Anterior cord syndrome is an incomplete cord syndrome that predominantly affects the anterior 2/3 of the spinal cord, characteristically resulting in motor paralysis below the level of the lesion as well as the loss of pain and temperature at and below the level of the lesion. The patient presentation typically includes these two findings; however, there is variability depending on the portion of the spinal cord affected. Other findings include back pain, or autonomic dysfunction such as hypotension, neurogenic bowel or bladder, and sexual dysfunction.[1] The severity of motor dysfunction can vary, typically resulting in paraplegia or quadriplegia. Anterior cord syndrome is caused by ischemia within the anterior spinal artery (ASA), which supplies blood to the anterior 2/3of the spinal cord. The ASA forms from the bilateral vertebral arteries at the foramen magnum. It runs as an uninterrupted artery within the anterior median sulcus of the spinal cord to the conus medullaris. Radicular arteries enter the spinal canal through the intervertebral foramen and primarily supply the nerve roots; however, some also anastomose and contribute to the ASA. The largest of these radicular arteries is the artery of Adamkiewicz, which most commonly arises off of a left intercostal artery between T9-T12 but can vary anatomically. The ASA gives off small sulcal and penetrating arteries that enter the body of the spinal cord to supply blood.[2] The anterior spinal artery supplies blood to the bilateral anterior and lateral horns of the spinal cord, as well as the bilateral spinothalamic tracts and corticospinal tracts. The anterior horns and corticospinal tracts control the somatic motor system from the neck to the feet. The lateral horns span T1-L2 of the spinal cord and house the neuronal cell bodies of the sympathetic nervous system. The spinothalamic tracts relay pain and temperature sensory information. The anterior spinal artery, with a few radicular artery contributions, is the sole source of blood supply to these areas of the spinal cord via its sulcal and penetrating arteries. Ischemia of the ASA causes symptoms consistent with the dysfunction of these tracts. Since the ASA is formed from the more cephalad vertebral arteries and runs caudally, the higher the location at which ischemia occurs, the more widespread or severe the symptoms will be. Since the lateral horns are located only between T1-L2 of the spinal cord, autonomic symptoms are not always present if ischemia does not involve this region.[1] Proprioception, vibratory sense, two-point discrimination, and fine touch are not affected in anterior cord syndrome. These sensations are under the control of the dorsal column of the spinal cord, which is supplied by two posterior spinal arteries running in the posterior lateral sulci.[3]