Vertebral artery dissection (VAD) is rare in children but is increasingly recognized as a cause of stroke in the pediatric population. Traditionally, VAD was thought to be attributable to either trauma or spontaneous dissections. Recently, several underlying causes, such as bony cervical abnormalities, connective tissue diseases, and infection, have been determined to account for spontaneous VAD or those cases associated with only minor trauma. Two pediatric cases of VAD are presented, both caused by bony cervical abnormalities and each treated with different surgical procedures for symptom resolution. The first case required suboccipital decompression and endovascular sacrifice of the vertebral artery. The second case was treated with surgical decompression of the foramen transversarium at C-1 and C-2. The treatment of both of these patients required accurate diagnosis via cervical spine CT to define the bone anatomy and delineate a cause for what was originally theorized to be spontaneous VAD.
Report of 2 cases
Cara L. Sedney and Charles L. Rosen
Cara L. Sedney, Scott D. Daffner, Jared J. Stefanko, Hesham Abdelfattah, Sanford E. Emery and John C. France
As spinal fusions become more common and more complex, so do the sequelae of these procedures, some of which remain poorly understood. The authors report on a series of patients who underwent removal of hardware after CT-proven solid fusion, confirmed by intraoperative findings. These patients later developed a spontaneous fracture of the fusion mass that was not associated with trauma. A series of such patients has not previously been described in the literature.
An unfunded, retrospective review of the surgical logs of 3 fellowship-trained spine surgeons yielded 7 patients who suffered a fracture of a fusion mass after hardware removal. Adult patients from the West Virginia University Department of Orthopaedics who underwent hardware removal in the setting of adjacent-segment disease (ASD), and subsequently experienced fracture of the fusion mass through the uninstrumented segment, were studied. The medical records and radiological studies of these patients were examined for patient demographics and comorbidities, initial indication for surgery, total number of surgeries, timeline of fracture occurrence, risk factors for fracture, as well as sagittal imbalance.
All 7 patients underwent hardware removal in conjunction with an extension of fusion for ASD. All had CT-proven solid fusion of their previously fused segments, which was confirmed intraoperatively. All patients had previously undergone multiple operations for a variety of indications, 4 patients were smokers, and 3 patients had osteoporosis. Spontaneous fracture of the fusion mass occurred in all patients and was not due to trauma. These fractures occurred 4 months to 4 years after hardware removal. All patients had significant sagittal imbalance of 13–15 cm. The fracture level was L-5 in 6 of the 7 patients, which was the first uninstrumented level caudal to the newly placed hardware in all 6 of these patients. Six patients underwent surgery due to this fracture.
The authors present a case series of 7 patients who underwent surgery for ASD after a remote fusion. These patients later developed a fracture of the fusion mass after hardware removal from their previously successfully fused segment. All patients had a high sagittal imbalance and had previously undergone multiple spinal operations. The development of a spontaneous fracture of the fusion mass may be related to sagittal imbalance. Consideration should be given to reimplanting hardware for these patients, even across good fusions, to prevent spontaneous fracture of these areas if the sagittal imbalance is not corrected.
James D. Mills, Julian E. Bailes, Cara L. Sedney, Heather Hutchins and Barry Sears
Traumatic brain injury remains the most common cause of death in persons under 45 years of age in the Western world. Recent evidence from animal studies suggests that supplementation with omega-3 fatty acid (O3FA) (particularly eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) improves functional outcomes following focal neural injury. The purpose of this study is to determine the benefits of O3FA supplementation following diffuse axonal injury in rats.
Forty adult male Sprague-Dawley rats were used. Three groups of 10 rats were subjected to an impact acceleration injury and the remaining group underwent a sham-injury procedure (surgery, but no impact injury). Two of the groups subjected to the injury were supplemented with 10 or 40 mg/kg/day of O3FA; the third injured group served as an unsupplemented control group. The sham-injured rats likewise received no O3FA supplementation. Serum fatty acid levels were determined from the isolated plasma phospholipids prior to the injury and at the end of the 30 days of supplementation. After the animals had been killed, immunohistochemical analysis of brainstem white matter tracts was performed to assess the presence of β-amyloid precursor protein (APP), a marker of axonal injury. Immunohistochemical analyses of axonal injury mechanisms—including analysis for caspase-3, a marker of apoptosis; RMO-14, a marker of neurofilament compaction; and cytochrome c, a marker of mitochondrial injury—were performed.
Dietary supplementation with a fish oil concentrate rich in EPA and DHA for 30 days resulted in significant increases in O3FA serum levels: 11.6% ± 4.9% over initial levels in the 10 mg/kg/day group and 30.7% ± 3.6% in the 40 mg/kg/day group. Immunohistochemical analysis revealed significantly (p < 0.05) decreased numbers of APP-positive axons in animals receiving O3FA supplementation: 7.7 ± 14.4 axons per mm2 in the 10 mg/kg/day group and 6.2 ± 11.4 axons per mm2 in the 40 mg/kg/day group, versus 182.2 ± 44.6 axons per mm2 in unsupplemented animals. Sham-injured animals had 4.1 ± 1.3 APP-positive axons per mm2. Similarly, immunohistochemical analysis of caspase-3 expression demonstrated significant (p < 0.05) reduction in animals receiving O3FA supplementation, 18.5 ± 28.3 axons per mm2 in the 10 mg/kg/day group and 13.8 ± 18.9 axons per mm2 in the 40 mg/kg/day group, versus 129.3 ± 49.1 axons per mm2 in unsupplemented animals.
Dietary supplementation with a fish oil concentrate rich in the O3FAs EPA and DHA increases serum levels of these same fatty acids in a dose-response effect. Omega-3 fatty acid supplementation significantly reduces the number of APP-positive axons at 30 days postinjury to levels similar to those in uninjured animals. Omega-3 fatty acids are safe, affordable, and readily available worldwide to potentially reduce the burden of traumatic brain injury.