A study found that rotavirus infection is associated with lesions in the splenium of the corpus callosum in patients with benign convulsions with mild gastroenteritis (CwG). The findings from this study were published in Pediatric Neurology.
Patients with CwG (n=32) or benign infantile epilepsy (n=22) were included in the study if they had undergone a brain MRI within a 7-day period of seizure onset. Child neurologists from 12 hospitals of the Tokai Pediatric Neurology Society answered a questionnaire that inquired about clinical characteristics, seizure manifestations, neurological examination, laboratory exams, and electroencephalogram findings. Medical records were used to identify the number of seizures in the cohort. All patients with CwG were tested for rotavirus and adenovirus.
In 7 patients with CwG, diffusion-weighted imaging demonstrated signal hyperintensity in the splenium of the corpus callosum. Researchers observed no abnormalities in the benign infantile epilepsy patient group. Compared with patients with CwG without splenial lesions, patients with CwG who presented with splenial lesions had higher rates of rotavirus (P =.006), higher C-reactive protein (P =.04), and shorter periods between seizure onset and MRI (P =.002). The presence of rotavirus infection was found to be a risk factor for splenial lesions in patients with CwG (P =.02), according to the multivariate analysis.
Limitations of the study include the small sample size and the reliance on questionnaire data, as well as the retrospective nature of the analysis.
The researchers concluded that “splenial lesions on DWI are seen more frequently in patients with CwG than in those with [benign infantile epilepsy].” Further, rotavirus may play a role in causing edema in the corpus callosum, and as such, it should not go overlooked as a risk factor for splenial lesions in patients with CwG.
Ogawa C, Kidokoro H, Ishihara N, et al. Splenial lesions in benign convulsions with gastroenteritis associated with rotavirus infection [published online May 9, 2019]. Pediatric Neurol. doi:10.1016/j.pediatrneurol.2019.05.002.