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Myogenic potentials generated by a click evoked vestibulospinal reflex can be easily recorded from the tonically contracting ipsilateral sternocleidomastoid muscle (SCM). These “vestibular evoked myogenic potentials” (VEMPs) are abolished by selective vestibular nerve section1 as well as by certain peripheral vestibular diseases.2-4 Click sensitive primary vestibular neurons arise from the saccular macula in the guinea pig5 and electrical stimulation of these neurons in the cat evokes inhibitary postsynaptic potentials in ipsilateral SCM motor neurons which are abolished by transection of the medial vestibulospinal tract.6 These clinical and neurophysiological data suggest that VEMPs are mediated by a pathway consisting of the saccular macula, its primary neurons, vestibulospinal neurons from the lateral vestibular nucleus, the medial vestibulospinal tract, and finally motor neurons of the ipsilateral SCM. Therefore a lesion anywhere in this pathway could result in abnormal VEMPs. We studied VEMPs in three patients with definite multiple sclerosis7 to search for lesions in the vestibulospinal pathways.
Patient 1, a woman aged 30, and patient 2, a man aged 32, both showed dysarthria, cerebellar ataxia, bilateral internuclear ophthalmoplegia, and a spastic tetraparesis. Patient 3, a woman aged 36, showed cerebellar ataxia and a spastic tetraparesis only. Apart from VEMPs, all patients underwent auditory evoked potential (AEP) testing as well as MRI.
Our recording methods have been described previously.2 3Briefly, surface EMG activity was recorded in the supine patient from symmetric sites over the upper half of each SCM with a reference electrode on the lateral end of the upper sternum. During the recording, the patients were instructed to rotate their heads to the opposite side to the stimulated ear to activate the SCM. Rarefaction clicks (0.1 ms, 95 dB normal hearing level) were presented through a headphone. The responses to 100 stimuli were averaged twice. Our normal control values have been reported previously.2 3 Briefly, all normal subjects show a biphasic response (p13-n23) from the ipsilateral SCM. The mean (SD) of the positive peak (p13)=11.4 (0.8) ms; the mean (SD) of the negative peak (n23)=20.8 (2.3) ms. We defined the mean+2 SD as the upper limit of the normal range—that is, p13=13 ms and n23=25.4 ms.
All of the six sides in three patients showed biphasic responses (p13-n23) with significantly prolonged latencies. Patient 1 showed prolonged p13 and n23 on both sides (right p13=16.7, n23=26.9 ms; left p13=19.8, n23=29.2 ms, figure A). Patients 2 and 3 showed bilaterally prolonged p13 (right p13=15.3, left p13=16.5 ms (patient 2), and right p13=15.0, left p13=18.5 ms (patient 3). In patient 1 the latency of the left p13 (19.8 ms) was longer than that of the right p13 (16.7ms); in this patient the interpeak latency between waves I and V of the AEP was significantly prolonged only on the right (right=5.14 ms, left=4.30 ms, figure B).
T2 weighted MRI of patient 1 showed high intensity areas in the tegmentum of the pons on both sides involving the vestibulospinal tracts bilaterally (figure C). Patients 2 and 3 also had high intensity areas in the same areas. Apart from lesions in this area, all showed high signal intensity areas in the cerebral white matter.
This preliminary study shows that latencies of a vestibulospinal reflex can be prolonged in multiple sclerosis. As in these three patients the VEMPs were remarkably delayed rather than simply abolished as occurs in patients with peripheral vestibular lesions,2-4 the VEMP delay could be attributed to demyelination either of primary afferent axons at the root entry zone or secondary vestibulospinal tract axons rather than to lesions involving vestibular nucleus neurons. The MRI findings in these patients were not inconsistent with this proposition. Measurement of VEMPs could be a useful clinical test to evaluate function of the vestibulospinal pathway and for detecting subclinical vestibulospinal lesions in suspected multiple sclerosis.
This study was supported by a Research Grant from the Intractable Diseases Fund (Vestibular Disorders) of the Ministry of Health and Welfare, Japan (1999).
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