LATERAL MEDULLARY INFARCTS - DISTRIBUTION , ETIOLOGIES AND PROGNOSIS IN 40 CASES IDENTIFIED BY MRI

Citation
L. Milandre et al., LATERAL MEDULLARY INFARCTS - DISTRIBUTION , ETIOLOGIES AND PROGNOSIS IN 40 CASES IDENTIFIED BY MRI, Revue neurologique, 151(12), 1995, pp. 714-721
Citations number
35
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00353787
Volume
151
Issue
12
Year of publication
1995
Pages
714 - 721
Database
ISI
SICI code
0035-3787(1995)151:12<714:LMI-D,>2.0.ZU;2-N
Abstract
Recent advances in lateral medullary syndrome have focused on otoneuro -ophtalmology and magnetic resonance imaging (MRI). To reevaluate late ral medullary infarcts, 40 non fatal cases (30 men and 10 women, in an age 57.5 years) accounting for 4.5 p. 100 of overall cerebral infarct s were consecutively included in a prospective study using MRI in all cases. Thirty three patients were investigated using transfemoral or m agnetic resonance angiography Besides classical symptomatology visual disorders were usually noted: diplopia (n = 18), transient visual tilt of the surrounding (n = 4), skew deviation (= 4), esotropia (n = 2) o r conjugate gaze deviation (n = 2). The middle part of the medulla was affected in 35 cases. When associated, ipsilateral peripheral facial palsy and/or deafness were linked to tile involvement of the pontomedu llary junction (n = 3) while ipsilateral hemiparesis (Opalski's syndro me, n = 4) was inked to the involvement of the lower medulla and the c ervicomedullary junction. MRI showed an associated cerebellar infarct in 35 p. 100 of cases. Of 33 patients angiographically investigated, 2 7 (82 p. 100) had stenosis or occlusion of the ipsilateral vertebral a rtery, usually affecting the intracranial portion, when 3 had isolated posterior inferior cerebellar artery occlusion. Atherosclerosis was r ecognized as the main cause of lateral medullary infarcts (n = 25). Ot her miscellaneous etiologies were diagnosed : coagulopathy (n = 2), sp ontaneous arterial dissection (n = 2), dolichoectatic artery (n = 1), arteriolopathy (n = 1) or cardiogenic embolism (n = 1). At the term of follow-up (mean : 35 +/- 24 months), 33 patients were free of residua l handicap, 8 had experienced recurrent vertebrobasilar infarcts, incl uding 3 medullary infarcts (median ipsilateral, n = 1 or lateral contr alateral, n = 2), and 3 were died of basilar artery thrombosis complic ating extensive atherosclerosis of the intracranial vertebrobasilar sy stem.