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Reversible Splenial Lesion Associated
with Subarachnoid Hemorrhage
EP-31 #1780
J Starkey1, Y Moteki1, Y Numaguchi1, J Kim2, T Moritani3, A Uemura4
Luke's International Hospital, Tokyo, Japan, 2Brighmam & Women’s Hospital, Boston, MA, 3University of Iowa Hospital &
Clinics, Iowa City, IA
1St.
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 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 - patients
Patient 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 - lesions
Patient 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 DWI
Initial (10 days after SAH)
Axial FLAIR
Initial
Axial DWI
+
Follow-up (6 weeks later)
+
Follow-up 1
Axial FLAIR
Axial DWI
+
Follow-up 2 (10 weeks later)
+
Follow-up 2
Axial FLAIR
+
+
Patient 2
Axial CT
+
Axial DWI
Initial (10 days after SAH)
Axial FLAIR
Initial
Axial DWI
+
Follow-up 1 (4 weeks later)
+
Follow-up 1 (4 weeks later)
Axial FLAIR
+
+
Patient 3
Axial CT
+
Axial DWI
Initial (7 days after SAH)
Axial FLAIR
Initial
Axial DWI
+
Follow-up 1 (2 weeks later)
+
Follow-up 1
Axial FLAIR
Axial DWI
+
Follow-up 2 (4 weeks later)
+
Follow-up 2
Axial FLAIR
+
+
Discussion
We present three patients with reversible lesions of
the posterior corpus callosum. In all cases, the DWI
abnormality nearly completely resolved at followup 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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