to evaluate recording conditions most likely to permit CSD detection, and identify likely events during the course of neurosurgical procedures using standard criteria.

RESULTS

Eleven patients underwent ECoG monitoring during elective neurosurgical procedures. During the periods of monitoring, 2 definite CSDs were observed to occur in 1 patient and 8 suspicious events were detected in 4 patients. In other patients, either no events were observed or artifact limited interpretation of the data. The DC-coupled amplifier system represented an improvement in stability of data compared with AC-coupled systems. Compared with more widely used postoperative ICU monitoring, there were additional challenges with artifact from saturation during bipolar cautery as well as additional noise peaks detected.

CONCLUSIONS

CSD can occur during elective neurosurgical procedures even in brain regions distant from the immediate operative site. ECoG monitoring with a DC-coupled full-spectrum amplifier seemed to provide the most stable signal despite significant challenges to the operating room environment. CSD may be responsible for some cases of secondary surgical injury. Though further studies on outcome related to the occurrence of these events is needed, efforts to decrease the occurrence of CSD by modification of anesthetic regimen may represent a novel target for study to increase the safety of neurosurgical procedures.

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Andrew P. Carlson, Mohammad Abbas, Robert L. Alunday, Fares Qeadan and C. William Shuttleworth

OBJECTIVE

Retrospective clinical data and case studies support a therapeutic effect of ketamine in suppression of spreading depolarization (SD) following brain injury. Preclinical data strongly support efficacy in terms of frequency of SD as well as recovery from electrocorticography (ECoG) depression. The authors present the results of the first prospective controlled clinical trial testing the role of ketamine used for clinical sedation on occurrence of SD.

METHODS

Ten patients with severe traumatic brain injury (TBI) or aneurysmal subarachnoid hemorrhage (SAH) were recruited for this pilot trial. A standard ECoG strip was placed at the time of craniotomy, and the patients were then placed on an alternating every-6-hour schedule of ketamine or other sedation agent. The order of treatment was randomized. The ketamine dose was adjusted to clinical effect or maintained at a subanesthetic basal dose (0.1 mg/kg/hr) if no sedation was required. SD was scored using standard criteria, blinded to ketamine dosing. Occurrence of SD was compared with the hourly dose of ketamine to determine the effect of ketamine on SD occurrence.

RESULTS

Successful ECoG recordings were obtained in all 10 patients: 8 with SAH and 2 with TBI. There were a total of 1642 hours of observations with adequate ECoG: 833 hours off ketamine and 809 hours on ketamine. Analysis revealed a strong dose-dependent effect such that hours off ketamine or on doses of less than 1.15 mg/kg/hr were associated with an increased risk of SD compared with hours on doses of 1.15 mg/kg/hr or more (OR 13.838, 95% CI 1.99–1000). This odds ratio decreased with lower doses of 1.0 mg/kg/hr (OR 4.924, 95% CI 1.337–43.516), 0.85 mg/kg/hr (OR 3.323, 95% CI 1.139–16.074), and 0.70 mg/kg/hr (OR 2.725, 95% CI 1.068–9.898) to a threshold of no effect at 0.55 mg/kg/hr (OR 1.043, 95% CI 0.565–2.135). When all ketamine data were pooled (i.e., on ketamine at any dose vs off ketamine), a nonsignificant overall trend toward less SD during hours on ketamine (χ2 = 3.86, p = 0.42) was observed.

CONCLUSIONS

Ketamine effectively inhibits SD over a wide range of doses commonly used for sedation, even in nonintubated patients. These data also provide the first prospective evidence that the occurrence of SD can be influenced by clinical intervention and does not simply represent an unavoidable epiphenomenon after injury. These data provide the basis for future studies assessing clinical improvement with SD-directed therapy.

Clinical trial registration no.: NCT02501941 (clinicaltrials.gov)

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Daniel San-Juan, Andres Jaramillo-Gonzalez, Roberto Diaz-Peregrino, Arturo Olivares Rivera and Edgar Santos

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Dominic A. Harris, Danielle E. Sorte, Sandi K. Lam and Andrew P. Carlson

OBJECTIVE

The incidence of blunt cerebrovascular injury (BCVI) has not been well characterized in the pediatric population. The goal of this study was to describe the incidence, patient characteristics, and risk factors for pediatric patients with cerebrovascular injuries.

METHODS

The authors collected data from the Kids’ Inpatient Database (KID), a nationally representative database of pediatric admissions, for years 2000, 2003, 2006, 2009, and 2012.

RESULTS

Among an estimated 646,549 admissions for blunt trauma, 2150 were associated with BCVI, an overall incidence of 0.33%. The incidence of BCVI nearly doubled from 0.24% in 2000 to 0.49% in 2012. Patients 4 to 13 years of age were less likely to have BCVI than those in the youngest (0–3 years) and oldest age groups comprising adolescents (14–17 years) and young adults (18–20 years). BCVIs were associated with cervical (adjusted OR [aOR] 4.6, 95% CI 3.8–5.5), skull base (aOR 3.0, 95% CI 2.5–3.6), clavicular (aOR 1.4, 95% CI 1.1–1.8), and facial (aOR 1.2, 95% CI 1.0–1.5) fractures, as well as intracranial hemorrhage (aOR 2.7, 95% CI 2.2–3.2) and traumatic brain injury (aOR 2.0, 95% CI 1.7–2.3). Mechanism of injury was also independently associated with BCVI: motor vehicle collision (aOR 1.7, 95% CI 1.3–2.2) and struck pedestrian (aOR 1.4, 95% CI 1.0–1.9). Among pediatric patients with BCVI, 37.4% had cerebral ischemic infarction with an in-hospital mortality of 12.7%, and patients with stroke had 20% mortality.

CONCLUSIONS

The incidence of pediatric BCVI is increasing, likely due to increased use of screening, but remains lower than that in the adult population. Risk factors include the presence of cervical, facial, clavicular, and skull base fractures, similar to that of the adult population. Diagnosed BCVI is associated with a relatively high incidence of stroke with increased morbidity and mortality. The use of adult screening criteria is likely reasonable given the similarity in the risk factors identified in this study. Further studies are needed to investigate the role of treatment with antiplatelet agents or anticoagulation.

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Andrew P. Carlson, C. William Shuttleworth, Sebastian Major, Coline L. Lemale, Jens P. Dreier and Jed A. Hartings

The authors report on a 57-year-old woman in whom progression to brain death occurred on day 9 after aneurysmal subarachnoid hemorrhage without evidence of significant brain edema or vasospasm. Neuromonitoring demonstrated that brain death was preceded by a series of cortical spreading depolarizations that occurred in association with progressive hypoxic episodes. The depolarizations induced final electrical silence in the cortex and ended with a terminal depolarization that persisted > 7 hours. To the authors’ knowledge, this is the first report of terminal spreading depolarization in the human brain prior to clinical brain death and major cardiopulmonary failure.