Medial medullary syndromes

Introduction
Article section 1 of 5.  Next

By Douglas J Lanska MD MS MSPH

The medial medulla is supplied from the anterior spinal artery and penetrating branches of the vertebral arteries. Classically, the so-called Déjèrine syndrome is associated with medial medullary infarcts that cause hemisensorimotor stroke crossed or alternating paralysis of the ipsilateral tongue (hypoglossal nerve nucleus or fascicle) and the contralateral body (medullary pyramidal tract rostral to the decussation), sparing the face, with associated posterior column sensory loss on the contralateral body (medial lemniscus).

Vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the predominant vascular pathologies (Vuilleumier et al 1995; Toyoda et al 1996; Kumral et al 2002). The syndrome has been reported with occlusion of the anterior spinal artery (including 1 case of fibrocartilaginous embolism to the anterior spinal artery) (Kase et al 1983), occlusion of penetrating branches of vertebral or basilar arteries (including as a result of meningovascular syphilis) (Roh and Lee 1996; Bassetti et al 1997; Ikeda et al 1998), occlusion of the vertebral artery (Kim et al 1995), vertebral artery stenosis and presumed artery-to-artery emboli (Nakajima et al 2005), dolicoectatic vertebrobasilar arteries (Kumral et al 2002), vertebral artery dissection (Toyoda et al 1996; Leppert and Radue 2001; Yokota et al 2003; Kameda et al 2004; Kinoshita et al 2007) (with 1 case of vertebral artery dissection causing medial medullary infarction due to chiropractic neck manipulation) (Yokota et al 2003), and rare cases of cardiac embolism (Veilleumeier et al 1995; Kumral et al 2002) and paradoxical embolism (eg, with talc emboli in an intravenous drug user, and in a weight lifter with a patent foramen ovale) (Mizutani et al 1980; Sweeney and Rossor 1996).

The advent of modern MRI has considerably broadened the clinical spectrum of medial medullary infarcts, and at the same time raised recognition that a significant proportion of cases of medial medullary infarction have incomplete presentations, at least according to the classic conception of the disorder (Kim et al 1995; Roh and Lee 1996; Toyoda et al 1996; Wada et al 1996; Arai and Shichi 1999; Kumral et al 2002). In reality, the "typical" crossed or alternating paralysis of the ipsilateral tongue and the contralateral body is rare among all patients with medial medullary syndrome (Kim et al 1995; Roh and Lee 1996). Previous expectations of a poor prognosis have also improved as a group with recognition of milder cases with small nonembolic lesions (Kim et al 1995; Roh and Lee 1996; Toyoda et al 1996; Arai and Shichi 1999; Kumral et al 2002).