Clinical and anatomical factors associated with thalamic dyskinesias

• Published in: Journal of the neurological sciences 2001, Vol.182 (2), p.137-142
• Main Authors: Lee, M.S, Kim, Y.D, Yang, J.W, Lyoo, C.H, Oh, S.H, Kim, H.S
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aged, 80 and over; Biological and medical sciences; Brain Infarction - pathology; Brain Infarction - physiopathology; Dyskinesia; Dystonia; Female; Humans; Infarction; Magnetic Resonance Imaging; Male; Medical sciences; Middle Aged; Movement Disorders - pathology; Movement Disorders - physiopathology; Neural Pathways - pathology; Neural Pathways - physiopathology; Neurology; Thalamic Diseases - pathology; Thalamic Diseases - physiopathology; Thalamus; Thalamus - pathology; Thalamus - physiopathology; Tropical medicine; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/S0022-510X(00)00463-9

To define the clinical and anatomical factors associated with dyskinesias following thalamic infarction, we performed neurological examination and three-dimensional brain magnetic resonance imaging for 23 patients with thalamic infarction. We measured the total volumes and the largest diameters of the lesions on axial and coronal images. Using the atlas of human thalamus, we investigated the damaged thalamic nuclei. We compared the means of the volumes and the largest diameters of the lesions, and the frequencies of damaged thalamic nuclei between patients with and without thalamic dyskinesias. Seven (two pseudochoreoathetosis and five dystonia) of the 23 patients with thalamic infarction developed dyskinesias. No specific neurological deficits at the onset of stroke predicted the development of dyskinesias. The mean volume of the lesions of patients with dyskinesias (739 mm 3) was significantly larger than that of those without dyskiensias (92.9 mm 3). The means of the largest axial (11.6 mm) and coronal (10.8 mm) diameters were significantly larger in patients with dyskinesias, compared to those (axial, 7.1 mm; coronal, 6.4 mm) of patients without dyskinesias. Patients with dyskinesias had damage in the centromedian (CM) thalamic nucleus more frequently compared to those without dyskinesias. Patients with a large thalamic infarction involving the CM nucleus are more likely to develop dyskinesias.