PURPOSE: This article discusses the possible pathophysiological conditions responsible for magnetic resonance imaging (MRI) finding of transient focal lesions in the splenium of the corpus callosum on the basis of our experience and a review of the literature. MATERIALS AND METHODS: In six patients undergoing computed tomography (CT) and MRI examinations, focal nonhemorrhagic lesions of the splenium of the corpus callosum were incidentally discovered. Patients had been referred for suspected encephalitis (n=2), dural sinus thrombosis (n=1) and multiple sclerosis (n=3). MRI examinations were repeated after 4, 8 and 12 weeks and in two cases also after 6 and 9 months. MRI and medical records were retrospectively reviewed with respect to patients' clinical history, medication and laboratory findings to define lesion aetiology. RESULTS: In all patients, the lesions were isolated, reversible and with no contrast enhancement. In four patients, the lesion disappeared after complete remission of the underlying disease, whereas in two patients, they persisted for 6 and 9 months, respectively. CONCLUSIONS: To our knowledge and according to previous reports, the fact that these lesions are detected in a relatively large number of conditions with heterogeneous etiopathogenetic factors leads to the hypothesis that a common underlying pathophysiological mechanism that, considering signal characteristic, reversibility and white matter location, could be represented by vasogenic oedema.
PURPOSE: This article discusses the possible pathophysiological conditions responsible for magnetic resonance imaging (MRI) finding of transient focal lesions in the splenium of the corpus callosum on the basis of our experience and a review of the literature. MATERIALS AND METHODS: In six patients undergoing computed tomography (CT) and MRI examinations, focal nonhemorrhagic lesions of the splenium of the corpus callosum were incidentally discovered. Patients had been referred for suspected encephalitis (n=2), dural sinus thrombosis (n=1) and multiple sclerosis (n=3). MRI examinations were repeated after 4, 8 and 12 weeks and in two cases also after 6 and 9 months. MRI and medical records were retrospectively reviewed with respect to patients' clinical history, medication and laboratory findings to define lesion aetiology. RESULTS: In all patients, the lesions were isolated, reversible and with no contrast enhancement. In four patients, the lesion disappeared after complete remission of the underlying disease, whereas in two patients, they persisted for 6 and 9 months, respectively. CONCLUSIONS: To our knowledge and according to previous reports, the fact that these lesions are detected in a relatively large number of conditions with heterogeneous etiopathogenetic factors leads to the hypothesis that a common underlying pathophysiological mechanism that, considering signal characteristic, reversibility and white matter location, could be represented by vasogenic oedema.
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