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Basilar Artery Stenosis Mimicking the Lacunar Syndrome of Pure Motor Hemiparesis

Published online by Cambridge University Press:  16 December 2016

David K. Chan
Affiliation:
Division of Neurology, Department of Medicine, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada
Frank L. Silver*
Affiliation:
Division of Neurology, Department of Medicine, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada
*
University Health Network Stroke Program, Toronto Western Hospital, 5 W, 399 Bathurst Street, Toronto, Ontario, Canada M5T 2S8
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Abstract:

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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.

Case description:

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.

Résumé:

RÉSUMÉ:Contexte:

Des accès ischémiques transitoires cérébraux répétés et stéréotypés sous forme d'hémiparésie motrice pure sont le plus souvent attribués à une ischémie de la capsule interne ou du pont antérieur résultant d'une maladie in situ des petites artères perforantes.

Description de cas:

Nous rapportons le cas d'un homme de 61 ans qui a consulté pour des épisodes récurrents de faiblesse du côté gauche compatible avec un syndrome lacunaire d'hémiparésie motrice pure. La neuroimagerie a montré un infarctus de la portion ventrale droite du pont et une sténose critique de l'artère basilaire. Malgré une thérapie antithrombotique maximale, il a continué à présenter des symptômes. On a tenté une angioplastie et la mise en place d'une endoprothèse, mais sans succès à cause de la rétraction d'une plaque athéromateuse et de difficultés techniques. Après l'intervention, le patient n'a pas présenté d'autre épisode ischémique et il est toujours asymptomatique deux mois plus tard.

Conclusions:

Ce cas illustre une relation imprécise et discordante entre le mode de présentation d'un syndrome d'accident vasculaire cérébral et sa physiopathologie présumée. Le syndrome lacunaire d'hémiparésie motrice pure devrait être reconnu par les cliniciens comme le mode de présentation d'un accident vasculaire cérébral dû non seulement à une maladie des petits vaisseaux, mais également à la maladie athéromateuse de grosses artères telle la sténose de l'artère basilaire. Un traitement rapide peut donner de bons résultats cliniques.

Type
Case Report
Copyright
Copyright © The Canadian Journal of Neurological 2003

References

REFERENCES

1. Caplan, LR. Posterior Circulation Disease: Clinical Findings, Diagnosis, and Management. Blackwell Science. 1996;340.Google Scholar
2. Fisher, CM. The ‘herald hemiparesis’ of basilar artery occlusion. Arch Neurol 1988;45:13011303.Google Scholar
3. Donnan, GA, O’Malley, HM, Quang, L, Hurley, S, Bladin, PF. The capsular warning syndrome: pathogenesis and clinical features. Neurology 1993;43:957962.CrossRefGoogle ScholarPubMed
4. Farrar, J, Donnan, GA. Capsular warning syndrome preceding pontine infarction (Letter). Stroke 1993;24:762.Google Scholar
5. Bamford, JM, Warlow, CP. Evolution and testing of the lacunar hypothesis. Stroke 1988;19:10741082.CrossRefGoogle ScholarPubMed
6. Boiten, J, Lodder, J. Lacunar infarcts: pathogenesis and validity of the clinical syndromes. Stroke 1991;22:13741378.CrossRefGoogle ScholarPubMed
7. Lodder, J, Bamford, J, Kappelle, J, Boiten, J. What causes false clinical prediction of small deep infarcts? Stroke 1994;25:8691.CrossRefGoogle ScholarPubMed
8. Gan, R, Sacco, RL, Kargman, DE, et al. Testing the validity of the lacunar hypothesis: the Northern Manhattan Stroke Study experience. Neurology 1997;48:12041211.Google Scholar
9. Toni, D, Del Duca, R, Fiorelli, M, et al. Pure motor hemiparesis and sensorimotor stroke: accuracy of very early clinical diagnosis of lacunar strokes. Stroke 1994;25:9296.CrossRefGoogle ScholarPubMed
10. Millikan, C, Futrell, N. The fallacy of the lacune hypothesis. Stroke 1990;21:12511257.Google Scholar
11. Fisher, CM. Capsular infarcts: the underlying vascular lesions. Arch Neurol 1979;36:6573.Google Scholar
12. Fisher, CM. Occlusion of the internal carotid artery. Arch Neurol 1951;65:346377.Google Scholar
13. Alazzaz, A, Thornton, J, Aletich, VA, et al. Intracranial percutaneous transluminal angioplasty for arteriosclerotic stenosis. Arch Neurol 2000;57:16251630.Google Scholar
14. Joseph, GJ, Goldstein, J, Cloft, H, Tong, F, Dion, J. Endovascular stenting of atherosclerotic stenosis in a basilar artery after unsuccessful angioplasty. AJR Am J Roentgenol 2000;174:383385.Google Scholar
15. Wafarin-Aspirin Symptomatic Intracranial Disease (WASID) study group. Prognosis of patients with symptomatic vertebral or basilar artery stenosis. Stroke 1998;29:13891392.Google Scholar