STUDY DESIGN: Three case reports. OBJECTIVE: To elucidate the pathophysiology of cervical spondylotic amyotrophy. SUMMARY OF BACKGROUND DATA: Cervical spondylotic amyotrophy is the clinical syndrome in cervical spondylosis characterized by severe muscular atrophy in the upper extremities, with an absent or insignificant sensory deficit. Pathophysiology of this particular syndrome has not been well understood. METHODS: Three cases of cervical spondylotic amyotrophy are presented in which magnetic resonance imaging confirmed the intrinsic cord disease as the cause of the syndrome. RESULTS: The patients had segmental muscular atrophy of the proximal upper extremities, with an absent or insignificant sensory deficit. After initial disease progression, the symptoms stabilized for years. Sagittal T2-weighted magnetic resonance images showed multi-segmental linear high-signal intensity within the compressed spinal cord. These high-signal intensity lesions appeared to be located at the anterior horns on axial images. The spinal cord compression was less severe in the neck-neutral position, but spinal canal stenosis increased when the neck was extended. CONCLUSIONS: The results suggest that one pathophysiology of this syndrome may be multisegmental damage to the anterior horns caused by dynamic cord compression, possibly through circulatory insufficiency.
STUDY DESIGN: Three case reports. OBJECTIVE: To elucidate the pathophysiology of cervical spondylotic amyotrophy. SUMMARY OF BACKGROUND DATA: Cervical spondylotic amyotrophy is the clinical syndrome in cervical spondylosis characterized by severe muscular atrophy in the upper extremities, with an absent or insignificant sensory deficit. Pathophysiology of this particular syndrome has not been well understood. METHODS: Three cases of cervical spondylotic amyotrophy are presented in which magnetic resonance imaging confirmed the intrinsic cord disease as the cause of the syndrome. RESULTS: The patients had segmental muscular atrophy of the proximal upper extremities, with an absent or insignificant sensory deficit. After initial disease progression, the symptoms stabilized for years. Sagittal T2-weighted magnetic resonance images showed multi-segmental linear high-signal intensity within the compressed spinal cord. These high-signal intensity lesions appeared to be located at the anterior horns on axial images. The spinal cord compression was less severe in the neck-neutral position, but spinal canal stenosis increased when the neck was extended. CONCLUSIONS: The results suggest that one pathophysiology of this syndrome may be multisegmental damage to the anterior horns caused by dynamic cord compression, possibly through circulatory insufficiency.