Reversible Splenial Lesion Associated with Subarachnoid Hemorrhage

J Starkey1, Y Moteki1, Y Numaguchi1, J Kim2, T Moritani3, A Uemura4

1St. Luke's International Hospital, Tokyo, Japan, 2Brighmam & Women’s Hospital, Boston, MA, 3University of Iowa Hospital & Clinics, Iowa City, IA

EP-31 #1780

PurposeClinically 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 MethodsWe 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 2014. Initial noncontrast MRI/MRA imaging following CT imaging for the purpose of localizing possible aneurysms and subsequent follow-up imaging studies were reviewed.

Results - patientsPatient 1 Patient 2 Patient 3

Age 42 53 68

Social History Smoking 1 pack/day, heavy alcohol use

None Smoking 1 pack/day, heavy alcohol use

Past medical history Untreated hypertension None None

Presentation Acute onset headache and nausea

Acute onset headache and nausea

Acute onset headache and nausea after drinking

SAH Grade Hunt & Kosnik grade II / Fisher group 3

Hunt & Kosnik grade IV / Fisher group 3

Hunt & Kosnik grade II / Fisher group 3

Angiogram Negative Right vertebral artery dissection Negative

Medications Nicardipine for neuroprotection Nicardipine for neuroprotection Nicardipine for neuroprotection

Recent labs Glu 154, otherwise WNL Glu 140, otherwise WNL Glu 154, otherwise WNL

Outcome Back to baseline Nearly back to baseline but developed severe hydrocephalus requiring long-term shunting

Nearly back to baseline but developed severe hydrocephalus requiring long-term shunting

Results - lesionsPatient 1 Patient 2 Patient 3

Location Body/splenium junction Splenium Splenium

Lesion characteristics Localized, central Localized, larger and eccentric to the left

Localized, central

ADC initial (10-6 mm2/s) 495 525 525

ADC follow-up (10-6 mm2/s) 800 (4 weeks later) 740 (4 weeks later) 663 (2 weeks later)

Timing of initial MRI 3 days after SAH 7 days after SAH 10 days after SAH

Symptoms prior to MRI No change; lesion discovered on routine follow-up

No change; lesion discovered on routine follow-up

No change; lesion discovered on routine follow-up

Patient 1

Axial CT+

Axial DWIInitial (10 days after SAH) +

Axial FLAIRInitial +

Axial DWIFollow-up (6 weeks later) +

Axial DWIFollow-up 2 (10 weeks later) +

Axial FLAIRFollow-up 1 +

Axial FLAIRFollow-up 2 +

Patient 2

Axial CT+

Axial DWIInitial (10 days after SAH) +

Axial FLAIRInitial +

Axial DWIFollow-up 1 (4 weeks later) +

Axial FLAIRFollow-up 1 (4 weeks later) +

Patient 3

Axial CT+

Axial DWIInitial (7 days after SAH) +

Axial FLAIRInitial +

Axial DWIFollow-up 1 (2 weeks later) +

Axial DWIFollow-up 2 (4 weeks later) +

Axial FLAIRFollow-up 1 +

Axial FLAIRFollow-up 2 +

DiscussionWe 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.

DiscussionTo 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.

DiscussionPathogenesis 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.

DiscussionThe 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.

SummaryWe 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.

THANK YOU!

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