J Neurosurg Pediatrics 13:408–413, 2014

©AANS, 2014

Hypertrophic olivary degeneration in a child following

midbrain tumor resection: longitudinal diffusion tensor
imaging studies
Case report

Gunes Orman, M.D.,1 Thangamadhan Bosemani, M.D.,1 George I. Jallo, M.D., 2

Thierry A. G. M. Huisman, M.D.,1 and Andrea Poretti, M.D.1
Section of Pediatric Neuroradiology, Division of Pediatric Radiology, Russell H. Morgan Department of
1

Radiology and Radiological Science; and 2Division of Pediatric Neurosurgery, The Johns Hopkins School of
Medicine, Baltimore, Maryland

Hypertrophic olivary degeneration (HOD) is a dynamic process caused by disruptive lesions affecting compo-
nents of the Guillain-Mollaret triangle (GMT). The authors applied diffusion tensor imaging (DTI) to investigate
longitudinal changes of the GMT components in a child with HOD after neurosurgery for a midbrain tumor. Diffu-
sion tensor imaging data were acquired on a 1.5-T MRI scanner using a balanced pair of diffusion gradients along
20 noncollinear directions 1 day and 3, 6, and 9 months after surgery. Measurements from regions of interest (ROIs)
were sampled in the affected inferior olivary nucleus, ipsilateral red nucleus, and contralateral superior and inferior
cerebellar peduncles and dentate nucleus. For each ROI, fractional anisotropy and the mean, axial, and radial dif-
fusivities were calculated. In the affected inferior olivary nucleus, the authors found a decrease in fractional anisot-
ropy and an increase in mean, axial, and radial diffusivities 3 months after surgery, while 3 months later fractional
anisotropy increased and diffusivities decreased. For all other GMT components, changes in DTI scalars were less
pronounced, and fractional anisotropy mildly decreased over time. A detailed analysis of longitudinal DTI scalars in
the various GMT components may shed light on a better understanding of the dynamic complex histopathological
processes occurring in pediatric HOD over time.
(http://thejns.org/doi/abs/10.3171/2014.1.PEDS13490)

Key Words      •      diffusion tensor imaging      •      magnetic resonance imaging      •     

children      •      hypertrophic olivary degeneration      •      inferior olivary nucleus      •     
Guillain-Mollaret triangle

H
ypertrophic olivary degeneration (HOD) is a sec-
ondary transsynaptic deafferentation of the inferior
olivary nucleus that occurs after disruption of the
dentato-rubro-olivary pathway, or Guillain-Mollaret trian-
gle (GMT).7 The GMT is defined by 3 gray matter nuclei:
the dentate nucleus, the red nucleus, and the inferior oli-
vary nucleus.8 These anatomical structures are connected
by 3 pathways: 1) olivary-dentate fibers, or olivocerebellar
fibers, arising from the hilum of the inferior olivary nucle-
us and crossing the midline through the inferior cerebel-
lar peduncle to reach the contralateral dentate nucleus, 2)
dentatorubral fibers arising from the contralateral dentate
nucleus, entering their own superior cerebellar peduncle
and decussating within the midbrain to reach the opposite
Abbreviations used in this paper: DTI = diffusion tensor imaging;
GMT = Guillain-Mollaret triangle; HOD = hypertrophic olivary de­­
generation; ROI = region of interest.
red nucleus, and 3) the ipsilateral central tegmental tract, or
rubro-olivary tract, descending from the red nucleus to the
original inferior olivary nucleus.8
Diffusion tensor imaging (DTI) is an advanced MRI
technique that allows investigation of the organization,
microstructure, and integrity of gray and white matter
structures in vivo.5,13,15 Recent cross-sectional studies in
children and adults with HOD showed that DTI can dem-
onstrate and quantify the disruption of the GMT’s com-
ponents.4,12,17 However, HOD is a dynamic process, and
progressive changes have been shown by neuropathologi-
cal examination and conventional MRI.6,7 The purpose of
this study is to investigate longitudinal DTI changes of
the GMT’s components in a child with HOD after neuro-
surgery for a midbrain tumor.
This article contains some figures that are displayed in color
on­line but in black-and-white in the print edition.

408 J Neurosurg: Pediatrics / Volume 13 / April 2014

Diffusion tensor imaging in hypertrophic olivary degeneration

Case Report

Presentation. This 14-year-old boy presented with

new-onset subtle intention tremor and dysdiadochokine-
sia of the left hand and bilateral horizontal gaze–evoked
nystagmus 3 months after resection of a midbrain pilocyt-
ic astrocytoma. Additionally, neurological examination
re­­vealed truncal ataxia, dysarthria, and increased muscle
tone in the right upper and lower extremities that became
apparent shortly after neurosurgery. Palatal myoclonus
was not present.
Conventional MRI and DTI. The MRI studies were
acquired on a 1.5-T clinical MR scanner (Avanto, Sie-
mens) using a standard 8-channel head coil. The standard
departmental protocols included multiplanar T1- and T2-
weighted images, an axial FLAIR sequence, multiplanar
T1-weighted images obtained after intravenous injection
of a Gd-based contrast agent and a single-shot spin echo,
and an echo planar axial DTI sequence with diffusion
gradients along 20 noncollinear directions. An effective
high b-value of 1000 sec/mm2 was used for each of the
20 diffusion-encoding directions. We performed an ad-
ditional measurement without diffusion weighting (b = 0
sec/mm2). For the acquisition of the DTI data, the follow-
ing parameters were used: TR 7100 msec, TE 84 msec,
slice thickness 2.5 mm, FOV 240 × 240 mm, and matrix
size 192 × 192. Parallel imaging iPAT factor 2 (Siemens)
with GRAPPA (generalized auto-calibrating partial par- Fig. 1.  Axial T2- (A) and postcontrast T1- (B) weighted images show-
allel acquisition reconstruction) was used. The acquisition ing a multilobulated, predominantly cystic tumor centered in the left mid-
was repeated twice to enhance the signal-to-noise ratio. brain extending superiorly into the left cerebral peduncle and inferiorly
Diffusion tensor imaging data were acquired 1 day to the level of the pons. The solid, nodular component of the tumor
and 3, 6, and 9 months after neurosurgery of a neoplasm demonstrates heterogeneous enhancement (arrow in B). Axial T2- (C)
affecting the left GMT. and postcontrast T1- (D) weighted images obtained 9 months after neu-
rosurgery, demonstrating a postsurgical disruptive lesion involving the
Quantitative DTI Analysis. Diffusion tensor imaging left midbrain with a T2-hyperintense lesion (arrow in C) that most likely
data of the patient were transferred to an offline work- represents residual tumor unchanged in size over time. Additionally,
station for further postprocessing. DtiStudio, DiffeoMap, minimal linear enhancement along the resection cavity is noted (arrow
in D).
and RoiEditor software (available at www.MriStudio.org)
were used. After correcting for eddy currents and motion
artifacts, all images were coregistered to one another us- 2). T2 hyperintensity and enlargement of the left inferior
ing a 12-mode affine transformation. Subsequently, the olivary nucleus were noted 3 months later, confirming left
following maps were generated: fractional anisotropy, HOD. The last follow-up MRI study obtained 9 months
vector, color-coded fractional anisotropy, mean diffusiv- after surgery revealed no interval changes in T2 hyper-
ity, axial diffusivity, and radial diffusivity. After rigid intensity and degree of enlargement of the left inferior
transformation for adjustment of position and rotation of olivary nucleus. Contrast enhancement in the left inferior
images, regions of interest (ROIs) were drawn manually olivary nucleus was absent on all studies.
using the color-coded fractional anisotropy maps and the Absolute values of DTI scalars derived from the
T2-weighted images, which have been coregistered to the GMT components are shown in Table 1, and their chang-
es over time are illustrated in Fig. 3. In the inferior olivary
DT images. Regions of interest were positioned within
nucleus, fractional anisotropy prominently decreased at 3
the inferior olivary nucleus, the ipsilateral red nucleus,
months postsurgery, increased without achieving the ini-
contralateral inferior cerebellar peduncle, dentate nucle-
tial value 3 months later, and remained stable at 9 months
us, and superior cerebellar peduncle. For each ROI, frac- after surgery. The mean diffusivity, axial diffusivity,
tional anisotropy, mean diffusivity, axial diffusivity, and and radial diffusivity had an opposite course from that
radial diffusivity values were extracted. of fractional anisotropy. Compared with the left inferior
Imaging Findings. Conventional MRI showed a CSF- olivary nucleus, fractional anisotropy values in the other
filled postsurgical defect involving the medial portion of GMT components were less prominently altered.
the left midbrain with residual tumor that was stable in
size over time (Fig. 1). A mild T2 hyperintense signal and Discussion
enlargement of the left inferior olivary nucleus was first
seen 3 months after surgery and suggested left HOD (Fig. Hypertrophic olivary degeneration is an intriguing

J Neurosurg: Pediatrics / Volume 13 / April 2014 409

 G. Orman et al.

Fig. 2.  Axial T2-weighted images (A–D) and color-coded fractional anisotropy maps (E–H) at the level of the medulla 1 day
and 3, 6, and 9 months after surgery. Three months after surgery, the left inferior olivary nucleus appeared mildly enlarged and
exhibited T2 hyperintensity (arrow in B). Enlargement and T2 hyperintensity of the left inferior olivary nucleus became more
prominent 6 and 9 months after surgery (arrows in C and D). Retrocerebellar artifacts after midline suboccipital craniotomy are
seen in panel A. Axial color-coded fractional anisotropy maps show a mild attenuation in signal of the left inferior olivary nucleus
(arrows in E–H) at 3, 6, and 9 months after surgery compared with the right inferior olivary nucleus.

phenomenon affecting the inferior olivary nucleus. It is this causes the removal of inhibition of the electrotonic
caused by disruptive lesions of the afferent GMT com- gap junctions in the inferior olivary nucleus.3,18 On his-
ponents (dentatorubral tract and central tegmental tract) topathology, disinhibition and deafferentation of the in-
resulting in a transsynaptic deafferentation of the infe- ferior olivary nucleus result in vacuolar degeneration
rior olivary nucleus.7 In children, disruptive lesions of and enlargement of neurons and an increase in glial cells
the GMT may include low- and high-grade tumors and and hypertrophy of astrocytes.6 Hypertrophic olivary
vascular malformations.10,12,14,16,21 Neurophysiologically, degeneration is not static, but it is a reactive, dynamic,
TABLE 1: Diffusion tensor imaging scalars derived from the left GMT components on 4 postsurgical follow-up studies*

GMT Component Time Since Op FA MD† AD† RD†

ION 1 day 0.253 1.154 1.459 1.001
3 mos 0.111 1.325 1.483 1.246
6 mos 0.202 0.929 1.124 0.831
9 mos 0.201 1.034 1.220 0.941
ICP 1 day 0.634 0.936 1.725 0.541
3 mos 0.577 0.975 1.677 0.624
6 mos 0.538 1.016 1.708 0.670
9 mos 0.532 1.025 1.714 0.680
DN 1 day 0.188 1.051 1.262 0.945
3 mos 0.175 1.117 1.309 1.021
6 mos 0.182 1.013 1.317 0.861
9 mos 0.172 1.009 1.330 0.848
SCP 1 day 0.711 0.880 1.763 0.439
3 mos 0.712 0.973 2.037 0.442
6 mos 0.709 0.986 1.941 0.508
9 mos 0.671 0.978 1.893 0.521
RN 1 day 0.293 0.984 1.306 0.824
3 mos 0.245 1.004 1.343 0.834
6 mos 0.236 1.436 1.766 1.271
9 mos 0.234 1.464 1.812 1.291

*  AD = axial diffusivity; DN = dentate nucleus; FA = fractional anisotropy; ICP = inferior cerebellar peduncle; ION = inferior olivary
nucleus; MD = mean diffusivity; RD = radial diffusivity; RN = red nucleus; SCP = superior cerebellar peduncle.
†  Values are × 10−3 mm2/sec.

410 J Neurosurg: Pediatrics / Volume 13 / April 2014

Diffusion tensor imaging in hypertrophic olivary degeneration
Fig. 3.  Longitudinal evolution of DTI scalars for the different components of the left GMT. AD = axial diffusivity; DN = dentate
nucleus; FA = fractional anisotropy; ICP = inferior cerebellar peduncle; ION = inferior olivary nucleus; MD = mean diffusivity; RD
= radial diffusivity; RN = red nucleus; SCP = superior cerebellar peduncle.
and evolving process that may take months to years to
progress.1,7 Goto et al.6 classified the pathological changes
in HOD into 6 phases: 1) no olivary changes, observed
within 24 hours after onset; 2) degeneration of the oli-
vary amiculum (the capsule of white matter composing
the periphery of the oliva) at 2 to 7 days or more; 3) oli-
vary hypertrophy (the stage of mild olivary enlargement
with neuronal hypertrophy and no glial reaction) at about
3 weeks; 4) culminant olivary enlargement (the stage of
hypertrophy of both neurons and astrocytes) at about 8.5
months; 5) olivary pseudohypertrophy (the stage of neu-
ronal dissolution with gemistocytic astrocytes) at about
9.5 months and later; and 6) olivary atrophy (the stage of
neuronal disappearance with olivary atrophy and prom-
inent degeneration of the amiculum olivae) after a few
years.
Neuroimaging is necessary for diagnosis and con-
firmation of HOD and allows for study of the pathobi-
ology of HOD in vivo. Conventional neuroimaging is
mandatory for the diagnosis of HOD.2,7,11,16 Hypertrophic
olivary degeneration is characterized by enlargement and
increased T2 hyperintense signal of the inferior olivary
nucleus.7,11,16 On postcontrast T1-weighted images, hyper-
trophic inferior olivary nuclei are typically not enhanc-
ing.19 Familiarity with HOD and its neuroimaging ap-
pearance in pediatric patients will help to avoid potential
misdiagnosis of HOD as tumor recurrence, or, in high-
grade primary tumors, for example, medulloblastomas, as
metastatic lesions.
Conventional neuroimaging allows only a limited
understanding of the pathobiology of HOD. In our pa-
tient, a mild enlargement and T2 hyperintensity of the left
inferior olivary nucleus was visible 3 months after sur-
gery, which subsequently increased 6 months after sur-
gery. On conventional MRI, 3 distinct stages with specific
time intervals have been described: 1) T2 hyperintense
signal of the inferior olivary nucleus without hypertro-
J Neurosurg: Pediatrics / Volume 13 / April 2014
phy within the first 6 months after the disruptive event,
2) T2 hyperintense signal and hypertrophy of the infe-
rior olivary nucleus up to 3–4 years after HOD onset, and
3) T2 hyperintense signal with progressive resolution of
inferior olivary nucleus hypertrophy.7 These stages take
into account the dynamic course of HOD and match mac-
roscopic changes of the inferior olivary nucleus in HOD,
such as increased content of water as part of vacuolar de-
generation and gliosis (both are depicted by a hyperin-
tense signal on T2-weighted images). Conventional MRI,
however, does not provide detailed information about
the microscopic structural change in the inferior olivary
nucleus and involvement of the other GMT components.
As in the studied patient, the other components of the
GMT appear unremarkable on conventional MRI except
for the component directly affected by the primary lesion
or neurosurgical procedure. However, the involvement of
the other GMT components plays an important role in
the manifestation of HOD symptoms. Secondary damage
of the olivary-dentate tract may cause over-excitation of
the dentate nucleus and result in functional impairment of
the patient’s ability to estimate the direction of gravity as
recently demonstrated in a patient with HOD.20
Diffusion tensor imaging was shown to shed light on
the pathobiology of HOD and microstructural changes
occurring in the GMT components. At the mean post-
surgical time of 20 months, Dinçer et al. demonstrated
an increase in radial diffusivity, mean diffusivity, and
axial diffusivity and a decrease in fractional anisotropy
in all anatomical components of the GMT in 10 adults
with HOD.4 A decrease in fractional anisotropy and an
increase in radial diffusivity most likely represent demy-
elination in the late phase of HOD. Eight months after
surgery, Meoded et al. found higher fractional anisotropy
and axial diffusivity values of the inferior olivary nuclei
and lower fractional anisotropy but higher radial diffusiv-
ity values of all other GMT components in a child with
411

bilateral HOD compared with age-matched controls.12 An
increase in fractional anisotropy in the inferior olivary
nuclei may reflect rearrangement of regenerating axons
and shrunken neurons. Decreased fractional anisotropy
and increased radial diffusivity in the other GMT com-
ponents most likely reflect the demyelination process
associated with axonal degeneration in accordance with
histopathological studies. In this article, we applied DTI
to investigate dynamic changes of the different GMT
components in a child with HOD. In the left inferior oli-
vary nucleus, fractional anisotropy had a variable course
and decreased at 3 months after surgery. A decrease in
fractional anisotropy, an increase in radial diffusivity
and mean diffusivity, and an almost unchanged axial dif-
fusivity may reflect transsynaptic deafferentation at an
early stage of HOD with only mild olivary enlargement,
which was depicted on conventional MRI. Six months
after surgery, fractional anisotropy mildly increased and
mean diffusivity, axial diffusivity, and radial diffusivity
decreased. At this time, culminant olivary enlargement
secondary to hypertrophy of both neurons and astrocytes
was achieved.6 Olivary hypertrophy is expected to in-
crease fractional anisotropy, while astrocytic prolifera-
tion or gliosis is expected to reduce it. Because fractional
anisotropy increased in our patient 6 months after surgery,
it is arguable that neuronal hypertrophy may play a pre-
ponderant role in comparison with gliosis. Nine months
after surgery, fractional anisotropy remained stable, but
mean diffusivity, axial diffusivity, and radial diffusivity
increased. The lack of further increase in fractional an-
isotropy may represent a modified balance between neu-
ronal hypertrophy and astrocytic proliferation. At about 9
months and later after surgery, neuronal dissolution and
gemistocytic astrocytes represent the prominent histolog-
ical findings.6 In the other GMT components, changes in
DTI scalars are present but are less pronounced than in
the inferior olivary nucleus. A decrease in fractional an-
isotropy and an increase in radial diffusivity (particularly
in the inferior cerebellar peduncle and superior cerebel-
lar peduncle) most likely reflect secondary demyelination
associated with axonal degeneration, which occurs in
transneuronal degeneration. This finding is in accordance
with histopathological studies and previous DTI stud-
ies.4,12 In the red nucleus, however, changes in DTI scalars
over time are more prominent, particularly the increase in
mean diffusivity, axial diffusivity, and radial diffusivity.
The marked, global increase of the diffusivity in the red
nucleus is likely due to the primary lesion and postsurgi-
cal changes with resolution of necrotic tissue and forma-
tion of cystic spaces.
Neurological symptoms in patients with HOD in-
clude palatal myoclonus, truncal and limb ataxia, and
ocular movement disorders. These symptoms may be
severe, have a major impact on activities of daily living,
and consequently decrease the patient’s quality of life sig-
nificantly. In adults with HOD, symptomatic therapeutic
approaches using, for example, benzodiazepines or anti-
epileptic drugs have been attempted with varying results.9
A more detailed understanding of the pathobiology of
HOD and its dynamic changes over time using noninva-
sive techniques such as DTI may allow the development
412
G. Orman et al.
of more causative treatments. Additionally, longitudinal,
quantitative DTI studies may monitor therapeutic results
in patients with HOD.
Preoperative DTI and fiber tractography allow the
study of the integrity and course of the GMT as well as
the study of the GMT’s anatomical relationship to the
mass lesion, and these modalities determine children at
risk for HOD. In a similar approach, DTI and fiber trac-
tography are used to assess the risk of superior quadrantic
visual field deficits by injury of the Meyer’s loop in tem-
poral lobe resection.22,23 Integration of GMT fiber trac-
tography into stereo-navigational systems together with
T1-weighted anatomical images may reduce the risk of
HOD due to GMT injury by neurosurgery. The feasibil-
ity of integration of GMT fiber tractography into stereo-
navigational systems for patients with brainstem lesions
as well as its capability to prevent occurrence of HOD has
to be addressed by future prospective studies.
We are aware of some limitations in our report, in-
cluding the study of only 1 child with HOD, the retro-
spective nature of the study and the ROI-based analysis,
which is investigator dependent.
Conclusions
Our study shows that longitudinal detailed DTI anal-
ysis of the various components of GMT may shed light
on the dynamic complex histopathological processes oc-
curring in pediatric HOD over time. Future studies with
a larger number of subjects and dedicated high angular
DTI study of the brainstem may better address this issue.
Disclosure
The authors report no conflict of interest concerning the mate-
rials or methods used in this study or the findings specified in this
paper.
Author contributions to the study and manuscript preparation
include the following. Conception and design: Poretti, Huisman.
Acquisition of data: all authors. Analysis and interpretation of data:
Poretti, Orman, Bosemani. Drafting the article: Orman. Critically
revising the article: all authors. Reviewed submitted version of man-
uscript: all authors. Approved the final version of the manuscript on
behalf of all authors: Poretti. Study supervision: Poretti.
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Manuscript submitted September 23, 2013.
Accepted January 14, 2014.
Please include this information when citing this paper: published
online February 14, 2014; DOI: 10.3171/2014.1.PEDS13490.
Address correspondence to: Andrea Poretti, M.D., Section of
Pediatric Neuroradiology, Division of Pediatric Radiology, Russell
H. Morgan Department of Radiology and Radiological Science,
Charlotte R. Bloomberg Children’s Center, Sheikh Zayed Tower,
Rm. 4174, 1800 Orleans St., Baltimore, MD 21287. email: aporett1
@jhmi.edu.
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