MRI findings in Susac’s syndrome

J.O. Susac, MD; F.R. Murtagh, MD; R.A. Egan, MD; J.R. Berger, MD; R. Bakshi, MD; N. Lincoff, MD;
A.D. Gean, MD; S.L. Galetta, MD; R.J. Fox, MD; F.E. Costello, MD; A.G. Lee, MD; J. Clark, DO;
R.B. Layzer, MD; and R.B. Daroff, MD

Abstract—Background: Susac syndrome (SS) is a self-limited syndrome, presumably autoimmune, consisting of a clinical
triad of encephalopathy, branch retinal artery occlusions, and hearing loss. All three elements of the triad may not be
present or recognized, and MR imaging is often necessary to establish the diagnosis. Objective: To determine the spectrum
of abnormalities on MRI in SS. Methods: The authors reviewed the MR images of 27 previously unreported patients with
the clinical SS triad, and 51 patients from published articles in which the MR images were depicted or reported. Results:
All 27 patients had multifocal supratentorial white matter lesions including the corpus callosum. The deep gray nuclei
(basal ganglia and thalamus) were involved in 19 (70%). Nineteen (70%) also had parenchymal enhancement and 9 (33%)
had leptomeningeal enhancement. Of the 51 cases from the literature, at least 32 had callosal lesions. The authors could
not determine the presence of callosal lesions in 18 of these patients, and only one was reported to have a normal MRI at
the onset of encephalopathy. Conclusions: The MR scans in SS show a rather distinctive pattern of supratentorial white
matter lesions that always involve the corpus callosum. There is often deep gray matter, posterior fossa involvement, and
frequent parenchymal with occasional leptomeningeal enhancement. The central callosal lesions differ from those in
demyelinating disease, and should support the diagnosis of SS in patients with at least two of the three features of the
clinical triad.
NEUROLOGY 2003;61:1783–1787

Susac syndrome (SS) consists of the triad of enceph- elements may not all be present at the onset. More-
alopathy, branch retinal artery occlusions (BRAO), over, the encephalopathy may prevent patients from
and hearing loss.1-42 The encephalopathy manifests complaining of visual and hearing difficulty. Periph-
with headache, confusion, memory loss, behavioral erally located BRAO may not result in visual symp-
changes, dysarthria, and occasional mutism. The toms, and may only be recognized by an
BRAO may be extensive or subtle; if the posterior ophthalmologist. Thus, MR imaging is often neces-
pole of the retina is involved, patients may complain sary to establish the diagnosis.
of impaired vision. These BRAO are usually bilateral MR images are invariably abnormal, particularly
and may be the presenting features of the illness, or in encephalopathic onset patients, but the white
occur later in the clinical course. Likewise, the hear- matter lesions are often attributed to demyelination
ing loss is usually bilateral and frequently associated (multiple sclerosis [MS] or acute disseminated en-
with tinnitus and vertigo; like the BRAO, it may be cephalomyelitis [ADEM]). Proper interpretation of
the presenting feature or develop later. Although SS the MRI should increase the diagnostic yield of SS.
usually occurs in young women between the ages of Toward that end, we describe the MR images of 27
20 and 40, it may also afflict men. The age range in previously unreported patients, all of whom pre-
both sexes is from 16 to 58 years, and the female-to- sented with the SS clinical triad. We also reviewed
male ratio is 3:1. The clinical course is self-limited, the MR reports from the literature.
usually ranging 2 to 4 years, after which patients
will then stabilize with varying degrees of cognitive Methods. Brain MR images in 27 patients with the complete
disturbance, impaired hearing, and vision loss. An clinical SS triad were reviewed by F.R.M., A.D.G., R.B., and J.O.S.
There were 17 women and 10 men with an age range of 22 to 58
immune response etiology is presumed.3 years, median age 29 years. All patients had 5 mm axial T2,
The classic triad of encephalopathy, BRAO, and proton density, T1, and axial/sagittal T1-weighted images with
hearing loss is pathognomonic for SS but the three gadolinium. Ten patients had fluid-attenuated inversion recovery
(FLAIR) images in the axial/sagittal planes; one patient had
double-dose gadolinium with magnetization transfer.
Additional material related to this article can be found on the Neurology
Web site. Go to www.neurology.org and scroll down the Table of Con- Results. Multifocal supratentorial white matter lesions,
tents for the December 23 issue to find the title link for this article.
including the corpus callosum (figure 1), were present in

From Neurology and Neurosurgery Associates (Dr. Susac), Winter Haven, FL; University of South Florida (Dr. Murtagh), Tampa; Casey Eye Institute (Dr. Egan),
Portland, OR; University of Kentucky (Dr. Berger), Lexington; Buffalo General Hospital (Drs. Bakshi and Lincoff), NY; University of California (Drs. Gean and
Layzer), San Francisco; University of Pennsylvania (Dr. Galetta), Philadelphia; Cleveland Clinic (Dr. Fox), OH; The Ottawa Hospital (Dr. Costello), Canada;
University of Iowa (Dr. Lee), Iowa City; Scott & White Clinic (Dr. Clark), Temple, TX; and Case Western Reserve University (Dr. Daroff), Cleveland, OH.
Received July 28, 2003. Accepted in final form October 17, 2003.
Address correspondence and reprint requests to Dr. John O. Susac, Neurology and Neurosurgery Associates, 50 Second Street, S.E., Winter Haven, FL 33880;
[email protected]

Copyright © 2003 by AAN Enterprises, Inc. 1783

Figure 1. (A) Axial T2 and (B, C) axial fluid-attenuated inversion recovery showing evolving lesions in the brainstem
and middle cerebellar peduncles: sequential images, 1 month apart.

all 27 patients, and there was frequent involvement of the in the splenium. Linear defects were sometimes seen,
cerebellum, middle cerebellar peduncles, and brainstem probably reflecting microinfarction of obliquely radiating
(see figure 1, table). The lesions were numerous and axons within the callosum. The central holes (see figure 4)
tended to be small (3 to 7 mm) but some small lesions are presumed to be due to microinfarcts of transversely
became confluent and some were larger (⬎7 mm). Nine- radiating axons of the callosum.
teen patients had parenchymal enhancement, which, when There were deep gray basal ganglia and thalamus le-
pronounced, resulted in a miliary appearance of the brain sions in 19 patients (see the table) that typically mani-
(figure 2). The lesions of the corpus callosum were typically fested with increased signal intensity on T2, proton
small and involved the central fibers with relative sparing density, and FLAIR images. Larger lesions resembled “gi-
of the periphery; enhancement was variable. The acute ant lacunes”43 and suggested extensive involvement of the
callosal lesions (figure 3) observed during the active en- lenticulostriate arteries. Three such patients showed dra-
cephalopathy were replaced by a “riddled”/punched out ap- matic enhancement of these lesions, accompanied by lepto-
pearance on follow-up MR in all 27 patients (figure 4), meningeal enhancement. Parenchymal enhancement (see
presumably representing microinfarctions, which were not figure 2) involved all areas of the brain, and was occasion-
present in other locations. The riddled callosum, best seen ally associated with leptomeningeal enhancement (see the
on thin section (3 mm thick) sagittal T1 or sagittal T2/ table). Had serial scanning been performed, enhancement
proton density weighted images, consisted of a series of might have been even more common. As the encephalopa-
small (3 mm) central holes separated by 7 mm on sagittal thy waned and the patients began to recover, the only
T1 and sagittal T2/proton density images. These extended residual lesions were the central callosal holes (see figure
over the entire length of the corpus callosum. When larger 4) and a few white matter lesions. In two patients, in-
acute (“snowball”) (see figure 3) callosal lesions were creased signal intensity changes within the callosum were
present, the chronic residual holes were larger, especially accompanied by central callosal holes on the initial MRI
examination. In the more severely affected patients, cere-
bral and cerebellar atrophy ensued. In two such instances,
Table MRI findings in 27 Susac’s syndrome patients
the callosum became so atrophied that the previously
Patients Percentage noted callosal holes virtually disappeared.

1. White-matter lesions 27 100%

Periventricular, centrum semiovale and 27 100% Discussion. All 27 patients had cerebral white
subcortical location matter lesions with involvement of the corpus callo-
Corpus callosum 27 100% sum. Nineteen (70%) also had deep gray lesions, and
9 (33%) had leptomeningeal enhancement. The corre-
Cerebellum 14 52%
lation of these MR findings with the clinical triad of
Brainstem 8 30% SS, or even elements of the triad, seems pathogno-
Middle cerebellar peduncles 8 30% monic. SS is often misdiagnosed as MS or ADEM
2. Deep gray matter involvement 19 70% because of the prominent white matter lesions.1,3,40
3. Leptomeningeal enhancement 9 33%
Callosal lesions, specifically, were regarded as “a
sensitive and specific indicator of MS” in a report44
4. Gadolinium enhancing gray and white 19 70%
written to differentiate age-related microvascular is-
matter lesions
chemic changes (which do not involve the corpus cal-
1784 NEUROLOGY 61 December (2 of 2) 2003
 Figure 2. Double-dose gadolinium
T1-weighted image with magnetiza-
tion transfer showing numerous en-
hancing lesions of white, deep, and
gray matter, and leptomeninges.

losum) from those of demyelinating disease. One of Only one patient has been reported with a normal
our patients was a 58-year-old man whose white scan.22 The patient presented with memory loss, diz-
matter lesions could have easily been misinterpreted ziness, ataxia, and visual blurring and later devel-
as being age related, except for the characteristic oped BRAO and hearing loss. The patient has been
callosal findings of SS. stable for 15 years; a follow-up scan several years
We attempted to review all previous case reports ago was said to have shown several “white spots”
of patients with SS to determine how many had cal- (personal communication with J. Bogousslavsky).
losal involvement. This was difficult because many Early generation scanners might have missed small
authors simply described widespread white matter lesions and gadolinium was not available. The scan
lesions without specifically mentioning the corpus might have been obtained too early for the radiologic
callosum. At times, the published MR images did findings to develop, but based upon all other pub-
show callosal involvement. Table E-1 (available on- lished reports, a patient with full-blown encephalop-
line at www.neurology.org) breaks down 51 SS pa- athy from SS should not have a normal MR, at least
tients with MR from a total of 35 separate reports. with current imaging techniques.
Of the 51 patients, 32 had callosal lesions that were In some patients, the degree of white matter
either specifically mentioned in the text or evident change was minimal compared to the severe degree
from the published figures or upon our personal re- of encephalopathy. Double-dose gadolinium with
view of the actual scans. We could not determine magnetization transfer may show more extensive
callosal involvement in 20 patients. changes (see figure 2), which would help explain this

Figure 3. (A) Sagittal proton density weighted image showing larger lesions (“snowballs”) in corpus callosum with corre-
sponding (B) axial view.
December (2 of 2) 2003 NEUROLOGY 61 1785
 rioles that are under 100 ␮m in the corpus
callosum.44-46 This small size is beyond the resolution
of arteriography, which is almost always normal in
patients with SS. These callosal microinfarcts show up
best on 3 mm sagittal (T1/T2/proton density/FLAIR)
sections, but the larger sagittal “snowball” lesions are
also evident on the axial views (see figure 3).

Acknowledgment
The authors thank the following doctors for referral of patients,
MRI, and clinical data on their patients with Susac syndrome:
Susan Andracchi, MD, Wilmington, NC; Richard Bernstein, MD,
Chicago, IL; Nancy Bonachier, MD, Florence, SC; J.P. Cavalier,
PA, Pittsburgh, PA; James J. Corbett, MD, Jackson, MS; Brad
Farris, MD, Oklahoma City, OK; Scott S. Ferer, MD, Newport
Beach, CA; Doreen Fialho, MD, London, UK; Josef Flammer, MD,
Basel, Switzerland; Benjamin A. Frishberg, MD, Washington, DC;
Figure 4. Sagittal T1-weighted image showing the central Richard M. Garcia, MD, Sarasota, FL; T. Haufschild, MD, Basel,
Switzerland; T. Heckman, MD, Oroville, CA; George J. Hutton,
callosal holes that result from acute microinfarctions. MD, Dallas, TX; Eric Kraus, MD, Seattle, WA; Paul Latkany, MD,
New York, NY; Richard P. Lenahan, MD, Temple, TX; Leah Levi,
MD, San Diego, CA; Claudia F. Luchinetti, MD, Rochester, MN;
apparent clinical/MR disparity. We used this se- Peter McCluskey, MD, Sydney, Australia; Jerry Maitland, MD,
quence in only one of our patients, however. Tallahassee, FL; Charles A. Mango, MD, Syracuse, NY; Clyde
A normal MR might be predicted in patients with Markowitz, MD, Philadelphia, PA; Luis Mejico, MD, Syracuse,
NY; Hani A. Midani, MD, Albany, NY; Douglas J. Mogle, MD,
only hearing loss and BRAO, but without encepha- Melbourne, FL; Carlos L. Perez, MD, Dallas, TX; George Petty,
lopathy. Two of us (J.O.S. and F.E.C.) have seen MD, Rochester, MN; Steven Putnam, MD, Charlotte, NC; S.R.
three patients without encephalopathy who had cen- Rana, MD, Pittsburgh, PA; George P. Rice, MD, Ottawa, Canada;
tral callosal changes. Eric J. Russell, MD, Chicago, IL; Rosa Tang, MD, Houston, TX;
Daniel Tesfaye, MD, Wilmington, NC; E. Uyama, MD, Kumamoto,
In 1991, one of us (A.D.G.) published MR images Japan; James P. Valeriano, MD, Pittsburgh, PA; John Watson,
with central holes in the callosum that were errone- MD, Sydney, Australia; Brian G. Weinshenker, MD, Rochester,
ously attributed to ADEM.44 The patient’s diagnosis MN; Max H. Williams, MD, Queensland, Australia; James M.
was never clear and, in retrospect, was almost cer- Winkley, MD, Crestview Hills, KY; and Mitchell P. Wolin, MD,
Greenville, SC.
tainly SS. The central callosal holes in SS are not a
feature of ADEM or MS. In contrast to SS, the cal- The following references are non-peer reviewed material that
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December (2 of 2) 2003 NEUROLOGY 61 1787

 MRI findings in Susac's syndrome
J. O. Susac, F. R. Murtagh, R. A. Egan, et al.
Neurology 2003;61;1783-1787
DOI 10.1212/01.WNL.0000103880.29693.48

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