Case Re

Truncal Ataxia From InfarctiOlivary N

Jae Hyun Park, MD,* Sookyung Ryoo

Sand Won Seo, MD, PhD,* an

ay b

atax

arat

llary

ral t

tibu

edul

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

(TBM). Antitubercul

time. After 6 weeks

had improved, and h

activities of daily liv

while still receiving

to exhibit unsteadine

tilted to the left si

was admitted to our hospital, he was unable to walk with-

out assistance. His neurologic examination revealed

left side regardless

d. He demonstrated

tongue weakness.

ealed lymphocyte-

, 96% lymphocytes)

(93 mg/dL), normal

tio (60:115 mg/dL),

compared with previous findings. Brain magnetic reso-

nance imaging revealed a lesion in the right medial region

involve the medial lemniscus, leading to sensory ataxia.

Suwon, Korea.

School of Medicine, 50 Ilwon-dong, Kangnam-gu, Seoul 135-710,

Korea. E-mail: sangwonseo@empal.com.1052-3057/$ - see front matter

However, the patients gait disturbance remained un-

changed regardless ofwhetherhis eyeswere openorclosed. 2012 by National Stroke AssociationDiscussion

The present case suggests that lesions in the ION can

cause contralesional truncal ataxia. Such lesions might

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 Universityof the medulla involving the inferior olivary nucleus

(ION) (Figure 1). High-dose intravenous corticosteroid

therapy was initiated, and the patient demonstrated re-

markable clinical improvement after 2 days of treatment.

From the *Department of Neurology, Samsung Medical Center,

Sungkyunkwan University School of Medicine, Seoul, Korea; and

Department of Neurology, Ajou University School of Medicine,frequently slipped down to the left.

The patients symptoms progressed, and by the time he

and normal adenosine deaminase level (4.7 IU/L; normal

range, 0-10 IU/L), which were significantly improveddoi:10.1016/j.jstrokece

Journal of Stroke and Cosed with tuberculosis meningitis

osis therapy was initiated at that

of therapy, the patients symptoms

e was able to participate in normal

ing. At 1 month before admission,

antituberculosis therapy, he began

ss of gait. His wife reported that he

de when sitting or standing and

minimally decreased proprioception

He showed a tendency to fall to the

of whether his eyes were open or close

no nystagmus, ophthalmoplegia, or

Cerebrospinal fluid analysis rev

dominant pleocytosis (33 cells/mm3

with a mildly elevated protein level

cerebrospinal fluid:serum glucose rawith unsteadiness of gait. At 5 months before admission,

he had been diagn

prominent axial truncal ataxia, minimal limb ataxia, and

in all 4 extremities.Truncal ataxia in medullary infarction m

part of the medulla; however, truncal

olivary nucleus (ION) has received comp

with truncal ataxia due to medial medu

in the ION could produce a contralate

tory input to the contralesional ves

flocculus. Key Words: Tuberculosism

2012 by National Stroke Associationrebrovasdis.2010.11.001

erebrovascular Diseases, Vol. 21, No. 6 (Augu, MD,* So Young Moon, MD, PhD,

d Duk L. Na, MD, PhD*

e caused by involvement of the lateral

ia in infarction involving the inferior

ively little attention.We report a patient

infarction located in the ION. A lesion

runcal ataxia due to increased inhibi-

lar nucleus from the contralesional

latuberculosis meningitis.port

on Involving the InferiorucleusHow can we explain the truncal ataxia in ION? An earlier

st), 2012: pp 507-508 507

experimental study showed that the ION sends inhibitory

projections to the Purkinje cells of the contralateral floccu-

lus, which in turn inhibit the ipsilateral vestibular nu-

cleus.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 indi-

cating that contralesional truncal ataxia can be accompa-

nied 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 sup-

ported by a previous case involving a patient exhibiting

truncal ataxia with involvement of olivocerebellar fibers.4

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 asso-ciated with a lesion in the nucleus prepositus hypoglossiarea. Arch Neurol 2004;61:1440-1443.

2. Arts MP, De Zeeuw CI, Lips J, et al. Effects of nucleus pre-positus hypoglossi lesions on visual climbing fiber activityin the rabbit flocculus. J Neurophysiol 2000;84:2552-2563.

3. Bassetti C, Bogousslavsky J, Mattle H, et al. Medial medul-lary stroke: Report of seven patients and review of theliterature. Neurology 1997;48:882-890.

Figure 1. (A) T2-weighted brain magnetic reso-

nance imaging showing a small lesion in the right

medial region of the medulla involving the ION.

(B) Axial diagram of the medulla showing the loca-

tion of the ION and adjacent structures.

J.H. PARK ET AL.508In 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-4. LeeH, SohnCH.Axial lateropulsion as a solemanifestationof lateral medullary infarction: A clinical variant related torostral-dorsolateral lesion. Neurol Res 2002;24:773-774.

5. Lammie GA, Hewlett RH, Schoeman JF, et al. Tuberculouscerebrovascular disease: A review. J Infect 2009;59:156-166.

Truncal Ataxia From Infarction Involving the Inferior Olivary NucleusDiscussionReferences