Rapid improvement of diffusion-weighted imaging abnormalities after glucose infusion in hypoglycaemic coma

Acute symptomatic hypoglycaemia mimicking ischaemic stroke on imaging: a systemic review

“…Most lesions were bilateral [14,21,28-30,32,34,35,37] but seven patients had unilateral [4,25,31,41] lesions mimicking stroke. Lesions were located anywhere along the corticospinal tracts, including the motor cortex [29], corona radiate [29,30,34,42], posterior limb of the internal capsule [4,14,21,28,29,31,32,34,35,41], pyramidal tracts [25,37], splenium of the corpus callosum [21,30,32,34,35,41] or middle cerebellar peduncles [32,37]. A few patients had isolated lesions in the splenium [38,40,42].…”

“…Those with bilateral lesions were more likely to present with coma, although two with asymmetrical internal capsule lesions presented with hemiparesis [28,30]. Where neuroimaging was repeated after symptom recovery (all within 3 days of presentation), there was either complete [4,14,21,25,30-32,34,35,37,40,41] or partial [28,29] resolution of the imaging abnormalities. …”

“…Amongst the 55 patients (34 papers) imaged on the day of admission, lesions were seen on MR DWI as early as 45 minutes after symptom onset [25,31,34,35,41], but were not apparent on T2w imaging until at least 12 hours after symptom onset [8,11,37,38]. Of the 21 CTs performed on the day of admission, only one showed a low attenuation lesion [4], whilst two showed generalised cerebral swelling [17,26].…”

“…Our first new case, imaged at 14 days after initial presentation, showed unilateral cortical low attenuation and swelling. Patients with good clinical outcome who had repeat imaging showed resolution of lesions as early as 6 hours after clinical recovery [4,21,28-31,34,35,37,40,41]. Patients with intermediate outcome showed no lesion resolution.…”

Neuroimaging Correlates of Acute Encephalopathy

“…In patients with hypoglycemia-related encephalopathy, the CT is usually unremarkable, whereas the pathophysiologic changes include hyperintense T2 signals and restrictions on DWI in the cortex, the internal capsules, the basal ganglia, the hippocampi, or the splenium of the corpus callosum, reflecting cytotoxic edema and neuronal death (Aoki et al, 2004;Bottcher et al, 2005;Fujioka et al, 1997;Kang et al, 2010;Kim et al, 2007;Lim et al, 2009;Lo et al, 2006;Maruya et al, 2007;Terakawa et al, 2007). Large DWI changes in the deep white matter and the basal ganglia can be seen in patients with poor outcome (Lim et al, 2009;Ma et al, 2009).…”