No abstract

Background and Purpose: The ‘capsular warning syndrome’ (CWS) of recurrent stereotyped episodes of motor or sensory dysfunction is clinically well recognized, and is associated with a high risk of imminent lacunar infarction with permanent deficits resembling those of CWS. However, the pathophysiology of CWS has not been well characterized. We report a clinicoanatomic correlation with MR imaging studies in the acute and chronic phases in patients with CWS. Material and Methods: Between April 1997 and March 2001, we prospectively studied 8 patients, mean age 73.3 years, presenting with 4–17 motor or sensorimotor transient ischemic attacks (TIAs; duration 2–90 min) up to 3 days after onset of the first episode. Four patients were free of symptoms between the attacks and had no residua, whereas 4 patients developed a pure motor or sensorimotor stroke within 1–3 days after symptom onset. Diffusion-weighted echoplanar MRI (DWI) and T₂-weighted MRI studies were performed within 1 week after symptom onset and were repeated 1–2 months later. Results: Seven of the 8 patients had an appropriate lesion on DWI in the acute phase. DWI abnormalities in the 3 patients with TIAs were 4–10 mm in diameter and confined to the lateral thalamus or medial globus pallidus without involving the internal capsule, whereas 4 patients who developed a stroke had abnormalities localized to the putamen extending to corona radiata (3 patients), or the pontomesencephalic junction (1 patient). All 6 patients who underwent follow-up MRI had an infarct on T₂-weighted images corresponding to, but usually smaller than, the acute phase DWI abnormality. Conclusions: Small infarcts in the basal ganglia or the pons, close to central motor pathways, appear to be the primary lesion in CWS. The pathophysiology of CWS is complex, and may involve hemodynamic mechanisms in penetrating arterial territories, as well as molecular mechanisms, such as peri-infarct depolarizations affecting adjacent motor pathways.

Diffusion-weighted imaging (DWI) has been reported to be useful in the differential diagnosis between abscesses and cystic or necrotic tumours. However, experience is still limited and the true sensitivity and specificity remain to be determined. Our purpose is to describe a ring-enhancing metastasis of adenocarcinoma with a DWI pattern similar to that reported for abscesses. The tumour had a diameter of 1.5 cm and give signal from its centre similar to that of normal brain on T1-weighted images, whereas it was increased on T2-weighted images, and surrounded by a low signal ring, suggesting a capsule. The signal was high on DWI and the apparent diffusion coefficient (ADC) was low (0.55 x 10(-3) mm2/s). The findings were misinterpreted as representing an abscess in the early capsule-formation stage, but the signal pattern probably represented early tumour necrosis with intracellular oedema, but without liquefaction. Findings on DWI during the early capsule formation stage in abscesses and early tumour necrosis are probably similar and must be interpreted with caution.

Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.

The use of prospective diastolic ECG triggering significantly improves the accuracy of quantitative diffusion measurements but for routine clinical diffusion imaging, where quantitative data is of less importance, the accuracy obtained without ECG triggering can be considered adequate.