Brain, Vol. 116, No. 1, 161-186, 1993
© 1993 Oxford University Press
research-article |
Very small (border zone) cerebellar infarcts
Distribution, causes, mechanisms and clinical features
1Service de Neurologie, Hôpital Saint-Antoine, Université Pierre et Marie Curie Paris, France 2Department of Neurology, Boston University Medical Center, Boston University School of Medicine Boston, USA 3Department of Neurology, New England Medical Center, Tufts University School of Medicine Boston, USA
Correspondence to:
Correspondence to: Dr P. Amarenco, Service de Neurologie, Hôpital Saint-Antoine, 184 rue du faubourg Saint-Antoine, 75571 Paris Cédex 12, France.
Computerized tomography (CT) and magnetic resonance imaging (MRI) allow accurate anatomical localization of large thromboembolic cerebellar infarcts in the territories of the cerebellar arteries and their branches. In addition, MRI and CT show very small cerebellar infarcts as discrete foci of signal change that are not easily localizable within well-defined arterial territories. They could be border zone infarcts. Their anatomy, mechanism and clinical features have not been studied. By reviewing our CT and MRI files over a 2-year period, we found 47 patients with very small cerebellar infarcts; 23 patients had angiography. Infarcts were cortical (32 patients), deep (10 patients) and both (five patients). Most lesions corresponded to border zone cerebellar infarcts. The mechanisms of infarction were (i) global hypoperfusion due to cardiac arrest (two patients); (ii) small or end (pial) artery disease due to intracranial atheroma or hypercoagulable states (nine patients); (iii) focal cerebellar hypoperfusion due to large artery (vertebral or basilar) occlusive disease (16 patients) or brain embolism (11 patients) resulting in infarcts in the watershed areas (27 patients total); (iv) unknown mechanism (nine patients, 19%). Large artery occlusive disease was more frequently observed in deep than in cortical infarcts (9 out of 15 versus 11 out of 37; P < 0.0001). The most frequent symptoms were dizziness, lightheadedness, unsteadiness with axial lateropulsion, dysarthria and limb clumsiness. These symptoms were either transient or recurrent, at times related to positional changes of the head or trunk. Position-related symptoms often persisted for weeks or months after the ischaemic event, and occurred mainly in patients with combined carotid and verte brobasilar occlusive disease. Physical findings were either absent or included wide-based gait, lateropulsion, mild ipsilateral dysmetria, dysarthria or dysdiadochokinesia. We conclude that very small cerebellar infarcts are often found on CT and MRI. Their border zone distribution and frequent posturally related symptoms most often result from large or pial artery disease rather than from systemic hypotension.
Received April 13, 1992. Revised May 29, 1992. Accepted July 5, 1992.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J M Hong, C-S Chung, O Y Bang, S W Yong, I S Joo, and K Huh Vertebral artery dominance contributes to basilar artery curvature and peri-vertebrobasilar junctional infarcts J. Neurol. Neurosurg. Psychiatry, October 1, 2009; 80(10): 1087 - 1092. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B M Seemungal and A M Bronstein A practical approach to acute vertigo Practical Neurology, August 1, 2008; 8(4): 211 - 221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. C. Kruit, L. J. Launer, M. D. Ferrari, and M. A. van Buchem Infarcts in the posterior circulation territory in migraine. The population-based MRI CAMERA study Brain, September 1, 2005; 128(9): 2068 - 2077. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Koch, M. Amir, A. A. Rabinstein, Y. Reyes-Iglesias, J. G. Romano, and A. Forteza Diffusion-Weighted Magnetic Resonance Imaging in Symptomatic Vertebrobasilar Atherosclerosis and Dissection Arch Neurol, August 1, 2005; 62(8): 1228 - 1231. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. S. Hayreh Posterior Ciliary Artery Circulation in Health and Disease The Weisenfeld Lecture Invest. Ophthalmol. Vis. Sci., March 1, 2004; 45(3): 749 - 757. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Soeda, N. Sakai, K. Murao, H. Sakai, K. Ihara, N. Yamada, S. Imakita, and I. Nagata Thromboembolic Events Associated with Guglielmi Detachable Coil Embolization with Use of Diffusion-Weighted MR Imaging. Part II. Detection of the Microemboli Proximal to Cerebral Aneurysm AJNR Am. J. Neuroradiol., November 1, 2003; 24(10): 2035 - 2038. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. H. Wong, P. M. Pullicino, and R. Benedict Deep Cerebral Infarcts Extending to the Subinsular Region Stroke, October 1, 2001; 32(10): 2272 - 2277. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Akiyama, S. Takizawa, K. Tokuoka, Y. Ohnuki, N. Kobayashi, and Y. Shinohara Bilateral middle cerebellar peduncle infarction caused by traumatic vertebral artery dissection Neurology, March 13, 2001; 56(5): 693 - 693. [Full Text] [PDF]
|
|
|
|
|
|
W. K. Min, Y. S. Kim, J. Y. Kim, S. P. Park, and C. K. Suh Atherothrombotic Cerebellar Infarction : Vascular Lesion-MRI Correlation of 31 Cases Stroke, November 1, 1999; 30(11): 2376 - 2381. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Canaple and J. Bogousslavsky Multiple large and small cerebellar infarcts J. Neurol. Neurosurg. Psychiatry, June 1, 1999; 66(6): 739 - 745. [Abstract] [Full Text]
|
|
|
|
|
|
F. Barinagarrementeria, L. E. Amaya, and C. Cantu Causes and Mechanisms of Cerebellar Infarction in Young Patients Stroke, December 1, 1997; 28(12): 2400 - 2404. [Abstract] [Full Text]
|
|
|
|
 |
|
 M. J. G. Harrison Neurologic Complications of Coronary Artery Bypass Grafting: Diffuse or Focal Ischemia? Ann. Thorac. Surg., May 1, 1995; 59(5): 1356 - 1358. [Abstract] [Full Text]
|
|