- Email: [email protected]
Progression of acute cochleovestibulopathy into anterior inferior cerebellar artery infarction
Journal of the Neurological Sciences 278 (2009) 119–122
Contents lists available at ScienceDirect
Journal of the Neurological Sciences j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / j n s
Short communication
Progression of acute cochleovestibulopathy into anterior inferior cerebellar artery infarction☆ Hyung Lee a, Hyo-Jung Kim b, Ja-Won Koo c, Ji Soo Kim b,⁎ a b c
Department of Neurology, Keimyung University School of Medicine, Republic of Korea Department of Neurology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Republic of Korea Department of Otolaryngology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Republic of Korea
a r t i c l e
i n f o
Article history: Received 15 September 2008 Received in revised form 18 November 2008 Accepted 19 November 2008 Available online 23 December 2008 Keywords: Labyrinthitis Anterior inferior cerebellar artery Internal auditory artery Infarction
a b s t r a c t Antemortem diagnosis of isolated inner ear infarction remains a diagnostic challenge since current imaging techniques do not permit differentiation of isolated labyrinthine infarction from other more benign disorders involving the inner ear. An 81-year-old woman with diabetes, hypertension and hypercholesterolemia presented with vertigo and hearing loss. Initial examination revealed findings of left cochleovestibular labyrinthitis without brainstem or cerebellar signs. MRIs including the diffusion-weighted images were normal. Five days later, however, she developed dysarthria, and decreased facial sensation, subtle facial palsy, and dysmetria in the left side. Follow-up MRI was consistent with acute infarctions in the territory of anterior inferior cerebellar artery (AICA), involving the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum. AICA infarction should be considered in acute audiovestibular syndrome, especially in aged patients with vascular risk factors, even though the classic brainstem or cerebellar signs are absent. © 2008 Elsevier B.V. All rights reserved.
1. Introduction In infarctions involving the anterior inferior cerebellar artery (AICA) territory, vertigo or deafness is usually associated with other brainstem and cerebellar signs [1]. However, partial ischemia of AICA may give rise to isolated vertigo or hearing loss since the internal auditory artery (IAA) supplying the inner ear is an end artery of AICA with minimal collaterals from other major arterial branches [2,3], and the cochlea and vestibular apparatus are supplied by different branches of IAA. As current imaging techniques do not permit differentiation of isolated labyrinthine infarction from other more benign disorders involving the inner ear, antemortem diagnosis of labyrinthine infarction remains a diagnostic challenge. Transient hearing loss or vertigo preceding AICA infarction has been described [1,3–5]. However, only a prior report described progression of isolated labyrinthine infarction to AICA infarction involving the other areas supplied by AICA [6].
☆ This study was supported by a grant of the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (A080750). ⁎ Corresponding author. Department of Neurology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 300 Gumi-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-707, Republic of Korea. Tel.: +82 31 787 7463; fax: +82 31 719 6828. E-mail address: [email protected] (J.S. Kim). 0022-510X/$ – see front matter © 2008 Elsevier B.V. All rights reserved. doi:10.1016/j.jns.2008.11.019
In view of different therapeutic strategies and potentially grave prognosis of the strokes involving the vertebrobasilar artery territory, it is of great importance to differentiate labyrinthine infarction from more benign disorders involving the inner ear [7]. We report on a patient with AICA infarction who initially presented with acute vestibulocochlear syndrome which progressed into pontocerebellar infarction over several days. Our patient indicates that AICA infarction should be considered in acute audiovestibular syndrome, especially in elderly patients with vascular risk factors, even though MRIs do not demonstrate acute infarction in the pontocerebellum. 2. Case report An 81-year-old woman with diabetes, hypertension and hypercholesterolemia presented with dizziness and vomiting, which developed seven days before. She also noticed tinnitus and hearing loss in the left ear. She was taking aspirin 100 mg a day with antihypertensives, and oral hypoglycemic and lipid-lowering agents. Examination revealed leftward head tilt and right beating nystagmus with clockwise (from the patient's perspective) torsional component. The nystagmus increased without fixation. Head impulse tests revealed corrective catch-up saccades during stimulations of the left horizontal, anterior and posterior semicircular canals (Video). Head heave was also positive leftward. Horizontal head shaking augmented the spontaneous nystagmus. Positioning maneuvers, including lying down, head-turning to either side while supine,
120
H. Lee et al. / Journal of the Neurological Sciences 278 (2009) 119–122
Fig. 1. Fundus photography shows an abnormal intorsion of the right eye (−11.1°, normal range O to 12.6°, negative value indicates an intorsion) and increased extorsion of the left eye (22.3°).
straight head hanging, and Dix–Hallpike in either direction, modulated intensity of the spontaneous nystagmus mildly without changing the direction. She fell to the left during attempted tandem gait. Other findings of neurological and neurotological examinations were normal. The patient also showed counterclockwise torsion of both eyes (Fig. 1) and counterclockwise rotation of the subjective visual vertical when viewing with right (−18.3°, normal range: −3.1°–3.0°, The negative value indicates a counterclockwise rotation) and both eyes (−7.6°, normal range: −2.4°–2.6°) [8]. Pure tone audiometry showed profound hearing loss in the left ear (Fig. 2A). Brainstem auditory evoked potential was not obtained in the left side. Bithermal caloric tests documented 70% caloric paresis in the left ear (Fig. 2B). Vestibular-evoked myogenic potential was absent in the left side (Fig. 2C). MRIs including the diffusion-weighted images performed 7 days after the onset of symptoms were normal (Fig. 3A). MR angiography disclosed multiple stenosis in the petrous portion of right internal carotid artery (curved arrow), right vertebral artery (thick arrow), right vertebrobasilar junction (arrow head), and basilar artery (thin arrow, Fig. 3C). The initial impression was cochleovestibular labyrinthitis and she was on conservative managements with previous medications. The vertigo and imbalance improved gradually. Five days later, however, she reported dysarthria and left sided hand clumsiness without aggravation of the dizziness. On examination, she had spontaneous nystagmus only without fixation. However, she had decreased sensation in the left mouth angle and tongue, decreased taste sensation, subtle left-sided facial palsy, dysmetria of the left upper and lower extremities. She still fell to the left during attempted tandem gait. In view of the newly developed neurological findings, she underwent another diffusion-weighted MRI, which disclosed acute infarctions in the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum (Fig. 3B). Clopidogrel 75 mg per day was added on her previous medication. Three months later, her symptoms almost resolved without spontaneous nystagmus. Audiometry and bithermal caloric tests also showed mildly improved hearing and caloric asymmetry (Fig. 2A–B). However, head impulse tests remained positive. 3. Discussion Our patient initially presented with acute audiovestibular syndrome and developed pontine infarction several days later. AICA is important for vascular supply to the peripheral and central vestibular structures [9]. It usually irrigates the inner ear, lateral pons, middle cerebellar peduncle, and anterior inferior cerebellum including the flocculus [10]. Accordingly, in contrast to other cerebellar artery territory lesions, complete AICA infarction usually results in combined peripheral and central vestibular damage in addition to hearing loss,
facial weakness, limb and facial sensory loss, ataxia, and cerebellar dysmetria [1,10]. When vertigo or hearing loss is associated with other brainstem or cerebellar signs, the diagnosis of AICA infarction is straightforward. However, since IAA supplying the inner ear is a branch of the AICA and is an end artery with minimal collaterals from other major arterial branches [2,9], partial ischemia of AICA may lead to isolated deafness or vertigo, mimicking more common vestibular disorders including Meniere's syndrome, vestibular neuritis, or labyrinthitis, especially when the pontine territory is not involved [1]. Most common mechanism of AICA infarction is the thrombotic narrowing of AICA itself or the extension of the basilar artery plaque into the AICA, which blocks AICA orifice [9,11], even though embolic IAA infarction has been documented [12]. Previously, six of seven patients with isolated vertigo from presumed vertebrobasilar insufficiency showed atherosclerotic narrowing of the vertebral arteries that extended up to the proximal basilar artery where AICA takes off [5]. Our patients also showed stenosis in the right vertebral artery, vertebrobasilar junction, and basilar artery. We speculate that hypoperfusion of AICA induced the labyrinthine infarction initially and further aggravation of the ischemia resulted in the progression to pontine infarction in our patient. Rarely, AICA infarction causes sudden deafness and vertigo without brainstem or cerebellar signs, in which case an acute infarct may still be seen on brain MRI [13]. However, the sensorineural hearing loss is predominantly of cochlear origin in most patients with AICA infarction [1]. The severe sensorineural hearing loss and severe caloric paresis, observed during the initial presentation in our patient, are consistent with a cochlear site of injury. The normal MRIs including the diffusionweighted images on initial presentation also indicate a labyrinthine infarction. In addition to hearing loss as a permanent symptom of AICA stroke, transient auditory symptoms with hearing loss may precede AICA infarction. A recent report showed that 31% (5/16) of patients with AICA infarction had either recurrent transient episodes or single episode of prolonged hearing loss 1 to 10 days before the onset of other brainstem or cerebellar symptoms [4]. Likewise, isolated recurrent vertigo spells may develop prior to permanent AICA infarction [9]. Accordingly, the episodic vertigo and hearing loss may serve as prodromes of AICA infarction. Since current diagnostic methods (including MRI) cannot confirm labyrinthine infarction among the acute audiovestibular syndrome, clinicians should consider all the clinical evidences when attempting to determine the etiology of acute vertigo and hearing loss. Our patient indicates that AICA infarction should be considered, particularly in elderly patients with vascular risk factors and acute vestibulocochlear syndrome, even when the classic brainstem or cerebellar signs are absent and MRIs do not demonstrate acute infarction in the brain.
H. Lee et al. / Journal of the Neurological Sciences 278 (2009) 119–122
121
Fig. 2. A. Pure tone audiometry on initial presentation demonstrates profound sensorineural hearing loss (SNHL) with a pure tone average at 83 dB in the left ear. Also, moderate SNHL was observed in the right ear, probably due to presbycusis. Follow-up audiometry, three months later, shows mildly improved hearing. The patient's hearing levels are plotted against stimulus frequency on a logarithmic scale. Measurements were made according to the American National Standards Institute, 1989. Circle, air conduction on the right side; cross, air conduction on the left side. B. Video-oculographic recordings (ICS medical, IL, USA) of bithermal caloric tests show left canal paresis (70%) on initial presentation. Three months later, the left canal paresis improved to 33%. SPV, slow phase velocity. C. Vestibular evoked myogenic potential recorded on the contracting ipsilateral sternocleidomastoid muscle exhibits no wave formation with left ear stimulation. The stimuli were short alternating tone bursts (95 dB nHL, 108 dB SPL; 500 Hz; ramp = 2 ms; plateau = 3 ms) given at 2.1 Hz monaurally. Lt, left; Rt, right.
122
H. Lee et al. / Journal of the Neurological Sciences 278 (2009) 119–122
Fig. 3. A. Diffusion-weighted MRIs are normal on initial presentation. B. Follow-up diffusion-weighted MRI demonstrates acute infarctions in the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum. C. MR angiography discloses multiple stenoses in the petrous portion of right internal carotid artery (curved arrows), right vertebral artery (thick arrow), right vertebrobasilar junction (arrow head), and midbasilar artery (thin arrow).
Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.jns.2008.11.019. References [1] Lee H, Sohn SI, Jung DK, Cho YW, Lim JG, Yi SD, et al. Sudden deafness and anterior inferior cerebellar artery infarction. Stroke 2002;33:2807–12. [2] Kim JS, Lopez I, DiPatre PL, Liu F, Ishiyama A, Baloh RW. Internal auditory artery infarction: clinical-pathologic correlation. Neurology 1999;52:40–4. [3] Grad A, Baloh RW. Vertigo of vascular origin: clinical and electronystagmographic features in 84 cases. Arch Neurol 1989;46:281–4. [4] Lee H, Cho YW. Auditory disturbance as a prodrome of anterior inferior cerebellar artery infarction. J Neurol Neurosurg Psychiatry 2003;74:1644–8. [5] Fife TD, Baloh RW, Duckwiler GR. Isolated dizziness in vertebrobasilar insufficiency: clinical features, angiography, and follow-up. J Stroke Cerebrovasc Dis 1994;4:4–12.
[6] Yi HA, Lee H, Lee SR, Ahn BH, Park BR, Whitman GT. Sudden deafness as a sign of stroke with normal diffusion-weighted brain MRI. Acta Oto-laryngol 2005;125:1119–21. [7] Kim HA, Lee SR, Lee H. Acute peripheral vestibular syndrome of a vascular cause. J Neurol Sci 2007;254:99–101. [8] Choi KD, Oh SY, Kim HJ, Park SH, Koo JW, Kim JS. Recovery of vestibular imbalances after vestibular neuritis: one-year follow-up. Laryngoscope 2007;117:1307–12. [9] Oas JG, Baloh RW. Vertigo and the anterior inferior cerebellar artery syndrome. Neurology 1992;42:2274–9. [10] Amarenco P, Hauw JJ. Cerebellar infarction in the territory of the anterior and inferior cerebellar artery. Brain 1990;113:139–55. [11] Amarenco P, Rosengart A, DeWitt LD, Pessin MS, Caplan LR. Anterior inferior cerebellar artery territory infarcts: mechanisms and clinical features. Arch Neurol 1993;50:154–61. [12] Choi KD, Chun JU, Han MG, Park SH, Kim JS. Embolic internal auditory artery infarction from vertebral artery dissection. J Neurol Sci 2006;246:169–72. [13] Lee H, Ahn BH, Baloh RW. Sudden deafness with vertigo as a sole manifestation of anterior inferior cerebellar infarction. J Neurol Sci 2004;222:105–7.
Contents lists available at ScienceDirect
Journal of the Neurological Sciences j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / j n s
Short communication
Progression of acute cochleovestibulopathy into anterior inferior cerebellar artery infarction☆ Hyung Lee a, Hyo-Jung Kim b, Ja-Won Koo c, Ji Soo Kim b,⁎ a b c
Department of Neurology, Keimyung University School of Medicine, Republic of Korea Department of Neurology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Republic of Korea Department of Otolaryngology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Republic of Korea
a r t i c l e
i n f o
Article history: Received 15 September 2008 Received in revised form 18 November 2008 Accepted 19 November 2008 Available online 23 December 2008 Keywords: Labyrinthitis Anterior inferior cerebellar artery Internal auditory artery Infarction
a b s t r a c t Antemortem diagnosis of isolated inner ear infarction remains a diagnostic challenge since current imaging techniques do not permit differentiation of isolated labyrinthine infarction from other more benign disorders involving the inner ear. An 81-year-old woman with diabetes, hypertension and hypercholesterolemia presented with vertigo and hearing loss. Initial examination revealed findings of left cochleovestibular labyrinthitis without brainstem or cerebellar signs. MRIs including the diffusion-weighted images were normal. Five days later, however, she developed dysarthria, and decreased facial sensation, subtle facial palsy, and dysmetria in the left side. Follow-up MRI was consistent with acute infarctions in the territory of anterior inferior cerebellar artery (AICA), involving the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum. AICA infarction should be considered in acute audiovestibular syndrome, especially in aged patients with vascular risk factors, even though the classic brainstem or cerebellar signs are absent. © 2008 Elsevier B.V. All rights reserved.
1. Introduction In infarctions involving the anterior inferior cerebellar artery (AICA) territory, vertigo or deafness is usually associated with other brainstem and cerebellar signs [1]. However, partial ischemia of AICA may give rise to isolated vertigo or hearing loss since the internal auditory artery (IAA) supplying the inner ear is an end artery of AICA with minimal collaterals from other major arterial branches [2,3], and the cochlea and vestibular apparatus are supplied by different branches of IAA. As current imaging techniques do not permit differentiation of isolated labyrinthine infarction from other more benign disorders involving the inner ear, antemortem diagnosis of labyrinthine infarction remains a diagnostic challenge. Transient hearing loss or vertigo preceding AICA infarction has been described [1,3–5]. However, only a prior report described progression of isolated labyrinthine infarction to AICA infarction involving the other areas supplied by AICA [6].
☆ This study was supported by a grant of the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (A080750). ⁎ Corresponding author. Department of Neurology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 300 Gumi-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-707, Republic of Korea. Tel.: +82 31 787 7463; fax: +82 31 719 6828. E-mail address: [email protected] (J.S. Kim). 0022-510X/$ – see front matter © 2008 Elsevier B.V. All rights reserved. doi:10.1016/j.jns.2008.11.019
In view of different therapeutic strategies and potentially grave prognosis of the strokes involving the vertebrobasilar artery territory, it is of great importance to differentiate labyrinthine infarction from more benign disorders involving the inner ear [7]. We report on a patient with AICA infarction who initially presented with acute vestibulocochlear syndrome which progressed into pontocerebellar infarction over several days. Our patient indicates that AICA infarction should be considered in acute audiovestibular syndrome, especially in elderly patients with vascular risk factors, even though MRIs do not demonstrate acute infarction in the pontocerebellum. 2. Case report An 81-year-old woman with diabetes, hypertension and hypercholesterolemia presented with dizziness and vomiting, which developed seven days before. She also noticed tinnitus and hearing loss in the left ear. She was taking aspirin 100 mg a day with antihypertensives, and oral hypoglycemic and lipid-lowering agents. Examination revealed leftward head tilt and right beating nystagmus with clockwise (from the patient's perspective) torsional component. The nystagmus increased without fixation. Head impulse tests revealed corrective catch-up saccades during stimulations of the left horizontal, anterior and posterior semicircular canals (Video). Head heave was also positive leftward. Horizontal head shaking augmented the spontaneous nystagmus. Positioning maneuvers, including lying down, head-turning to either side while supine,
120
H. Lee et al. / Journal of the Neurological Sciences 278 (2009) 119–122
Fig. 1. Fundus photography shows an abnormal intorsion of the right eye (−11.1°, normal range O to 12.6°, negative value indicates an intorsion) and increased extorsion of the left eye (22.3°).
straight head hanging, and Dix–Hallpike in either direction, modulated intensity of the spontaneous nystagmus mildly without changing the direction. She fell to the left during attempted tandem gait. Other findings of neurological and neurotological examinations were normal. The patient also showed counterclockwise torsion of both eyes (Fig. 1) and counterclockwise rotation of the subjective visual vertical when viewing with right (−18.3°, normal range: −3.1°–3.0°, The negative value indicates a counterclockwise rotation) and both eyes (−7.6°, normal range: −2.4°–2.6°) [8]. Pure tone audiometry showed profound hearing loss in the left ear (Fig. 2A). Brainstem auditory evoked potential was not obtained in the left side. Bithermal caloric tests documented 70% caloric paresis in the left ear (Fig. 2B). Vestibular-evoked myogenic potential was absent in the left side (Fig. 2C). MRIs including the diffusion-weighted images performed 7 days after the onset of symptoms were normal (Fig. 3A). MR angiography disclosed multiple stenosis in the petrous portion of right internal carotid artery (curved arrow), right vertebral artery (thick arrow), right vertebrobasilar junction (arrow head), and basilar artery (thin arrow, Fig. 3C). The initial impression was cochleovestibular labyrinthitis and she was on conservative managements with previous medications. The vertigo and imbalance improved gradually. Five days later, however, she reported dysarthria and left sided hand clumsiness without aggravation of the dizziness. On examination, she had spontaneous nystagmus only without fixation. However, she had decreased sensation in the left mouth angle and tongue, decreased taste sensation, subtle left-sided facial palsy, dysmetria of the left upper and lower extremities. She still fell to the left during attempted tandem gait. In view of the newly developed neurological findings, she underwent another diffusion-weighted MRI, which disclosed acute infarctions in the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum (Fig. 3B). Clopidogrel 75 mg per day was added on her previous medication. Three months later, her symptoms almost resolved without spontaneous nystagmus. Audiometry and bithermal caloric tests also showed mildly improved hearing and caloric asymmetry (Fig. 2A–B). However, head impulse tests remained positive. 3. Discussion Our patient initially presented with acute audiovestibular syndrome and developed pontine infarction several days later. AICA is important for vascular supply to the peripheral and central vestibular structures [9]. It usually irrigates the inner ear, lateral pons, middle cerebellar peduncle, and anterior inferior cerebellum including the flocculus [10]. Accordingly, in contrast to other cerebellar artery territory lesions, complete AICA infarction usually results in combined peripheral and central vestibular damage in addition to hearing loss,
facial weakness, limb and facial sensory loss, ataxia, and cerebellar dysmetria [1,10]. When vertigo or hearing loss is associated with other brainstem or cerebellar signs, the diagnosis of AICA infarction is straightforward. However, since IAA supplying the inner ear is a branch of the AICA and is an end artery with minimal collaterals from other major arterial branches [2,9], partial ischemia of AICA may lead to isolated deafness or vertigo, mimicking more common vestibular disorders including Meniere's syndrome, vestibular neuritis, or labyrinthitis, especially when the pontine territory is not involved [1]. Most common mechanism of AICA infarction is the thrombotic narrowing of AICA itself or the extension of the basilar artery plaque into the AICA, which blocks AICA orifice [9,11], even though embolic IAA infarction has been documented [12]. Previously, six of seven patients with isolated vertigo from presumed vertebrobasilar insufficiency showed atherosclerotic narrowing of the vertebral arteries that extended up to the proximal basilar artery where AICA takes off [5]. Our patients also showed stenosis in the right vertebral artery, vertebrobasilar junction, and basilar artery. We speculate that hypoperfusion of AICA induced the labyrinthine infarction initially and further aggravation of the ischemia resulted in the progression to pontine infarction in our patient. Rarely, AICA infarction causes sudden deafness and vertigo without brainstem or cerebellar signs, in which case an acute infarct may still be seen on brain MRI [13]. However, the sensorineural hearing loss is predominantly of cochlear origin in most patients with AICA infarction [1]. The severe sensorineural hearing loss and severe caloric paresis, observed during the initial presentation in our patient, are consistent with a cochlear site of injury. The normal MRIs including the diffusionweighted images on initial presentation also indicate a labyrinthine infarction. In addition to hearing loss as a permanent symptom of AICA stroke, transient auditory symptoms with hearing loss may precede AICA infarction. A recent report showed that 31% (5/16) of patients with AICA infarction had either recurrent transient episodes or single episode of prolonged hearing loss 1 to 10 days before the onset of other brainstem or cerebellar symptoms [4]. Likewise, isolated recurrent vertigo spells may develop prior to permanent AICA infarction [9]. Accordingly, the episodic vertigo and hearing loss may serve as prodromes of AICA infarction. Since current diagnostic methods (including MRI) cannot confirm labyrinthine infarction among the acute audiovestibular syndrome, clinicians should consider all the clinical evidences when attempting to determine the etiology of acute vertigo and hearing loss. Our patient indicates that AICA infarction should be considered, particularly in elderly patients with vascular risk factors and acute vestibulocochlear syndrome, even when the classic brainstem or cerebellar signs are absent and MRIs do not demonstrate acute infarction in the brain.
H. Lee et al. / Journal of the Neurological Sciences 278 (2009) 119–122
121
Fig. 2. A. Pure tone audiometry on initial presentation demonstrates profound sensorineural hearing loss (SNHL) with a pure tone average at 83 dB in the left ear. Also, moderate SNHL was observed in the right ear, probably due to presbycusis. Follow-up audiometry, three months later, shows mildly improved hearing. The patient's hearing levels are plotted against stimulus frequency on a logarithmic scale. Measurements were made according to the American National Standards Institute, 1989. Circle, air conduction on the right side; cross, air conduction on the left side. B. Video-oculographic recordings (ICS medical, IL, USA) of bithermal caloric tests show left canal paresis (70%) on initial presentation. Three months later, the left canal paresis improved to 33%. SPV, slow phase velocity. C. Vestibular evoked myogenic potential recorded on the contracting ipsilateral sternocleidomastoid muscle exhibits no wave formation with left ear stimulation. The stimuli were short alternating tone bursts (95 dB nHL, 108 dB SPL; 500 Hz; ramp = 2 ms; plateau = 3 ms) given at 2.1 Hz monaurally. Lt, left; Rt, right.
122
H. Lee et al. / Journal of the Neurological Sciences 278 (2009) 119–122
Fig. 3. A. Diffusion-weighted MRIs are normal on initial presentation. B. Follow-up diffusion-weighted MRI demonstrates acute infarctions in the left lateral pons, left middle cerebellar peduncle, and inferolateral cerebellum. C. MR angiography discloses multiple stenoses in the petrous portion of right internal carotid artery (curved arrows), right vertebral artery (thick arrow), right vertebrobasilar junction (arrow head), and midbasilar artery (thin arrow).
Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.jns.2008.11.019. References [1] Lee H, Sohn SI, Jung DK, Cho YW, Lim JG, Yi SD, et al. Sudden deafness and anterior inferior cerebellar artery infarction. Stroke 2002;33:2807–12. [2] Kim JS, Lopez I, DiPatre PL, Liu F, Ishiyama A, Baloh RW. Internal auditory artery infarction: clinical-pathologic correlation. Neurology 1999;52:40–4. [3] Grad A, Baloh RW. Vertigo of vascular origin: clinical and electronystagmographic features in 84 cases. Arch Neurol 1989;46:281–4. [4] Lee H, Cho YW. Auditory disturbance as a prodrome of anterior inferior cerebellar artery infarction. J Neurol Neurosurg Psychiatry 2003;74:1644–8. [5] Fife TD, Baloh RW, Duckwiler GR. Isolated dizziness in vertebrobasilar insufficiency: clinical features, angiography, and follow-up. J Stroke Cerebrovasc Dis 1994;4:4–12.
[6] Yi HA, Lee H, Lee SR, Ahn BH, Park BR, Whitman GT. Sudden deafness as a sign of stroke with normal diffusion-weighted brain MRI. Acta Oto-laryngol 2005;125:1119–21. [7] Kim HA, Lee SR, Lee H. Acute peripheral vestibular syndrome of a vascular cause. J Neurol Sci 2007;254:99–101. [8] Choi KD, Oh SY, Kim HJ, Park SH, Koo JW, Kim JS. Recovery of vestibular imbalances after vestibular neuritis: one-year follow-up. Laryngoscope 2007;117:1307–12. [9] Oas JG, Baloh RW. Vertigo and the anterior inferior cerebellar artery syndrome. Neurology 1992;42:2274–9. [10] Amarenco P, Hauw JJ. Cerebellar infarction in the territory of the anterior and inferior cerebellar artery. Brain 1990;113:139–55. [11] Amarenco P, Rosengart A, DeWitt LD, Pessin MS, Caplan LR. Anterior inferior cerebellar artery territory infarcts: mechanisms and clinical features. Arch Neurol 1993;50:154–61. [12] Choi KD, Chun JU, Han MG, Park SH, Kim JS. Embolic internal auditory artery infarction from vertebral artery dissection. J Neurol Sci 2006;246:169–72. [13] Lee H, Ahn BH, Baloh RW. Sudden deafness with vertigo as a sole manifestation of anterior inferior cerebellar infarction. J Neurol Sci 2004;222:105–7.