Visual vertigo and motion sickness is different between persistent postural-perceptual dizziness and vestibular migraine.

INTRODUCTION: Persistent postural-perceptual dizziness (PPPD) and vestibular migraine (VM) share symptoms of visual vertigo and motion sickness that can be confusing for clinicians to distinguish. We compare the severity of these symptoms and dynamic subjective visual vertical (dSVV) in these two common vestibular conditions. METHOD: Twenty-nine patients with PPPD, 37 with VM, and 29 controls were surveyed for subjective symptoms using the visual vertigo analogue scale (VVAS) and motion sickness susceptibility questionnaire during childhood (MSA) and the past 10 years (MSB). dSVV is a measure of visual dependence measures perception of verticality against a rotating background (5 deg./s). RESULTS: VVAS revealed contextual differences for dizziness between those with PPPD and VM. Ratings of visual vertigo were most severe in PPPD, less in VM, and mild in controls (VVAS PPPD 27.1, VM 11.2, control 4.6, p < 0.001). MSA was more severe in VM than in PPPD or control (12.8 vs 7.6 vs 8.5, p = 0.01). MSB was more severe in VM than controls (MSB score 12.9 VS 8.1 p = 0.009) but was not different than PPPD (MSB score 10.0, p = 0.10). dSVV alignment was similar among the three groups (p = 0.83). Both VM and PPPD groups had greater simulator sickness than controls after completing the dSVV. CONCLUSIONS: Patients with PPPD report more visual vertigo than those with VM, but a history of motion sickness as a child is more common in VM. Additionally, the environmental context that induces visual vertigo is different between PPPD and VM.

Subjective visual vertical imprecision during lateral head tilt in patients with chronic dizziness.

Most prior studies of the subjective visual vertical (SVV) focus on inaccuracy of subjects' SVV responses with the head in an upright position. Here we investigated SVV imprecision during lateral head tilt in patients with chronic dizziness compared to healthy controls. Forty-five dizzy patients and 45 healthy controls underwent SVV testing wearing virtual reality (VR) goggles, sitting upright (0°) and during head tilt in the roll plane (± 30°). Ten trials were completed in each of three static head positions. The SVV inaccuracy and SVV imprecision were analyzed and compared between groups, along with systematic errors during head tilt, i.e., A-effect and E-effect (E-effect is a typical SVV response during head tilts of ± 30°). The SVV imprecision was found to be affected by head position (upright/right head tilt/left head tilt, p < 0.001) and underlying dizziness (dizzy patients/healthy controls, p = 0.005). The SVV imprecision during left head tilt was greater in dizzy patients compared to healthy controls (p = 0.04). With right head tilt, there was a trend towards greater SVV imprecision in dizzy patients (p = 0.08). Dizzy patients were more likely to have bilateral (6.7%) or unilateral (22.2%) A-effect during lateral head tilt than healthy controls (bilateral (0%) or unilateral (6.7%) A-effect, p < 0.01). Greater SVV imprecision in chronically dizzy patients during head tilts may be attributable to increased noise of vestibular sensory afferents or disturbances of multisensory integration. Our findings suggest that SVV imprecision may be a useful clinical parameter of underlying dizziness measurable with bedside SVV testing in VR.

Pendular Oscillation and Ocular Bobbing After Pontine Hemorrhage.

The pathophysiology of acute, vertical spontaneous eye movements following pontine hemorrhage is not well understood. Here, we present and discuss the video-oculography findings of a patient with acute pontine hemorrhage who developed vertical pendular oscillation and ocular bobbing while comatose. The amplitudes, peak velocities, frequency distribution, and phase planes (velocity versus position) of the eye movements were analyzed. The vertical pendular oscillation was rhythmic with a peak frequency of 1.7 Hz, but amplitudes (mean 1.9°, range 0.2-8.2°) and peak velocities (mean 20.6°/s; range 5.9-60.6°/sec) fluctuated. Overall, their peak velocities were asymmetric, faster with downward than upward. Higher peak velocities were seen with larger amplitudes (downward phase r = 0.95, p < 0.001; upward phase r = 0.91, p < 0.001) and with movements beginning at eye positions lower in the orbit (downward phase r = - 0.64, p < 0.001; upward phase r = - 0.86, p < 0.001). Interspersed were typical ocular bobbing waveforms with a fast (peak velocity 128.8°/s), large-amplitude (17.5°) downward movement, sometimes followed by a flat interphase interval (0.5 s) when the eye was nearly stationary, and then a slow return to mid-position with a decaying velocity waveform. To account for the presence and co-existence of pendular oscillations and bobbing, we present and discuss three hypothetical models, not necessarily mutually exclusive: (1) oscillations originating in the inferior olives due to disruption of the central tegmental tract(s); (2) unstable neural integrator function due to pontine cell group damage involving neurons involved in gaze-holding; (3) low-frequency saccadic intrusions following omnipause neuron damage.

Statistical insights for crude-rate-based operational measures of misdiagnosis-related harms.

In longitudinal event data, a crude rate is a simple quantification of the event rate, defined as the number of events during an evaluation window, divided by the at-risk population size at the beginning or mid-time point of that window. The crude rate recently received revitalizing interest from medical researchers who aimed to improve measurement of misdiagnosis-related harms using administrative or billing data by tracking unexpected adverse events following a "benign" diagnosis. The simplicity of these measures makes them attractive for implementation and routine operational monitoring at hospital or health system level. However, relevant statistical inference procedures have not been systematically summarized. Moreover, it is unclear to what extent the temporal changes of the at-risk population size would bias analyses and affect important conclusions concerning misdiagnosis-related harms. In this article, we present statistical inference tools for using crude-rate based harm measures, as well as formulas and simulation results that quantify the deviation of such measures from those based on the more sophisticated Nelson-Aalen estimator. Moreover, we present results for a generalized multibin version of the crude rate, for which the usual crude rate is a single-bin special case. The generalized multibin crude rate is more straightforward to compute than the Nelson-Aalen estimator and can reduce potential biases of the single-bin crude rate. For studies that seek to use multibin measures, we provide simulations to guide the choice regarding number of bins. We further bolster these results using a worked example of stroke after "benign" dizziness from a large data set.

Convergence Vestibulo-ocular Reflex in Unilateral Vestibular Hypofunction: Behavioral Evidence in Support of a Novel Gaze Stability Exercise.

BACKGROUND AND PURPOSE: Convergence of the eyes during head rotation increases the gain (eye velocity/head velocity) of the vestibulo-ocular reflex (VOR). We sought to know whether convergence would increase the VOR gain (mean + SD) in unilateral vestibular hypofunction (UVH). METHODS: Vestibulo-ocular reflex gain during ipsi- and contralesional horizontal head rotation at near (15 cm) and far (150 cm) targets was measured in 22 subjects with UVH and 12 healthy controls. Retinal slip was estimated (retinal slip index [RSI]) as the difference between ideal VOR gain (no retinal slip) and the actual VOR gain. RESULTS: Convergence did not significantly enhance VOR gain for ipsilesional rotation (mean difference, 0.04; 95% confidence interval [CI], -0.01 to 0.09), near viewing (0.77 ± 0.34) versus far viewing (0.72 ± 0.29), yet the VOR gain during contralesional rotation was greater for near viewing (1.20 ± 0.23) than for far viewing (0.97 ± 0.21; mean difference, 0.23; 95% CI, 0.13-0.32). In the 36% of subjects with recovery of their ipsilesional VOR gain, the vergence effect trended to recover (far VOR gain: 1.06 ± 0.17 vs near VOR gain 1.16 ± 0.21; mean difference, 0.10; 95% CI, -0.02 to 0.22). Ipsilesional head rotation induced greater retinal slip for near (RSI = 0.90 ± 0.34) targets than for far targets (RSI = 0.35 ± 0.29; mean difference, 0.56; 95% CI, 0.51-0.61). DISCUSSION AND CONCLUSIONS: The convergence-mediated VOR gain enhancement is preserved during contralesional but impaired during ipsilesional head rotation. Recovery of ipsilesional passive VOR gain does not equate to restored convergence enhancement, although it did increase ∼10%. These data suggest head motion viewing near targets will increase retinal slip, which warrants consideration as a gaze stability exercise for subjects with UVH.Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A325).

The fixation suppression test can uncover vertical nystagmus of central origin in some patients with dizziness.

BACKGROUND: Identifying dangerous causes of dizziness is a challenging task for neurologists, as it requires interpretation of subtle bedside exam findings, which become even more subtle with time. Nystagmus can be instrumental in differentiating peripheral from central vestibular disorders. Conventional teaching is that peripheral vestibular nystagmus is accentuated by removal of visual fixation. We sought to systematically test the hypothesis that, in some cases, vertical nystagmus due to central vestibular disorders may also be easier to identify when fixation is removed. METHODS: To identify patients with vertical nystagmus, we retrospectively reviewed clinical, MRI, and VNG data of consecutive patients undergoing VNG in our vestibular clinic over a 9-month period. We analyzed clinical features, bedside neuro-otological examination, MRI results, and VNG findings in fixation as well as those with fixation removed. RESULTS: Two hundred and fourteen charts were reviewed. Twenty-six patients had vertical nystagmus with fixation removed on VNG. Only three (11.5%) of these patients had vertical nystagmus apparent with fixation (and only two had nystagmus observed clearly at the bedside with the unaided eye). Thirteen (50%) of the patients had posterior fossa lesions on MRI and eight of the rest (30.8%) were diagnosed with central vestibular disorders. Of the 13 patients with MRI-confirmed lesions, 3 patients (23.1%) had no neurological signs or conventional bedside oculomotor signs; in these cases, vertical nystagmus without fixation was the only sign of a central lesion. CONCLUSIONS: Our findings go against conventional teaching and show that removing fixation can uncover subtle vertical nystagmus due to central vestibular disease, particularly from focal or chronic lesions.

The bucket test differentiates patients with MRI confirmed brainstem/cerebellar lesions from patients having migraine and dizziness alone.

BACKGROUND: Amongst the most challenging diagnostic dilemmas managing patients with vestibular symptoms (i.e. vertigo, nausea, imbalance) is differentiating dangerous central vestibular disorders from benign causes. Migraine has long been recognized as one of the most common causes of vestibular symptoms, but the clinical hallmarks of vestibular migraine are notoriously inconsistent and thus the diagnosis is difficult to confirm. Here we conducted a prospective study investigating the sensitivity and specificity of combining standard vestibular and neurological examinations to determine how well central vestibular disorders (CVD) were distinguishable from vestibular migraine (VM). METHOD: Twenty-seven symptomatic patients diagnosed with CVD and 36 symptomatic patients with VM underwent brain imaging and clinical assessments including; 1) SVV bucket test, 2) ABCD2, 3) headache/vertigo history, 4) presence of focal neurological signs, 5) nystagmus, and 6) clinical head impulse testing. RESULTS: Mean absolute SVV deviations measured by bucket testing in CVD and VM were 4.8 ± 4.1° and 0.7 ± 1.0°, respectively. The abnormal rate of SVV deviations (> 2.3°) in CVD was significantly higher than VM (p < 0.001). Using the bucket test alone to differentiate CVD from VM, sensitivity was 74.1%, specificity 91.7%, positive likelihood ratio (LR+) 8.9, and negative likelihood ratio (LR-) 0.3. However, when we combined the SVV results with the clinical exam assessing gaze stability (nystagmus) with an abnormal focal neurological exam, the sensitivity (92.6%) and specificity (88.9%) were optimized (LR+ (8.3), LR- (0.08)). CONCLUSION: The SVV bucket test is a useful clinical test to distinguish CVD from VM, particularly when interpreted along with the results of a focal neurological exam and clinical exam for nystagmus.

Sudden Hearing Loss with Vertigo Portends Greater Stroke Risk Than Sudden Hearing Loss or Vertigo Alone.

BACKGROUND: Because it is unknown whether sudden hearing loss (SHL) in acute vertigo is a "benign" sign (reflecting ear disease) or a "dangerous" sign (reflecting stroke), we sought to compare long-term stroke risk among patients with (1) "SHL with vertigo," (2) "SHL alone," and (3) "vertigo alone" using a large national health-care database. METHODS: Patients with first-incident SHL (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] 388.2) or vertigo (ICD-9-CM 386.x, 780.4) were identified from the National Health Insurance Research Database of Taiwan (2002-2009). We defined SHL with vertigo as a vertigo-related diagnosis ±30 days from the index SHL event. SHL without a temporally proximate vertigo diagnosis was considered SHL alone. The vertigo-alone group had no SHL diagnosis. All the patients were followed up until stroke, death, withdrawal from the database, or current end of the database (December 31, 2012) for a minimum period of 3 years. The hazards of stroke were compared across groups. RESULTS: We studied 218,656 patients (678 SHL with vertigo, 1998 with SHL alone, and 215,980 with vertigo alone). Stroke rates at study end were 5.5% (SHL with vertigo), 3.0% (SHL alone), and 3.9% (vertigo alone). Stroke hazards were higher in SHL with vertigo than in SHL alone (hazard ratio [HR], 1.93; 95% confidence interval [CI], 1.28-2.91) and in vertigo alone (HR, 1.63; 95% CI, 1.18-2.25). Defining a narrower window between SHL and vertigo (±3 days) increased the hazards. CONCLUSIONS: The combination of SHL plus vertigo in close temporal proximity is associated with increased subsequent stroke risk over SHL alone and vertigo alone. This suggests that SHL in patients with vertigo is not necessarily a benign peripheral vestibular sign.

Vestibular migraine has higher correlation with carsickness than non-vestibular migraine and Meniere's disease.

PURPOSE: To investigate whether patients with vestibular migraine (VM) are more susceptible to carsickness than patients with non-vestibular migraine (NVM) or Meniere's disease (MD). METHODS: Consecutive patients with a diagnosis of definite VM, probable VM, NVM, or MD at our Headache and Dizziness clinics were interviewed using the same three questions to investigate the history of carsickness. The patients who had experienced carsickness in their lifetime and those who had still experienced carsickness in the past ten years were identified. The rates of carsickness were compared between groups. RESULTS: 78.4% of the VM patients had experienced carsickness in their lifetime, which was significantly higher than the patients with NVM (43.6%) and MD (18.2%). Both the lifetime rate of carsickness and the rate in the past ten years were highest in the patients with definite VM, followed by probable VM, NVM, and MD (p less than 0.05, chi-square test). The odds ratio of lifetime carsickness for VM versus MD was high (8.7). CONCLUSION: Both patients with definite VM and probable VM were more susceptible to carsickness than the patients with NVM or MD. This reinforces the theory of vestibular hypersensitivity in VM. We suggest that a past history of carsickness may help in the diagnosis of VM, and especially in distinguishing VM from MD.

Prevalence of cavum septum pellucidum and/or cavum Vergae in brain computed tomographies of Taiwanese.

OBJECTIVE: The reported prevalence of cavum septum pellucidum (CSP) and cavum Vergae (CV) in brain computed tomography (CT) is 5.5% in Great Britain and 1.24% in China but unknown in Taiwan. Moreover, CSP and/or CV has generally been thought to decrease as age progresses, but the evidence of actual prevalence at different age levels is still limited in the literature. METHODS: A total of 19,031 patients with brain CT at a regional hospital in northern Taiwan from July 2008 to August 2010 were included in this study. Their radiological official reports were retrospectively reviewed to check for CSP and/or CV. An X2 test was used for statistical analysis (α = .05). RESULTS: The prevalence of CSP and/or CV in all brain CT was 0.93% (n = 177), which was lower. than that in the Chinese and British studies. Among them, 2.8% (n = 5) had only CSP, 1.7% (n = 3) had only CV, and 95.5% (n = 169) had coexistent CSP and CV. There is a significant difference in prevalence between the age groups (p = .009), and the prevalence is the highest in the group aged 20-29 years (1.56%) and lowest in the group aged above 80. After age 20-29, the prevalence tends to decrease with increasing age. CONCLUSION: This is not only the first study of CSP and CV in the Taiwanese population but the study population is also larger than those in the literature. The prevalence was found to approximately decrease as age progresses, but would reach the peak in the young adult group rather than the children or adolescent group.

Risk of Cervical Dizziness in Patients With Cervical Spondylosis.

Importance: The dizziness associated with cervical spondylosis is a controversial topic given that many experts believe that cervical spondylosis is a common cause of dizziness, whereas others do not believe it exists. Objective: To compare the risk of dizziness between patients with cervical spondylosis and matched controls (ie, patients with lumbar spondylosis after propensity score matching [PSM]). Design, Setting, and Participants: This cohort study used medical claims data from the National Health Insurance Research Database of Taiwan for patients 60 years or older with cervical or lumbar spondylosis newly diagnosed in any outpatient department between January 1, 2010, and December 31, 2015. Patients diagnosed with cervical spondylosis were included as the study cohort, and those diagnosed with lumbar spondylosis who were matched to the study cohort via PSM were selected as the control cohort. Both cohorts were followed up for 1 year unless they were diagnosed with dizziness, censored by death, or withdrew from the health insurance program. Data analysis was performed from August 9 to September 20, 2022. Main Outcomes and Measures: The main outcome was the date of outpatient diagnosis of dizziness. The risks of dizziness were compared between groups. The relative risk and incidence rate difference were calculated. Results: A total of 3638 patients with cervical spondylosis (mean [SD] age, 67.9 [7.1] years; 2024 [55.6%] male) and 3638 patients with lumbar spondylosis (mean [SD] age, 68.0 [7.1] years; 2024 [55.6%] male) after PSM were selected as the study and control cohorts, respectively. The patients with cervical spondylosis had higher risk of dizziness than matched controls, with a 1-year relative risk of 1.20 (95% CI, 1.03-1.39). The 1-year incidence of dizziness was 10.2% (95% CI, 9.2%-11.2%) in patients with cervical spondylosis and 8.6% (95% CI, 7.7%-9.5%) in the matched group of lumbar spondylosis. The incidence rate difference between the groups was 1.6% (95% CI, 0.3%-3.0%). Conclusions and Relevance: These data support the association between dizziness and cervical spondylosis, but the small difference between groups reveals that dizziness associated with cervical spondylosis is uncommon. Clinicians should be wary of diagnosing a cervical cause for dizziness based on an actual history of cervical spondylosis.

Vestibular paroxysmia associated with paroxysmal pulsatile tinnitus: a case report and review of the literature.

PURPOSE: Vestibular paroxysmia is defined as paroxysmal, brief, and carbamazepine-responsive vertigo. Although neurovascular cross-compression (NVCC) of the vestibulocochlear nerve is believed to be the cause of vestibular paroxysmia, the mechanism remains controversial. Herein, we describe the case of a man with NVCC who presented with paroxysmal vertigo associated with paroxysmal pulsatile tinnitus. CASE REPORT: A 68-year-old man presented with paroxysmal vertigo for one month. Paroxysmal pulsatile tinnitus in the right ear occurred simultaneously with the vertigo. Magnetic resonance imaging demonstrated that the right anterior inferior cerebellar artery was compressing the right vestibulocochlear nerve. The vertigo and tinnitus completely disappeared within one week after treatment with carbamazepine. CONCLUSION: The pulsatile nature of the patient's tinnitus implied that the auditory nerve was being compressed by a pulsating artery and was found to consolidate the causal relationship between NVCC and vestibular paroxysmia.

Weak nystagmus in the dark persists for months after acute unilateral vestibular loss.

Background: Weak nystagmus with fixation removed can be seen both in normal individuals and in recovery from a unilateral vestibular insult, thus its clinical significance is unclear in patients with dizziness. We thus sought to compare features of nystagmus at various stages following unilateral vestibular loss (UVL). Methods: We enrolled thirty consecutive patients after acute UVL with impaired vestibulo-ocular reflex (VOR) gain. The patients were allocated into three groups according to time from onset of symptoms: acute (1-7 days), subacute (8-30 days), and chronic (>30 days). Patients underwent video-oculography (with and without fixation) and video head impulse testing (vHIT) to determine VOR gain. We examined the relationships amongst SPV, VOR gain, and time from symptom onset across groups. Results: There were 11, 10, and 9 patients in the acute, subacute, and chronic stages of UVL, respectively. With visual fixation, only 8 patients (26.7%) demonstrated nystagmus, all from the acute group. With fixation removed, 26 patients (86.7%) exhibited spontaneous nystagmus, including 90.9%, 90%, and 77.8% of the patients from the acute, subacute, and chronic groups, respectively. Horizontal nystagmus was paralytic (i.e., fast phase contralesional) in 25 (96.7%) cases. Horizontal SPV was negatively correlated with logarithm of time from onset to examination (r = -0.48, p = 0.007) and weakly negatively correlated with ipsilesional VOR gain (r = -0.325, p = 0.08). Conclusion: In the subacute or chronic stages of UVL, paralytic nystagmus with fixation removed persisted at a low intensity. Therefore, weak nystagmus in the dark may have diagnostic value in chronic dizziness.

Positive horizontal-canal head impulse test is not a benign sign for acute vestibular syndrome with hearing loss.

Background: Diagnosis of acute vestibular syndrome (AVS) with hearing loss is challenging because the leading vascular cause-AICA territory stroke-can appear benign on head impulse testing. We evaluated the diagnostic utility of various bedside oculomotor tests to discriminate imaging-positive and imaging-negative cases of AVS plus hearing loss. Method: We reviewed 13 consecutive inpatients with AVS and acute unilateral hearing loss. We compared neurologic findings, bedside and video head impulse testing (bHIT, vHIT), and other vestibular signs (including nystagmus, skew deviation, and positional testing) between MRI+ and MRI- cases. Results: Five of thirteen patients had a lateral pontine lesion (i.e., MRI+); eight did not (i.e., MRI-). Horizontal-canal head impulse test showed ipsilateral vestibular loss in all five MRI+ patients but only in three MRI- patients. The ipsilesional VOR gains of horizontal-canal vHIT were significantly lower in the MRI+ than the MRI- group (0.56 ± 0.11 vs. 0.87 ± 0.24, p = 0.03). All 5 MRI+ patients had horizontal spontaneous nystagmus beating away from the lesion (5/5). One patient (1/5) had direction-changing nystagmus with gaze. Two had skew deviation (2/5). Among the 8 MRI- patients, one (1/8) presented as unilateral vestibulopathy, four (4/8) had positional nystagmus and three (3/8) had isolated posterior canal hypofunction. Conclusion: The horizontal-canal head impulse test poorly discriminates central and peripheral lesions when hearing loss accompanies AVS. Paradoxically, a lateral pontine lesion usually mimics unilateral peripheral vestibulopathy. By contrast, patients with peripheral lesions usually present with positional nystagmus or isolated posterior canal impairment, risking misdiagnosis as central vestibulopathy.

Automated nystagmus detection: Accuracy of slow-phase and quick-phase algorithms to determine the presence of nystagmus.

PURPOSE: To verify the accuracy of automated nystagmus detection algorithms. METHOD: Video-oculography (VOG) plots were analyzed from consecutive patients with dizziness presenting to a neurology clinic. Data were recorded for 30 s in upright position with fixation block. For automated nystagmus detection, slow-phase algorithm parameters included mean and median slow-phase velocity (SPV), and slow-phase duration ratio. Quick-phase algorithm parameters included saccadic difference and saccadic ratio. For verification, two independent blinded assessors reviewed VOG traces and videos and coded presence or absence of nystagmus. Assessor consensus was used as reference standard. Accuracy of slow-phase and quick-phase algorithm parameters were compared, and ROC analysis was performed. RESULTS: Among 524 analyzed VOG traces, 99 were verified as nystagmus present and 425 were verified as nystagmus absent. Prevalence of nystagmus in the sample population was 18.9%. In ROC analysis, areas under the curve of individual algorithm parameters were 0.791-0.896. With optimal thresholds for determining presence or absence of nystagmus, algorithm sensitivity (70.7-87.9%), specificity (71.8-84.0%), and negative predictive value (91.7-96.4%) were ideal, but positive predictive value (38.8-53.4%) was not ideal. Combining algorithm parameters using logistic regression models mildly improved detection accuracy. CONCLUSION: Both slow-phase and fast-phase algorithms were accurate for detecting nystagmus. Due to low positive predictive value, the utility of independent automated nystagmus detection systems is limited in clinical settings with low prevalence of nystagmus. Combining parameters using logistic regression models appears to improve detection accuracy, indicating that machine learning may potentially optimize the accuracy of future automated nystagmus detection systems.

Vestibular paroxysmia: Long-term clinical outcome after treatment.

Objective: To study the long-term treatment outcome of vestibular paroxysmia (VP). Study design: Retrospective study. Setting: Tertiary referral hospital. Methods: We analyzed records of 29 consecutive patients who were diagnosed with VP and who were treated with VP-specific anticonvulsants for at least 3 months. Patients were followed for a minimum of 6 months. We recorded and assessed starting and target dosage of medications, time to achieve adequate therapeutic response, adverse effects, and the rates of short-term and long-term remission without medication. Results: All 29 patients were started on oxcarbazepine as first-line treatment, and 93.1% and 100% of patients reported good-to-excellent therapeutic response within 2 and 4 weeks, respectively. Three patients switched to other anticonvulsants at 3 months. At long-term follow-up (8-56 months), most (84.6%) oxcarbazepine-treated patients maintained good therapeutic response at doses between 300 and 600 mg/day. Eleven (37.9%) patients experienced complete remission without medication for more than 1 month, of which six (20.7%) had long-term remission off medication for more than 12 months. Nineteen (65.5%) patients had neurovascular compression (NVC) of vestibulocochlear nerve on MRI, but its presence or absence did not predict treatment response or remission. Conclusion: Low-dose oxcarbazepine monotherapy for VP is effective over the long term and is generally well-tolerated. About 20% of patients with VP in our study had long-term remission off medication.

Test-retest reliability of subjective visual vertical measurements with lateral head tilt in virtual reality goggles.

OBJECTIVE: The objective is to investigate the test-retest reliability of subjective visual vertical (SVV) in the upright position and with lateral head tilts through a computerized SVV measuring system using virtual reality (VR) goggles. MATERIALS AND METHODS: Thirty healthy controls underwent SVV test in upright position, with the head tilted to the right 30°, and with the head tilted to the left 30°. Subjects wore SVV VR goggles, which contained a gyroscope for monitoring the angle of head tilt. Each subject completed 10 adjustments in each head position. The mean value of SVV deviations and SVV imprecision (the intra-individual variability of SVV deviations from the 10 adjustments) were recorded and compared across different head positions. The participants then repeated the same SVV protocol at least 1 week later. The test-retest reliability of SVV deviation and SVV imprecision were analyzed. RESULTS: The SVV deviation (mean ± standard deviation) was 0.22° ± 1.56° in upright position, -9.64° ± 5.91° in right head tilt, and 7.20° ± 6.36° in left head tilt. The test-retest reliability of SVV deviation was excellent in upright position (intra-class correlation coefficient [ICC] = 0.77, P < 0.001), right head tilt (ICC = 0.83, P < 0.001) and left head tilt (ICC = 0.84, P < 0.001). The SVV values from the 10 adjustments made during right and left head tilts were less precise than when measured at upright (P < 0.001). The test-retest reliability of SVV imprecision was poor at upright (ICC = 0.21, P = 0.26) but fair-to-good in right head tilt (ICC = 0.72, P < 0.001) and left head tilt (ICC = 0.44, P = 0.04). CONCLUSION: The test-retest reliability of SVV deviation during lateral head tilts via VR goggles is excellent, which supports further research into the diagnostic value of head-tilt SVV in various vestibular disorders. In addition, the degree of SVV imprecision during head tilt has fair-to-good test-retest reliability, which suggests SVV imprecision may have clinical applicability.

Stroke hospitalization after misdiagnosis of "benign dizziness" is lower in specialty care than general practice: a population-based cohort analysis of missed stroke using SPADE methods.

OBJECTIVES: Isolated dizziness is a challenging stroke presentation in the emergency department, but little is known about this problem in other clinical settings. We sought to compare stroke hospitalizations after treat-and-release clinic visits for purportedly "benign dizziness" between general and specialty care settings. METHODS: This was a population-based retrospective cohort study from a national database. We included clinic patients with a first incident treat-and-release visit diagnosis of non-specific dizziness/vertigo or a peripheral vestibular disorder (ICD-9-CM 780.4 or 386.x [not 386.2]). We compared general care (internal medicine, family medicine) vs. specialty care (neurology, otolaryngology) providers. We used propensity scores to control for baseline stroke risk differences unrelated to dizziness diagnosis. We measured excess (observed>expected) stroke hospitalizations in the first 30 d (i.e., missed strokes associated with an adverse event). RESULTS: We analyzed 144,355 patients discharged with "benign dizziness" (n=117,117 diagnosed in general care; n=27,238 in specialty care). After propensity score matching, patients in both groups were at higher risk of stroke in the first 30 d (rate difference per 10,000 treat-and-release visits for "benign dizziness" 24.9 [95% CI 18.6-31.2] in general care and 10.6 [95% CI 6.3-14.9] in specialty care). Short-term stroke risk was higher in general care than specialty care (relative risk, RR 2.2, 95% CI 1.5-3.2) while the long-term risk was not significantly different (RR 1.3, 95% CI 0.9-1.9), indicating higher misdiagnosis-related harms among dizzy patients who initially presented to generalists after adequate propensity matching. CONCLUSIONS: Missed stroke-related harms in general care were roughly twice that in specialty care. Solutions are needed to address this care gap.

Unilateral paresthesia after isolated infarct of the splenium: case report.

PURPOSE: We describe a patient who presented with unilateral paresthesia after acute isolated infarct of the splenium. CASE REPORT: A 74-year-old woman presented with acute onset of right sided numbness and tingling. MR imaging of the brain showed hypointensity on T1-weighted images and on apparent diffusion coefficient maps, and hyperintensity on T2-weighted and on diffusion-weighted images in the splenium, suggestive of acute infarction. MR angiography showed narrowing of left posterior cerebral artery with decreased branches. On detailed high cortical function assessment, she did not have frontal lobe dysfunction, alien hand syndrome, apraxia, optic ataxia, cortical sensation dysfunction, alexia, agraphia, visual field defect, nor color agnosia. CONCLUSION: Infarcts of the splenium are not common. Splenial lesion may be associated with altered mental status, ataxia, recent seizure, hemispheric disconnection, and dysarthria. The presentation of isolated unilateral paresthesia makes the patient different from those previously described. The paresthesia could be caused by selective lacunar infarcts in the diencephalic and mesencephalic regions or could be caused by the diaschisis in the parietal cortex. Single photon emission CT may be indicated to provide further information of central nervous system dysfunction in splenial lesion.