Persistent Nystagmus in Chronic Phase of Lateral Medullary Infarction
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Background and Purpose We aimed to determine the patterns and mechanisms of persistent nystagmus (PN) lasting >1 year in lateral medullary infarction (LMI). Methods We recruited 13 patients with PN due to LMI and another 13 with transient nystagmus (TN) (<1 year) as control. All patients underwent oculography, rotatory chair test, caloric test, bedside head impulse test, dizziness handicap inventory (DHI), and brain MRI. Results All patients had spontaneous, contralesional, horizontal-torsional nystagmus during the acute phase. Although two patients exhibited consistent contralesional torsional nystagmus, most patients (11/13, 85%) with PN evolved from the initial contralesional to ipsilesional nystagmus. During horizontal gaze, the patterns of ipsilesional PN were diverse; torsional (n=5), torsional-downbeat (n=2), horizontal (n=2), and horizontal nystagmus while looking at the lesion side, and torsional nystagmus while looking at the opposite side (n=2). During rotatory chair test, the gains of the vestibulo-ocular reflex in the PN group were lower than those in the TN group to the lesion side at 0.02 and 0.64 Hz. The caudal and ventrolateral parts of the vestibular nuclei were mostly involved in patients with PN. The DHI score did not differ between the groups. Conclusions PN patterns frequently change in LMI. Resultant vestibular asymmetry after vestibular afferents or cerebellar inhibitory pathway damage and/or inappropriate vestibular compensation may be responsible for PN in LMI. Impairment of the horizontal or vertical neural integrators may be another cause. The presence of PN does not necessarily indicate more severe dizziness in LMI.
Abstract
Background and Purpose We aimed to determine the patterns and mechanisms of persistent nystagmus (PN) lasting >1 year in lateral medullary infarction (LMI). Methods We recruited 13 patients with PN due to LMI and another 13 with transient nystagmus (TN) (<1 year) as control. All patients underwent oculography, rotatory chair test, caloric test, bedside head impulse test, dizziness handicap inventory (DHI), and brain MRI. Results All patients had spontaneous, contralesional, horizontal-torsional nystagmus during the acute phase. Although two patients exhibited consistent contralesional torsional nystagmus, most patients (11/13, 85%) with PN evolved from the initial contralesional to ipsilesional nystagmus. During horizontal gaze, the patterns of ipsilesional PN were diverse; torsional (n=5), torsional-downbeat (n=2), horizontal (n=2), and horizontal nystagmus while looking at the lesion side, and torsional nystagmus while looking at the opposite side (n=2). During rotatory chair test, the gains of the vestibulo-ocular reflex in the PN group were lower than those in the TN group to the lesion side at 0.02 and 0.64 Hz. The caudal and ventrolateral parts of the vestibular nuclei were mostly involved in patients with PN. The DHI score did not differ between the groups. Conclusions PN patterns frequently change in LMI. Resultant vestibular asymmetry after vestibular afferents or cerebellar inhibitory pathway damage and/or inappropriate vestibular compensation may be responsible for PN in LMI. Impairment of the horizontal or vertical neural integrators may be another cause. The presence of PN does not necessarily indicate more severe dizziness in LMI.
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