Devon A. Hoover and Asim Mahmood
✓ Pericranium is frequently used in duraplasty and is considered superior to the many other alternatives because of its easy availability and because it offers a watertight dural closure while minimizing the problems of adhesion, infection, and rejection. Although the osteogenic potential of all periosteal tissues is recognized, a review of the literature did not reveal a reported case of osseous formation following use of pericranium for duraplasty.
The authors report the case of a 17-year-old man who presented with a self-inflicted gunshot wound to the head. He was obtunded, but moving all extremities purposefully. Computerized tomography scanning demonstrated bifrontal injury. A bicoronal craniotomy with debridement was performed on an emergency basis, with vascularized pericranium used for a duraplasty. Follow-up cranioplasty demonstrated significant ossification of the pericranium 5 months after the original surgery. Pericranium is an attractive material for duraplasty; however, its osteogenic potential may interfere with future cranioplasty and cosmesis. This may be especially relevant in young persons.
Ghaus M. Malik, Asim Mahmood, and Bharat A. Mehta
✓ Intracranial arteriovenous malformations (AVM's) have been classified as pure pial, pure dural, and mixed pial and dural. Dural AVM's are relatively uncommon, with 377 cases documented up to 1990. These lesions were believed to be situated within the walls of the sinuses, but during the last decade researchers discovered a small subgroup of dural AVM's in extrasinusal locations such as the skull base and tentorium. Two of the 17 patients who were studied between 1976 and 1993 had dural AVM's that were entirely intraosseous except for their venous drainage, which was via the dural venous sinuses. Although such intraosseous dural AVM's have not been previously described, the authors elected to group these malformations with dural AVM's because their venous drainage was intracranial and angiograms revealed identical features.
Asim Mahmood, Dario V. Caccamo, and Jay K. Morgan
✓ A case of tenosynovial giant-cell tumor affecting the cervical spine is reported. The lesion is seen primarily in the fingers, knee, or ankle, and there are no previous reports of it occurring in the spine. The histological and radiological features of this tumor are discussed along with a brief description of the disease entity.
Asim Mahmood, Hongtao Wu, Changsheng Qu, Selina Mahmood, Ye Xiong, David L. Kaplan, and Michael Chopp
Neurocan is a major form of growth-inhibitory molecule (growth-IM) that suppresses axonal regeneration after neural injury. Bone marrow stromal cells (MSCs) have been shown to inhibit neurocan expression in vitro and in animal models of cerebral ischemia. Therefore, the present study was designed to investigate the effects of treatment of MSCs impregnated with collagen scaffolds on neurocan expression after traumatic brain injury (TBI).
Adult male Wistar rats were injured with controlled cortical impact and treated with saline, human MSCs (hMSCs) (3 × 106) alone, or hMSCs (3 × 106) impregnated into collagen scaffolds (scaffold + hMSCs) transplanted into the lesion cavity 7 days after TBI (20 rats per group). Rats were sacrificed 14 days after TBI, and brain tissues were harvested for immunohistochemical studies, Western blot analyses, laser capture microdissections, and quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) to evaluate neurocan protein and gene expressions after various treatments.
Animals treated with scaffold + hMSCs after TBI showed increased axonal and synaptic densities compared with the other groups. Scaffold + hMSC treatment was associated with reduced TBI-induced neurocan protein expression and upregulated growth-associated protein 43 (GAP-43) and synaptophysin expression in the lesion boundary zone. In addition, animals in the scaffold + hMSC group had decreased neurocan transcription in reactive astrocytes after TBI. Reduction of neurocan expression was significantly greater in the scaffold + hMSC group than in the group treated with hMSCs alone.
The results of this study show that transplanting hMSCs with scaffolds enhances the effect of hMSCs on axonal plasticity in TBI rats. This enhanced axonal plasticity may partially be attributed to the downregulation of neurocan expression by hMSC treatment after injury.
Asim Mahmood, Manuel Dujovny, Maximo Torche, Ljubisa Dragovic, and James I. Ausman
✓ The foramen caecum (FC) is a triangular-shaped fossa situated in the midline on the base of the brain stem, at the pontomedullary junction. Although this area is known to have a very high concentration of brainstem perforating vessels, its microvascular anatomy has not been studied in detail. The purpose of this study was to detail the microvasculature of this territory. Twenty unfixed brains were injected with silicone rubber solution and dissected under a microscope equipped with a camera. The origin, course, outer diameter, and branching pattern of the perforators were examined.
The total number of perforators found in the 20 brains was 287, with an average (± standard deviation) of 14.35 ± 1.24 perforators per brain (range seven to 28). Their origin was as follows: right vertebral artery in 52 perforators (18.11%); left vertebral artery in 35 (12.19%); basilar artery below the anterior inferior cerebellar artery (AICA) in 139 (48.43%); basilar artery above the AICA in 46 (16.02%); AICA in 10 (3.48%); and anterior spinal artery in five (1.74%). Most of the perforators arose as sub-branches of larger trunks; their average outer diameter was 0.16 ± 0.006 mm while that of trunks was 0.35 ± 0.02 mm.
These anatomical data are important for those wishing 1) to study the pathophysiology of vascular insults to this area caused by atheromas, thrombi, and emboli; 2) to plan vertebrobasilar aneurysm surgery; 3) to plan surgery for vertebrobasilar insufficiency; and 4) to study foramen magnum neoplasms.
Victor Chang, Paul Hartzfeld, Marianne Langlois, Asim Mahmood, and Donald Seyfried
Hemicraniectomy is a commonly practiced neurosurgical intervention with a wide range of indications and clinical data supporting its use. The extensive use of this procedure directly results in more cranioplasties to repair skull defects. The complication rate for cranial repair after craniectomy seems to be higher than that of the typical elective craniotomy. This finding prompted the authors to review their experience with patients undergoing cranial repair.
The authors performed a retrospective review of 212 patients who underwent cranial repair over a 13-year period at their institution. A database tracking age, presenting diagnosis, side of surgery, length of time before cranial repair, bone graft material used, presence of a ventricular shunt, presence of a postoperative drain, and complications was created and analyzed.
The overall complication rate was 16.4% (35 of 213 patients). Patients 0–39 years of age had the lowest complication rate of 8% (p = 0.028). For patients 40–59 years of age and older than 60, complication rates were 20 and 26%, respectively. Patients who originally presented with traumatic injuries had a lower rate of complications than those who did not (10 vs 20%; p = 0.049). Conversely, patients who presented with tumors had a higher complication rate than those without (38 vs 15%; p = 0.027). Patients who received autologous bone graft placement had a statistically significant lower risk of postoperative infection (4.6 vs 18.4%; p = 0.002). Patients who underwent cranioplasty with a 0–3 month interval between operations had a complication rate of 9%, 3–6 months 18.8%, and > 6 months 26%. Pairwise comparisons showed that the difference between the 0–3 month interval and the > 6-month interval was significant (p = 0.007). The difference between the 0–3 month interval and the 4–6 month interval showed a trend (p = 0.07). No difference was detected between the 4–6 month interval and > 6-month interval (p = 0.35).
The overall rate of complications related to cranioplasty after craniectomy is not negligible, and certain factors may be associated with increased risk. Therefore, when evaluating the need to perform a large decompressive craniectomy, the surgeon should also be aware that the patient is not only subject to the risks of the initial operation, but also the risks of subsequent cranioplasty.
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.
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.
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.