Sequential changes of ascending myelopathy after spinal cord injury on magnetic resonance imaging: a case report of neurologic deterioration from paraplegia to tetraplegia

Abstract

Background contextMarked neurologic deterioration within a few days of traumatic spinal cord injury, known as subacute posttraumatic ascending myelopathy, is rare. Although several hypotheses regarding the pathogenesis of this condition have been proposed, the details remain elusive. PurposeTo report a case of ascending myelopathy in which a series of magnetic resonance images (MRIs) taken through the course of the illness helped follow the course of the disease and discuss possible pathogenesis. Study designCase report and review of the literature. Patient sampleA 75-year-old woman involved in a motor vehicle collision sustained a fracture dislocation of T7–T8 with complete paraplegia below T8. MethodsNeurologic examination and radiologic imaging taken by various means. ResultsPosterior surgical stabilization was performed 18 hours after the injury. Both the surgical and postsurgical courses were uneventful. Four days after the injury, however, the patient reported feeling a tingling sensation in the right-hand fingers and gradually suffered from motor weakness of the upper extremities, deteriorating within a few hours to complete tetraplegia and ventilator dependence. Subsequent cervicothoracic MRI showed abrupt cord swelling with abnormal areas of signal intensity in the cervical and upper thoracic spinal cord during the interval between the onset of tingling and the development of motor paralysis in the arms. On the 20th postsurgical day, an area of hypointensity within the region of high intensity was observed on T2-weighted MRIs, indicating intramedullary spinal cord hemorrhage. ConclusionsOur MRI findings suggest that systemically increased intraspinal pressure resulting from the impairment of spinal venous drainage is involved in the pathogenesis of ascending myelopathy. Although ascending myelopathy is often thought to be partly reversible, persisting increase of the intraspinal pressure may result in intramedullary hemorrhage and irreversible neurologic deficit.