Restricted diffusion in Splenium of Corpus Callosum

A 18 yo male, known case of GTCS under treatment with anti epileptic drugs (which drug i am deliberately not mentioning), comes now with very recent history of seizure, at the time of admission conscious and well oriented.
Vitals normal.
No neurological signs.
No fall or significant head injury during seizure episode.
No any cardio pulmonary resuscitation required.
Immediate post admission MRI Brain done show a focal restricted diffusion in the region of splenium of corpus callosum.

Rest of the brain parenchyma normal.
Csf evaluation done turned out normal.
Managed conservatively, continued the same AEDs and discharged.

Discussion about the case: 

Differentials for Splenial signal abnormality are Ischemia, Diffuse axonal injury, Multiple sclerosis, Marchiafava-Bignami disease, Wernicke's encephalopathy , Encephalitis, Post ictal and long term antiepileptic drug usage.

Now in this case we’ll rule out one by one to cut short the list of differentials. 

• Ischemia is unlikely as pt was stable, vitals were normal. No history of cardiac arrest or cardio pulmonary resisutation.
• Diffuse axonal injury unlikely as there was no history of significant trauma. Pts was not unconscious, Glass-Glow Coma score.
• Multiple sclerosis unlikely as there were no plaques elsewhere.
• For Marchiafava-Bignami disease patient is non alcoholic.
• Wernicke's encephalopathy (WE) caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia.
• Encephalitis, yes milder form of encephalitis is possible and mentioned in literature with reversible restricted diffusion in SCC. ( Reference: American Journal of Neuroradiology 27:1983-1986, October 2006)
• Long term use of Antiepileptic drungs, may be, as mentioned in most of the literature as possible cause for restricted diffusion in SCC which also mentions that it reverses with discontinuation of AEDs. But there are certain literatures reports presence of restricted diffusion in SCC in patients not using AEDs (reference: Epilepsia, 44(6):1–3, 2003, Blackwell Publishing, Inc.C 2003 International League Against Epilepsy) which support that it is related to seizure activity itself and not the result of long term use of AEDs, Drug toxicity or Demyelination. They also mention that it’s a transient signal abnormality with intramyelinic vasogenic edema as possible mechanism.

So the post ictal transient signal abnormality appears to be the most convincing.

A follow up MRI after 1 month showed complete regression of the signal abnormality again supports that the signal abnormality which was seen in splenium of corpus callosum is a reversible signal abnormality and can be correlated to seizure activity itself and not the result of use of AEDs.