Reversible Splenial Lesion Associated with Subarachnoid Hemorrhage J Starkey 1, Y Moteki 1, Y Numaguchi 1, J Kim 2, T Moritani 3, A Uemura 4 1 St. Luke's International Hospital, Tokyo, Japan, 2 Brighmam & Women’s Hospital, Boston, MA, 3 University of Iowa Hospital & Clinics, Iowa City, IA EP-31 #1780

Purpose Clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS), otherwise known as a transient lesion of the splenium (TLS) has been described for many entities, including epilepsy, demyelination, posterior reversible encephalopathy, diffuse axonal injury, AIDS dementia complex, various viral and nonviral infections, and hypoglycemia. However, to date such splenial lesions have not been described in association with subarachnoid hemorrhage. We present three cases of isolated transient splenial lesions associated with subarachnoid hemorrhage.

Materials and Methods We retrospectively reviewed the medical records and imaging findings in patients who presented with SAH and subsequently were found to have splenial lesions with reduced diffusion between July and December Initial noncontrast MRI/MRA imaging following CT imaging for the purpose of localizing possible aneurysms and subsequent follow-up imaging studies were reviewed.

Results - patients Patient 1Patient 2Patient 3 Age Social HistorySmoking 1 pack/day, heavy alcohol use NoneSmoking 1 pack/day, heavy alcohol use Past medical historyUntreated hypertensionNone PresentationAcute onset headache and nausea Acute onset headache and nausea after drinking SAH GradeHunt & Kosnik grade II / Fisher group 3 Hunt & Kosnik grade IV / Fisher group 3 Hunt & Kosnik grade II / Fisher group 3 AngiogramNegativeRight vertebral artery dissectionNegative MedicationsNicardipine for neuroprotection Recent labsGlu 154, otherwise WNLGlu 140, otherwise WNLGlu 154, otherwise WNL OutcomeBack to baselineNearly back to baseline but developed severe hydrocephalus requiring long-term shunting

Results - lesions Patient 1Patient 2Patient 3 LocationBody/splenium junctionSplenium Lesion characteristicsLocalized, centralLocalized, larger and eccentric to the left Localized, central ADC initial ( mm 2 /s) ADC follow-up ( mm 2 /s) 800 (4 weeks later)740 (4 weeks later)663 (2 weeks later) Timing of initial MRI3 days after SAH7 days after SAH10 days after SAH Symptoms prior to MRINo change; lesion discovered on routine follow-up

Patient 1 Axial CT + + Axial DWI Initial (10 days after SAH) + + Axial FLAIR Initial + + Axial DWI Follow-up (6 weeks later) + + Axial DWI Follow-up 2 (10 weeks later) + + Axial FLAIR Follow-up Axial FLAIR Follow-up 2 + +

Patient 2 Axial CT + + Axial DWI Initial (10 days after SAH) + + Axial FLAIR Initial + + Axial DWI Follow-up 1 (4 weeks later) + + Axial FLAIR Follow-up 1 (4 weeks later) + +

Patient 3 Axial CT + + Axial DWI Initial (7 days after SAH) + + Axial FLAIR Initial + + Axial DWI Follow-up 1 (2 weeks later) + + Axial DWI Follow-up 2 (4 weeks later) + + Axial FLAIR Follow-up Axial FLAIR Follow-up 2 + +

Discussion We present three patients with reversible lesions of the posterior corpus callosum. In all cases, the DWI abnormality nearly completely resolved at follow- up exam within several weeks to a month. Patients had acute issues related to their SAH, so the “mild encephalopathy” often described with such lesions is less applicable. These lesions were all noted on routine MRI follow-up exams. Such routine MRI follow-up has been recently implemented at our institution to assess for vasospasm on MRA and infarct on DWI in patients with SAH.

Discussion To our knowledge, these types of lesions have not previously been described in patients with SAH. Our patients where on nicardipine for neuroprophylaxis, but otherwise had no unifying medical regimens to explain the findings. They also had no suspicious laboratory results. In particular, they did not have hypoglycemia (at least when laboratory values were drawn) and were not diabetic, so hypoglycemia as an etiology seems unlikely.

Discussion Pathogenesis of such lesions is unknown. Influx of inflammatory mediators/cytokines, intramyelinic edema, arginine-vasopressin fluid balance systems, and toxin-mediated immune activation causing endothelial injury have been suggested. These lesions are not infarctions and should not be mistaken as such.

Discussion The high frequency of these lesions is somewhat unexpected and likely related to recent institution of post-SAH routine MR evaluation. We suspect that the incidence of these lesions is likely high but previously undetected. We also hypothesize that these lesions are likely related to irritating properties of blood products and the severity of SAH in the basal cisterns (in which our patients had extensive hemorrhages) and may be less likely to occur with SAH limited only to the Sylvian fissure, such as with MCA aneurysm rupture.

Summary We present three cases of isolated transient splenial lesions associated with subarachnoid hemorrhage. These should not be mistaken for acute infarct. Further research about corpus callosum lesions in SAH needs to be conducted with regards frequency, relationship to SAH severity, clinical significance, and relationship to other similar lesions.

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