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Daniel C. Lu and Michael T. Lawton


Intramedullary cavernous malformation (CM) is a rare entity, accounting for 5% of all intraspinal lesions. The objective in this study was to define the clinical characteristics of this disease, detail the surgical approach and technique, and present the clinical outcome.


Retrospective chart review was performed in 22 patients with histologically confirmed CMs. The authors used a laminectomy approach for midline dorsal lesions, with unilateral radical facetectomy and dentate ligament resection for laterally or ventrally located lesions. Patient profiles, operative indications, surgical approaches, operative findings, complications, and long-term follow-up were reviewed.


The average age of patients in the cohort was 43 ± 14 years, the average duration of symptoms was 7 ± 7 months, and the average follow-up was 6 ± 4 years. The average size of the lesion was 1 ± 0.4 cm, the average surgical time was 4 ± 0.96 hours, and the average estimated blood loss was 350 ± 131 ml. The rate of complication was 5% (1 patient; due to a wound infection). According to the McCormick classification, the score for the cohort was 1.8 ± 1.2 preoperatively, 2.1 ± 1.2 postoperatively, and 1.3 ± 0.65 at late follow-up. (All preceding values are given as the mean ± SD.) There was a significant neurological improvement at follow-up compared with the preoperative state (p < 0.05). The majority of patients (50%) had a stable outcome compared with their preoperative state, with a large proportion (41%) having an improved outcome. A minority of patients (9%) had a worsened outcome due to dysesthetic pain. Patients with dysesthesia had a longer duration of clinical symptoms prior to surgery compared with patients without dysesthesia (p < 0.05).


The authors demonstrated the safety, efficacy, and durability of their surgical approach for resection of spinal intramedullary CM. Proper examination, preoperative imaging, and prompt surgical intervention were necessary for a satisfactory outcome.

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Dunyue Lu, Asim Mahmood, Changsheng Qu, Anton Goussev, Mei Lu and Michael Chopp

Object. Atorvastatin, a β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitor, has pleiotropic effects such as improving thrombogenic profile, promoting angiogenesis, and reducing inflammatory responses and has shown promise in enhancing neurological functional improvement and promoting neuroplasticity in animal models of traumatic brain injury (TBI), stroke, and intracranial hemorrhage. The authors tested the effect of atorvastatin on intracranial hematoma after TBI.

Methods. Male Wistar rats were subjected to controlled cortical impact, and atorvastatin (1 mg/kg) was orally administered 1 day after TBI and daily for 7 days thereafter. Rats were killed at 1, 8, and 15 days post-TBI. The temporal profile of intraparenchymal hematoma was measured on brain tissue sections by using a MicroComputer Imaging Device and light microscopy.

Conclusions. Data in this study showed that intraparenchymal and intraventricular hemorrhages are present 1 day after TBI and are absorbed at 15 days after TBI. Furthermore, atorvastatin reduces the volume of intracranial hematoma 8 days after TBI.

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Asim Mahmood, Dunyue Lu, Changsheng Qu, Anton Goussev, Zheng Gang Zhang, Chang Lu and Michael Chopp


This study was designed to investigate the neuroprotective properties of recombinant erythropoietin (EPO) and carbamylated erythropoietin (CEPO) administered following traumatic brain injury (TBI) in rats.


Sixty adult male Wistar rats were injured with controlled cortical impact, and then EPO, CEPO, or a placebo (phosphate-buffered saline) was injected intraperitoneally. These injections were performed either 6 or 24 hours after TBI. To label newly regenerating cells, bromodeoxyuridine was injected intraperitoneally for 14 days after TBI. Blood samples were obtained on Days 1, 2, 3, 7, 14, and 35 to measure hematocrit. Spatial learning was tested using the Morris water maze. All rats were killed 35 days after TBI. Brain sections were immunostained as well as processed for the enzyme-linked immunosorbent assay to measure brain-derived neurotrophic factor (BDNF).


A statistically significant improvement in spatial learning was seen in rats treated with either EPO or CEPO 6 or 24 hours after TBI (p < 0.05); there was no difference in the effects of EPO and CEPO. Also, these drugs were equally effective in increasing the number of newly proliferating cells within the dentate gyrus at both time points. A statistically significant increase in BDNF expression was seen in animals treated with both EPO derivatives at 6 or 24 hours after TBI. Systemic hematocrit was significantly increased at 48 hours and 1 and 2 weeks after treatment with EPO but not with CEPO.


These data demonstrate that at the doses used, EPO and CEPO are equally effective in enhancing spatial learning and promoting neural plasticity after TBI.

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Donald Seyfried, Yuxia Han, Dunyue LU, Jieli Chen, Ali Bydon and Michael Chopp

Object. Atorvastatin, a β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitor, improves neurological functional outcome, reduces cerebral cell loss, and promotes regional cellular plasticity when administered after intracerebral hemorrhage (ICH) in rats.

Methods. Autologous blood was stereotactically injected into the right striatum in rats, and atorvastatin was administered orally beginning 24 hours after ICH and continued daily for 1 week. At a dose of 2 mg/kg, atorvastatin significantly reduced the severity of neurological deficit from 2 to 4 weeks after ICH. The area of cell loss in the ipsilateral striatum was also significantly reduced in these animals. Consistent with previous study data, higher doses of atorvastatin (8 mg/kg) did not improve functional outcome or reduce the extent of injury. Histochemical stains for markers of synaptogenesis, immature neurons, and neuronal migration revealed increased labeling in the region of hemorrhage in the atorvastatin-treated rats.

Conclusions. Analysis of the data in this study indicates that atorvastatin improves neurological recovery after experimental ICH and may do so in part by increasing neuronal plasticity.

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Dunyue Lu, Yi Li, Asim Mahmood, Lei Wang, Tahir Rafiq and Michael Chopp

Object. This study was designed to investigate the effect of treatment with a novel composite material consisting of embryonic neurospheres and bone marrow—derived stromal cell spheres (NMSCSs) in a rat model of traumatic brain injury (TBI).

Methods. The NMSCS composite was injected into the TBI contusion site 24 hours after injury, and all rats were killed on Day 14 after the transplantation. The Rotarod test and the neurological severity score were used to evaluate neurological function. The transplanted NMSCS was analyzed in recipient rat brains by using histological staining and laser scanning confocal microscopy. The lesion volumes in the brains were also calculated using computer image analysis.

Conclusions. Rats that received NMSCS transplants had reduced lesion volume and showed improved motor and neurological function when compared with control groups 14 days after the treatment. These results suggest that transplantation of this novel biological material (NMSCS) may be useful in the treatment of TBI.

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Dunyue Lu, Asim Mahmood, Ruilan Zhang, Yi Li and Michael Chopp

Object. Neurogenesis, which is upregulated by neural injury in the adult mammalian brain, may be involved in the repair of the injured brain and functional recovery. Therefore, the authors sought to identify agents that can enhance neurogenesis after brain injury, and they report that (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA/NONOate), a nitric oxide donor, upregulates neurogenesis and reduces functional deficits after traumatic brain injury (TBI) in rats.

Methods. The agent DETA/NONOate (0.4 mg/kg) was injected intraperitoneally into 16 rats daily for 7 days, starting 1 day after TBI induced by controlled cortical impact. Bromodeoxyuridine (100 mg/kg) was also injected intraperitoneally daily for 14 days after TBI to label the newly generated cells in the brain. A neurological functional evaluation was performed in all rats and the animals were killed at 14 or 42 days postinjury. Immunohistochemical staining was used to identify proliferating cells.

Conclusions. Compared with control rats, the proliferation, survival, migration and differentiation of neural progenitor cells were all significantly enhanced in the hippocampus, subventricular zone, striatum, corpus callosum, and the boundary zone of the injured cortex, as well as in the contralateral hemisphere in rats with TBI that received DETA/NONOate treatment. Neurological functional outcomes in the DETA/NONOate-treated group were also significantly improved compared with the untreated group. These data indicate that DETA/NONOate may be useful in the treatment of TBI.

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Asim Mahmood, Dunyue Lu, Changsheng Qu, Anton Goussev and Michael Chopp


This study was designed to follow the effects of bone marrow stromal cell (BMSC) administration in rats after traumatic brain injury (TBI) for a 3-month period.


Forty adult female Wistar rats were injured by a controlled cortical impact and, 1 week later, were injected intravenously with one of three different doses of BMSCs (2 × 106, 4 × 106, or 8 × 106 cells per animal) obtained in male rats. Control rats received phosphate-buffered saline (PBS). Neurological function in these rats was studied using a neurological severity scale (NSS). The rats were killed 3 months after injury, and immunohistochemical stains were applied to brain samples to study the distribution of the BMSCs. Additional brain samples were analyzed by quantitative enzyme-linked immunosorbent assays to measure the expression of the growth factors brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF).

Three months after injury, BMSCs were present in the injured brain and their number was significantly greater in animals that received 4 × 106 or 8 × 106 BMSCs than in animals that received 2 × 106 BMSCs. The cells were primarily distributed around the lesion boundary zone. Functional outcome was significantly better in rats that received 4 × 106 or 8 × 106 BMSCs, compared with control animals, although no improvement was seen in animals that received 2 × 106 BMSCs. All doses of BMSCs significantly increased the expression of BDNF but not that of NGF; however, this increase was significantly larger in animals that received 4 × 106 or 8 × 106 BMSCs than in controls or animals that received 2 × 106 BMSCs.


In summary, when injected in rats after TBI, BMSCs are present in the brain 3 months later and significantly improve functional outcome.

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Asim Mahmood, Dunyue Lu, Yi Li, Jae Li Chen and Michael Chopp

Object. The authors tested the hypothesis that intracranial bone marrow (BM) transplantation after traumatic brain injury (TBI) in rats provides therapeutic benefit.

Methods. Sixty-six adult Wistar rats, weighing 275 to 350 g each, were used for the experiment. Bone marrow prelabeled with bromodeoxyuridine (BrdU) was harvested from tibias and femurs of healthy adult rats. Other animals were subjected to controlled cortical impact, and BM was injected adjacent to the contusion 24 hours after the impact. The animals were killed at 4, 7, 14, or 28 days after transplantation. Motor function was evaluated both before and after the injury by using the rotarod test. After the animals had been killed, brain sections were examined using hemotoxylin and eosin and immunohistochemical staining methods. Histological examination revealed that, after transplantation, BM cells survived, proliferated, and migrated toward the injury site. Some of the BrdU-labeled BM cells were reactive, with astrocytic (glial fibrillary acid protein) and neuronal (NeuN and microtubule-associated protein) markers. Transplanted BM expressed proteins phenotypical of intrinsic brain cells, that is, neurons and astrocytes. A statistically significant improvement in motor function in rats that underwent BM transplantation, compared with control rats, was detected at 14 and 28 days posttransplantation.

Conclusions. On the basis of their findings, the authors assert that BM transplantation improves neurological outcome and that BM cells survive and express nerve cell proteins after TBI.

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Changsheng Qu, Dunyue Lu, Anton Goussev, Timothy Schallert, Asim Mahmood and Michael Chopp

Object. Atorvastatin administered after traumatic brain injury (TBI) induced by controlled cortical impact promotes functional improvement in male rats. Note, however, that parallel studies have not been performed in female rats. Therefore, the authors tested the effect of atorvastatin on TBI in female rats.

Methods. Atorvastatin (1 mg/kg/day) was orally administered for 7 consecutive days in female Wistar rats starting 1 day after TBI; control animals received saline. Modified neurological severity scores, the corner turn test, and the Morris water maze test were used to evaluate functional response to treatment. Rats were killed on Day 15 post-TBI, and brain tissue samples were processed for immunohistochemical staining. Atorvastatin administration after brain injury significantly promoted the restoration of spatial memory but did not reduce sensorimotor functional deficits. Treatment of TBI with atorvastatin increased neuronal survival in the CA3 region and the lesion boundary zone and prevented the loss of neuronal processes of damaged neurons in the hippocampal CA3 region but not in the lesion boundary zone on Day 15 after TBI. The protective effect of atorvastatin on the injured neurons perhaps is mediated by increasing the density of vessels in the lesion boundary zone and the hippocampus after TBI.

Conclusions. These data indicate that atorvastatin is beneficial in the treatment of TBI in female rats, although the effect may differ between sexes.

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Kevin T. Huang, Michael A. Silva, Alfred P. See, Kyle C. Wu, Troy Gallerani, Hasan A. Zaidi, Yi Lu, John H. Chi, Michael W. Groff and Omar M. Arnaout


Recent advances in computer vision have revolutionized many aspects of society but have yet to find significant penetrance in neurosurgery. One proposed use for this technology is to aid in the identification of implanted spinal hardware. In revision operations, knowing the manufacturer and model of previously implanted fusion systems upfront can facilitate a faster and safer procedure, but this information is frequently unavailable or incomplete. The authors present one approach for the automated, high-accuracy classification of anterior cervical hardware fusion systems using computer vision.


Patient records were searched for those who underwent anterior-posterior (AP) cervical radiography following anterior cervical discectomy and fusion (ACDF) at the authors’ institution over a 10-year period (2008–2018). These images were then cropped and windowed to include just the cervical plating system. Images were then labeled with the appropriate manufacturer and system according to the operative record. A computer vision classifier was then constructed using the bag-of-visual-words technique and KAZE feature detection. Accuracy and validity were tested using an 80%/20% training/testing pseudorandom split over 100 iterations.


A total of 321 total images were isolated containing 9 different ACDF systems from 5 different companies. The correct system was identified as the top choice in 91.5% ± 3.8% of the cases and one of the top 2 or 3 choices in 97.1% ± 2.0% and 98.4 ± 13% of the cases, respectively. Performance persisted despite the inclusion of variable sizes of hardware (i.e., 1-level, 2-level, and 3-level plates). Stratification by the size of hardware did not improve performance.


A computer vision algorithm was trained to classify at least 9 different types of anterior cervical fusion systems using relatively sparse data sets and was demonstrated to perform with high accuracy. This represents one of many potential clinical applications of machine learning and computer vision in neurosurgical practice.