Evaluation of a Patient With Spinal Cord Infarction After a Hypotensive Episode

Abstract

A 72-year-old man with past medical history significant for peripheral vascular disease, bilateral carotid stenosis, hypertension, dyslipidemia, and heavy tobacco use developed sudden severe chest pain and received sublingual nitroglycerin with pain resolution. The patient was able to walk to the ambulance, but on arrival in the emergency room had a systolic blood pressure of 60 mm Hg, which was thought to be secondary to nitroglycerin. He was given intravenous fluids. A few hours later, he complained of being unable to move his legs and was found to be paraplegic with urinary retention and a T4 sensory level to pain and temperature with preserved light touch, vibration, and joint position sense. Additional intravenous fluids resulted in minimal improvement. Emergent MRI of the spine was nondiagnostic, but a follow-up MRI the next day showed abnormal signal intensity within the anterior gray matter on T2-weighted images from the T2 through T5 level, with corresponding signal on diffusion weighted imaging. A computed tomography of the chest showed no aortic dissection. Cardiac telemetry and echocardiogram were unremarkable. A fasting low density lipoprotein was 120. He was treated with intravenous fluids, aspirin 81 daily, an increased statin dose, and eventually discharged to an acute rehabilitation facility. Six month later, his lower extremity strength had improved. He was able to walk 45 feet with a wheeled walker and required intermittent urinary catheterization. DiscussionAcute spinal cord infarction (SCI) is uncommon, accounting for 1.2% of stroke admissions and 5% to 8% of acute myelopathies.1 The vast majority of spinal infarcts involve the anterior spinal artery (ASA) and have distinct clinical features because of sparing of the posterior columns. These patients have preserved posterior column function despite loss of pain and temperature with bilateral lower extremity weakness. Recognizing spinal cord ischemia early is critical so that the processes causing ischemia can be addressed to limit SCI. Vascular Anatomy of the Spinal CordTo understand the mechanisms of spinal cord ischemia, one must first understand the vascular supply of the cord, which leaves the thoracic cord particularly vulnerable to ischemia (Figure). There is a single ASA and 2 or 4 posterior spinal arteries (PSAs). The ASA is derived from branches of the vertebral arteries arising at the level of the foramen magnum. Segmental vessels at the level of each spinal nerve roots divide into anterior and posterior radicular arteries. At variable levels these course medially and anastomose with either the ASA or the PSAs. During development the majority of anterior radicular arteries regress leaving only 4 to 8 arteries to feed into the ASA. Fewer anastomoses make this territory more susceptible to ischemia. In the cervical cord the anterior radicular arteries are branches of the vertebral and ascending cervical arteries. In the rostral thoracic cord they are branches of the deep and ascending cervical arteries. In the middle and lower thorac...

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Spinal Cord Infarction Following Total Hysterectomy Due to Severe Postpartum Hemorrhage

“…Rao Shailaja et al 8 dalities. 3,6,7 The patient in this case was close to the transverse infarction.…”

“…2 Patients typi cally present with acute back or neck pain at the onset of symptoms, and areflexic flaccid paraplegia or tetraplegia with loss of bowel and bladder continence. 3 The research reports a 34yearold woman developed spinal cord infarction after total hysterectomy, due to severe postpartum hemorrhage.…”

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“…The classic symptoms of SCI when the anterior spinal artery is involved are sudden ridiculer pain at the level involved, motor weakness, loss of sphincter control, spinothalamic deficits with sparing of dorsal column related vibration and Proprioception [12]. A retrospective review of 27 patients with confirmed spinal cord ischemia revealed that the majority of patients had anterior spinal artery syndrome with only a minority having transverse infarcts that caused a more severe central cord syndrome [13]. Symptom onset was usually acute (minutes to hours) with some reporting TIA symptoms in the preceding years.…”