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Neurodegeneration in the spinal ventral horn prior to motor impairment in cervical spondylotic myelopathy

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Mohammadi,  Siawoosh
Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Germany;
Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, United Kingdom;
Department Neurophysics (Weiskopf), MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Freund,  Patrick
Balgrist Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland;
Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, United Kingdom;
Department Neurophysics (Weiskopf), MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Department of Brain Repair & Rehabilitation, University College London, United Kingdom;

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Citation

Grabher, P., Mohammadi, S., David, G., & Freund, P. (2017). Neurodegeneration in the spinal ventral horn prior to motor impairment in cervical spondylotic myelopathy. Journal of Neurotrauma, 34(15), 2329-2334. doi:10.1089/neu.2017.4980.


Cite as: http://hdl.handle.net/21.11116/0000-0004-A6B2-7
Abstract
Remote gray matter pathology has been suggested rostral to the compression site in cervical spondylotic myelopathy (CSM). We therefore assessed neurodegeneration in the gray matter ventral and dorsal horns. Twenty patients with CSM and 18 healthy subjects underwent a high-resolution structural and diffusion magnetic resonance imaging protocol at vertebra C2/C3. Patients received comprehensive clinical assessments. T2*-weighted data provided cross-sectional area measurements of gray matter ventral and dorsal horns to identify atrophy. At the identical location, mean diffusivity (MD) and fractional anisotropy (FA) determined the microstructural integrity. Finally, the relationships between neurodegeneration occurring in the gray and white matter and clinical impairment were investigated. Patients suffered from mild-to-moderate CSM with mainly sensory impairment. In the ventral horns, cross-sectional area was not reduced (p = 0.863) but MD was increased (p = 0.045). The magnitude of MD changes within the ventral horn was associated with white matter diffusivity changes (MD: p = 0.013; FA: p = 0.028) within the lateral corticospinal tract. In contrast, dorsal horn cross-sectional area was reduced by 16.0% (p < 0.001) without alterations in diffusivity indices, compared with controls. No associations between the magnitude of ventral and dorsal horn neurodegeneration and clinical impairment were evident. Focal cord gray matter pathology is evident remote to the compression site in vivo in CSM patients. Microstructural changes in the ventral horns (i.e., motoneurons) related to corticospinal tract integrity in the absence of atrophy and marked motor impairment. Dorsal horn atrophy corresponded to main clinical representation of sensory impairment. Thus, neuroimaging biomarkers of cord gray matter integrity reveal focal neurodegeneration prior to marked clinical impairment and thus could serve as predictors of ensuing impairment in CSM patients.