Search

Background and Purpose: The recognition of clinical features of transient vestibular symptoms (TVSs) preceding posterior circulation stroke (PCOS) would be informative to discriminate dizziness/vertigo due to vertebrobasilar transient ischemic attack from the acute transient vestibular syndrome. We sought to determine the prevalence and characteristics of TVSs preceding PCOS., Methods: We performed a prospective multicenter observational study that had recruited 447 patients with PCOS from referral-based 4 university hospitals in Korea. We investigated the timing, pattern, frequency, duration, and accompanying neurological symptoms of TVSs during the 3 months preceding PCOS., Results: The prevalence of TVSs preceding PCOS was 12% (55/447) during the previous 3 months. The TVSs preceding PCOS occurred within 1 week (33%), between 1 week and 1 month (16%), or between 1 and 3 months (51%). The TVSs were mostly dizziness/vertigo with (36%) or without (60%) imbalance, while the remaining 4% had an isolated imbalance. The dizziness/vertigo was spinning in 38% and was aggravated during head position in 45%. The duration of TVSs was mostly a few seconds (55%) or minutes (38%). Approximately 72% of the patients with PCOS had TVSs 1 to 5 times, while 16% had >10 times. Accompanying neurological symptoms, including headache, tinnitus, limb weakness, sensory change, dysarthria, visual field defect, and diplopia, were reported in 11%., Conclusions: Preceding TVSs can occur in 12% of PCOS during the previous 3 months. Isolated dizziness/vertigo of unknown cause needs to be considered as a vertebrobasilar transient ischemic attack symptom, especially in patients with vascular risk factors. The characteristics of isolated vestibular symptom in vertebrobasilar transient ischemic attacks is highly variable and atypical compared with other transient ischemic symptoms.

Isolated dizziness and vertigo due to vascular mechanisms are frequently misdiagnosed as peripheral vestibulopathy or vestibular migraine. For diagnosis of strokes presenting with an acute prolonged (≥ 24 hours) vestibular syndrome, findings on clinical examination, such as HINTS (negative head impulse tests, detection of direction-changing gaze-evoked nystagmus, and presence of skew deviation), are more sensitive than findings on neuroimaging. Since HINTS alone cannot securely detect anterior inferior cerebellar artery strokes, additional attention should be paid to the patients with unexplained hearing loss in addition to acute prolonged vestibulopathy. For diagnosis of transient (< 24 hours) spontaneous vestibular syndrome due to vascular mechanisms, the presence of associated craniocervical pain and focal neurological symptoms/signs is the clue. Even without these symptoms or signs, however, vascular imaging combined with perfusion- and diffusion-weighted MRI should be performed in patients with multiple vascular risk factors or a high ABCD2 score (age, blood pressure, clinical features, duration of symptom, and presence of diabetes)., Competing Interests: H.A.K. and H.L. report no disclosure. J-S.K. serves as an associate editor of Frontiers in Neuro-otology and on the editorial boards of the Journal of Clinical Neurology, Frontiers in Neuro-ophthalmology, Journal of Neuro-ophthalmology, Journal of Vestibular Research, Journal of Neurology, and Medicine., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

This paper presents the diagnostic criteria for hemodynamic orthostatic dizziness/vertigo to be included in the International Classification of Vestibular Disorders (ICVD). The aim of defining diagnostic criteria of hemodynamic orthostatic dizziness/vertigo is to help clinicians to understand the terminology related to orthostatic dizziness/vertigo and to distinguish orthostatic dizziness/vertigo due to global brain hypoperfusion from that caused by other etiologies. Diagnosis of hemodynamic orthostatic dizziness/vertigo requires: A) five or more episodes of dizziness, unsteadiness or vertigo triggered by arising or present during upright position, which subsides by sitting or lying down; B) orthostatic hypotension, postural tachycardia syndrome or syncope documented on standing or during head-up tilt test; and C) not better accounted for by another disease or disorder. Probable hemodynamic orthostatic dizziness/vertigo is defined as follows: A) five or more episodes of dizziness, unsteadiness or vertigo triggered by arising or present during upright position, which subsides by sitting or lying down; B) at least one of the following accompanying symptoms: generalized weakness/tiredness, difficulty in thinking/concentrating, blurred vision, and tachycardia/palpitations; and C) not better accounted for by another disease or disorder. These diagnostic criteria have been derived by expert consensus from an extensive review of 90 years of research on hemodynamic orthostatic dizziness/vertigo, postural hypotension or tachycardia, and autonomic dizziness. Measurements of orthostatic blood pressure and heart rate are important for the screening and documentation of orthostatic hypotension or postural tachycardia syndrome to establish the diagnosis of hemodynamic orthostatic dizziness/vertigo.

Cerebellar ischemic stroke is one of the common causes of vascular vertigo. It usually accompanies other neurological symptoms or signs, but a small infarct in the cerebellum can present with vertigo without other localizing symptoms. Approximately 11 % of the patients with isolated cerebellar infarction simulated acute peripheral vestibulopathy, and most patients had an infarct in the territory of the medial branch of the posterior inferior cerebellar artery (PICA). A head impulse test can differentiate acute isolated vertigo associated with PICA territory cerebellar infarction from more benign disorders involving the inner ear. Acute hearing loss (AHL) of a vascular cause is mostly associated with cerebellar infarction in the territory of the anterior inferior cerebellar artery (AICA), but PICA territory cerebellar infarction rarely causes AHL. To date, at least eight subgroups of AICA territory infarction have been identified according to the pattern of neurotological presentations, among which the most common pattern of audiovestibular dysfunction is the combined loss of auditory and vestibular functions. Sometimes acute isolated audiovestibular loss can be the initial symptom of impending posterior circulation ischemic stroke (particularly within the territory of the AICA). Audiovestibular loss from cerebellar infarction has a good long-term outcome than previously thought. Approximately half of patients with superior cerebellar artery territory (SCA) cerebellar infarction experienced true vertigo, suggesting that the vertigo and nystagmus in the SCA territory cerebellar infarctions are more common than previously thought. In this article, recent findings on clinical features of vertigo and hearing loss from cerebellar ischemic stroke syndrome are summarized.

Orthostatic hypotension (OH), a proxy for sympathetic adrenergic failure, is the most incapacitating sign of autonomic failure. Orthostatic dizziness (OD) is known to be the most common symptom of OH. However, recent studies have demonstrated that 30-39 % of patients with OH experienced rotatory vertigo during upright posture (i.e., orthostatic vertigo, OV), which challenges the dogma that OH induces dizziness and not vertigo. A recent population-based study on spontaneously occurring OD across a wide age range showed that the one-year and lifetime prevalence of OD was 10.9 and 12.5 %, respectively. Approximately 83 % of patients with OD had at least one abnormal autonomic function test result. So far, 11 subtypes of OD have been proposed according to the pattern of autonomic dysfunction, and generalized autonomic failure of sympathetic adrenergic and parasympathetic cardiovagal functions was the most common type. Four different patterns of OH, such as classic, delayed, early, and transient type have been found in patients with OD. The head-up tilt test and Valsalva maneuver should be performed for a comprehensive evaluation of sympathetic adrenergic failure in patients with OD/OV. This review summarizes current advances in OH presenting OD/OV, with a particular focus on the autonomic dysfunction associated with OD.

Background and Purpose: Vertebrobasilar ischemic stroke (VBIS) can cause acute hearing loss (AHL) because the vertebrobasilar system supplies most of the auditory system including the inner ear. The aim of this study was to assess the long-term prognosis of AHL associated with VBIS., Methods: Over 12.5 years, 62 patients with AHL of a vascular cause who were followed for at least 1 year (mean, 49.2 months; SD, 24.4 months) were enrolled in this study. Quantitative audiovestibular function testing was performed during the acute (mostly within 10 days after symptom onset) and last follow-up periods in all patients., Results: On the last follow-up, approximately 65% (39/62) of the patients showed a partial (n=24) or complete (n=15) hearing recovery. All but 2 (97%) patients had acute vertigo and 56 (56/62, 90%) had a unilateral canal paresis to caloric stimulation on the side of the AHL. The most commonly infarcted territory on brain MRI was in the distribution of the anterior inferior cerebellar artery (55/62, 89%). Multivariable analysis showed that multiple risk factors for stroke [odds ratio (OR) 10.46, 95% confidence interval (CI) 1.72 to 13.7, p=0.011] and profound hearing loss [OR 3.92, 95% CI 1.03 to 14.97, p<0.046] predicted a poor outcome for recovery of hearing loss., Conclusions: Acute hearing loss associated with posterior circulation ischemic stroke exhibits a relatively good long-term outcome. Two or more risk factors for stroke and profound hearing loss are adverse prognostic factors for recovery of hearing loss of a vascular cause., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Objective: To investigate whether residual dizziness after successful treatment in patients with benign paroxysmal positional vertigo (BPPV) was associated with autonomic dysfunction., Methods: Fifty-eight consecutive patients with BPPV who had successful canal repositioning procedures (CRPs) and showed no nystagmus or positional vertigo at the next follow-up visit were enrolled and divided into two groups with and without residual dizziness. We performed a standardized autonomic function test., Results: Of the 58 patients, 25 (43%) complained of residual dizziness after successful CRPs, in which postural lightheadedness when righting from sitting, or short-lasting nonspecific dizziness that occurred during head movement or walking were common complaints. Orthostatic hypotension (OH) occurred in 11 patients (19%). Incidence of OH was significantly higher in patients with residual dizziness at the next follow-up than those without residual dizziness (40% and 3%, p=0.000). Compared to patients without residual dizziness, patients with residual dizziness had larger falls in systolic BP during the valsalva maneuver and head-up tilt test. However, cardiovagal parasympathetic function was not different between the patients with and without residual dizziness., Conclusion: In BPPV, residual dizziness after successful treatment may be associated with sympathoneural autonomic dysfunction., Significance: This investigation could be useful in understanding the mechanism of residual dizziness in patients with BPPV., (Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Rotational vertebral artery syndrome (RVAS) is characterized by recurrent attacks of paroxysmal vertigo, nystagmus, and ataxia induced by head rotation. Although recent report has described the RVAS as an important but unrecognized cause of isolated vascular vertigo, the locus of injury site responsible for isolated vertigo in RVAS is still unclear. We report here two patients with RVAS who had a stereotypic clinical presentation characterized by recurrent attacks of isolated vertigo induced by head rotation. The pattern of nystagmus observed in our patients with RVAS can be best explained by the stimulation of the vestibular labyrinth bilaterally or unilaterally. In RVAS, the isolated vertigo may occur due to transient ischemia of the superior vestibular labyrinth. RAVS should be considered in the differential diagnosis of positional vertigo, especially when vertigo is developed while sitting or standing position.

The incidence and characteristics of acute vestibular symptoms, responsible structures, and lateralization of the causative lesions in supratentorial stroke remain unknown. This study aimed to determine the incidence, clinical features, and anatomical correlation of acute vestibular symptoms in supratentorial stroke. We performed a prospective, multicenter, observational study that had recruited patients with supratentorial stroke from the neurology clinics of referral-based four university hospitals in Korea. All patients received a constructed neuro-otological evaluations, and neuroimaging. We analyzed the incidence of acute vestibular symptoms, abnormal ocular motor and vestibular function tests, and stroke lesions. Of 1301 patients with supratentorial stroke, 48 (3.7%) presented with acute vestibular symptoms, and 13 of them (1%) had the vestibular symptoms in isolation. In patients with acute vestibular symptoms, abnormal findings included spontaneous nystagmus (5%), impaired horizontal smooth pursuit (41%), and abnormal tilt of the subjective visual vertical (SVV) (20%). Video head impulse and caloric tests were normal in all the patients. There was no clear correlation between acute vestibular symptoms and involvement of specific vestibular cortex. In patients with unilateral stroke, there was also no lateralization of the causative lesions of acute vestibular symptoms (left vs. right; 52 vs. 48%), even in patients with vertigo (left vs. right; 58 vs. 42%). This study demonstrates that the incidence of acute vestibular symptoms in supratentorial stroke is 3.7%, with being isolated in 1%. The widespread lesions responsible for acute vestibular symptoms implicate diffuse multisensory cortical–subcortical networks in the cerebral hemispheres without a lateralization. [ABSTRACT FROM AUTHOR]

Early identification of cardiogenic vertigo (CV) is necessary to prevent serious complications of cardiovascular diseases. However, the literature is limited to case reports without detailed clinical features or diagnostic criteria. The aim of this study was to define characteristics of CV and propose diagnostic criteria. This study included patients with CV diagnosed at Pusan National University and Keimyung University Hospitals. Demographic, clinical, laboratory, and treatment data were analyzed. Of 72 patients with clinically suspicious CV, 27 were finally included. The age ranged from 63 to 88 years (75.1 ± 7.2 years). Recurrent vertigo occurred without syncopal attacks in 52% [95% CI, 32–71], while it preceded (37% [19–58]) or followed (11% [2–29]) syncope. The patients with recurrent isolated vertigo had suffered from symptoms from 15 days to 5 years until final diagnosis (median 122 days). The vertigo lasted only for a few seconds (93% [76–99]) or a few minutes (7% [1–24]). Fourteen patients presented with spinning vertigo, and one of them showed spontaneous downbeat nystagmus during the attack. Accompanying symptoms including chest discomfort, palpitation, headache, arm twitching, and lightheadedness were found in 70% [50–86]. Between patients with and without syncope, there was no difference in clinical parameters and results of cardiac function tests. The most common cardiac abnormality during the attacks of vertigo was bradyarrhythmia (89% [71–98]). Cardiovascular diseases can develop recurrent isolated vertigo without or preceding syncope. Onset age, duration of vertigo, accompanying symptoms, and underlying cardiac diseases can aid in differentiation from other vestibular disorders. Early identification of CV would reduce morbidity and mortality associated with cardiac syncope. [ABSTRACT FROM AUTHOR]

Background: It was the aim of this study to investigate the pattern of evolution of hyperventilation-induced nystagmus (HIN) in vestibular neuritis (VN) and to determine whether HIN influences the dizziness outcome at the last follow-up visit. Methods: Fifty-three consecutive patients with VN underwent a quantitative vestibular function test including hyperventilation and the Korean version of the Dizziness Handicap Inventory during the acute period and the follow-up visit. Results: The incidence of HIN was higher in the acute (62%, 33/53) than in the chronic (17%, 9/53) stages of VN. Approximately 70% (6/9) of patients who continued to have persistent HIN at the last follow-up reported dizziness compared to only 27% (12/44) of patients who had no HIN. Patients who complained of persistent dizziness were significantly more likely to have persistent HIN and high Korean Dizziness Handicap Inventory scores at the last follow-up compared with patients who did not suffer from dizziness. In terms of the degree of recovery of dizziness, patients with HIN initially beating toward the contralesional side exhibited significantly more improvement than patients with HIN initially beating toward the ipsilesional side. Conclusions: The presence of either HIN beating toward the ipsilesional side at the acute stage of VN or persistent HIN at the follow-up visit is associated with persistent dizziness. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract: Background: Acute peripheral vestibular syndrome (APVS) is an idiopathic peripheral vestibulopathy characterized by prolonged vertigo (over 24 h), nausea, vomiting, and postural instability. There has been no previous report of APVS presumably of a vascular cause. Objectives: To describe APVS presumably resulting from a vascular disturbance with embolic cerebral infarction. Patient: A 67-year-old woman developed sudden onset of severe isolated vertigo, nausea, and vomiting, which lasted for 3 days. Ten days earlier, she had had 4 episodes of transient vertigo lasting a few minutes. She had a spontaneous right-beating horizontal nystagmus with a torsional component, in the primary position and on gaze to the right or left. Caloric test showed a decreased response on the left side. Diffusion-weighted brain MRI showed 2 tiny acute infarcts in the left hippocampus and basal ganglia. Magnetic resonance angiogram showed no abnormalities. Continuous electrocardiographic monitoring for 24 h showed paroxysmal atrial fibrillation. Conclusion: In this patient, clinical and laboratory findings were consistent with APVS. Considering the simultaneous onset of acute silent infarcts on brain MRI, the definite cardioembolic source with atrial fibrillation, and the episodic transient vertigo attacks before APVS, we speculate that small emboli arising from the heart may have lodged selectively in the anterior vestibular artery, producing APVS. [Copyright &y& Elsevier]