Clinical Manifestations of Vertebrobasilar Territory Ischemia

Medial Medullary Infarction

This third syndrome is much less common. The anterior spinal artery supplying the medial medulla arises from the distal intracranial vertebral artery. The medial medullary syndrome is characterized by a hemiparesis that affects the contralateral arm and leg attributable to ischemia of the medullary pyramid, and ipsilateral weakness of the tongue and contralateral loss of position sense explained by involvement of the hypoglossal nerve and the medial lemniscus. In some patients with intracranial vertebral artery occlusion, ischemia of the medial medulla accompanies lateral medullary infarction, forming a hemimedullary syndrome. This occurs when an intracranial vertebral artery occlusion is extensive and both the lateral medullary penetrators and the anterior spinal artery branches are concomitantly involved. Rarely, medial medullary infarction is bilateral and can extend caudally into the rostral spinal cord, causing a syndrome of quadriparesis difficult to separate from basilar artery occlusion with pontine infarction.

PROXIMAL AND MIDBASILAR ARTERY OCCLUSION

The basilar artery forms after merging of the two intracranial vertebral arteries at the medullo-pontine junction. The basilar artery ends at the junction of the pons and midbrain. The major territory of supply of the basilar artery is the pons, especially the basis pontis. The tegmentum of the pons has a rich collateral supply of blood vessels. The superior cerebellar arteries at the distal end of the basilar artery provide much supply to the pontine and midbrain tegmentum. Occlusion of the basilar artery often causes ischemia in the pontine base bilaterally, sometimes extending into the medial tegmentum on one or both sides. The most important neurologic signs and symptoms that accompany basilar artery occlusion are:

1. Limb paralysis. Limb paralysis is usually bilateral but often asymmetric; stiffness, hyperreflexia, and extensor plantar reflexes are found when examining the weak limbs. Some patients present with a hemiparesis, but examination shows weakness and reflex changes in the contralateral limbs.

2. Bulbar or pseudobulbar paralysis. Infarction may affect cranial motor nuclei, causing paralysis of the face, palate, pharynx, neck, or tongue on one or both sides. The 9th- to 12th-nerve nuclei are located within the medullary tegmentum, which is usually below the level of infarction. Weakness of the cranial musculature innervated by these nuclei causes dysarthria, dysphonia, hoarseness, dysphagia, and tongue weakness. The pontine lesion interrupts corticofugal descending fibers destined for these cranial nerve nuclei. The resulting weakness is referred to as pseudobulbar because it involves the descending pathways controlling the bulbar nuclei rather than the nuclei themselves. Exaggerated jaw and facial reflexes, increased gag reflex, and easily induced emotional incontinence with excessive laughing and/or crying are found. The limb and bulbar paralysis may be so severe that the patient cannot communicate verbally or by gesture. Such patients have been referred to as having the locked-in syndrome because of their loss of motor function.

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