Otology & Neurotology 35:1633Y1637 Ó 2014, Otology & Neurotology, Inc.
Cervical Vestibular Evoked Myogenic Potentials in Cerebellar Lesions Savvas S. Papacostas, Eleftherios Stelios Papathanasiou, Theodoros Kyriakides, and Marios Pantzaris Clinical Sciences, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus
Introduction: Reports about cervical vestibular evoked myogenic potentials (cVEMPs) in central nervous system lesions are scarce. Our experience with cerebellar lesions is still evolving, with only a few cases published. The purpose of this article is to present our cVEMP findings of 3 cases with cerebellar lesions. Materials and Methods: cVEMPs were performed using unilateral 120-dB peak SPL intensity 1 kHz tone air-conducted sound stimulation with contralateral masking noise, with recording from the tonically active sternocleidomastoid muscle. Results: Brain MRI scans showed a small focal lesion in the right middle cerebellar peduncle in our first case, 2 foci in the right middle cerebellar peduncle and cerebellar hemisphere in our second case, and lesions in the right superior and inferior
cerebellar peduncles near the fourth ventricle in our final case. All cVEMPs were normal. Discussion: cVEMPs seem to be unaffected by at least certain cerebellar peduncle and hemispheric lesions. Although an abnormal cVEMP result may suggest noncerebellar dysfunction, further work is needed, as the lesions reported may not be interrupting the known cerebellovestibular pathways. Normal cVEMP responses may also or otherwise be due to affected vestibular nuclei influenced by the above cerebellar lesions not being part of the cVEMP pathway. Key Words: Cerebellar hemisphereVCerebellar peduncleVMedial vestibulospinal tractV SacculeVsternocleidomastoid muscleVSound stimulation. Otol Neurotol 35:1633Y1637, 2014.
Cervical vestibular evoked myogenic potentials (cVEMPs) represent a noninvasive method of evaluating vestibular nervous system function. Using air-conducted sound, the response is thought to occur because the saccule is located close to the oval window (1). cVEMPs are recorded from the tonically active sternocleidomastoid muscle ipsilateral to the ear being examined and likely represents a short period of inhibition (2,3). cVEMPs are used routinely in the assessment of the functional integrity of the vestibular pathway, specifically that which involves the saccule, inferior vestibular nerve, vestibular nuclear complex, medial vestibulospinal tract, and the spinal accessory nerve (4,5). Reports about cVEMPs in central nervous system lesions are scarce, and our experience is dominated by peripheral vestibular system disorders such as Me´nie`re’s disease, vestibular neuritis, superior semicircular canal dehiscence, and other inner ear perilymphatic fistulas (6). Our experience in patients with cerebellar lesions is evolving, with only a few cases published (7,8), and more illustrative cases are required. Other studies involving lesions in the
posterior fossa have focused on the brainstem either alone or together with the cerebellum (9Y15). We describe 3 cases, two with isolated cerebellar vascular lesions and one probably with demyelinating lesions, which all had cVEMPs performed. MATERIALS AND METHODS BAEPs were performed in the standard manner (16). cVEMPs were performed using unilateral 120 dB peak SPL (pSPL) intensity 1 kHz tone air-conducted sound stimulation with contralateral 90 dB pSPL masking noise. The stimulation rate was 5 Hz in condensation mode, with a plateau of 3 cycles and a ramp of 2 cycles. Recording was performed from the tonically active sternocleidomastoid muscle (SCM) ipsilateral to the ear receiving tone stimuli, with the active recording electrode placed over the midpoint of the muscle, the reference electrode on the clavicle, and the ground on the forehead. The SCM was activated by asking the patient to lift their head up slightly from the pillow while in a supine position. Parallel recording of rectified EMG activity from the SCM was performed from the same recording electrodes and averaged. The response from 100 stimulations was averaged per trial, and for each ear, 2 trials were obtained and superimposed. The bandpass was 10 Hz to 1.5 kHz with a time base of 5 ms per division and a gain of 2,000. The first major positive peak was labeled p13, and the following negative peak was labeled n23. For the rectified EMG, the bandpass was 10 Hz
Address correspondence and reprint requests to Eleftherios Stelios Papathanasiou, Ph.D., The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus; E-mail: [email protected] The authors disclose no conflicts of interest. Supplemental digital content is available in the text.
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to 1.5 kHz, with a time base of 2 ms per division and a gain of 2,000. The final result with regard to amplitude was calculated as the ratio of the amplitude of the actual or ‘‘raw’’ cVEMP response (amplitude between p13 and n23) over the rectified averaged EMG amplitude. As the amplitude of both the ‘‘raw’’ cVEMP response and the EMG response is in microvolts (uV), the resulting ratio (called the corrected amplitude) is a dimensionless number. Statistical analysis was performed using the Student’s t test at the 5% significance level.
RESULTS The first case was a 28-year-old man with a patent foramen ovale and evidence of intra-atrial shunt. He presented with blurred vision in the right eye and severe headache 2 months previously. His brain MRI scan revealed a small focal lesion in the right middle cerebellar peduncle (see Figure, Supplemental Digital Content 1, http://links.lww.com/MAO/A237). The BAEP was within normal limits with left ear stimulation but poorly organized with right ear stimulation (see Figure, Supplemental Digital Content 2, http://links.lww.com/MAO/A238). Cervical vestibular evoked myogenic potentials were within normal limits bilaterally (see Figure, Supplemental Digital Content 2, http://links.lww.com/MAO/A238). The p13 peak times were 18.3 and 18.1 ms on the left (mean, 18.2 ms) and 14.6 and 13.2 ms on the right (mean, 13.9 ms). For our laboratory, the mean value of p13 from physiologically normal volunteers is 15.9 T 3.6 ms (mean oˆT standard deviation). This gives an upper limit of normal of 24.9 ms when adding 2.5 standard deviations to the mean. The mean interside difference, calculated at 4.3 ms, is within normal limits for our laboratory. The normal range for our laboratory, calculated after subtracting the right side from the left side, is -5.7 to 5.8 ms, after obtaining a mean of 0.07 T 2.29 ms. The range is calculated as mean T2.5 times the standard deviation. The corrected P13-N23 amplitude was 1.43 and 1.18 on the left (mean, 1.3) and 1.78 and 1.49 on the right (mean, 1.6). The normal range for the laboratory is 0.3 to 13.2, after a mean of 2.5 T 1.8 standard deviations. As amplitude is known to be skewed (17), the upper and lower limits of normal were calculated after logarithmic transformation. The interside amplitude difference (left side/right side) was found to be -0.3. The normal range for our laboratory is 0.3 to 4.4, after a mean of 0.03 T 0.24 standard deviations and with the same logarithmic transformation. Our second case was a 65-year-old man who experienced a cerebrovascular accident 2 months previously after warfarin discontinuation for cardiac catheterization. An MRI scan at 1.5 T revealed 2 foci in the right middle cerebellar peduncle and right cerebellar hemisphere respectively (see Figure, Supplemental Digital Content 3, http://links.lww.com/MAO/A239). Both the BAEPs and cVEMPs (see Figure, Supplemental Digital Content 4, http://links.lww.com/MAO/A240) were normal bilaterally. For the cVEMP specifically, the p13 peak times
were 12.8 and 14.8 ms on the left (mean, 13.8 ms) and 11.9 and 12.1 ms on the right (mean, 12.0 ms). The corrected P13-N23 amplitude was 1.02 and 0.78 on the left (mean, 0.9) and 0.94 and 0.61 on the right (mean, 0.8). Our third case was a 20-year-old man who had an episode of diplopia probably because of demyelinating disease. This event happened 1.5 months before our evoked examinations. On examination, there was no ophthalmoplegia of note or any cerebellar signs. An MRI scan at 1.5 T (Fig. 1) showed circumscribed lesions in the right superior and inferior cerebellar peduncles near the fourth ventricle. Both the BAEPs and cVEMPs (Fig. 2) were normal bilaterally. For the cVEMP specifically, the P13 peak times were 13.6 and 14.1 ms on the left (mean, 13.9 ms) and 14.5 and 14.6 ms on the right (mean, 14.6 ms). The corrected P13-N23 amplitude was 4.0 and 2.9 on the left (mean, 3.5), and 2.3 and 1.8 on the right
FIG. 1. T2-weighted MRI images of this manuscript’s third case, with transverse (bottom figures) and sagittal (top figure) sections. In all figures, the white arrow points to the area of the lesions located in the right superior and inferior cerebellar peduncles.
Otology & Neurotology, Vol. 35, No. 9, 2014
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FIG. 2. Brainstem auditory evoked potentials, cVEMPs, and rectified EMG recordings shown as detailed in supplemental digital content 2 and 4 (http://links.lww.com/MAO/A238 and http://links.lww.com/MAO/A240). All responses were within normal limits.
(mean, 2.1). The interside corrected amplitude difference ratio was 1.7. When the values from all 3 cases were pooled, the mean value for the p13 absolute latency was calculated at 14.4 ms T 1.58 standard deviations. The p13-n23 corrected amplitude was found to be 1.53 T 0.60. With the Student’s t test, this gives t values of 0.67 and -0.03 for latency and corrected amplitude, respectively, when
compared with our control values, which is not statistically significant ( p 9 0.05). DISCUSSION In confirming and contributing to past studies, cVEMPs are unaffected by at least certain cerebellar peduncle and cerebellar hemispheric lesions. Otology & Neurotology, Vol. 35, No. 9, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
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It is known that the vestibulocerebellum (the flocculonodular lobe) receives afferent fibers from the ipsilateral vestibular ganglion and from the vestibular nuclei (18), via the inferior cerebellar peduncle (19). It is believed that the flocculus communicates with the superior vestibular nucleus (20Y22) via an inhibitory pathway (23). Efferent connections in the rhesus macaque have also been demonstrated between the flocculus and the ygroup of the vestibular nuclear complex, medial vestibular nucleus, and to a small extent, the inferior vestibular nucleus (20,24). These projections have been shown to course specifically along the caudal surface of the middle cerebellar peduncle and the lateral surface of the inferior cerebellar peduncle. The reason the cVEMPs remain normal in our and other similar articles may be because the lesions spare cerebellovestibular or vestibulocerebellar pathways, which course in specific areas of the peduncles and cerebellar hemispheres. In our first case, the lesion on MRI was located on the medial aspect of the middle cerebellar peduncle and midway rather than caudal or rostral. Our second case revealed one lesion on the lateral aspect of the middle cerebellar peduncle and midway between rostral and caudal and a second lesion within the right cerebellar hemisphere but at an appreciable distance from the midline ‘‘vestibulocerebellum.’’ Our third case revealed lesions on the medial aspects of the superior and inferior cerebellar peduncles. All of these cases would be expected to spare the above pathways. Previous studies do not describe the location of cerebellar lesions (7,8). This makes a comparison difficult to rule out the involvement of pathways between the vestibular nuclear complex and cerebellum. Another reason for the normal cVEMP may be due to the affected vestibular nuclei influenced by the above cerebellar lesions not being located along the cVEMP pathway. It is known from animal studies that secondary neurons within the lateral vestibular nucleus receive vestibular primary afferents from the ipsilateral sacculus (25Y28). Yet, from the literature, we know that the lateral vestibular nucleus does not receive projections from the flocculus (20), although projections do exist from the ‘‘b-zone’’ of the vermis (29,30). Projections to the flocculus are also absent from the lateral ventricular nucleus (31). The normal cVEMPs can be explained by the lateral vestibular nucleus as mediating this response. Also, the medial vestibulospinal tract, which is believed to be responsible for transmitting signals to the sternocleidomastoid muscle (5,32), receives contributions from the lateral nucleus (25,33Y42). Acknowledgments: The authors thank Ms. Elena Polycarpou and Ms. Christina Hadjiyianni for help with figure preparations.
REFERENCES 1. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentials generated by a click-evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatr 1994;57:190Y7.
2. Colebatch JG, Rothwell JC. Motor unit excitability changes mediating vestibulocollic reflexes in the sternocleidomastoid muscle. Clin Neurophysiol 2004;115:2567Y73. 3. Wit HP, Kingma CM. A simple model for the generation of the vestibular-evoked myogenic potential (VEMP). Clin Neurophysiol 2006;117:1354Y8. 4. Welgampola MS. Evoked potential testing in neuro-otology. Curr Opin Neurol 2008;21:29Y35. 5. Govender S, Rosengren SM, Colebatch JG. Vestibular neuritis has selective effects on air- and bone-conducted cervical and ocular vestibular evoked myogenic potentials. Clin Neurophysiol 2011; 122:1246Y55. 6. Baier B, Dieterich M. Vestibular-evoked myogenic potentials in ‘‘vestibular migraine’’ and Meniere’s disease. Ann N Y Acad Sci 2009;1164:324Y7. 7. Pollak L, Kushnir M, Stryjer R. Diagnostic value of vestibular evoked myogenic potentials in cerebellar and lower-brainstem strokes. Neurophysiologie Clinique 2006;36:227Y33. 8. Su CH, Young YH. Differentiating cerebellar and brainstem lesions with ocular vestibular-evoked myogenic potential test. Eur Arch Otorhinolaryngol 2011;268:923Y30. 9. Matsuzaki M, Murofushi T, Mizuno M. Vestibular evoked myogenic potentials in acoustic tumor patients with normal auditory brainstem responses. Euro Arch Otorhinolaryngol 1999;256:1Y4. 10. Itoh A, Kim YS, Yoshioka K, et al. Clinical study of vestibular-evoked myogenic potentials and auditory brainstem responses in patients with brainstem lesions. Acta Otolaryngol Suppl 2001;545:116Y9. 11. Chen CH, Young YH. Vestibular evoked myogenic potentials in brainstem stroke. Laryngoscope 2003;113:990Y3. 12. Sazgar AA, Akrami K, Akrmi S, Mehdizadeh J, Fezi A. Evaluation of brainstem function in patients with spasmodic dysphonia using vestibular evoked myogenic potentials and auditory brainstem responses. Acta Otolaryngol 2008;128:177Y80. 13. Eleftheriadou A, Deftereos N, Zarikas V, et al. The diagnostic value of earlier and later components of vestibular evoked myogenic potentials (VEMP) in multiple sclerosis. J Vestib Res 2009;19:59Y66. 14. Heide G, Luft B, Franke J, Schmidt P, Witte OW, Axer H. Brainstem representation of vestibular evoked myogenic potentials. Clin Neurophysiol 2010;121:1102Y8. 15. Gazioglou S, Boz C. Ocular and cervical vestibular evoked myogenic potentials in multiple sclerosis patients. Clin Neurophysiol 2012;123:1872Y9. 16. Chiappa KH. Evoked Potentials in Clinical Medicine, 3rd ed. Philadelphia, PA: Lippincott-Raven Press, 1997. 17. Oken BS. Statistics for evoked potentials. In Chiappa KH ed, Evoked Potentials in Clinical Medicine, 3rd ed. Philadelphia, PA: Lippincott-Raven publications, 1997;565Y77. 18. Kiernan JA. The Human Nervous System: An Anatomical Viewpoint. Baltimore, MD: Lippincott Williams & Wilkins Press, 2005. 19. Nolte J. The Human Nervous System: An Introduction to its Functional Anatomy. 3rd ed., St. Louis, MO: Mosby Year Book Press, 1993. 20. Langer T, Fuchs AF, Chubb MC, Scudder CA. Floccular efferents in the rhesus macaque as revealed by autoradiography and horseradish peroxidase. J Comp Neurol 1985; 235:26Y37. 21. Brodal A, Pompeiano O, Walberg F. The Vestibular Nuclei and their Connections, Anatomy and Functional Correlations. London, UK: The William Henderson Trust Lecture. Oliver & Boyd, 1962. 22. Zhang Y, Partasalis AM, Highstein SM. Properties of superior vestibular nucleus flocculus target neurons in the squirrel monkey. I. General properties in comparison with flocculus projecting neurons. J Neurophysiol 1995;73:2261Y78. 23. Pierrot-Deseilligny C, Milea D. Vertical nystagmus: clinical facts and hypothesis. Brain 2005;128:1237Y46. 24. Angaut P, Brodal A. The projection of the ‘‘vestibulocerebellum’’ onto the vestibular nuclei in the cat. Arch Ital Biol 1967; 105:441Y79. 25. Barmack NH. Central vestibular system: vestibular nuclei and posterior cerebellum. Brain Res Bull 2003;60:511Y41. 26. Wilson VJ, Gacek RR, Uchino Y, Susswein AJ. Properties of
Otology & Neurotology, Vol. 35, No. 9, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
CVEMPS AND CEREBELLAR LESIONS central vestibular neurons fired by stimulation of the saccular nerve. Brain Res 1978;251Y61. 27. Sato H, Imagawa M, Isu N, Uchino Y. Properties of saccular nerve-activated vestibulospinal neurons in cats. Exp Brain Res 1997;116:381Y8. 28. Uchino Y, Sato H, Suwa H. Excitatory and inhibitory inputs from saccular afferents to single vestibular neurons in the cat. J Neurophysiol 1997;78:2186Y92. 29. Andersson G, Oscarsson O. Climbing fiber microzones in cerebellar vermis and their projection to different groups of cells in the lateral vestibular nucleus. Exp Brain Res 1978;32:565Y79.
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30. Andersson G, Oscarsson O. Projections to lateral vestibular nucleus and cerebellar climbing fiber zones. Exp Brain Res 1978;32:549Y64. 31. Langer T, Fuchs AF, Scudder CA, Chubb MC. Afferents to the flocculus of the cerebellum in the rhesus macaque as revealed by retrograde transport of horseradish peroxidase. J Comp Neurol 1985;235:1Y25. 32. Kushiro K, Zakir M, Ogawa Y, Sato H, Uchino Y. Saccular and utricular inputs to SCM motoneurons of decerebrate cats. Exp Brain Res 1999;126:410Y6. 33. Brodal A. Neurological Anatomy, 3rd ed. New York, NY: Oxford University Press, 1981.
Otology & Neurotology, Vol. 35, No. 9, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
Cervical Vestibular Evoked Myogenic Potentials in Cerebellar Lesions Savvas S. Papacostas, Eleftherios Stelios Papathanasiou, Theodoros Kyriakides, and Marios Pantzaris Clinical Sciences, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus
Introduction: Reports about cervical vestibular evoked myogenic potentials (cVEMPs) in central nervous system lesions are scarce. Our experience with cerebellar lesions is still evolving, with only a few cases published. The purpose of this article is to present our cVEMP findings of 3 cases with cerebellar lesions. Materials and Methods: cVEMPs were performed using unilateral 120-dB peak SPL intensity 1 kHz tone air-conducted sound stimulation with contralateral masking noise, with recording from the tonically active sternocleidomastoid muscle. Results: Brain MRI scans showed a small focal lesion in the right middle cerebellar peduncle in our first case, 2 foci in the right middle cerebellar peduncle and cerebellar hemisphere in our second case, and lesions in the right superior and inferior
cerebellar peduncles near the fourth ventricle in our final case. All cVEMPs were normal. Discussion: cVEMPs seem to be unaffected by at least certain cerebellar peduncle and hemispheric lesions. Although an abnormal cVEMP result may suggest noncerebellar dysfunction, further work is needed, as the lesions reported may not be interrupting the known cerebellovestibular pathways. Normal cVEMP responses may also or otherwise be due to affected vestibular nuclei influenced by the above cerebellar lesions not being part of the cVEMP pathway. Key Words: Cerebellar hemisphereVCerebellar peduncleVMedial vestibulospinal tractV SacculeVsternocleidomastoid muscleVSound stimulation. Otol Neurotol 35:1633Y1637, 2014.
Cervical vestibular evoked myogenic potentials (cVEMPs) represent a noninvasive method of evaluating vestibular nervous system function. Using air-conducted sound, the response is thought to occur because the saccule is located close to the oval window (1). cVEMPs are recorded from the tonically active sternocleidomastoid muscle ipsilateral to the ear being examined and likely represents a short period of inhibition (2,3). cVEMPs are used routinely in the assessment of the functional integrity of the vestibular pathway, specifically that which involves the saccule, inferior vestibular nerve, vestibular nuclear complex, medial vestibulospinal tract, and the spinal accessory nerve (4,5). Reports about cVEMPs in central nervous system lesions are scarce, and our experience is dominated by peripheral vestibular system disorders such as Me´nie`re’s disease, vestibular neuritis, superior semicircular canal dehiscence, and other inner ear perilymphatic fistulas (6). Our experience in patients with cerebellar lesions is evolving, with only a few cases published (7,8), and more illustrative cases are required. Other studies involving lesions in the
posterior fossa have focused on the brainstem either alone or together with the cerebellum (9Y15). We describe 3 cases, two with isolated cerebellar vascular lesions and one probably with demyelinating lesions, which all had cVEMPs performed. MATERIALS AND METHODS BAEPs were performed in the standard manner (16). cVEMPs were performed using unilateral 120 dB peak SPL (pSPL) intensity 1 kHz tone air-conducted sound stimulation with contralateral 90 dB pSPL masking noise. The stimulation rate was 5 Hz in condensation mode, with a plateau of 3 cycles and a ramp of 2 cycles. Recording was performed from the tonically active sternocleidomastoid muscle (SCM) ipsilateral to the ear receiving tone stimuli, with the active recording electrode placed over the midpoint of the muscle, the reference electrode on the clavicle, and the ground on the forehead. The SCM was activated by asking the patient to lift their head up slightly from the pillow while in a supine position. Parallel recording of rectified EMG activity from the SCM was performed from the same recording electrodes and averaged. The response from 100 stimulations was averaged per trial, and for each ear, 2 trials were obtained and superimposed. The bandpass was 10 Hz to 1.5 kHz with a time base of 5 ms per division and a gain of 2,000. The first major positive peak was labeled p13, and the following negative peak was labeled n23. For the rectified EMG, the bandpass was 10 Hz
Address correspondence and reprint requests to Eleftherios Stelios Papathanasiou, Ph.D., The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus; E-mail: [email protected] The authors disclose no conflicts of interest. Supplemental digital content is available in the text.
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to 1.5 kHz, with a time base of 2 ms per division and a gain of 2,000. The final result with regard to amplitude was calculated as the ratio of the amplitude of the actual or ‘‘raw’’ cVEMP response (amplitude between p13 and n23) over the rectified averaged EMG amplitude. As the amplitude of both the ‘‘raw’’ cVEMP response and the EMG response is in microvolts (uV), the resulting ratio (called the corrected amplitude) is a dimensionless number. Statistical analysis was performed using the Student’s t test at the 5% significance level.
RESULTS The first case was a 28-year-old man with a patent foramen ovale and evidence of intra-atrial shunt. He presented with blurred vision in the right eye and severe headache 2 months previously. His brain MRI scan revealed a small focal lesion in the right middle cerebellar peduncle (see Figure, Supplemental Digital Content 1, http://links.lww.com/MAO/A237). The BAEP was within normal limits with left ear stimulation but poorly organized with right ear stimulation (see Figure, Supplemental Digital Content 2, http://links.lww.com/MAO/A238). Cervical vestibular evoked myogenic potentials were within normal limits bilaterally (see Figure, Supplemental Digital Content 2, http://links.lww.com/MAO/A238). The p13 peak times were 18.3 and 18.1 ms on the left (mean, 18.2 ms) and 14.6 and 13.2 ms on the right (mean, 13.9 ms). For our laboratory, the mean value of p13 from physiologically normal volunteers is 15.9 T 3.6 ms (mean oˆT standard deviation). This gives an upper limit of normal of 24.9 ms when adding 2.5 standard deviations to the mean. The mean interside difference, calculated at 4.3 ms, is within normal limits for our laboratory. The normal range for our laboratory, calculated after subtracting the right side from the left side, is -5.7 to 5.8 ms, after obtaining a mean of 0.07 T 2.29 ms. The range is calculated as mean T2.5 times the standard deviation. The corrected P13-N23 amplitude was 1.43 and 1.18 on the left (mean, 1.3) and 1.78 and 1.49 on the right (mean, 1.6). The normal range for the laboratory is 0.3 to 13.2, after a mean of 2.5 T 1.8 standard deviations. As amplitude is known to be skewed (17), the upper and lower limits of normal were calculated after logarithmic transformation. The interside amplitude difference (left side/right side) was found to be -0.3. The normal range for our laboratory is 0.3 to 4.4, after a mean of 0.03 T 0.24 standard deviations and with the same logarithmic transformation. Our second case was a 65-year-old man who experienced a cerebrovascular accident 2 months previously after warfarin discontinuation for cardiac catheterization. An MRI scan at 1.5 T revealed 2 foci in the right middle cerebellar peduncle and right cerebellar hemisphere respectively (see Figure, Supplemental Digital Content 3, http://links.lww.com/MAO/A239). Both the BAEPs and cVEMPs (see Figure, Supplemental Digital Content 4, http://links.lww.com/MAO/A240) were normal bilaterally. For the cVEMP specifically, the p13 peak times
were 12.8 and 14.8 ms on the left (mean, 13.8 ms) and 11.9 and 12.1 ms on the right (mean, 12.0 ms). The corrected P13-N23 amplitude was 1.02 and 0.78 on the left (mean, 0.9) and 0.94 and 0.61 on the right (mean, 0.8). Our third case was a 20-year-old man who had an episode of diplopia probably because of demyelinating disease. This event happened 1.5 months before our evoked examinations. On examination, there was no ophthalmoplegia of note or any cerebellar signs. An MRI scan at 1.5 T (Fig. 1) showed circumscribed lesions in the right superior and inferior cerebellar peduncles near the fourth ventricle. Both the BAEPs and cVEMPs (Fig. 2) were normal bilaterally. For the cVEMP specifically, the P13 peak times were 13.6 and 14.1 ms on the left (mean, 13.9 ms) and 14.5 and 14.6 ms on the right (mean, 14.6 ms). The corrected P13-N23 amplitude was 4.0 and 2.9 on the left (mean, 3.5), and 2.3 and 1.8 on the right
FIG. 1. T2-weighted MRI images of this manuscript’s third case, with transverse (bottom figures) and sagittal (top figure) sections. In all figures, the white arrow points to the area of the lesions located in the right superior and inferior cerebellar peduncles.
Otology & Neurotology, Vol. 35, No. 9, 2014
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FIG. 2. Brainstem auditory evoked potentials, cVEMPs, and rectified EMG recordings shown as detailed in supplemental digital content 2 and 4 (http://links.lww.com/MAO/A238 and http://links.lww.com/MAO/A240). All responses were within normal limits.
(mean, 2.1). The interside corrected amplitude difference ratio was 1.7. When the values from all 3 cases were pooled, the mean value for the p13 absolute latency was calculated at 14.4 ms T 1.58 standard deviations. The p13-n23 corrected amplitude was found to be 1.53 T 0.60. With the Student’s t test, this gives t values of 0.67 and -0.03 for latency and corrected amplitude, respectively, when
compared with our control values, which is not statistically significant ( p 9 0.05). DISCUSSION In confirming and contributing to past studies, cVEMPs are unaffected by at least certain cerebellar peduncle and cerebellar hemispheric lesions. Otology & Neurotology, Vol. 35, No. 9, 2014
Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
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It is known that the vestibulocerebellum (the flocculonodular lobe) receives afferent fibers from the ipsilateral vestibular ganglion and from the vestibular nuclei (18), via the inferior cerebellar peduncle (19). It is believed that the flocculus communicates with the superior vestibular nucleus (20Y22) via an inhibitory pathway (23). Efferent connections in the rhesus macaque have also been demonstrated between the flocculus and the ygroup of the vestibular nuclear complex, medial vestibular nucleus, and to a small extent, the inferior vestibular nucleus (20,24). These projections have been shown to course specifically along the caudal surface of the middle cerebellar peduncle and the lateral surface of the inferior cerebellar peduncle. The reason the cVEMPs remain normal in our and other similar articles may be because the lesions spare cerebellovestibular or vestibulocerebellar pathways, which course in specific areas of the peduncles and cerebellar hemispheres. In our first case, the lesion on MRI was located on the medial aspect of the middle cerebellar peduncle and midway rather than caudal or rostral. Our second case revealed one lesion on the lateral aspect of the middle cerebellar peduncle and midway between rostral and caudal and a second lesion within the right cerebellar hemisphere but at an appreciable distance from the midline ‘‘vestibulocerebellum.’’ Our third case revealed lesions on the medial aspects of the superior and inferior cerebellar peduncles. All of these cases would be expected to spare the above pathways. Previous studies do not describe the location of cerebellar lesions (7,8). This makes a comparison difficult to rule out the involvement of pathways between the vestibular nuclear complex and cerebellum. Another reason for the normal cVEMP may be due to the affected vestibular nuclei influenced by the above cerebellar lesions not being located along the cVEMP pathway. It is known from animal studies that secondary neurons within the lateral vestibular nucleus receive vestibular primary afferents from the ipsilateral sacculus (25Y28). Yet, from the literature, we know that the lateral vestibular nucleus does not receive projections from the flocculus (20), although projections do exist from the ‘‘b-zone’’ of the vermis (29,30). Projections to the flocculus are also absent from the lateral ventricular nucleus (31). The normal cVEMPs can be explained by the lateral vestibular nucleus as mediating this response. Also, the medial vestibulospinal tract, which is believed to be responsible for transmitting signals to the sternocleidomastoid muscle (5,32), receives contributions from the lateral nucleus (25,33Y42). Acknowledgments: The authors thank Ms. Elena Polycarpou and Ms. Christina Hadjiyianni for help with figure preparations.
REFERENCES 1. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentials generated by a click-evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatr 1994;57:190Y7.
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