Spinal Cord Vascular Disease

Intrinsic Spinal Cord Arterial Supply

The main blood supply to spinal gray matter, as well as to anterior and lateral funiculi, is derived from the anterior sulcal arteries. These arise from the ASA in the midline and course into the ventral median fissure. Each anterior sulcal artery distributes blood to only the left or right half of the spinal cord. The greatest distance between sulcal arteries is in the thoracic segments; the vascularity is proportional to the number of neurons located throughout the cord at that level. The dorsal columns and extreme dorsal horns (approximately the posterior one-third of the cord cross-section) are supplied by penetrating branches from the posterior spinal arteries. The superficial white matter also receives blood flow via the circumflex anastomotic vessels. This arrangement leads to a clinically relevant border zone between the territories of the sulcal and superficial arterial distributions. As a result, many spinal cord infarctions do not follow the conventional boundaries between anterior and posterior arterial distributions.

Venous Drainage

The venous system of the spinal cord parallels the arterial supply. A group of radial veins flows outward to the surface of the cord, ending in a coronal plexus. Deep parenchymal veins empty into central sulcal veins in the median fissure. However, unlike the arteries, each parenchymal vein drains both the right and left sides of the cord. There are few venous anastomoses within the substance of the cord, but sulcal veins often have intersegmental anastomoses. The anterior median spinal vein, which lies external to its corresponding artery, is filled from the sulcal veins. As with the other spinal veins, the median spinal vein is more irregular than the corresponding artery and may be doubled at some levels. Extramedullary venous channels are also prominent along the dorsal cord, and the dominant vessel is usually the posterior median spinal vein. Eight to 12 major anterior radiculomedullary veins arise from the anterior median spinal vein. They are joined by anterolateral anastomoses from the coronal venous plexus at the nerve roots before passing through the dura. There is typically a large vein that drains the levels of the lumbar enlargement (vena radicularis magna). Posterior radicular veins are present throughout but are particularly prominent in the cervical region.

Venous blood from the entire cord runs into the epidural and paravertebral venous plexuses, forming a large valveless system from sacrum to occiput, known as the vertebral venous plexus or Batson plexus . The absence of valves to resist retrograde flow in this continuous venous network may be a factor in the pathogenesis of some spinal cord vascular disease.

Presentation and Initial Course

Similar to cerebral infarction, most patients present with sudden onset of neurological dysfunction that evolves over minutes to hours. In rare cases of spontaneous spinal cord infarction, transient symptoms referred to as “spinal transient ischemic attacks” have been reported. Symptoms depend on the vascular territory involved, with the ASA territory being most often affected. The ASA syndrome is characterized by loss of strength and pain/temperature sensation, with sparing of vibration/proprioception below the level of the infarction. This syndrome is most often bilateral but may be unilateral or incomplete, depending on the degree of collateral vessels. Autonomic dysfunction including hypotension, bowel/bladder dysfunction, or sexual dysfunction may also occur. The posterior spinal artery (PSA) syndrome is less common and typically presents with isolated loss of vibration and proprioception below the level of the lesion.

Weakness (89%–100%), sensory loss (89%–95%), back pain at onset (72%–82%), and urinary complaints requiring catheterization (75%) are the most common presenting symptoms of cord ischemia in multiple series ( ; ; ). Hyperacute onset is the clue to the diagnosis, with most patients reaching a nadir of their symptoms within 12 hours. The most common location to be affected is the mid-to-low thoracic spine. Lower cervical lesions are less common and upper thoracic spinal infarcts are rare. Cervical lesions may cause respiratory failure and quadriparesis. Pain and sensory changes occur first in most cases, followed by weakness within minutes or hours. More than 80% of back pain with spinal infarction follows a radicular pattern, but in cases of acute aortic disease, pain may have a more visceral character. Back pain typically occurs at the level of the infarction, which may assist with localization. Urinary retention is typical in the acute phase, but involuntary voiding or defecation may be associated with the onset of the ischemic insult.

The dominant clinical presentation depends on the vascular territory involved. ASA distribution infarction typically presents with weakness (ventral gray matter involvement), loss of pain and temperature sensation (spinothalamic tract involvement), and areflexia with bladder and bowel dysfunction. Asymmetry of these symptoms is not uncommon. Posterior spinal infarctions result in loss of proprioception and vibration sense, paresis, and sphincter dysfunction. Acute severe hypotension and aortic surgery can present as bilateral sensory symptoms with preserved motor function (central infarction) or focal combined motor and sensory symptoms (complete transverse infarction).

Examination Findings

Weakness most commonly affects both lower limbs. Examination typically reveals flaccid paresis acutely accompanied by diminished superficial and tendon reflexes below the level of the lesion. Preservation of strength and reflexes suggests PSA territory infarction. Upper motor neuron signs, including spasticity and hyperreflexia, may develop in the subsequent weeks. Sensory changes, when present, nearly always affect spinothalamic modalities. Isolated proprioceptive loss is rare. Hypotension may be present, suggesting autonomic involvement, and respiratory function may be compromised with cervical cord lesions.