Cortical laminar necrosis detected by diffusion-weighted imaging in a dog suspected of having hypoglycemic encephalopathy

Abstract

We describe a 5-year-old castrated male dog suspected hypoglycemic encephalopathy that was evaluated by using diffusion-weighted imaging (DWI). The dog experienced hypoglycemia after prolonged generalized and continued partial seizures. In the acute phase, DWI showed hyperintensity in the left temporal lobe. After about a month, DWI maintained hyperintensity, and left middle cerebral artery dilation was noted on magnetic resonance angiography (MRA). In the chronic phase, the left temporal lobe lesion was replaced by cerebrospinal fluid. In humans, it was reported that cortical laminar necrosis (CLN) with hypoglycemic encephalopathy presents hyperintensity in the cerebral cortex on DWI and increased vascularity of the middle cerebral artery branches on MRA. In conclusion, DWI has detected CLN in a dog suspected hypoglycemic encephalopathy.

Keywords: diffusion-weighted imaging; hypoglycemic encephalopathy; magnetic resonance imaging.

Fig. 1.

The region of interest (ROI) locations for the apparent diffusion coefficient (ADC) values. A) These images were DWI. The ROI was set on the piriform lobe (a), gyrus sylvius (b), amygdala (c), gyrus ectosylvius medialis (d), and hippocampus (e). DWI, diffusion-weighted imaging; L, left side; R, right side. B) These images were ADC maps. The ADC values were observed by these images.

Fig. 2.

Transverse images obtained at the temporal lobe level. Images were acquired on the A) second day, B) 39th day, and C) 133rd day after the epilepsy onset by a) T2WI, b) FLAIR, c) T1WI, d) post-contrast T1WI, and e) DWI. A) On the second day after onset, T2WI, FLAIR, and DWI showed hyperintensity respectively in the left temporal lobe, including the gyrus sylvius and gyrus ectosylvius medialis (arrow). T1WI showed isointensity, which was not enhanced by contrast medium. The hyperintensity was clearer on DWI than on T2WI and FLAIR, and showed in the left temporal lobe and bilateral hippocampi (asterisk). B) On day 39 after onset, the temporal lobe showed hyperintensity on T2WI. The center of the left temporal lobe showed hypointensity on FLAIR and T1WI respectively (dotted arrow). The periphery of the temporal cortex showed hyperintensity on FLAIR, with linear contrast enhancement on T1WI (arrowhead). Hyperintensity on DWI was maintained in the left temporal lobe. C) On day 133 after onset, the center of lesion in the temporal lobe showed hyperintensity on T2WI. The lesion was observed hypointensity on FLAIR and T1WI respectively (dotted arrow). The cortex periphery was hyperintense on FLAIR, with linear contrast enhancement on T1WI (arrowhead). The hyperintense lesion in the left temporal lobe was not seen on DWI. T1WI, T1-weighted imaging; T2WI, T2-weighted imaging; FLAIR, fluid attenuated inversion recovery; DWI, diffusion-weighted imaging; L, left; R, right.

Fig. 3.

The periphery of the cortical lesion on T1-weighted imaging (WI). These images showed a), b) Transverse images acquired on T1WI at the temporal lobe level on day 39 after epilepsy onset and c) Transverse image on T1WI at the occipital lobe level on day 133 after epilepsy onset. The center of lesion was hypointensity, but the periphery of the cortical lesion was hyperintense on T1WI slightly (arrow). R, right; T1WI, T1-weighted imaging.

Fig. 4.

Magnetic resonance angiography (MRA) on day 39 after epilepsy onset. The images show (a) ventral view, and (b) rostral view. The left middle cerebral artery was clearer than the right one (arrows). Tortuous small vessels were observed in the left temporal lobe (arrowheads). R, right side; L, left side.