Diffusion-Weighted MRI Findings in Patients with Capsular Warning SyndromeStaaf G.a · Geijer B.b · Lindgren A.a · Norrving B.a
Departments of aNeurology and bNeuroradiology, Lund University Hospital, Lund, Sweden
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.
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