Inflammatory responses are a major component of secondary injury and play a central role in mediating the pathogenesis of acute and chronic spinal cord injury (SCI). The nuclear factor-kappaB (NF-kappaB) family of transcription factors is required for the transcriptional activation of a variety of genes regulating inflammatory, proliferative, and cell death responses of cells. In this study we examined the temporal and cellular expression of activated NF-kappaB after traumatic SCI. We used a contusion model (N.Y.U. Impactor) to initiate the early biochemical and molecular changes that occur after traumatic injury to reproduce the pathological events associated with acute inflammation after SCI. The activation and cellular distribution of activated NF-kappaB was evaluated by using a monoclonal antibody that selectively recognizes activated p65 in a NF-kappaB dimer. Immunohistochemical and Western blot analyses demonstrated that NF-kappaB activation occurred as early as 0.5 hr postinjury and persisted for at least 72 hr. Using electrophoretic mobility shift assays (EMSA), we demonstrate that NF-kappaB is activated after SCI. In our immunohistochemical, Western, and EMSA experiments there are detectable levels of activated NF-kappaB in our control animals. Using double-staining protocols, we detected activated NF-kappaB in macrophages/microglia, endothelial cells, and neurons within the injured spinal cord. Colocalization of activated NF-kappaB with the NF-kappaB-dependent gene product, inducible nitric oxide synthase (iNOS), suggests functional implications for this transcription factor in the pathogenesis of acute spinal cord injury. Although there is considerable evidence for the involvement of an inflammatory reaction after traumatic SCI, this is the first evidence for the activation of NF-kappaB after trauma. Strategies directed at blocking the initiation of this cascade may prove beneficial as a therapeutic approach for the treatment of acute SCI.

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Intracellular fluid within single human erythrocytes is analyzed by capillary electrophoresis with laser-excited native protein fluorescence. Good signal-to-noise is achieved, allowing even minor components to be quantified. Non-Gaussian distributions were found for total protein, fraction carbonic anhydrase, fraction hemoglobin A0, and an unidentified component. Variations among a group of 29 cells for each quantity are as much as 1 order of magnitude, even though erythrocytes are known to be fairly homogeneous in size distribution. Variations in fraction hemoglobin A0 reflect differences in in vitro oxidation rates to methemoglobin. A positive correlation was observed between carbonic anhydrase and hemoglobin A0 for individual cells. This is consistent with the presence of erythrocytes of different ages within the population, with the older cells being less capable of maintaining enzyme activity and preventing oxidative damage.

Patients with progressive posttraumatic myelomalacic myelopathy (PPMM), or tethered cord syndrome, present with symptoms and signs similar to those observed in case of progressive posttraumatic cystic myelopathy, that is, sensorimotor function deterioration, local and/or radicular pain, increased spasticity, increased autonomic dysreflexia, and sphincter dysfunction. The authors investigated surgical outcomes of untethering combined with expansive duraplasty. Forty patients with PPMM who presented with functional deterioration underwent untethering of the spinal cord and nerve roots with an expansive duraplasty. Meticulous dissections of adhesions on the dorsal and lateral aspects of the spinal cord and nerve roots were performed. Intraoperative ultrasonography was used to detect the presence of a confluent cyst and to assess the success of untethering. After surgery, the patients were treated using a protocol that involved frequent turning for 48 hours and subsequently mobilization. Preoperative magnetic resonance (MR) imaging, with and without administration of a contrast agent, was obtained in all patients, except one patient who underwent immediate and delayed computerized tomography (CT) myelography. The mean follow-up period was 3 years (range 20-57 months) for the 36 patients available for follow-up review. Spinal cord tethering was observed in all patients preoperatively. Trauma was the most common cause of this pathology, accounting for 31 of the 40 cases. Preoperative MR imaging did not demonstrate tumor recurrence in the group of five patients who had undergone an initial operation for tumor excision. The interval between the causative event and the operation was less than 5 years in half of the patients (20 of 40), with the longest interval lasting up to 37 years. Motor function deterioration was the most frequent manifestation; it was present in 31 of 40 patients. Improvements in motor function, autonomic dysreflexia, pain, sphincter dysfunction, and sensory function were found during the most recent follow-up examination in 79%, 75%, 62%, 50%, and 43% of the patients, respectively. Two patients experienced retethering of the spinal cord and one underwent a second operation. Surgical untethering and expansive duraplasty, followed by postoperative position rotation to avoid retethering, provide symptomatic relief for patients with PPMM.

Isolated stable burst fracture of the atlas can be treated effectively with a rigid cervical collar alone for 10 to 12 weeks with good neurologic recovery and segmental stability. Unstable Jefferson fractures with concurrent unstable fracture of other cervical vertebrae, especially C2, requires surgical stabilization.