Kim J. Burchiel
James W. Leiphart, Cynthia V. Dills, Ofer M. Zikel, Daniel L. Kim, and Robert M. Levy
✓ The antinociceptive actions of morphine and tizanidine (an α2-adrenergic agonist) administered intrathecally in a rat model of mononeuropathic pain were investigated. Tizanidine increased to normal levels the intensity of a noxious pressure stimulus required to induce paw withdrawal (p < 0.01) and decreased the duration of limb withdrawal from both normal-temperature and cooled floors in a dose-dependent manner (p < 0.01). Tizanidine had virtually no effect on the latency of paw withdrawal from a noxious heat stimulus. In comparison, morphine significantly decreased, in a dose-dependent manner, limb withdrawal from the normal-temperature and cooled floors and increased to cutoff values the withdrawal latencies of both noxious heat and pressure stimuli (p < 0.01). The effect of tizanidine was limited to the hyperalgesic limb and served to normalize reactive latencies, whereas morphine affected both hindlimbs and increased latencies to supranormal cutoff values. These data suggest that intrathecal tizanidine may be more specific than morphine in reversing the allodynia and hyperpathia associated with neuropathic pain states and may be of value in the management of patients with these clinical syndromes.
Robert B. Kim, Riann Robbins, Michael D. Rollins, and Douglas L. Brockmeyer
Currarino syndrome is an autosomal dominant condition with variable expressivity and penetrance that is associated with several classic features: sacral dysgenesis, presacral mass, and/or anorectal anomalies. The authors present a unique case in which the patient’s initial presentation was a CSF leak from a sinus tract. The sinus tract was identified and disconnected from the thecal sac, obliterating the anterior sacral meningocele. This case represents a unique scenario in which Currarino syndrome manifested as a CSF leak from a dermal sinus tract.
Jeffrey G. Ojemann, Robert L. Grubb, Michael Kyriakos, and Kim B. Baker
✓ This 52-year-old woman developed crystal deposition disease involving the cervical vertebrae. She presented with symptomatic spinal cord compression secondary to extensive calcified lesions in the posterior elements of the cervical spine. Surgical decompression with posterior fusion was performed. Histological examination showed hardened deposits of calcium carbonate involving the soft tissue, and dissolution of the vertebral bone trabeculae. There was no inflammatory response to these deposits. One year postoperatively the patient developed severe pulmonary disease associated with the collagen-vascular disorder, scleroderma (calcinosis, Raynaud's phenomenon, esophageal hypomotility, sclerodactyly, and telangiectasia [CREST] syndrome). Calcium carbonate deposition disease represents an unusual clinical entity that is possibly associated with scleroderma or other collagen-vascular diseases, and it is distinct from ligamentum flavum calcification, calcium pyrophosphate deposition disease, and hydroxyapatite deposition disease.
Roel H. L. Haeren, Jim Dings, M. Christianne Hoeberigs, Robert G. Riedl, and Kim Rijkers
Intraosseous cavernous hemangiomas of the skull are rare lesions for which the origin is unclear. The authors present a case in which there was a radiologically documented history of trauma preceding the development of a hemangioma in the frontal bone.
In a review of the literature the authors found 83 cases of skull hemangiomas, and 43% of the lesions were located in the frontal bone. In 25% of these lesions, previous trauma was reported anamnestically. The present case and radiological findings related to it suggest a causal relationship between trauma and the development of intraosseous hemangioma.
Terrence T. Kim, Doniel Drazin, Faris Shweikeh, Robert Pashman, and J. Patrick Johnson
Intraoperative CT image–guided navigation (IGN) has been increasingly incorporated into minimally invasive spine surgery (MIS). The vast improvement in image resolution and virtual real-time images with CT-IGN has proven superiority over traditional fluoroscopic techniques. The authors describe their perioperative MIS technique using the O-arm with navigation, and they report their postoperative experience, accuracy results, and technical aspects.
A retrospective review of 48 consecutive adult patients undergoing minimally invasive percutaneous posterior spinal fusion with intraoperative CT-IGN between July 2010 and August 2013 at Cedars-Sinai Medical Center was performed. Two surgeons assessed 290 screws in a blinded fashion on intraoperative O-arm images and postoperative CT scans for bony pedicle wall breach. Grade 1 breach was defined to be < 2 mm, Grade 2 breach to be between 2 and 4 mm, and a Grade 3 breach to be > 4 mm. Additionally, anterior vertebral body breach was recorded.
Of 290 pedicle screws placed, 280 (96.6%) were in an acceptable position without cortical wall or anterior breach. Of the 10 breaches (3.4%) 5 were lateral (50%), 4 were medial, and 1 was anterior; 90% of breaches were Grade 1–2 and all medial breaches were Grade 1. The one Grade 3 breach was lateral. No vascular or neurological complications were observed intraoperatively, and no significant postoperative complications were noted. The mean clinical follow-up period was 18 months (range 3–39 months). The overall clinical outcomes, measured using the visual analog scale (back pain scores), were improved significantly postoperatively at 3 months compared with preoperatively (visual analog score 6.35 vs 3.57; p < 0.0001). No revision surgery was performed for screw misplacement or neurological deterioration.
New CT-IGN with the mobile O-arm scanner has increased the accuracy of pedicle screw/instrumentation placement using MIS techniques. The authors' high (96.6%) accuracy rate in MIS compares favorably with historical published accuracy rates for fluoroscopy-based techniques. Additional advantages of CT-IGN over fluoroscopic imaging methods are lower occupational radiation exposure for the surgical team, reduced need for postoperative imaging, and decreased rates of revision surgery. For now, the authors simply conclude that use of intraoperative CT-IGN is safe and accurate.
Bum-Tae Kim, Vemuganti L. Raghavendra Rao, Kurt A. Sailor, Kellie K. Bowen, and Robert J. Dempsey
Object. The purpose of this study was to evaluate whether glial cell line—derived neurotrophic factor (GDNF) can protect against hippocampal neuronal death after traumatic brain injury (TBI).
Methods. Male Sprague—Dawley rats were subjected to moderate TBI with a controlled cortical impact device while in a state of halothane-induced anesthesia. Then, GDNF or artificial cerebrospinal fluid ([aCSF]; vehicle) was infused into the frontal horn of the left lateral ventricle. In eight brain-injured and eight sham-operated rats, GDNF was infused continuously for 7 days (200 ng/day intracerebroventricularly at a rate of 8.35 ng/0.5 µl/hour). An equal volume of vehicle was infused at the same rate into the remaining eight brain-injured and eight sham-operated rats. Seven days post-injury, all rats were killed. Their brains were sectioned and stained with cresyl violet, and the hippocampal neuronal loss was evaluated in the CA2 and CA3 regions with the aid of microscopy. A parallel set of sections from each brain was subjected to immunoreaction with antibodies against glial fibrillary acidic protein (GFAP; astroglia marker). In the aCSF-treated group, TBI resulted in a significant neuronal loss in the CA2 (60%, p < 0.05) and CA3 regions (68%, p < 0.05) compared with the sham-operated control animals. Compared with control rats infused with aCSF, GDNF infusion significantly decreased the TBI-induced neuronal loss in both the CA2 (58%, p < 0.05) and CA3 regions (51%, p < 0.05). There was no difference in the number of GFAP-positive astroglial cells in the GDNF-infused rats in the TBI and sham-operated groups compared with the respective vehicle-treated groups.
Conclusions. The authors found that GDNF treatment following TBI is neuroprotective.
Phyo Kim, Robert R. Lorenz, Thoralf M. Sundt Jr., and Paul M. Vanhoutte
✓ The purpose of this study was to determine the cause of the loss of endothelium-dependent relaxation observed in chronic cerebral vasospasm. A bioassay system was developed to measure the release of endothelium-derived relaxing factor (EDRF) from canine basilar arteries. Subarachnoid hemorrhage (SAH) was induced in dogs by two injections of autologous blood into the cisterna magna. Angiograms were performed on the 7th day after SAH to check the presence of chronic vasospasm. The animals were sacrificed on the 8th day, and in vitro experiments were performed on rings harvested from the basilar artery. These confirmed loss of endothelium-dependent relaxation in response to bradykinin and arginine vasopressin in the group with SAH. The basilar arteries were perfused with modified Krebs-Ringer solution. The perfusate was bioassayed with a ring of coronary artery without endothelium (bioassay ring). The release of the EDRF was detected by relaxation of the bioassay ring contracted with prostaglandin F2α. Arginine vasopressin and bradykinin added to the perfusate upstream of the basilar artery caused concentration-dependent release of the EDRF. The direct effect of these peptides on the smooth muscle of the bioassay ring was to cause contraction. The release of the EDRF was identical in basilar arteries from the control and the SAH groups. These results indicate that the release of the EDRF is not impaired during chronic vasospasm, and thus that the loss of the endothelium-dependent relaxation is due to a decreased transfer of the EDRF or a reduced responsiveness of the smooth muscle to the factor.
Doniel Drazin, Ali Shirzadi, Sunil Jeswani, Harry Ching, Jack Rosner, Alexandre Rasouli, Terrence Kim, Robert Pashman, and J. Patrick Johnson
Athletes present with back pain as a common symptom. Various sports involve repetitive hyperextension of the spine along with axial loading and appear to predispose athletes to the spinal pathology spondylolysis. Many athletes with acute back pain require nonsurgical treatment methods; however, persistent recurrent back pain may indicate degenerative disc disease or spondylolysis. Young athletes have a greater incidence of spondylolysis. Surgical solutions are many, and yet there are relatively few data in the literature on both the techniques and outcomes of spondylolytic repair in athletes. In this study, the authors undertook a review of the surgical techniques and outcomes in the treatment of symptomatic spondylolysis in athletes.
A systematic review of the MEDLINE and PubMed databases was performed using the following key words to identify articles published between 1950 and 2011: “spondylolysis,” “pars fracture,” “repair,” “athlete,” and/or “sport.” Papers on both athletes and nonathletes were included in the review. Articles were read for data on methodology (retrospective vs prospective), type of treatment, number of patients, mean patient age, and mean follow-up.
Eighteen articles were included in the review. Eighty-four athletes and 279 nonathletes with a mean age of 20 and 21 years, respectively, composed the population under review. Most of the fractures occurred at L-5 in both patient groups, specifically 96% and 92%, respectively. The average follow-up period was 26 months for athletes and 86 months for nonathletes. According to the modified Henderson criteria, 84% (71 of 84) of the athletes returned to their sports activities. The time intervals until their return ranged from 5 to 12 months.
For a young athlete with a symptomatic pars defect, any of the described techniques of repair would probably produce acceptable results. An appropriate preoperative workup is important. The ideal candidate is younger than 20 years with minimal or no listhesis and no degenerative changes of the disc. Limited participation in sports can be expected from 5 to 12 months postoperatively.