MRI findings of corticosubcortical lesions in osmotic myelinolysis: report of two cases

Abstract

ABSTRACT. Reports on the MRI findings of cerebral corticosubcortical lesions in osmotic myelinolysis (OM) are rare despite several pathological descriptions of this involvement. We report two patients with subcortical lesions associated with OM that were characteristically distributed along the crowns and sides of the cerebral gyri on T 2 weighted or fluid-attenuated inversion-recovery MRI. We also discuss the MRI characteristics of corticosubcortical lesions in OM. Osmotic myelinolysis (OM) is a demyelinating disorder characterised by acutely evolving corticospinal and bulbar dysfunction following the rapid correction of hyponatraemia [1]. In the literature, MRI findings of OM consist primarily of hyperintensity on T 2 weighted images (T 2 WI) or fluid-attenuated inversion-recovery (FLAIR) images in the central pons (central-pontine myelinolysis), midbrain, bilateral thalami and/or basal ganglia (extrapontine myelinolysis), or a combination of these [1]. Although cerebral corticosubcortical involvements have been described in pathological studies [1][2][3], a description of the MRI findings has been mostly limited to case reports [4][5][6][7][8].We report serial MRI findings in two patients with corticosubcortical lesions associated with OM. One patient's lesions were disclosed on MRI that included diffusion-weighted imaging (DWI) and T 1 weighted imaging (T 1 WI) with contrast enhancement that were obtained 8 days (late acute phase) and 26 days (subacute phase) after the onset of neurological symptoms. The other patient's lesions appeared on MRI 14 months (chronic phase) after symptom onset. Case 1Following 1 month of chemotherapy, a 28-year-old female with advanced colon cancer developed coma and myoclonus-like involuntary movement as a result of hyponatraemia of 110 mEq l -1 . This was presumably caused by water toxicosis derived from vasopressin therapy for diabetes insipidus. The clinicians tried to control the serum sodium level gradually, but it unexpectedly rapidly elevated to 178 mEq l -1 within 4 days. The patient remained comatose after returning to normonatraemia and underwent an MRI of the brain 8 days after the onset of neurological symptoms (late acute phase). DWI showed multiple hyperintense lesions in the striatum (putamen and caudate nucleus) and almost symmetrically distributed in the corticosubcortical regions (Figure 1a,b). These lesions also appeared hyperintense on T 2 WI and FLAIR imaging. Some of the corticosubcortical lesions showed contrast enhancement, especially those subjacent to the top (crown) of the cerebral gyri (Figure 1c). The clinical presentation and MRI findings led to a diagnosis of OM with extrapontine involvement. In the subacute phase (26 days after the onset of symptoms), the cortico-subcortical lesions became more evident on T 2 WI and FLAIR images (Figure 1d,e) but appeared hypointense on T 1 WI. The patient remains comatose. Case 2A 65-year-old female was admitted to the hospital with loss of consciousness and convulsion half a day after she drank a large amount of...

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