Upper Cervical Compression Myelopathy Caused by the Retro-Odontoid Pseudotumor With Degenerative Osteoarthritis and Calcium Pyrophosphate Dihydrate Disease: A Case Report and Literature Review

The retro-odontoid pseudotumor is often concurrent with atlantoaxial subluxation (AAS). Therefore, the pseudotumor is relatively common in rheumatoid arthritis (RA) but rare in primary osteoarthritis (OA). This is a case report of an elderly male patient suffering from neck pain and compression myelopathy caused by the craniocervical pseudotumor with OA but without atlantoaxial instability. He had long-lasting peripheral and spinal pain treated by nonsteroidal anti-inflammatory drugs. Imaging found upper cervical spondylosis without AAS or dynamic instability but with periodontoid calcifications and ossifications, suggesting calcium pyrophosphate dihydrate (CPPD) crystal deposition. Based on a comprehensive literature search and review, CPPD disease around the atlantodental joint is a possible contributor to secondary OA development and retro-odontoid pannus formation through chronic inflammation, which can be enough severe to induce compression myelopathy in non-RA patients without AAS. The global increase in the aged population advises caution regarding more prevalent upper cervical spine disorders associated with OA and CPPD.

Misdiagnosis of “White Cord Syndrome” following posterior cervical surgery for ossification of the posterior longitudinal ligament: A case report

Background: Following decompressive cervical surgery for significant spinal cord compression/myelopathy, patients may rarely develop the “White Cord Syndrome (WCS).” This acute postoperative reperfusion injury is characterized on T2W MRI images by an increased intramedullary cord signal. However, it is a diagnosis of exclusion, and WCS can only be invoked once all other etiologies for cord injury have been ruled out. Case Description: A 49-year-old male, 3 days following a C3-C7 cervical laminectomy and C2-T1 fusion for extensive cord compression due to ossification of the posterior longitudinal ligament (OPLL), developed acute quadriparesis. This new deficit should have been attributed to an intraoperative iatrogenic cord injury, not the WCS. Conclusion: Very rarely patients sustain postoperative significant/severe new neurological deficits attributable to the WCS. Notably, the WCS is a diagnosis of exclusion, and all other etiologies (i.e. intraoperative iatrogenic surgeon-based mechanical cord injury, graft/instrumentation extrusion, failure to adequately remove/resect OPLL thus stretching cord over residual disease, other reasons for continued cord compression, including the need for secondary surgery, etc.) of cord injury must first be ruled out.

A case of cervical myelopathy following chronic hypertrophic non-union type 2 odontoid fracture managed with posterior C1 decompression and C1-3 instrumentation: Case report and brief review of literature

Background: Type 2 odontoid fractures are the most common type of fracture of the axis. In rare cases, nonunion of a type 2 odontoid fracture can be hypertrophic resulting in myelopathy due to cervical cord compression. Case Description: A 48-year-old male presented with hypertrophic nonunion of a chronic type 2 odontoid fracture resulting in cord compression/myelopathy. This was adequately treated utilizing a C1 decompression and C1-3 instrumented fusion; no anterior procedure was necessary. Conclusion: Here, we successfully treated a patient with a hypertrophic nonunion of a chronic type 2 odontoid fracture utilizing a posterior only approach consisting of a C1 laminectomy with C1-C3 fusion.

Correlation analysis of clinical features and genotype in dogs with intervertebral disc degeneration

Most modern pet species have awide breed variability. The genetic aspect plays a signif-icant role in the development of individual pathologies. A retrogen encoding fibroblast growth factor 4 (FGF4), when inserted into the chromosome 18of dogs (CFA18), leads to chondrodysplasia, phenotypically mani-festing itself as shortened limbs in dogs. The incorporation of the FGF4 retrogene into chromosome 12 (CFA12) leads to a similar phenotype, but associated with an increased degeneration of the intervertebral discs. Although many retrogens are considered “silent”pseudogenes, the FGF4 retrogene in cases of chondrodysplasia and chondro-dystrophy is transcriptionally activated and leads to hyperactivation of the fi-broblast growth factor 3 receptor (FGFR3). Mutations are dominant, but links with spinal problems have been identified only for one, where the retro-gene is integrated into chromosome 12. Thus, dogs with the phenotype of short limbs are at risk for degenerative disease of the intervertebral discs, however, the disease recorded among animals is not related to chondrodystrophoids. The genetic predispo-sition of dogs of chondrodystrophoid breeds to degeneration of intervertebral discs is not a pathognomonic criterion for its presence. The study included genetic tests of dogs of different breeds, which were examined for compression myelopathy as a result of degeneration of the intervertebral discs. During testing, the purpose of which was to find correlation, the corresponding pedigree predispositions and clinical mani-festations of degenerative diseases of the intervertebral discs among 20 dogs (14 chondrodystrophoid and 6 non-chondrodystrophoid) wereconfirmed, in 14 cases (i.e. 70%) discogenic compres-sion was revealed during tomography.

Serum oxidative stress influences neurological recovery after surgery to treat acutely worsening symptoms of compression myelopathy: a cross-sectional human study

Background Recent reports indicate that oxidative stress induced by reactive oxygen species is associated with the pathobiology of neurodegenerative disorders that involve neuronal cell apoptosis. Here we conducted a cross-sectional study to evaluate serum levels of oxidative stress in cervical compression myelopathy. Methods Thirty-six serum samples were collected preoperatively from patients treated for acutely worsening compression myelopathy (AM) and chronic compression myelopathy (CM). Serum levels of oxidative stress markers were evaluated by measuring derivatives of reactive oxygen metabolites (ROM), which reflect concentrations of hydroperoxides. ROM in healthy individuals range from 250 to 300 (U. CARR), whereas ROM >340–400 and > 400 define moderate and severe levels of oxidative stress, respectively. Difference of ROM by the cause of disorders whether cervical spondylotic myelopathy (CSM) or cervical ossification of longitudinal ligament (OPLL), correlations between ROM and patient age, body mass index (BMI), history of smoking, existence of diabetes were examined. Neurological evaluations according to Japanese Orthopaedic Association (JOA) scores were performed and correlated with ROM. Results ROM increased to 349.5 ± 54.8, representing a moderate oxidative stress, in CM samples. ROM increased to 409.2 ± 77.9 in AM samples, reflecting severe oxidative stress which were significantly higher than for CM samples (p < 0.05). There was no significant difference by the cause of disorders (CSM or OPLL). ROM were significantly increased in AM serum samples from female patients versus AM male and CM patients (p < 0.05). There were no correlations between ROM and age, BMI, history of smoking, and existence of diabetes. A negative correlation between ROM and recovery rate of JOA score (R2 = 0.454, p = 0.047) was observed in the AM group. Conclusions Although moderate oxidative stress was present in patients with CM, levels of oxidative stress increased in severity in patients with AM. These results suggest that postsurgical neurological recovery is influenced by severe oxidative stress in AM.

Human recombinant erythropoietin improves motor function in rats with spinal cord compression myelopathy

OBJECTIVEErythropoietin (EPO) is a clinically available hematopoietic cytokine. The aim of this study was to evaluate the effect of EPO on a rat model of cervical cord compression myelopathy and to explore the possibility of its use as a pharmacological treatment.METHODSTo produce the chronic cervical cord compression model, thin polyurethane sheets were implanted under the C5-C6 laminae of rats and gradually expanded due to water absorption. In this model, motor functions significantly declined from 7 weeks after surgery. Based on the result, EPO administration was started 8 weeks after surgery. Motor function as seen with rotarod performance and grip strength was measured 16 weeks after surgery, and then motor neurons were stained with H-E and NeuN staining, and counted. Apoptotic cell death was assessed with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) staining. To assess transfer of EPO into spinal cord tissue, the EPO level in spinal cord tissue was measured with an enzyme-linked immunosorbent assay for each group after subcutaneous injection of EPO.RESULTSHigh-dose EPO (5000 IU/kg) administered from 8 weeks after surgery markedly restored and maintained motor function in the Compression groups (P < 0.01). EPO significantly prevented loss of motor neurons in the anterior horn (P < 0.05) and significantly decreased the number of TUNEL-positive apoptotic cells (P < 0.05). The EPO level in spinal cord tissue was significantly higher in the High-dose EPO group than other groups.CONCLUSIONSEPO improves motor function in rats with progressive chronic compression myelopathy. EPO protects anterior horn motor neurons and inhibits neuronal cell apoptosis in spinal cord compression. The neuroprotective effects can be produced through transfer of EPO into spinal cord tissue. These findings suggest that EPO has high potential as a treatment for developing compression myelopathy.