Contents lists available at ScienceDirect Clinical Biomechanics journal homepage: www.elsevier.com/locate/clinbiomech Short communication In vivo study of paraspinal muscle weakness using botulinum toxin in one primate model Sang Kuy Han a,1 , Youngjeon Lee b,1 , Jung-Joo Hong b,1 , Hyeon-Gu Yeo b,c , Jincheol Seo b,d , Chang-Yeop Jeon b,e , Kang-Jin Jeong b , Yeung Bae Jin b , Philyong Kang b , Sangil Lee b , Choongsoo S. Shin f , Young Eun Kim g , Keyoung Jin Chun a , Kyu-Tae Chang b,c, ⁎ , Sang-Rae Lee b,c, ⁎ a Korea Institute of Industrial Technology, Cheonan, Republic of Korea b National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea c Department of Functional Genomics, University of Science and Technology, Daejeon, Republic of Korea d School of Life Sciences, Kyungpook National University, Daegu, Republic of Korea e Department of Biomedical Engineering, College of Medicine, Chungbuk National University, Cheongju, Republic of Korea f Department of Mechanical Engineering, Sogang University, Seoul, Republic of Korea g Department of Mechanical Engineering, Dankook University, Yongin, Republic of Korea ABSTRACT Background: It has been generally speculated that paraspinal muscle weakness is related to the spinal degen- eration including intervertebral disc failure. The purpose of this study was to investigate the effects of paraspinal muscle weakness induced by the botulinum toxin type-A on the lumbar spine and behavior pattern in an in-vivo primate model which has an upright locomotion similar to that of humans. Methods: Botox injections into paraspinal muscle of one cynomolgus monkey were conducted biweekly up to 19 weeks at L2–L3, L3–L4 and L4–L5. MRIs were performed for measurement of muscle cross-sectional areas and behavioral data were collected using a high-resolution portable digital video camera. Findings: The cross-sectional areas of the paraspinal muscles at L2–L3, L3–L4 and L4–L5 decreased by 8%, 12% and 8% at 21 weeks after the Botox injection, respectively. Intervertebral disc thickness at L2–L3, L3–L4 and L4–L5 decreased by 6%, 8% and 5% at 21 weeks after initial Botox injection, respectively. After the Botox injections, locomotion and movement activity of the monkey was decreased. The duration of sitting increased from 21% to a maximum of 97% at 9 weeks after the Botox injection, while stance time decreased from 9% to a minimum of 1% at 11 weeks post Botox injection. Interpretation: The findings of this study revealed that paraspinal muscle atrophy affects intervertebral disc morphology and locomotion activity of a primate and may lead to an onset of intervertebral disc degeneration. 1. Introduction The spine is a complex anatomic structure and provides mobility and strength. The health of the spine depends on the integrity and proper function of structural components. The paraspinal muscles and spine are mutually dependent in a functional manner, as the paraspinal muscles play a role in moving and stabilizing the spine. It has been generally accepted that paraspinal muscle dysfunction, including muscle weakness, is related to the spinal degeneration such as inter- vertebral disc (IVD) failure (Crisco and Panjabi, 1991; Gracovetsky, 1986; Kalichman et al., 2010; Panjabi, 1992). Degeneration of spine is defined by structural failure, such as disc herniation or prolapse, disc height loss and affects other spinal structures including muscles and ligaments (Urban and Roberts, 2003). Since experimental approaches for examining the strength of the paraspinal muscle in an in-vivo model is technically difficult, most previous studies have been conducted using an in-vitro experiment and computational analysis, such as finite element modeling, for under- standing of IVD biomechanics (El-Rich et al., 2004; Kim and Choi, 2013; Kong et al., 1996; Shirazi-Adl et al., 2005; Wilke et al., 1995). Recently, a series of studies employing a muscle weakness model in- duced by the botulinum toxin type-A (Botox) has been reported to in- vestigate the relationship between adjacent muscle weakness and sy- novial joint health (Egloff et al., 2014; Rehan Youssef et al., 2009). https://doi.org/10.1016/j.clinbiomech.2018.01.021 Received 30 October 2016; Accepted 23 January 2018 ⁎ Corresponding authors at: National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea. 1 Co-first authors: Sang Kuy Han, Youngjeon Lee and Jung-Joo Hong equally contribute this work. E-mail addresses: changkt@kribb.re.kr (K.-T. Chang), srlee@kribb.re.kr (S.-R. Lee). Clinical Biomechanics 53 (2018) 1–6 0268-0033/ © 2018 Published by Elsevier Ltd. T