Achim Gass

Diffusion-weighted MRI (DWI) and perfusion MRI (PI) have been mainly applied in acute stroke, but may provide information in the peri-ictal phase in epilepsy patients. Both transient reductions of brain water diffusion, namely a low apparent diffusion coefficient (ADC), and signs of hyperperfusion have been reported in experimental and human epilepsy case studies. We studied 10 patients with complex partial status epilepticus (CPSE) with serial MRI including DWI and PI. All patients showed regional hyperintensity on DWI, and a reduction of the ADC in (i) the hippocampal formation and the pulvinar region of the thalamus (six out of 10 patients), (ii) the pulvinar and cortical regions (two out of 10), (iii) the hippocampal formation only (one out of 10), and (iv) the hippocampal formation, the pulvinar and the cortex (one out of 10). In all patients a close spatial correlation of focal hyperperfusion with areas of ADC/DWI change was present. In two patients hyperperfusion was confirmed in additional SPECT (single photon emission computed tomography) studies. All patients received follow-up MRI examinations showing partial or complete resolution of diffusion and perfusion abnormalities depending on the length of the follow-up interval. The clinical course, EEG and SPECT results all indicate that MRI detected changes related to prolonged epileptic activity. Combined PI and DWI can visualize haemodynamic and tissue changes after CPSE in the hippocampus, thalamus and affected cortical regions.

Objective: To study the site of the ischemic lesion, the underlying cause, and the prognosis of acute stroke with distal arm paresis. Method: The authors investigated 14 consecutive patients with acute distal arm paresis with a diagnostic stroke protocol and early MRI, including T2-weighted images, diffusion-weighted images (DWI), and perfusion-weighted images (PWI). Acute 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 cases, DWI identified small lesions located in the motor cortex. Topographic lesion analysis, which was correlated with the clinical deficit, showed lesions centered in the hand knob area (2/14), involving the lateral (6/14), medial (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 lesion. In six patients, DWI and PWI lesions were identical in size and location; no definite perfusion deficit was seen in eight patients. In agreement with PWI, no patient showed clinical worsening, and six patients recovered completely within a week. Further investigations showed a potential source of embolus in 11 cases. Conclusions: Acute ischemic distal arm paresis is usually caused by a small cortical lesion in the motor hand cortex attributable to distal Rolandic artery obstruction without additional tissue at risk. These findings confirm the observed benign clinical course and its apparent main cause (artery-to-artery or cardiac embolism).