Introduction
The diagnosis of spinal cord infarction (SCI) has changed significantly in the past decade, largely due to the contributions of neuroimaging. Historically SCI was considered to be rare, with the definitive diagnosis requiring postmortem examination and probable diagnosis requiring the appropriate clinical context (usually aortic dissection or surgery) and exclusion of other possibilities. With the advent of spinal cord diffusion-weighted imaging (DWI), however, improved diagnosis has resulted in the expansion of research into the underlying etiologies, natural history, and prognosis. SCI is now defined by the American Heart Association as “spinal cord cell death attributable to ischemia, based on pathological, imaging, or other objective evidence of spinal cord focal ischemic injury in a defined vascular distribution.” Although aortic surgery and dissection are still considered important risk factors, SCI is now known to result from numerous entities, including atherosclerosis and embolism, systemic hypotension, vascular malformations, coagulopathies, cocaine, sickle cell disease, diving, and idiopathic causes. The evolving diagnosis of SCI is explored here, with a review of the spinal cord vascular anatomy, clinical findings, imaging, natural history, and diagnostic mimics.
Evolution: Overview
The current understanding of SCI is based on knowledge of spinal cord vascular anatomy, which directly affects the clinical presentation.
Vascular Anatomy
The spinal cord is principally supplied by a single anterior spinal artery (ASA) and paired posterior spinal arteries (PSAs), which, together with contributing branches, form an extensive vascular network that anastomoses at the level of the conus medullaris. The ASA originates from the distal V4 segment of the vertebral artery, lies on the central anterior aspect of the spinal cord, enters the anterior median fissure as the central sulcal artery, and supplies the anterior two-thirds of the spinal cord. The paired PSAs can arise from distal vertebral arteries or posterior inferior cerebellar arteries; they lie along the posterolateral aspects of the spinal cord, sending small penetrating branches to supply the posterior third of the cord. Anastomoses between the ASA and PSA, called arterial vasocorona, supply the peripheral lateral aspect of the spinal cord.
As they progress distally, the small-caliber ASA and PSA receive collateral supply from the radicular arteries, which enter the spinal canal along with the nerve roots, dividing into anterior and posterior branches and forming an extensive pial network. Each radiculomedullary (RM) artery supplies a separate functional region of the spinal arteries, particularly the ASA ( Fig. 31.1 ). The first region extends from C1 until T3; it is supplied at the C3 level from the vertebral arteries and at the C6 to C7 level from the ascending cervical arteries. The second region extends from T3 until T7 and sometimes receives a branch from the intercostal artery at the T7 level. The third region, which extends from T8 to the conus, is supplied by the largest RM artery, the artery of Adamkiewicz (AKA), which arises from an intercostal artery, most frequently between T9 and T12 and between T8 and L2 in 75% of the population (see Fig. 31.1 ). Variably, there may be additional vascular supply to the conus medullaris originating from the internal iliac artery (Desproges-Gotteron artery) at the L2 or L5 level. In the event of arterial supply being interrupted from the aorta, collateral arterial flow can come from the internal thoracic and lateral thoracic arteries, which anastomose with the posterior intercostal arteries.
The venous system’s drainage largely follows the arterial supply ( Fig. 31.2 ). The anterior median spinal vein runs with the ASA. One posterior median vein, the greatest spinal vein, is accompanied by two posterior lateral spinal veins. Spinal veins drain into the anterior and posterior RM veins, which in turn drain into the paravertebral and intervertebral plexuses, eventually draining into the ascending lumbar veins, azygos system, and pelvic venous plexuses.
Clinical Syndromes
SCI is often abrupt and painful, likely because the radicular arteries also supply the ipsilateral hemivertebra, meninges, and paraspinal musculature. Other than pain, the neurologic manifestations of SCI are specific to the vascular territory involved.
Of the spinal cord vascular territories, SCI related to the ASA (the anterior spinal cord syndrome) is most common. The anterior two thirds of the spinal cord supplied by the ASA contains the anterior gray matter horns as well as the ventral and lateral corticospinal and spinothalamic white matter tracts. As a result, ASA syndrome presents clinically as bilateral loss of motor function as well as loss of pain and temperature sensation at and below the affected level. The acute stages are characterized by flaccidity and loss of deep tendon reflexes; spasticity and hyperreflexia develop during ensuing days and weeks. Autonomic dysfunction may be present and can manifest as hypotension, sexual dysfunction, and/or bowel and bladder dysfunction.
SCI related to the PSAs involves the posterior third of the spinal cord, either unilaterally or bilaterally. The associated PSA syndrome results from infarction of the dorsal horn gray matter as well as the dorsal column and lateral corticospinal/spinothalamic white matter tracts. Clinically this results in ipsilateral loss of fine touch and vibratory sensation below the affected level. Weakness and segmental reflex loss are also seen.
Ischemia to the watershed vascular territories is usually the sequela of prolonged hypotension, and results in central cord syndrome, with bilateral spinothalamic dysfunction and relative sparing of motor function.
Unilateral ASA infarction can occur secondary to an insult of the central sulcal artery ( Fig. 31.3 ) and clinically manifests as a Brown-Sequard syndrome with hemiparesis and contralateral spinothalamic sensory deficit. A summary of the clinical features and anatomic distributions of spinal cord stroke syndromes is included in Table 31.1 .
| Artery | Clinical Syndrome |
|---|---|
| Anterior spinal artery | Bilateral motor deficit with spinothalamic sensory deficit |
| Unilateral anterior spinal artery | Hemiparesis with contralateral spinothalamic sensory deficit |
| Transverse infarct | Bilateral motor deficit with complete sensory deficit |
| Central infarct | Bilateral spinothalamic sensory deficit without motor deficit |
| Posterior spinal artery | Unilateral or bilateral motor deficit with lemniscal sensory deficit |
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