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Case Report

Truncal Ataxia From Infarction Involving the Inferior


Olivary Nucleus
Jae Hyun Park, MD,* Sookyung Ryoo, MD,* So Young Moon, MD, PhD,
Sand Won Seo, MD, PhD,* and Duk L. Na, MD, PhD*

Truncal ataxia in medullary infarction may be caused by involvement of the lateral


part of the medulla; however, truncal ataxia in infarction involving the inferior
olivary nucleus (ION) has received comparatively little attention. We report a patient
with truncal ataxia due to medial medullary infarction located in the ION. A lesion
in the ION could produce a contralateral truncal ataxia due to increased inhibitory input to the contralesional vestibular nucleus from the contralesional
flocculus. Key Words: Tuberculosismedullatuberculosis meningitis.
2012 by National Stroke Association

A 49-year-old man was admitted to our hospital


with unsteadiness of gait. At 5 months before admission,
he had been diagnosed with tuberculosis meningitis
(TBM). Antituberculosis therapy was initiated at that
time. After 6 weeks of therapy, the patients symptoms
had improved, and he was able to participate in normal
activities of daily living. At 1 month before admission,
while still receiving antituberculosis therapy, he began
to exhibit unsteadiness of gait. His wife reported that he
tilted to the left side when sitting or standing and
frequently slipped down to the left.
The patients symptoms progressed, and by the time he
was admitted to our hospital, he was unable to walk with-

From the *Department of Neurology, Samsung Medical Center,


Sungkyunkwan University School of Medicine, Seoul, Korea; and
Department of Neurology, Ajou University School of Medicine,
Suwon, Korea.
Received September 27, 2010; accepted November 1, 2010.
Supported by Grant A050079 from the Korea Health 21 R&D
Project, Ministry of Health and Welfare, Republic of Korea.
Address reprint requests to Sand Won Seo, MD, PhD, Department
of Neurology, Samsung Medical Center, Sungkyunkwan University
School of Medicine, 50 Ilwon-dong, Kangnam-gu, Seoul 135-710,
Korea. E-mail: sangwonseo@empal.com.
1052-3057/$ - see front matter
2012 by National Stroke Association
doi:10.1016/j.jstrokecerebrovasdis.2010.11.001

out assistance. His neurologic examination revealed


prominent axial truncal ataxia, minimal limb ataxia, and
minimally decreased proprioception in all 4 extremities.
He showed a tendency to fall to the left side regardless
of whether his eyes were open or closed. He demonstrated
no nystagmus, ophthalmoplegia, or tongue weakness.
Cerebrospinal fluid analysis revealed lymphocytedominant pleocytosis (33 cells/mm3, 96% lymphocytes)
with a mildly elevated protein level (93 mg/dL), normal
cerebrospinal fluid:serum glucose ratio (60:115 mg/dL),
and normal adenosine deaminase level (4.7 IU/L; normal
range, 0-10 IU/L), which were significantly improved
compared with previous findings. Brain magnetic resonance imaging revealed a lesion in the right medial region
of the medulla involving the inferior olivary nucleus
(ION) (Figure 1). High-dose intravenous corticosteroid
therapy was initiated, and the patient demonstrated remarkable clinical improvement after 2 days of treatment.

Discussion
The present case suggests that lesions in the ION can
cause contralesional truncal ataxia. Such lesions might
involve the medial lemniscus, leading to sensory ataxia.
However, the patients gait disturbance remained unchanged regardless of whether his eyes were open or closed.
How can we explain the truncal ataxia in ION? An earlier

Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 6 (August), 2012: pp 507-508

507

J.H. PARK ET AL.

508

Figure 1. (A) T2-weighted brain magnetic resonance imaging showing a small lesion in the right
medial region of the medulla involving the ION.
(B) Axial diagram of the medulla showing the location of the ION and adjacent structures.

experimental study showed that the ION sends inhibitory


projections to the Purkinje cells of the contralateral flocculus, which in turn inhibit the ipsilateral vestibular nucleus.1,2 Thus, lesions in the ION reduce inhibitory input
to the contralesional flocculus, thereby disinhibiting
inhibitory projections to the vestibular nucleus and
resulting in contralesional vestibular dysfunction.
Our findings are consistent with previous reports indicating that contralesional truncal ataxia can be accompanied by medial medullary infarction.3 Those previous
reports did not suggest the exact locations of lesions,
however. Our explanation in this case also might be supported by a previous case involving a patient exhibiting
truncal ataxia with involvement of olivocerebellar fibers.4
In the present case, arteritis in TBM might have caused
infarction in the ION, considering that our patient had no
cardiovascular risk factors and responded well to steroid
treatment. Although the timing of onset of cerebral infarc-

tion is variable in TBM, cerebral infarction seems to be


most common in cases of longer duration, like our
patient.5

References
1. Seo SW, Shin HY, Kim SH, et al. Vestibular imbalance associated with a lesion in the nucleus prepositus hypoglossi
area. Arch Neurol 2004;61:1440-1443.
2. Arts MP, De Zeeuw CI, Lips J, et al. Effects of nucleus prepositus hypoglossi lesions on visual climbing fiber activity
in the rabbit flocculus. J Neurophysiol 2000;84:2552-2563.
3. Bassetti C, Bogousslavsky J, Mattle H, et al. Medial medullary stroke: Report of seven patients and review of the
literature. Neurology 1997;48:882-890.
4. Lee H, Sohn CH. Axial lateropulsion as a sole manifestation
of lateral medullary infarction: A clinical variant related to
rostral-dorsolateral lesion. Neurol Res 2002;24:773-774.
5. Lammie GA, Hewlett RH, Schoeman JF, et al. Tuberculous
cerebrovascular disease: A review. J Infect 2009;59:156-166.

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