Abstract
Spinal cord infarction (SCI) is a rare vascular condition that can lead to the sudden onset of myelopathy, manifesting as paraplegia, bladder and bowel dysfunction, and/or sensory impairments. The primary arteries supplying the spinal cord are the anterior spinal artery (ASA) and the posterior spinal artery (PSA). The ASA mainly provides blood to the anterior two-thirds of the spinal cord, excluding the posterior columns, while the PSA primarily supplies the posterior one-third, which includes the posterior columns. It is relatively uncommon for vascular SCI to result in complete sensory loss, as the area supplied by the ASA is mainly associated with superficial sensation, while the PSA is related to deep sensation. In this report, we describe a case of SCI with pansensory deficits and explore the potential causes of pansensory loss in SCI. The patient was a 51-year-old healthy woman who experienced sudden lower back discomfort, progressing to bilateral lower limb weakness within 30 minutes, accompanied by urinary retention after lifting a heavy object. She was transferred to the hospital with stable vitals except for high blood pressure. A neurological examination revealed significant weakness in her lower limbs, hypesthesia below the Th10 level, bathyanesthesia, and areflexia. Spinal MRI showed hyperintensities at the Th11-Th12 levels, leading to a diagnosis of spinal cord infarction. She was treated with methylprednisolone, heparin, and rehabilitation. Over time, her muscle strength and sensory loss improved, though dysesthesia persisted. After 80 days of treatment and rehabilitation, she was able to walk independently with assistance and was discharged.