A 49-year-old male presented with 8 years of progressive myelopathy; he had acutely deteriorated over the prior month. On examination, he exhibited a significant left hemiparesis accompanied by marked hyperreflexia (i.e. left-sided Hoffman’s and Babinski response). The cervical CT and MR scan both documented OPLL extending from C2-C3 to C7-T1 resulting in significant cervical canal stenosis/ cord compression []. He underwent a C3-C7 laminectomy with C2-T1 lateral mass/pedicle screw fusion. Unfortunately, this was performed without intraoperative neural monitoring (IONM) (i.e. no somatosensory evoked potentials, motor evoked potentials, or electromyography). Without IONM, the patient likely sustained a traumatic but unrecognized intraoperative iatrogenic cord injury. On postoperative day 1, his strength was 4/5 in the upper, and 5/5 in the lower extremities, and his spasticity had decreased. However, on postoperative day 3, he became acutely quadriparetic (i.e. 2/5 in the left and 3/5 in the right upper extremity, with 4/5 motor function in both lower extremities without an accompanying sensory deficit). The postoperative MRI documented adequate cord decompression, but new intramedullary cord edema on the T2-weighted image opposite the C3, C6, and C7 levels []. Notably, these abnormal high intrinsic cord signals were all located directly opposite foci of maximal preoperative OPLL-related cord compression. Therefore, the patient most likely sustained an iatrogenic traumatic cord injury and the deficit was not attributable to the WCS. Once the deficit appeared, the patient was started on high-dose intravenous steroids (Methylprednisolone). NO further surgery was performed (i.e. no surgical lesion was identified on the postoperative MR). The patient regained his preoperative neurological baseline within 7 postoperative days.