title: Basilar artery stenosis mimicking the lacunar syndrome of pure motor hemiparesis.
abstract: BACKGROUND
  Stereotyped, repeated transient ischemic attacks manifesting as pure motor hemiparesis are most often attributed to ischemia of the internal capsule or ventral pons resulting from in situ disease of the small penetrating arteries.
  
  
  METHODS
  We report a 61-year-old man presenting with recurrent episodes of left-sided weakness consistent with the lacunar syndrome of pure motor hemiparesis. Subsequent neuroimaging revealed infarction of the right ventral pons and a critical basilar artery stenosis as the inciting lesion. Despite maximal antithrombotic therapy, he continued to have repeated symptoms. Angioplasty and stenting were attempted but both failed due to plaque recoil and technical difficulties. After the procedure, the patient had no further ischemic episodes and remained symptom-free at two months.
  
  
  CONCLUSIONS
  This case illustrates the imprecise and discordant relationship between the mode of presentation of a stroke syndrome and its presumed pathophysiology. The lacunar syndrome of pure motor hemiparesis should be recognized by clinicians as a mode of stroke presentation due not only to small vessel disease, but also to large artery atherosclerotic disease such as basilar artery stenosis. Prompt institution of treatment can lead to a good clinical outcome.
authors.affiliation: Division of Neurology, Department of Medicine, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada.
authors.forename: David K
authors.initials: DK
authors.lastname: Chan
authors.forename: Frank L
authors.initials: FL
authors.lastname: Silver
mesh_terms: D000800:Angioplasty, Balloon; D001488:Basilar Artery / Q000473:pathology* / Q000503:physiopathology; D020520:Brain Infarction / Q000473:pathology / Q000503:physiopathology*; D020526:Brain Stem Infarctions / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002533:Cerebral Angiography; D002941:Circle of Willis / Q000473:pathology / Q000503:physiopathology; D003937:Diagnosis, Differential; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D020772:Internal Capsule / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009778:Occipital Lobe / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D010291:Paresis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D011149:Pons / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D011712:Pyramidal Tracts / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D015607:Stents; D016896:Treatment Outcome; D014715:Vertebrobasilar Insufficiency / Q000473:pathology* / Q000503:physiopathology*
chemical_list: D005343:Fibrinolytic Agents