Avinash G Patwardhan1,2,3, Saeed Khayatzadeh4, Robert M Havey4,5, Leonard I Voronov4,5, Zachary A Smith6, Olivia Kalmanson5, Alexander J Ghanayem4,5, William Sears7. 1. Musculoskeletal Biomechanics Laboratory, Edward Hines Jr. VA Hospital, Hines, IL, USA. apatwar@lumc.edu. 2. Loyola University Stritch School of Medicine, Maywood, IL, USA. apatwar@lumc.edu. 3. Department of Orthopaedic Surgery and Rehabilitation, Loyola University Medical Center, 2160 S. First Avenue, Maywood, IL, 60153, USA. apatwar@lumc.edu. 4. Musculoskeletal Biomechanics Laboratory, Edward Hines Jr. VA Hospital, Hines, IL, USA. 5. Loyola University Stritch School of Medicine, Maywood, IL, USA. 6. Northwestern Feinberg School of Medicine, Chicago, IL, USA. 7. Wentworth Spine Clinic, Sydney, NSW, Australia.
Abstract
PURPOSE: In this article, we summarize our work on understanding the influence of cervical sagittal malalignment on the mechanics of the cervical spine. METHODS: Biomechanical studies were performed using an ex vivo laboratory model to study the kinematic and kinetic response of human cervical spine specimens in the setting of cervical sagittal imbalance. The model allowed controlled variations of C2-C7 Sagittal Vertical Alignment (C2-C7 SVA) and T1-Slope so that clinically relevant sagittally malaligned profiles could be prescribed, while maintaining horizontal gaze, and their biomechanical consequences studied. RESULTS: Our results demonstrated that increasing C2-C7 SVA caused flexion of lower cervical (C2-C7) segments and hyperextension of suboccipital (C0-C1-C2) segments to maintain horizontal gaze. An increase in C2-C7 SVA increased the lower cervical neural foraminal areas. Conversely, increasing T1-slope predominantly influenced subaxial cervical lordosis and, as a result, decreased cervical neural foraminal areas. Therefore, we believe patients with increased upper thoracic kyphosis and radicular symptoms may respond with increased forward head posture (FHP) as a compensatory mechanism to increase their lower cervical neural foraminal area and alleviate nerve root compression as well as reduce the burden on posterior muscles and soft and bony structures of the cervical spine. Increasing FHP (i.e., increased C2-C7 SVA) was associated with shortening of the cervical flexors and occipital extensors and lengthening of the cervical extensors and occipital flexors, which corresponds to C2-C7 flexion and C0-C2 extension. The greatest shortening occurred in the suboccipital muscles, suggesting considerable load bearing of these muscles during chronic FHP. Regardless, there was no evidence of nerve compression within the suboccipital triangle. Finally, cervical sagittal imbalance may play a role in exacerbating adjacent segment pathomechanics after multilevel cervical fusion and should be considered during surgical planning. CONCLUSIONS: The results of our biomechanical studies have improved our understanding of the impact of cervical sagittal malalignment on pathomechanics of the cervical spine. We believe this improved understanding will assist in clinical decision-making.
PURPOSE: In this article, we summarize our work on understanding the influence of cervical sagittal malalignment on the mechanics of the cervical spine. METHODS: Biomechanical studies were performed using an ex vivo laboratory model to study the kinematic and kinetic response of human cervical spine specimens in the setting of cervical sagittal imbalance. The model allowed controlled variations of C2-C7 Sagittal Vertical Alignment (C2-C7 SVA) and T1-Slope so that clinically relevant sagittally malaligned profiles could be prescribed, while maintaining horizontal gaze, and their biomechanical consequences studied. RESULTS: Our results demonstrated that increasing C2-C7 SVA caused flexion of lower cervical (C2-C7) segments and hyperextension of suboccipital (C0-C1-C2) segments to maintain horizontal gaze. An increase in C2-C7 SVA increased the lower cervical neural foraminal areas. Conversely, increasing T1-slope predominantly influenced subaxial cervical lordosis and, as a result, decreased cervical neural foraminal areas. Therefore, we believe patients with increased upper thoracic kyphosis and radicular symptoms may respond with increased forward head posture (FHP) as a compensatory mechanism to increase their lower cervical neural foraminal area and alleviate nerve root compression as well as reduce the burden on posterior muscles and soft and bony structures of the cervical spine. Increasing FHP (i.e., increased C2-C7 SVA) was associated with shortening of the cervical flexors and occipital extensors and lengthening of the cervical extensors and occipital flexors, which corresponds to C2-C7 flexion and C0-C2 extension. The greatest shortening occurred in the suboccipital muscles, suggesting considerable load bearing of these muscles during chronic FHP. Regardless, there was no evidence of nerve compression within the suboccipital triangle. Finally, cervical sagittal imbalance may play a role in exacerbating adjacent segment pathomechanics after multilevel cervical fusion and should be considered during surgical planning. CONCLUSIONS: The results of our biomechanical studies have improved our understanding of the impact of cervical sagittal malalignment on pathomechanics of the cervical spine. We believe this improved understanding will assist in clinical decision-making.
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