Isolated Nodular Infarction
- Author(s)
- In Soo Moon; Ji Soo Kim; Kwang Dong Choi; Min-Jeong Kim; Sun-Young Oh; Hyung Lee; Hak-Seung Lee; Seong-Ho Park
- Keimyung Author(s)
- Lee, Hyung
- Department
- Dept. of Neurology (신경과학)
- Journal Title
- Stroke
- Issued Date
- 2009
- Volume
- 40
- Issue
- 2
- Keyword
- nodular infarction; cerebellum; vertigo; imbalance; head impulse test
- Abstract
- Background and Purpose: Isolated nodular infarction has rarely been described in human. The purpose of this study is to report clinical and laboratory findings of isolated nodular infarction.
Methods: Eight patients with isolated nodular infarction were recruited from 6 hospitals in Korea. All patients underwent a complete and standardized neurotological evaluation including ocular torsion, bithermal caloric tests, and rotatory chair test in addition to MRI and MR angiography.
Results: All patients presented with isolated vertigo and moderate to severe imbalance. The most common manifestation was unilateral nystagmus and falling in the opposite direction, which mimicked peripheral vestibulopathy. Six patients had unilateral lesion, and 2 showed bilateral lesions. The direction of the spontaneous nystagmus was all ipsilesional in the unilateral lesion. However, head impulse and bithermal caloric tests were normal. Other findings include periodic alternating nystagmus, perverted head shaking nystagmus, paroxysmal positional nystagmus, and impaired tilt suppression of the postrotatory nystagmus. Hypoplasia of the ipsilesional vertebral artery was the only abnormal finding on MR angiography in 3 patients. The prognosis was excellent.
Conclusions: Isolated nodular infarction mostly presents with isolated vertigo mimicking acute peripheral vestibulopathy. However, severe imbalance and a negative head impulse test are important clinical discriminants between nodular infarcts and peripheral vestibular dysfunction. The findings of isolated nodular infarctions are consistent with impaired gravito-inertial processing of the vestibular signals and disrupted nodular inhibition on the vestibular secondary neurons and the velocity storage mechanism.
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