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Asymmetric Optokinetic Afterresponse in Patients with Vestibular Neuritis
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The symmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 14 patients with vestibular neuritis, as well as in 50 normals. The patients were examined at onset of symptoms and at follow-up 3 and 12 months later. At onset, OKAN was found mainly to reflect the spontaneous nystagmus. Although the spontaneous nystagmus disappeared in all patients within 3 months, both OKAN I and OKAN II was asymmetric at the 3- and 12-month check-ups. OKAN beating toward the lesioned ear was weaker than the OKAN beating toward the healthy ear. Thus, the asymmetric vestibular function was reflected not only in the OKAN I, but also by an asymmetry in OKAN II. Between the 3- and 12-month check-ups, asymmetry in OKAN declined, even among those patients who showed no improvement in caloric response during that time. The decreasing asymmetry in OKAN with time after lesion was, however, related to the disappearance of a positional nystagmus. Hence, the results may be interpreted as suggesting OKAN not only to be affected by vestibular side-difference, but also to be modified by the process responsible for vestibular compensation following a peripheral vestibular lesion.
Title: Asymmetric Optokinetic Afterresponse in Patients with Vestibular Neuritis
Description:
The symmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 14 patients with vestibular neuritis, as well as in 50 normals.
The patients were examined at onset of symptoms and at follow-up 3 and 12 months later.
At onset, OKAN was found mainly to reflect the spontaneous nystagmus.
Although the spontaneous nystagmus disappeared in all patients within 3 months, both OKAN I and OKAN II was asymmetric at the 3- and 12-month check-ups.
OKAN beating toward the lesioned ear was weaker than the OKAN beating toward the healthy ear.
Thus, the asymmetric vestibular function was reflected not only in the OKAN I, but also by an asymmetry in OKAN II.
Between the 3- and 12-month check-ups, asymmetry in OKAN declined, even among those patients who showed no improvement in caloric response during that time.
The decreasing asymmetry in OKAN with time after lesion was, however, related to the disappearance of a positional nystagmus.
Hence, the results may be interpreted as suggesting OKAN not only to be affected by vestibular side-difference, but also to be modified by the process responsible for vestibular compensation following a peripheral vestibular lesion.
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