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

• Main Authors: Hiroshi Takahashi, Yasuchika Aoki, Junya Saito, Arata Nakajima, Masato Sonobe, Yorikazu Akatsu, Shinji Taniguchi, Manabu Yamada, Keita Koyama, Yuki Akiyama, Yasuhiro Shiga, Kazuhide Inage, Sumihisa Orita, Yawara Eguchi, Satoshi Maki, Takeo Furuya, Tsutomu Akazawa, Masao Koda, Masashi Yamazaki, Seiji Ohtori, Koichi Nakagawa
• Format: Article
• Language: English
• Published: BMC 2019-12-01
• Series: BMC Musculoskeletal Disorders
• Subjects: Compression myelopathy; Serum oxidative stress; Reactive oxygen metabolites; Surgical outcome
• Online Access: https://doi.org/10.1186/s12891-019-2966-5

Abstract 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.