Nystagmus-Based Approach to Vertebrobasilar Stroke Presenting as Vertigo without Initial Neurologic Signs

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1 Original Paper Received: April 10, 2013 Accepted: May 26, 2013 Published online: October 12, 2013 Nystagmus-Based Approach to Vertebrobasilar Stroke Presenting as Vertigo without Initial Neurologic Signs Min-Beom Kim a Sung Hyun Boo b Jae Ho Ban a a Department of Otorhinolaryngology, Head and Neck Surgery, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, and b Department of Otorhinolaryngology, Head and Neck Surgery, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Changwon, Korea Key Words Vertigo Nystagmus Stroke Cerebellum Brainstem Vestibular neuronitis Abstract Background: We aimed to investigate the clinical courses and common nystagmus of isolated vertigo patients with vertebrobasilar stroke. Methods: The patients who presented with isolated acute spontaneous vertigo with spontaneous nystagmus (acute vestibular syndrome) at the Emergency Department were retrospectively analyzed. They were referred to the Otolaryngology Department due to the absence of neurologic signs or even of imaging abnormalities after the initial examination at the Emergency Department. Various clinical features, including presenting symptoms, delayed neurologic signs, the site of infarction, and videonystagmographic (VNG) findings were analyzed. Results: Of the 468 cases of acute vestibular syndrome, 23 (4.9%) cases of radiologically proven vertebrobasilar stroke were identified. Of the 23 patients, 17 (74%) showed aggravation of vertigo or delayed neurologic signs during the admission. In the analysis of VNG, 11 (48%) cases of direction-changing gazeevoked nystagmus, 7 (30%) cases of fixation failure in the caloric test, 6 (27%) cases of periodic alternating nystagmus, karger@karger.com S. Karger AG, Basel /13/ $38.00/0 and 4 (17%) cases of atypical head-shaking nystagmus were presented. Stroke occurred in the cerebellum (n = 18, 78%), medulla (n = 4, 17%), and pons (n = 1, 4%). Conclusion: In the early stage of vertebrobasilar stroke, an accurate diagnosis was difficult in the Emergency Department even though a radiologic study was performed, but various VNG abnormalities and delayed neurologic signs could help to diagnose whether the origin is central or not. Introduction 2013 S. Karger AG, Basel Acute vertigo is a common symptom at the Emergency Department [1]. Also, many otolaryngologists see these patients first or they are referred from the Emergency Department. In a large study, 3.2% of patients who presented with dizziness at the Emergency Department were diagnosed as having a stroke, and the symptom of isolated dizziness was found only in 0.7% [2]. Although the stroke incidence in all dizzy patients is relatively low, the misdiagnosis of central vertigo may lead to serious morbidity and even mortality [3 5]. Nevertheless, it is difficult to diagnose in vertigo patients whether the origin is central or not, especially at the initial visit. Jae Ho Ban, MD, PhD 108 Pyoung-Dong Jongno-Gu Seoul (Korea) naver.com

2 Even though focal neurologic signs or symptoms may help to diagnose central vertigo, some reports have described isolated vertigo patients without initial neurologic signs of stroke [6 8]. In the Emergency Department, there are some limitations in the detailed neurootologic examinations due to a lack of equipment or neurootologic specialists. Furthermore, a radiologic study of acute stroke can be incorrect in some cases. The computedtomographic (CT) scan has a sensitivity of only 16 26% to detect acute ischemic infarction [9, 10], and even diffusion-weighted magnetic resonance imaging (MRI) has a false-negative ratio of 6 12% [11, 12]. In the very early stage, CT and even MRI show normal findings because a little time is necessary for recognizable imaging abnormality to show up [9]. Also, it is more difficult to diagnose brainstem infarction radiologically because of the surrounding bony structures and artifacts, even if it is one of the causes in acute vertigo [13]. Especially in isolated vertigo patients, the false negative ratio on the radiologic study could be increased because the ischemic area of the central nervous system might be relatively small. The purpose of this study was to investigate the clinical courses or characteristics of isolated vertigo patients with vertebrobasilar stroke, with the goal of preventing a misdiagnosis of acute peripheral vestibulopathy in these patients. We also suggest an appropriate practice for the radiologic investigation in these patients. Subjects and Methods Subjects A retrospective analysis of patients who had isolated acute spontaneous vertigo with spontaneous nystagmus (SN; acute vestibular syndrome) between January 2003 and December 2011 at our Otolaryngology Department was carried out. Among them, we found patients who had been diagnosed with vertebrobasilar stroke during the admission. The study population had no additional neurologic signs or symptoms at initial visit. We excluded tumor, old infarction, transient ischemic attack, and stroke in the anterior circulation that was not clearly correlated with vertigo. The study protocol was approved by the institutional review board. Analysis of Nystagmus in Central Vertigo Me t h o d s In all subjects, history taking included stroke risk factors and detailed neurologic examination at the emergency department by an attending neurologist before the admission to the Otolaryngology Department. After a neurologic examination, the patients were referred to our Otolaryngology Department because of an absence of neurologic signs and symptoms. All patients underwent an initial radiologic investigation for central lesion, such as contrast-enhanced brain CT or diffusion-weighted MRI at the Emergency Department. These patients were diagnosed as not having a significant central lesion by the radiologist or neurologist on duty in the Emergency Department. After the admission to our Otolaryngology Department, we conducted videonystagmography (VNG), audiometry and daily neurootologic examinations. VNG tested for SN, gaze-evoked nystagmus (GEN), and head-shaking nystagmus (HSN), and a caloric test and an oculomotor test including saccade, pursuit and optokinetic nystagmus were done. Unfortunately, the use of the head impulse test was begun late during this retrospective series and was performed in only 3 cases. Also, we checked delayed neurologic symptoms, signs, and the timing of the development of neurologic signs through daily neurootologic examinations. Upon a suspicious VNG finding of the central lesion or a neurologic sign, we immediately performed MRI (including diffusion-weighted images) and magnetic resonance angiography of the vertebral and basilar arteries. Finally, we evaluated the location of stroke and vascular territory. The location of the central lesion was divided into the cerebellum, the pons, and the medulla. The territories of the three major cerebellar arteries, posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), and superior cerebellar artery, were determined according to MR-anatomical templates [14]. R e s u l t s Demographics and Topography of Stroke In the study period, 468 patients who had been diagnosed with acute vestibular syndrome without initial neurologic signs were admitted to our department via the Emergency Department. Of these patients, 23 (4.9%) were finally diagnosed with vertebrobasilar stroke in our Otolaryngology Department, and they constituted the study population. The mean age of the study population was 64.8 years. There were 12 male and 11 female patients. According to the type of stroke, there were 22 cases of infarction and 1 case of hemorrhage. The most common risk factors were hypertension (n = 23) followed by diabetes mellitus (n = 9), cardiac arrhythmia (n = 3), valvular heart disease (n = 1), and a previous stroke history (n = 1). Stroke lesions included 18 cerebellar infarctions (17 infarctions and 1 hemorrhage), 4 medulla infarctions, and 1 pons infarction. Topographic analyses identified 19 cases of PICA involvement, 3 cases of AICA involvement, and 1 case of pontine artery involvement. Among the 19 cases of PICA involvement, in 14 cases the medial branch of PICA was involved, in 3 cases the lateral branch of PICA was involved, and in 2 cases both the medial and lateral branches of PICA were involved. Figure 1 provides a schematic illustration and MRI findings of this involvement in the vertebrobasilar system. 323

3 Fig. 1. Schematic illustration of the involvement in the vertebrobasilar system. Cerebellar infarction is the most frequent lesion in isolated vertigo patients. PICA involvement is more frequent than AICA involvement. PICA is divided into the medial and the lateral branch. Clinical Courses and VNG Findings Table 1 shows clinical features and VNG findings in 23 stroke patients. All patients initially presented with vertigo with or without hearing loss (table 1). Twenty cases showed isolated vertigo and 3 cases showed vertigo with sudden unilateral hearing loss. All these 3 sudden hearing loss patients were associated with AICA infarction. Including case 6 ( fig. 2, table 1 ), all patients with AICA infarction showed ipsilesional sensorineural hearing loss in audiometry and ipsilesional canal paresis in the caloric test. Nausea or vomiting was combined in all cases and 8 cases complained of a mild headache. The initial radiologic studies performed in the Emergency Department were six diffusion-weighted MRI and 17 contrast-enhanced CT. The initial radiologic diagnosis by the onduty radiologist or neurologist was normal in all cases. Four cases had a suspicious lesion in the initial diffusionweighted MRI compared with the follow-up image ( fig. 2 ). Two cases did not show an initial MRI abnormality, even upon a retrospective film review. All patients had SN in VNG after the admission to the Otolaryngology Department. It seemed that in the Emergency Department they were suspected of having acute unilateral vestibulopathy. Figure 3 shows the frequency of suspicious findings of VNG in the central lesion. The most common finding of a suspected stroke in VNG was SN without canal paresis (Jongkee s index >25) in caloric 324 test (n = 15) followed by direction-changing GEN (n = 11), fixation failure in caloric test (n = 7), and periodic alternating nystagmus (PAN; n = 6). Atypical head-shaking nystagmus (n = 4) was shown as perverted HSN [15], vigorous nystagmus after light head shaking and HSN beating in the opposite direction of SN [16]. Although we only performed a head impulse test in 3 cases, 1 of these cases (case 21, lateral medullary infarction) showed a positive head impulse test similar to peripheral vestibulopathy. Like VNG abnormality, delayed neurologic sign or aggravation of vertigo was also helpful for stroke diagnosis in the study population. Of the 23 stroke patients, 17 had delayed neurologic signs or aggravation of vertigo during the admission period. Fifteen of the delayed symptoms and signs occurred within 48 h and 2 occurred after 48 h. Various delayed neurologic signs were found in 7 patients and included facial numbness, diplopia, dysarthria, Horner s syndrome, unilateral paresthesia, and intention tremor. All signs were well correlated with abnormal lesions in MRI. Also, aggravation of vertigo or ataxia (n = 14) was frequently found in the study population. These patients were capable of independent walking at the initial admission but could not walk independently during the admission. Figure 4 is a schematic showing the suspicious central lesions in the study population. Except for 1 case (case 11, medial cerebellar infarction), 22 patients had two or more abnormalities considering VNG or delayed neurologic signs. Mean diagnostic delay was 2.6 days (range, 1 7 days) after visiting the hospital including the Emergency Department. When the diagnosis was confirmed, all stroke patients were referred to the Neurology or Neurosurgery Department for appropriate care. There were no mortalities after the transfer. D i s c u s s i o n In the present study, we document various presentations and clinical courses of vertebrobasilar stroke in acute vestibular syndrome. The initial accurate diagnosis of central vertigo is not easy, especially in the setting of the Emergency Department. All cases in this study were misdiagnosed in the Emergency Department. However, some clues for central disease were established through detailed history taking and serial neurootologic examinations, such as VNG, during the follow-up. As shown in figure 4, multiple considerations are important to prevent a misdiagnosis of vertebrobasilar stroke. Kim/Boo/Ban

4 Fig. 2. Misdiagnosis of initial diffusionweighted MRI in right AICA infarction. a A tiny focal lesion (arrow) in the right middle cerebellar peduncle on the initial diffusion-weighted MRI was missed until the follow-up image had been taken. b An evident lesion (arrow) was identified in the follow-up image 3 days after symptom onset. Delayed symptom aggravation was presented in this patient (case 6, table 1). a b Table 1. Clinical features and VNG findings in the study population Patient No. Sex/ age Risk factors Initial symptoms VNG findings Delayed signs Topography SN PAN HSN GEN fixation HIT in MRI without failure CP Time to diagnosis, days 1 F/63 HTN vertigo cerebellum 1 2 M/63 HTN, DM vertigo + + facial numbness medulla 2 3 M/61 DM vertigo + facial numbness pons 2 4 M/66 HTN vertigo + + cerebellum 2 5 F/51 HTN vertigo + vertigo aggravation, ataxia cerebellum 4 6 M/67 DM vertigo, hearing loss + + vertigo aggravation, ataxia cerebellum 3 7 M/60 DM vertigo diplopia cerebellum 2 8 F/59 HTN, DM vertigo + vertigo aggravation, ataxia cerebellum 5 9 F/63 HTN vertigo + ataxia cerebellum 2 10 F/56 HTN, AF vertigo + + ataxia cerebellum 3 11 M/60 HTN, DM vertigo vertigo aggravation cerebellum 7 12 F/62 HTN, DM vertigo + + Horner s syndrome medulla 2 13 F/62 HTN vertigo + + vertigo aggravation cerebellum 2 14 F/72 HTN, DM vertigo + + ataxia cerebellum 3 15 F/68 HTN, DM vertigo, hearing loss + + ataxia cerebellum 2 16 M/65 AF vertigo + facial numbness medulla 2 17 M/62 HTN, DM vertigo + vigorous after little shaking cerebellum 2 18 M/69 HTN vertigo + + cerebellum 3 19 M/60 HTN vertigo, hearing loss perverted + cerebellum 2 20 F/46 HTN, VHD vertigo cerebellum 2 21 F/83 HTN vertigo + opposite to SN positive ataxia medulla 3 22 M/72 HTN vertigo + + negative dysarthria cerebellum 2 23 M/64 HTN vertigo + perverted negative vertigo aggravation cerebellum 2 CP = Canal paresis; HIT = head impulse test; HTN = hypertension; DM = diabetes mellitus; AF = atrial fibrillation; VHD = valvular heart disease. Analysis of Nystagmus in Central Vertigo 325

5 Fig. 3. Frequency of VNG findings in the case of a suspicious central lesion in the study population. SN without canal paresis (CP) is the most frequent finding in vertebrobasilar stroke with isolated vertigo patients. Sequentially, direction-changing GEN, fixation failure, PAN, and atypical HSN were found. Although the head impulse test was performed in only 3 cases, 1 case even showed a positive head impulse test with SN (case 21, table 1). 0% SN without CP Direction-changing GEN Fixation failure PAN 15 (65%) 11 (48%) 7 (30%) 6 (27%) Atypical HSN 4 (17%) Negative HIT with SN 2 (66%) HIT (n = 3) 100% n = 23 Caloric test GEN Caloric test SN HSN Fig. 4. Schematic combination table for suspicious central lesions in the study population. Except for 1 case (case 11), 2 or more abnormalities were evident in the VNG findings as well as symptom aggravation or neurologic signs. The most frequent findings (74%) were delayed neurologic signs or vertigo aggravation. Delayed sign or symptom aggravation (n = 17) SN without CP (n = 15) Direction-changing GEN (n = 11) Fixation failure in caloric test (n = 7) PAN (n = 6) Atypical HSN (n = 4) Negative HIT with SN (n = 2, HIT was performed in only 3 cases) Of the 23 patients in our study, 17 cases underwent a contrast-enhanced CT scan for stroke. However, none of these cases had any abnormalities in the scan. Of the 6 cases of diffusion-weighted MRI, 4 cases missed the abnormality due to tiny lesions or artifacts. Also, 2 cases did not show any abnormalities unless the follow-up MRI was considered. A comparison between MRI and CT in the emergency assessment of acute stroke [9] reported a CT sensitivity of 16% in acute ischemic stroke. Although the sensitivity of MRI was 83%, the sensitivity was lower, that is 73%, within 3 h after symptom onset. Therefore, the clinicians need to investigate further when there is a suspicion of central disease even if the imaging findings are normal. Also, follow-up imaging should be done without hesitation if suspicious findings appeared during the follow-up period. 326 The mean age of our study population was 64.8 years. Although one woman was 46 years old (case 20, table 1), she had valvular heart disease with a history of open heart valve surgery. In our opinion, in elderly patients with other risk factors central disease should be considered and a careful serial follow-up is necessary to prevent misdiagnosis. Nystagmus evaluation by VNG is certainly necessary in dizzy patients. In our study, 45 VNG abnormalities were found in the study population. If we performed nystagmus evaluation with the naked eye or Frenzel s glass only, we could not find all these abnormalities. Although SN without caloric weakness is apparent in conditions including Ménière s disease and inferior vestibular neuritis, it could also be a clue for central disease because the vestibular-evoked myogenic potential test is useful for the diagnosis of inferior neuritis and isolated Kim/Boo/Ban

6 inferior neuritis is an extremely rare situation [17]. Also, Ménière s attack might not be continuous for a few days and can show typical hearing deterioration in audiometry. Direction-changing GEN in stroke patients was the second most common VNG abnormality in our study. It has been correlated with the failure of gaze-holding circuits in the cerebellum or brainstem [18]. Another study reported that one important sign for a central lesion is direction-changing GEN, and also reported 20% direction-changing GEN in central acute vestibular syndrome [19]. Failure of fixation suppression of caloric nystagmus can be seen in central disorders such as cerebellar disease. In our study, all cases of fixation failure were associated with cerebellar infarction as in a previous study [20]. PAN is demonstrated by a periodic reversal of horizontal SN with a null period of several seconds. It is related to damage of the uvulonodulus or to their connections with the brainstem vestibular nuclei [21]. We treated 6 cases of PAN, 1 with a lateral medullary infarction and 5 with medial cerebellum lesions. Central HSN presents many different features comparable with peripheral HSN [15]. Peripheral HSN is usually horizontal, monophasic, and beats towards the side with more caloric excitability by the velocity storage mechanism [22]. However, central HSN reportedly showed unusually strong HSN elicited by weak head shaking, strong HSN in patients without caloric paresis, HSN beating in the opposite direction of SN, and perverted HSN (e.g., downbeat nystagmus after horizontal head shaking). Central gain asymmetry, asymmetric central adaptation, and asymmetric velocity storage have been proposed as the mechanisms of central HSN. Also, asymmetric or unilateral impairment of uvulonodular inhibition over the vestibuloocular reflex is considered a mechanism. In our study, there was 1 case of vigorous HSN after weak head shaking and 1 case of HSN beating in the opposite direction of SN, and 2 cases of perverted HSN were identified (table 1). Although we could find many VNG abnormalities in our study population, there was no single consistent finding for stroke diagnosis. It seemed that there was no single consistent finding for stroke diagnosis, and numerous presentations were possible according to the site of the lesion in the central nervous system. In our study, delayed neurologic signs or aggravation of vertigo and ataxia are also important for the diagnosis of central lesions. Most of the delayed signs or symptom aggravations present within 48 h after the onset of dizziness [23, 24]. The most frequent signs were truncal ataxia in 6 cases and facial numbness in 3 cases. From the viewpoint Analysis of Nystagmus in Central Vertigo of cost-benefit analysis, we do not recommend MRI scanning for all cases of acute vestibular syndrome. However, some patients develop vertebrobasilar stroke even in the absence of focal neurologic signs and VNG abnormality for several days. We treated 1 patient (case 11, table 1) who did not have any neurologic signs in the follow-up period but who complained of an aggravation of vertigo 5 days after onset. He already had an initial diffusion-weighted MRI that did not reveal a central lesion. If we had not checked his MRI scan repeatedly, we could not have diagnosed him accurately. Although fortunately he did not have any sequelae, an accurate diagnosis was delayed up to 7 days. Some authors recommend MRI if vertigo does not improve after 48 h [25]. We strongly share this opinion and further suggest repeat MRI whenever vertigo has not improved after 48 h despite initial normal MRI findings. An interesting finding of our study was vertigo with sudden hearing loss. Three cases of vertigo combined with sudden hearing loss were all associated with AICA infarction (table 1). Lee et al. [26, 27] reported that AICA infarction can present as sudden deafness and vertigo. Our results were compatible with those of studies, and we also suggest that clinicians should be aware of the possibility of AICA infarction particularly in older patients with sudden deafness and vascular risk factors, even without initial neurologic signs. This study had some limitations. We did not perform a head impulse test and skew deviation in any of the cases. Recently, the head impulse test and skew deviation have attracted the clinician s attention for acute vestibular syndrome [19]. Head impulse test and evaluation of skew deviation are definitely good tools for the diagnosis of acute vestibular syndrome, but careful evaluation of other VNG findings and a neurologic test are also mandatory. Although we performed a head impulse test in only 3 cases, 1 case (case 21, table 1) showed a bilateral positive catch-up saccade that was thought be a peripheral vestibulopathy. In retrospect, this was likely to be due to the advanced age of this patient. If we did not conduct another VNG test, we could not have made an accurate diagnosis. As shown in figure 4, clinicians should not be bound by one test, but should rather consider multiple and various tests to prevent misdiagnosing vertebrobasilar stroke as peripheral vestibulopathy. Disclosure Statement This research did not receive financial support from any agency, grant, or other program. The authors have no conflict of interest to disclose. 327

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