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Spinal cord infarction: Clinical presentation and diagnosis

Michael T Mullen, MD
Michael L McGarvey, MD
Section Editor
Scott E Kasner, MD
Deputy Editor
Janet L Wilterdink, MD


Spinal cord infarction is a rare but often devastating disorder caused by a wide array of pathologic states. Patients typically present with acute paraparesis or quadriparesis, depending on the level of the spinal cord involved. The diagnosis is generally made clinically, with neuroimaging to confirm the diagnosis and exclude other conditions.

This topic discusses the clinical features and diagnosis of spinal cord infarction. The vascular anatomy of the spinal cord, and the etiologies, prognosis, treatment, and chronic complications of spinal cord infarction are discussed separately. Other causes of myelopathy are also discussed separately. (See "Spinal cord infarction: Vascular anatomy and etiologies" and "Spinal cord infarction: Prognosis and treatment" and "Chronic complications of spinal cord injury and disease" and "Disorders affecting the spinal cord" and "Anatomy and localization of spinal cord disorders".)


As with cerebral infarction, the onset of spinal cord infarction is typically abrupt [1,2]. In a few cases, symptoms progress over several minutes or even a few hours. The neurologic presentation of spinal cord infarction is largely defined by the vascular territory involved. The severity of the impairments can vary widely, from paraplegia to minor weakness. The involved cord level can be anywhere along the cord's length, depending in part on the underlying etiology. Back or neck pain often accompanies spinal cord ischemia, and has been reported in as many as 70 percent of patients, typically occurring at the level of the lesion [1-8].

Anterior spinal artery syndrome — The most common clinical presentation of a spinal cord infarction is anterior spinal artery (ASA) syndrome [1,5,9]. Consistent with its functional neuroanatomy, an ASA infarct typically presents as loss of motor function and pain/temperature sensation, with relative sparing of proprioception and vibratory sense below the level of the lesion [10]. The acute stages are characterized by flaccidity and loss of deep tendon reflexes; spasticity and hyperreflexia develop over ensuing days and weeks. Autonomic dysfunction may be present and can manifest as hypotension (either orthostatic or frank hypotension), sexual dysfunction, and/or bowel and bladder dysfunction [4,11,12]. Chest pain with ECG changes has been reported in a patient with C7 to T1 spinal cord infarction [13]. In the acute evaluation of patients, it is important to recognize that hypotension may be both a cause as well as a manifestation of spinal cord ischemia. If the lesion is in the rostral cervical cord, respiration is compromised.

While bilateral presentations are more common, unilateral ASA deficits are frequently reported [1,3-5,14]. This occurs either because of occlusion of a unilateral sulcal artery, or because incomplete collateralization with the PSA maintains perfusion on one side of the cord. Very rostral ASA infarctions produce sensory loss in all modalities because of involvement of the medial lemniscus in the medulla [3].

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Literature review current through: Nov 2017. | This topic last updated: Aug 11, 2016.
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