METHODS: Sixty healthy adult subjects aged 22-76-year-old (mean ± standard deviation=47.27 ± 18.29) participated in the head impulse paradigm and suppression head impulse paradigm using the video head impulse test. The Head impulse paradigm was used to assess all 6 semicircular canals, while suppression head impulse paradigm measured only the horizontal canals. Twenty subjects aged 22-40-year-old (25.25 ± 4.9) underwent a second session for the test-retest reliability.
RESULTS: There were good test-retest reliability for both measures (right horizontal head impulse paradigm, intraclass correlation coefficient=0.80; left horizontal head impulse paradigm, intraclass correlation coefficient=0.77; right anterior head impulse paradigm, intraclass correlation coefficient=0.86; left anterior head impulse paradigm, intraclass correlation coefficient=0.78; right posterior head impulse paradigm, intraclass correlation coefficient=0.78; left posterior head impulse paradigm, intraclass correlation coefficient=0.75; right horizontal suppression head impulse paradigm, intraclass correlation coefficient=0.76; left horizontal suppression head impulse paradigm, intraclass correlation coefficient=0.79). The test-retest reliability for suppression head impulse paradigmanti-compensatory saccade latency and amplitude were moderate (right latency, intraclass correlation coefficient=0.61; left latency, intraclass correlation coefficient=0.69; right amplitude, intraclass correlation coefficient=0.69; left amplitude, intraclass correlation coefficient=0.58). There were no significant effects of age on head impulse paradigm and suppression head impulse paradigm vestibulo-ocular reflex gain values and suppression head impulse paradigmsaccade latency. However, the saccade amplitude became smaller with increasing age, P < .001. The horizontal suppression head impulse paradigm vestibuloocular reflex gain values were significantly lower than the head impulse paradigm for both sides (right, P = .004; left, P = .004).
CONCLUSION: There was good test-retest reliability for both measures, and the gain values stabilized with age. However, suppression head impulse paradigm anti-compensatory saccade latency and amplitude had lower test-retest reliability than the gain. The suppression head impulse paradigm vestibulo-ocular reflex gain was lower than the head impulse paradigm and its anti-compensatory saccade amplitude reduced with increasing age.
PURPOSE: The aim of this study was to report a case of OTR with contralateral internuclear ophthalmoplegia (INO) and fifth and seventh cranial nerve palsies.
CASE REPORT: A 51-year-old gentleman with underlying diabetes mellitus presented with sudden onset of diplopia for 3 days. On examination, his visual acuity was 20/30 bilaterally without a relative afferent pupillary defect. He had a right OTR consisting of a right head tilt, a skew deviation with a left eye hypertropia, and bilateral ocular torsion (right excyclotorsion and left incyclotorsion) with nystagmus. He also had a left adduction deficit and right abduction nystagmus consistent with a left INO. Ocular examination revealed evidence of proliferative diabetic retinopathy bilaterally. Two days after the initial presentation, the patient developed left seventh and fifth cranial nerve palsies. MRI showed left pontine infarction and multiple chronic lacunar infarctions. There was an incidental finding of a vascular loop compression on cisternal portions of the left trigeminal, facial, and vestibulocochlear nerves. Antiplatelet treatment was started on top of a better diabetic control. The diplopia was gradually resolved with improved clinical signs. In this case, the left pontine infarction had likely affected the terminal decussated part of the vestibulocochlear nerve from the right VOR pathway, medial longitudinal fasciculus, and cranial nerve nuclei in the left pons.
CONCLUSIONS: The OTR can be ipsilateral to the lesion if the lesion is before the decussation of the VOR pathway in the pons, or it can be contralateral to the lesion if the lesion is after the decussation. In case of an OTR that is associated with contralateral INO and other contralateral cranial nerves palsy, a pathology in the pons that is contralateral to the OTR should be considered. Neuroimaging study can hence be targeted to identify the possible cause.