LAUSR

Introduction The true pathogenesis of cervical spondylotic amyotrophy (CSA) remains controversial. One of the current hypotheses for the etiology of CSA mainly involves selective compression of the ventral nerve roots and/or anterior horn cells by a bony spur or herniated disc. Some scholars have proposed that CSA may be ascribed to ischemia of anterior horn cells caused by compressive injury of anterior spinal artery. Recently published studies demonstrated that chronic incomplete cervical cord compression can cause the loss of motor neurons in the spinal anterior horn caudal to the level of the compressive injury, which was described as trans-synaptic damage. Although CSA was previously considered a neurological disease involving only lower motor neurons (LMNs), some authors revealed that approximately 28.6–66.7% of distal-type CSA patients had significant lower limb hyperreflexia, which is consistent with upper motor neuron (UMN) lesions. Therefore, trans-synaptic damage may be involved in the pathogenesis of distal-type CSA. The present study has been undertaken to evaluate central motor conduction in distal-type CSA patients and to analyze the role of trans-synaptic damage in the pathogenesis of distal-type CSA. Methods Central motor conduction time (CMCT) to both upper and lower limbs was measured in 28 distal-type CSA patients and 21 controls, and all subjects underwent further motor unit number estimation (MUNE), handgrip strength examination (HGS) and magnetic resonance imaging evaluation. Results Prolonged CMCT was recorded in 9/28 (32.1%) CSA patients, and both lower MUNE values and smaller HGS were observed in these 9 cases (P  Conclusion Distal-type CSA patients may have substantial corticospinal tract lesions, and trans-synaptic damage caused by these lesions may be involved in the pathogenesis of distal-type CSA. Therefore, clinicians should be cautious when evaluating and managing distal-type CSA patients, especially the cases with additional proximal cervical compression, because severe muscular atrophy may be caused by both trans-synaptic damage and selective compression.