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Vestibular Rehabilitation A forum for the discussion of vestibular dysfunction including dizziness, vertigo, and balance problems.

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Old 20-01-2016, 01:08 PM   #1
Jo Bowyer
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Default Papers related to examination of the Vestibular System

The video head impulse test during post-rotatory nystagmus: physiology and clinical implications
http://link.springer.com/article/10....ampaign=buffer
Abstract
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The aim of this study was to test the effects of a sustained nystagmus on the head impulse response of the vestibulo-ocular reflex (VOR) in healthy subjects. VOR gain (slow-phase eye velocity/head velocity) was measured using video head impulse test goggles. Acting as a surrogate for a spontaneous nystagmus (SN), a post-rotatory nystagmus (PRN) was elicited after a sustained, constant-velocity rotation, and then head impulses were applied. ‘Raw’ VOR gain, uncorrected for PRN, in healthy subjects in response to head impulses with peak velocities in the range of 150°/s–250°/s was significantly increased (as reflected in an increase in the slope of the gain versus head velocity relationship) after inducing PRN with slow phases of nystagmus of high intensity (>30°/s) in the same but not in the opposite direction as the slow-phase response induced by the head impulses. The values of VOR gain themselves, however, remained in the normal range with slow-phase velocities of PRN < 30°/s. Finally, quick phases of PRN were suppressed during the first 20–160 ms of a head impulse; the time frame of suppression depended on the direction of PRN but not on the duration of the head impulse. Our results in normal subjects suggest that VOR gains measured using head impulses may have to be corrected for any superimposed SN when the slow-phase velocity of nystagmus is relatively high and the peak velocity of the head movements is relatively low. The suppression of quick phases during head impulses may help to improve steady fixation during rapid head movements.
Posted on ACPIVR twitter feed this am. It is an issue that has given me cause for thought as a relative beginner in this field. I have seen several patients with spontaneous nystagmus underlying the presenting condition.
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Old 25-01-2016, 06:14 AM   #2
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interesting but it sounds weird to use a normal response like PRN and velocity storage to explain what happens during an abnormal condition SN. I am going to have to look up this article at some point
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Old 01-02-2016, 10:49 PM   #3
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Default The dorsal visual system predicts future and remembers past eye position.

http://journal.frontiersin.org/artic...00009/abstract

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Eye movements are essential to primate vision but introduce potentially disruptive displacements of the retinal image. To maintain stable vision, the brain is thought to rely on neurons that carry both visual signals and information about the current direction of gaze in their firing rates. We have shown previously that these neurons provide an accurate representation of eye position during fixation, but whether they are updated fast enough during saccadic eye movements to support real-time vision remains controversial. Here we show that not only do these neurons carry a fast and accurate eye-position signal, but also that they support in parallel a range of time-lagged variants, including predictive and postdictive signals. We recorded extracellular activity in four areas of the macaque dorsal visual cortex during a saccade task, including the lateral and ventral intraparietal areas (LIP, VIP), and the middle temporal (MT) and medial superior temporal (MST) areas. As reported previously, neurons showed tonic eye-position-related activity during fixation. In addition, they showed a variety of transient changes in activity around the time of saccades, including relative suppression, enhancement, and pre-saccadic bursts for one saccade direction over another. We show that a hypothetical neuron that pools this rich population activity through a weighted sum can produce an output that mimics the true spatiotemporal dynamics of the eye. Further, with different pooling weights, this downstream eye position signal could be updated long before (<100 ms) or after (<200 ms) an eye movement. The results suggest a flexible coding scheme in which downstream computations have access to past, current, and future eye positions simultaneously, providing a basis for visual stability and delay-free visually-guided behavior.
A short piece, but has finally enabled me to grok saccades.
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Old 01-03-2016, 02:57 PM   #4
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Default Dynamic causal modelling of eye movements during pursuit: Confirming precision-encoding in V1 using MEG.

http://www.ncbi.nlm.nih.gov/pubmed/26921713

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This paper shows that it is possible to estimate the subjective precision (inverse variance) of Bayesian beliefs during oculomotor pursuit. Subjects viewed a sinusoidal target, with or without random fluctuations in its motion. Eye trajectories and magnetoencephalographic (MEG) data were recorded concurrently. The target was periodically occluded, such that its reappearance caused a visual evoked response field (ERF). Dynamic causal modelling (DCM) was used to fit models of eye trajectories and the ERFs. The DCM for pursuit was based on predictive coding and active inference, and predicts subjects' eye movements based on their (subjective) Bayesian beliefs about target (and eye) motion. The precisions of these hierarchical beliefs can be inferred from behavioural (pursuit) data. The DCM for MEG data used an established biophysical model of neuronal activity that includes parameters for the gain of superficial pyramidal cells, which is thought to encode precision at the neuronal level. Previous studies (using DCM of pursuit data) suggest that noisy target motion increases subjective precision at the sensory level: i.e., subjects attend more to the target's sensory attributes. We compared (noisy motion-induced) changes in the synaptic gain based on the modelling of MEG data to changes in subjective precision estimated using the pursuit data. We demonstrate that imprecise target motion increases the gain of superficial pyramidal cells in V1 (across subjects). Furthermore, increases in sensory precision - inferred by our behavioural DCM - correlate with the increase in gain in V1, across subjects. This is a step towards a fully integrated model of brain computations, cortical responses and behaviour that may provide a useful clinical tool in conditions like schizophrenia.
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Old 27-03-2016, 09:13 AM   #5
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Default HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging.

http://www.ncbi.nlm.nih.gov/pubmed/?...1%29%3A3504-10

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BACKGROUND AND PURPOSE:
Acute vestibular syndrome (AVS) is often due to vestibular neuritis but can result from vertebrobasilar strokes. Misdiagnosis of posterior fossa infarcts in emergency care settings is frequent. Bedside oculomotor findings may reliably identify stroke in AVS, but prospective studies have been lacking.

METHODS:
The authors conducted a prospective, cross-sectional study at an academic hospital. Consecutive patients with AVS (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with >or=1 stroke risk factor underwent structured examination, including horizontal head impulse test of vestibulo-ocular reflex function, observation of nystagmus in different gaze positions, and prism cross-cover test of ocular alignment. All underwent neuroimaging and admission (generally <72 hours after symptom onset). Strokes were diagnosed by MRI or CT. Peripheral lesions were diagnosed by normal MRI and clinical follow-up.

RESULTS:
One hundred one high-risk patients with AVS included 25 peripheral and 76 central lesions (69 ischemic strokes, 4 hemorrhages, 3 other). The presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation (vertical ocular misalignment) was 100% sensitive and 96% specific for stroke. Skew was present in 17% and associated with brainstem lesions (4% peripheral, 4% pure cerebellar, 30% brainstem involvement; chi(2), P=0.003). Skew correctly predicted lateral pontine stroke in 2 of 3 cases in which an abnormal horizontal head impulse test erroneously suggested peripheral localization. Initial MRI diffusion-weighted imaging was falsely negative in 12% (all <48 hours after symptom onset).

CONCLUSIONS:
Skew predicts brainstem involvement in AVS and can identify stroke when an abnormal horizontal head impulse test falsely suggests a peripheral lesion. A 3-step bedside oculomotor examination (HINTS: Head-Impulse-Nystagmus-Test-of-Skew) appears more sensitive for stroke than early MRI in AVS.
posted on the ACPIVR twitter feed
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Old 24-04-2016, 02:15 PM   #6
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Default Comparison of the Bedside Head-Impulse Test with the Video Head-Impulse Test in a Clinical Practice Setting: A Prospective Study of 500 Outpatients

http://journal.frontiersin.org/artic...016.00058/full

Quote:
Objectives: The primary aim was to determine the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the bedside head-impulse test (bHIT) using the video HIT (vHIT) as the gold standard for quantifying the function of the vestibulo-ocular reflex (VOR). Secondary aims were to determine the bHIT inter-rater reliability and sensitivity in detecting unilateral and bilateral vestibulopathy.

Methods: In this prospective study, 500 consecutive outpatients presenting to a tertiary neuro-otology clinic with vertigo or dizziness of various vestibular etiologies who did not have any of the pre-defined exclusion criteria were recruited. Bedside HITs were done by three experienced neuro-otology clinicians masked to the diagnosis, and the results were compared with the vHIT. The patients were likewise blinded to the bHIT and vHIT findings. Patients with VOR deficits were identified on the vHIT by referencing to the pre-selected “pathological” gain of <0.7. The data were then analyzed using standard statistical methods.

Results: For the primary outcome (vHIT “pathological” VOR gain <0.7), the three-rater mean bHIT sensitivity = 66.0%, PPV = 44.3%, specificity = 86.2%, and NPV = 93.9%. Shifting the “pathological” threshold from 0.6 to 0.9 caused the bHIT sensitivity to decrease while the PPV increased. Specificity and NPV tended to remain stable. Inter-rater agreement was moderate (Krippendorff’s alpha = 0.54). For unilateral vestibulopathy, overall bHIT sensitivity = 69.6%, reaching 86.67% for severely reduced unilateral gain. For VOR asymmetry <40% and >40%, the bHIT sensitivity = 51.7 and 83%, respectively. For bilateral vestibulopathy, overall bHIT sensitivity = 66.3%, reaching 86.84% for severely reduced bidirectional gains.

Conclusion: For the primary outcome, the bHIT had moderate sensitivity and low PPV. While the study did not elucidate the best choice for vHIT reference, it demonstrated how the bHIT test properties varied with vHIT thresholds: selecting a lower threshold improved the sensitivity but diminished the PPV, while a higher threshold had the opposite effect. The VOR was most likely normal if the bHIT was negative due to its high NPV. The bHIT was moderately sensitive for detecting unilateral and bilateral vestibulopathy overall, but better for certain subgroups.
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Old 26-08-2016, 09:22 PM   #7
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Default The subscales and short forms of the dizziness handicap inventory: are they useful for comparison of the patient groups?

http://www.tandfonline.com/doi/abs/1...nalCode=idre20

Abstract
Quote:
Purpose: Dizziness Handicap Inventory (DHI) is one of the most frequently used surveys for vertigo. The aim of the study was re-analyze the consistency of subscales and correlation between original and different short forms.

Method: The data of 2111 patients were analyzed. Original three subscales, screening form of DHI and short form of DHI were evaluated. The suitability of the data set for factor analysis and factor structure was analyzed with Kaiser–Meyer–Olkin (KMO) coefficient, Bartlett’s Sphericity Test, and Varimax method. Pearson correlation analysis was performed.

Results: Factor analysis showed that two factor solutions are more prominent in our data. The factors proposed in different studies are not in harmony with each other. There is high correlation between the original and screening and short forms of DHI.

Conclusions: This study indicated that the factor structure of the scale was not consistent. It is not advised to use subscale scores for comparison especially in international level. Therefore, total score should be used rather than the scores of the subscales. Using DHI screening form instead of original 25 questions is more convenient, because it is highly correlated with the original one and has fewer questions.

Implications for rehabilitation
Factor structure of the DHI is not consistent enough for comparison of the international studies.

Total score of DHI is reliable.

Using the screening version of DHI is better, because it is highly correlated with the original form and has fewer questions (10 questions).
Keywords: Vertigo, dizziness, disability evaluation, surveys and questionnaires,
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Old 20-02-2017, 04:10 PM   #8
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Default Role of the Patient’s History of Vestibular Symptoms in the Clinical Evaluation of the Bedside Head-Impulse Test

http://journal.frontiersin.org/artic...017.00051/full

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Objective: Our aim was to identify the role of the investigators’ knowledge of the patient’s history of vestibular symptoms (PVH) in the clinical evaluation of the bedside head-impulse test (bHIT). We hypothesized that this knowledge will reduce uncertainty and improve bHIT accuracy when compared to quantitative analysis of the vestibulo-ocular reflex by video head-impulse test (vHIT).

Methods: We looked for changes in the clinical assessment of the bHIT in 594 consecutive patients before and after taking PVH. bHIT was performed by 12 clinical neurologists with various clinical experience in neuro-otological diseases (novices to long-standing experts). vHIT was analyzed by four experts being blinded for the patients’ clinical presentation and history of symptoms. The confidence of bHIT and vHIT was rated (0–100%).

Results: One hundred fifty-four (15%) of 1,030 bHIT of all eligible patients (n = 515) were rated pathological. Thirty-five (22.7%) of them were rated bilateral vestibulopathies. Sensitivity of bHIT reached 56.3%, its specificity 92.4%; the positive predictive value (PPV) was 41.5% and the negative predictive value 95.7%. These data did not differ between bHIT before and after PVH. bHIT after PVH (post-bHIT) differed from pre-bHIT in 44.3%, usually with regard to the level of confidence but also in polarity (5%). The accuracy of changes in bHIT depended on the direction of change: a “normal” post-bHIT was correct in 92.3% while only 39.8% of pathological post-bHIT were pathological on vHIT. However, sensitivity of a pathological post-bHIT depended on the clinical experience in taking PVH and bHIT: the PPV was 20.5% in novices as compared to 69.6% in experts.

Conclusion: The study shows that PVH changes the certainty and/or polarity of the clinical evaluation of bHIT. Unlike expected, the increase in confidence in post-bHIT is associated with a consistently high specificity but no increase in sensitivity. Accuracy of changes in post-bHIT depends on the investigators’ clinical experience: it increases only in experts but not novices. Since novices show only a poor PPV and moderate sensitivity of bHIT, pathological bHITs should be controlled by vHIT, even in patients with a positive PVH. By contrast, confirmed normal post-bHIT is usually correct.
Introduction
Quote:
The vestibulo-ocular reflex (VOR) stabilizes retinal images during head motion. It can be clinically assessed by the bedside head-impulse test (bHIT) (1). There are several quantitative recording methods, scleral search coil, and head mounted-video-oculography devices (2, 3), which can precisely identify abnormal VOR deficits that may be missed by the bHIT: covert compensatory and anti-compensatory saccades during the head impulse movement (4). According to these state of the art recordings of the high frequency VOR, there is a reasonable but moderate sensitivity (63–72%) (5), in particular in patients with mild vestibular hypofunction (6, 7). Some patients may exhibit only refixation saccades possibly reflecting a previous VOR deficit (8). This may account for the moderate sensitivity of bHIT which differs from video head-impulse test (vHIT) in about 30% (9). History of patients’ symptoms, specifically vestibular-related symptoms, is crucial in determining the clinical vestibular disease entity (10) and is—if not searched for—a major cause of false diagnostic assignments. Patients with vestibular hypofunction usually complain about unsteadiness on stance and gait, lateropulsion, and blurred vision or oscillopsia, particularly during rapid head movements.

The aim of this prospective double-blind study was to investigate if symptoms of vestibular hypofunction in the patient’s history change the clinical assessment of the bHIT. Vestibular-related symptoms may lead to a bias in the clinical assessment of bHIT provoking false positive or false negative results.

We hypothesized that the sensitivity of bHIT after knowing the patient’s history will improve both with respect to its positive predictive value (PPV) and negative predictive value (NPV). bHIT was rated pathological and negative from 0 to 100% certainty and compared to quantitative vHIT which was recorded by video-oculography (EyeSeeCam®) and analyzed anonymously by experienced neuro-otologists. Sensitivity, specificity, PPV, and NPV of bHIT were determined.
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Old 11-03-2017, 01:52 AM   #9
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Default The Skull Vibration-Induced Nystagmus Test of Vestibular Function—A Review

http://journal.frontiersin.org/artic...017.00041/full

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A 100-Hz bone-conducted vibration applied to either mastoid induces instantaneously a predominantly horizontal nystagmus, with quick phases beating away from the affected side in patients with a unilateral vestibular loss (UVL). The same stimulus in healthy asymptomatic subjects has little or no effect. This is skull vibration-induced nystagmus (SVIN), and it is a useful, simple, non-invasive, robust indicator of asymmetry of vestibular function and the side of the vestibular loss. The nystagmus is precisely stimulus-locked: it starts with stimulation onset and stops at stimulation offset, with no post-stimulation reversal. It is sustained during long stimulus durations; it is reproducible; it beats in the same direction irrespective of which mastoid is stimulated; it shows little or no habituation; and it is permanent—even well-compensated UVL patients show SVIN. A SVIN is observed under Frenzel goggles or videonystagmoscopy and recorded under videonystagmography in absence of visual-fixation and strong sedative drugs. Stimulus frequency, location, and intensity modify the results, and a large variability in skull morphology between people can modify the stimulus. SVIN to 100 Hz mastoid stimulation is a robust response. We describe the optimum method of stimulation on the basis of the literature data and testing more than 18,500 patients. Recent neural evidence clarifies which vestibular receptors are stimulated, how they cause the nystagmus, and why the same vibration in patients with semicircular canal dehiscence (SCD) causes a nystagmus beating toward the affected ear. This review focuses not only on the optimal parameters of the stimulus and response of UVL and SCD patients but also shows how other vestibular dysfunctions affect SVIN. We conclude that the presence of SVIN is a useful indicator of the asymmetry of vestibular function between the two ears, but in order to identify which is the affected ear, other information and careful clinical judgment are needed.
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