Reversible Pancallosal Signal Changes in Febrile Encephalopathy: Report of 2 Cases

Discussion

Prevalence of CC lesions has been reported at 3% in a large series of 450 patients undergoing MR imaging.¹ While the CC can be involved in vascular, traumatic, demyelinating, neoplastic, infective, and degenerative illnesses,² transient involvement has been reported with encephalitis of different etiologies,^3,5 antiepileptic drug use and a peri-ictal state. Among infectious etiologies, influenza has been most often associated with transient splenial involvement.^6,7

Tada et al⁸ proposed the terminology “MERS” to explain a clinical syndrome sharing common features of mild encephalopathy, seizures, and good outcome on follow-up. However, in all these reports, the involvement was restricted to the splenium, with some patients having adjacent white matter involvement as well.

Takanashi⁹ described another entity called “AESD” in children. Neuroimaging showed reduced diffusion in the frontal or frontoparietal subcortical white matter during days 3–9, which reversed on follow-up. Okumura et al⁴ described 2 patterns of lesions in AESD, a diffuse pattern with poor outcome and a central sparing pattern, which was clinically mild. None of their patients had CC involvement.

Both of our patients had similar clinical presentations, with a background of a febrile illness. The presentation with encephalopathy and minimal focal signs within the first week of illness and symmetric involvement of the CC makes postinfectious demyelination less likely. This clinical pattern has been described in most of the previously reported cases of MERS.^3,6–8

MR imaging showed pancallosal involvement with restricted diffusion in both of our patients. The first patient had a bulky CC, with patchy contrast enhancement, which was initially mistaken for glioma. The most consistently reported pathophysiologic mechanisms for CC involvement with restricted diffusion are transient intramyelinic edema and inflammatory infiltrates.¹⁰ Some of the recent reports of MERS have shown persistence of lesion/gliotic changes on follow-up, as in our first patient.^5,11

Imaging characteristics of neurodengue have rarely been reported, to our knowledge. In a large series of neurodengue,¹² no characteristic imaging pattern was noted. A similar observation was made by Wasay et al¹³ in their series of 6 patients. Their reported findings were cerebral edema and cortical and cord hyperintensities. Even though the findings of callosal hyperintensity with restricted diffusion have never been reported with neurodengue, we presume that the imaging finding may be related to AFE syndrome rather than the virus per se. More imaging studies on neurodengue would be required to clarify the observation.

We report these 2 cases to highlight a few points. Transient pancallosal involvement with restricted diffusion is a novel observation in AFE of any etiology. It may represent an extended spectrum of MERS because the presentation and outcome were similar. Encephalopathy associated with dengue has been linked to a poor outcome as opposed to our patient who had mild symptoms, which resolved spontaneously. Last, the appearance of the lesion can be mistaken for a glioma because of the associated swelling and contrast enhancement. However, the clinical setting and additional MR imaging sequences, including diffusion and perfusion, can differentiate the 2, thereby avoiding invasive biopsy.