Objective: To study the site of the ischemic lesion, the underlying cause,
and the prognosis of acute stroke with distal arm paresis. Methods: The aut
hors investigated 14 consecutive patients with acute distal arm paresis wit
h a diagnostic stroke protocol and early MRI, including T2-weighted images,
diffusion-weighted images (DWI), and perfusion-weighted images (PWI). Acut
e DWI lesions were shown on coregistered T2-weighted images for analysis of
the exact anatomic lesion location. Results: Patients showed a uniform (7/
14), radial (3/14), or ulnar (4/14) distribution of hand paresis. In all ca
ses, DWI identified small lesions located in the motor cortex. Topographic
lesion analysis, which was correlated with the clinical deficit, showed les
ions centered in the hand knob area (2/14), involving the lateral (6/14), m
edial (4/14), or both (2/14) borders of the hand knob. PWI (calculated time
-to-peak maps) did not show a mismatch between the DWI lesion and the PWI l
esion. In six patients, DWI and PWI lesions were identical in size and loca
tion; no definite perfusion deficit was seen in eight patients. In agreemen
t with PWI, no patient showed clinical worsening, and six patients recovere
d completely within a week. Further investigations showed a potential sourc
e of embolus in 11 cases. Conclusions: Acute ischemic distal arm paresis is
usually caused by a small cortical lesion in the motor hand cortex attribu
table to distal Rolandic artery obstruction without additional tissue at ri
sk. These findings confirm the observed benign clinical course and its appa
rent main cause (artery-to-artery or cardiac embolism).