Head Thrust Test Research Articles

Office vestibular tests: A battery approach to guide the diagnosis of dizzy patients

AbstractBackground: Laboratory vestibular tests are relatively expensive and may be not available in every clinic. On the other hand, office vestibular tests can be easily performed and are low-cost. Objectives: To measure the sensitivity of a proposed battery approach to be conducted as an office procedure to diagnose side and site of vestibular lesions. Methods: This study was conducted on 36 patients suffering from vertigo with a confirmed diagnosis of vestibular disorder by laboratory vestibular tests. These included a standard video nystagmography (VNG) test that entails recording of eye examination including gaze testing, saccadic eye movements and smooth pursuit together with positional and positioning examinations as well as bithermal calorics and Vestibular Evoked Myogenic Potential (VEMP) tests. Patients were evaluated independently by history, examination of eye movements and a battery of office vestibular tests that included the Head Shake nystagmus Test (HST), Head Thrust Test (HTT) and Fukud...

POC08 A case of central and peripheral vestibular vestibular failure

A 63-year old male presented with a 3-year history of worsening mobility due to difficulty maintaining balance and deterioration in his hearing. He had a past medical history of ankylosing...

P7-20 Central and peripheral sensory pathway function in familial amyotrophic lateral sclerosis

Aim: To assess the clinical and neurophysiological features of the peripheral neuropathy associated with Fabry disease (FD) and to examine the function of the VIII cranial nerve. Methods: We prospectively examined 38 adults with FD (17 male, 21 female; mean age, 35.6 years. Each patient was assessed clinically. Nerve conduction studies (NCS) and quantitative sensory testing (QST) were performed: cold, warmth, vibratory, cold pain and heat pain detection thresholds were evaluated in one hand and one foot. Neurootologic signs and symptoms were evaluated in a subgroup of 20 consecutive patients with FD (6 male, mean age, 32 years; 14 female, mean age, 37 years) from within the cohort studies using: head thrust test and conventional caloric testing. The VIII cranial nerve was investigated using vestibular evoked myogenic potentials, pure tone audiometry and BAER. Results: All patients had signs or symptoms of FD. The most frequent manifestation was acroparaesthesia. In total, 92.1% of patients with FD presented with abnormal QST results: 73.7% showed increased cold detection thresholds and 65.8% had altered warmth detection thresholds. NCS were normal. Neuro-otologic manifestations: 80% of the patients were affected by auditory manifestations, 13/19 patients (68%) had both cochlear and vestibular symptoms Neuro-otologic involvement was peripheral in 15 cases and central in one case. Only 2/15 patients showed a congruent peripheral unilateral involvement of the superior and inferior vestibular tests with compromise of the ipsilateral cochlea. The main finding was that in 15 patients there was a lack of neural or vascular pattern in the involvement of the peripheral labyrinth. Conclusion: We identified signs and symptoms of peripheral neuropathy in both heterozygous and hemiyzygous patients with Fabry disease. Neuropathy predominantly affects small A-delta and C fibers. Neuro otologic involvement is frequent in Fabry disease, affecting the vestibular cochlear labyrinth in the majority of patients.

Dynamic visual acuity during head-thrust test in canal planes in healthy subjects and patients with vestibular neuritis

Conclusions: Dynamic visual acuity (DVA) during the head-thrust test (htDVA) is reliable in normal subjects, having a high specificity for the horizontal canal, so it may be useful to monitor vestibular rehabilitation in patients with vestibular neuritis (VN). Objective: To obtain reference values for htDVA in healthy individuals and to investigate the potential application in subjects with unilateral VN. Methods: A total of 73 healthy individuals and 50 patients with unilateral VN were included. The DVA test was performed by adjusting a sensor on the subject's head to measure head velocity. During head thrust, the optotype flashed if the head velocity reached 150°/s, as previously defined, and a DVA score was obtained for each canal. Results: The htDVA was reliable in normal subjects (intra-class correlation coefficient (ICC) = 0.44–0.71; p = 0.001–0.007). The htDVA score showed an age-dependent increase for all canals (p < 0.0001). The 95th percentile of htDVA was used as the criterion to consider htDVA as abnormal in patients with VN. In all, 44%, 30%, and 16% of patients had an increase in htDVA score for one, two or all three canals on the affected side. The sensitivity and specificity of the htDVA test for the horizontal canal were 22% and 85%, respectively.

Pearls: Dizziness

Contrary to common belief, making a diagnosis in the patient with dizziness can be relatively straightforward. To do so, the clinician must be aware of the pitfalls in taking a history from the dizzy patient as well as be familiar with specific examination techniques, such as the Hallpike maneuver and the head thrust test. We summarize the important aspects of history taking and examination in the dizzy patient and relate these clinical aspects to the most common diagnoses that cause patients to complain of dizziness.

Evaluation and treatment of the patient with acute dizziness in primary care

Dizziness is a very common symptom encountered by primary care physicians. Dizziness can be divided into five subgroups according to symptoms. These subgroups can be determined by a patient's history and allow the physician to deduce the etiology. A careful and systematic approach to dizzy patients is the key to a correct diagnosis and finding the optimal treatment. Physicians should obtain a detailed history from the patient in an open-ended fashion. Brief and comprehensive bedside neuro-otologic examinations, such as cranial nerve examinations, the DixHallpike test, and the head thrust test cannot be omitted for an accurate diagnosis. Knowledge about the numerous disease entities that may contribute to dizziness can be essential for differential diagnosis. In addition, this article provides information about frequently prescribed drugs, including vestibular suppressants and antiemetics.

Manifestaciones audiovestibulares en las vasculitis sistémicas

Systemic vasculitides constitute a heterogeneous group of diseases with frequent overlapping in their clinical findings and the size of the vessels involved. They may be primary or secondary to other diseases. Their common characteristic is the inflammation of blood vessels, giving rise to ischaemia. In the present article, we have reviewed the most common audiovestibular features that may be observed in patients with systemic vasculitides. Audiovestibular manifestations may be the first symptom of a systemic vasculitis. Audiological manifestations include sudden hearing loss and progressive sensorineural hearing loss. Vertigo and nystagmus are vestibular symptoms that may be observed in several systemic vasculitides. Vestibular loss in caloric test, abnormal head-shaking nystagmus, head thrust test and positioning test (benign paroxysmal positioning vertigo) may also be found. Improvement of audiovestibular function is frequently observed in patients with giant cell arteritis following corticosteroid therapy.

Vestibular Hypofunction in the Initial Postoperative Period After Surgical Treatment of Superior Semicircular Canal Dehiscence

1) Determine the prevalence of vestibular hypofunction in the immediate postoperative period after surgical treatment of superior semicircular canal dehiscence syndrome. 2) Evaluate whether dehiscence length is associated with risk of postoperative vestibular hypofunction. 3) Compare the prevalences of immediate and late postoperative vestibular hypofunction. Clinical review. Tertiary referral center. Subjects with superior canal dehiscence syndrome (n = 42) based on history, physiologic testing, and computed tomography findings, who underwent middle fossa craniotomy and superior canal dehiscence plugging. Dehiscence length was measured intraoperatively. Bedside horizontal head thrust testing (hHTT) was administered between postoperative days 1 to 7 to diagnose immediate postoperative vestibular hypofunction. Both hHTT and quantitative vestibulo-ocular reflex testing were administered 6 to 29 weeks postoperatively to detect late vestibular hypofunction. Dehiscence length and hypofunction in response to hHTT. Thirty-eight percent of the subjects (95% confidence interval, 25-54) had hypofunction in response to hHTT within 1 week after surgery. Mean dehiscence lengths were 4.9 (range, 2.0-10.5 mm) and 3.4 mm (range, 1.0-5.5 mm) in subjects with and without postoperative hypofunction, respectively (p = 0.0018). Each 1-mm increase in dehiscence length increased the odds of immediate postoperative hypofunction 2.6-fold (95% confidence interval, 1.3-5.1). The prevalence of vestibular hypofunction was significantly higher in the early compared with the late postoperative period. Immediate postoperative vestibular hypofunction is common, particularly with larger dehiscences. This hypofunction may typically resolve, given that the prevalence of vestibular hypofunction 6 weeks postoperatively is low. Possible mechanisms include intraoperative loss of perilymph, which may be more likely with larger dehiscences.

Can active lateral canal benign paroxysmal positional vertigo mimic a false-positive head thrust test?

We present a patient with positive head thrust test (HTT) and video-oculography (VOG) findings suggestive of active lateral semicircular canal (LSCC) benign paroxysmal positional vertigo (BPPV). This patient was seen in a tertiary vestibular clinic for episodic vertigo. He exhibited robust corrective refixation saccades on HTT to the right and evidence of active contralateral LSCC BPPV on positional testing. Treatment of the LSCC BPPV led to immediate resolution of vertigo and near-normalization of the HTT on follow-up testing. The pathophysiologic basis and clinical implications of LSCC BPPV mimicking a false-positive HTT are discussed in detail.

Migrainous Vertigo: Results of Caloric Testing and Stabilometric Findings

Association between migraine and vertigo has been widely studied during the last years. A central or peripheral vestibular damage may occur in patients with migrainous vertigo. Despite much evidence, at present the International Headache Society classification does not include a specific category for migrainous vertigo. To assess the prevalence of central and peripheral vestibular disorders and postural abnormalities in patients diagnosed as affected by definite migrainous vertigo according to Neuhauser. Thirty patients with migraine and acute vertigo lasting from minutes to hours underwent a full otoneurological screening for spontaneous, positional, and positioning nystagmus with head-shaking and head-thrust (Halmagyi) tests, an audiometric examination, and videonystagmography with bithermal stimulation according to Freyss. Videonystagmographic findings were compared with those of 15 migraineurs without lifetime vertigo (group M). Next day, a static posturography was performed; posturographic results have been compared with those of a second control group of 30 healthy patients matched for age and sex (group C). In total, 14 subjects with migrainous vertigo showed otovestibular disorders; 6 subjects showed impaired vestibulo-oculomotor reflexes (20%). Five more patients had bilateral increased responses (16.6%). Five patients showed signs of central brainstem or cerebellar disorders for altered pursuit or saccades or positional direction changing nystagmus. Stabilometric results returned higher values of Length and Surface above all when testing was performed in eyes closed conditions compared with the normal control group. The subgroup of 14 subjects with migrainous vertigo and vestibular abnormalities performed poorly in stabilometric exams and seemed to rely more on visual cues in balance control than the subgroup of 16 subjects with migrainous vertigo but without abnormalities. Our results indicate that vestibular functional damage may occur in all vestibular pathways; central and peripheral signs are equally represented. Our data are not inconsistent with the hypothesis that a vestibulo-spinal dysfunction is the causal factor for the posturographic results. Moreover, the Visual Romberg Index is significant for increased visual cue dependence in migraineurs.

Vestibular impairments pre- and post-cochlear implant in children

Determine prevalence and types of vestibular impairments in sensorineural hearing loss (SNHL) in a large population of pediatric candidates for cochlear implants. Evaluate impact of cochlear implants on vestibular function. Retrospective and prospective study. Children with profound SNHL (n=224) underwent complete vestibular testing (clinical vestibular examination, bicaloric test, earth vertical axis rotation, off vertical axis rotation and vestibular evoked myogenic potentials) before cochlear implant. Changes in vestibular responses were measured after implants in 89 of these patients. In the SNHL population only 50% had normal bilateral vestibular function, while 20% had bilateral complete areflexia, 22.5% partial asymmetrical hypoexcitability and 7.5% partial symmetrical hypoexcitability. In the 71/89 follow-up patients showing vestibular responses prior to implant, 51 (71%) had changes in vestibular function including 7 (10%) who acquired ipsilateral areflexia. Others developed ipsilateral hypo- or hyperexcitability. Vestibular modifications occurred during the 3 months after surgery and were not clearly associated with clinical signs except for ipsilateral areflexia cases. In long-term follow-up, two of the 7 patients with ipsilateral areflexia partially recovered vestibular function. Since half of pediatric cochlear implant candidates have vestibular deficits and 51% of implants induce modifications of existing vestibular function, each implant should be preceded by canal and otolith functional tests to assure that the least functional vestibule is implanted. The tests provide baselines for follow-up monitoring of subsequent losses and recovery. This could be easily implemented with a clinical vestibular examination including the head thrust test associated with a bicaloric test and vestibular-evoked-myogenic-potentials.

Saccular function less affected than canal function in bilateral vestibulopathy

Bilateral vestibulopathy (BV) is characterized by impaired or lost function of both labyrinths or eighth nerves. The diagnosis is routinely established by the head-thrust test, caloric irrigation and rotational testing with electronystagmography to determine the high- and low-frequency deficit of the vestibulo-ocular reflex. All three methods evaluate semicircular canal function only. Vestibular-evoked myogenic potentials (VEMPs) provide a measure of saccular otolith function. The aim of this study was to evaluate the frequency and extent of saccular dysfunction in patients with BV and to correlate saccular with horizontal semicircular canal dysfunction. A total of 84 BV-patients (23 females, mean age 62 +/- 15 (SD) years at the time of diagnosis assessment) were examined with VEMPs, electronystagmography with caloric irrigation and a standardized neuro-ophthalmological and -otological examination; 47 healthy subjects (18 females, mean 56 +/- 19 years) served as controls. Amplitudes P1-N1 were significantly lower in patients with BV compared to controls (mean P1-N1 of all ears 82.1 +/- 50.7 microV in the patients vs. 130.8 +/- 85.9 microV in healthy volunteers). VEMPs were absent unilaterally in four patients with BV and in none bilaterally. In contrast, caloric responses were absent bilaterally in 40 patients. There was no correlation between amplitude P1-N1 and caloric-induced nystagmus. The latencies P1 and N1 were not significantly different between patients and controls. Thus, in our study population saccular function appeared to be less affected than horizontal semicircular canal function.

Bedside differentiation of vestibular neuritis from central “vestibular pseudoneuritis”

Acute unilateral peripheral and central vestibular lesions can cause similar signs and symptoms, but they require different diagnostics and management. We therefore correlated clinical signs to differentiate vestibular neuritis (40...

Mechanism of Dynamic Visual Acuity Recovery With Vestibular Rehabilitation

Schubert MC, Migliaccio AA, Clendaniel RA, Allak A, Carey JP. Mechanism of dynamic visual acuity recovery with vestibular rehabilitation. Objective To determine why dynamic visual acuity (DVA) improves after vestibular rehabilitation in people with vestibular hypofunction. Design Combined descriptive and intervention study. Setting Outpatient department in an academic medical institution. Participants Five patients (age, 42–66y) and 4 age-matched controls (age, 39–67y) were studied. Patients had vestibular hypofunction (mean duration, 177±188d) identified by clinical (positive head thrust test, abnormal DVA), physiologic (reduced angular vestibulo-ocular reflex [aVOR] gain during passive head thrust testing), and imaging examinations (absence of tumor in the internal auditory canals or cerebellopontine angle). Intervention Vestibular rehabilitation focused on gaze and gait stabilization (mean, 5.0±1.4 visits; mean, 66±24d). The control group did not receive any intervention. Main Outcome Measures aVOR gain (eye velocity/head velocity) during DVA testing (active head rotation) and horizontal head thrust testing (passive head rotation) to control for spontaneous recovery. Results For all patients, DVA improved (mean, 51%±25%; range, 21%–81%). aVOR gain during the active DVA test increased in each of the patients (mean range, 0.7±0.2 to 0.9±0.2 [35%]). aVOR gain during passive head thrust did not improve in 3 patients and improved only partially in the other 2. For control subjects, aVOR gain during DVA was near 1. Conclusions Our data suggest that vestibular rehabilitation increases aVOR gain during active head rotation independent of peripheral aVOR gain recovery.

Otoneurological findings in human immunodeficiency virus positive patients

To investigate vestibular function in human immunodeficiency virus positive subjects. We studied vestibular function in 60 human immunodeficiency virus positive subjects reporting dizziness. All three Center for Disease Control and Prevention categories of human immunodeficiency virus infection were represented in the study group (30 patients in class A, 20 in class B and 10 in class C). Subjects had had no previous history of acute vertigo. All subjects underwent: neurotological screening for spontaneous, positional and positioning nystagmus, using head-shaking and head-thrust (Halmagyi) tests; audiometrical examination; and electronystagmography with bithermal stimulation (Freyss' method). The results of the 30 class A subjects were compared with those of 30 human immunodeficiency virus negative patients reporting dizziness. Abnormal otoneurological findings increased progressively from the A to C categories, particularly regarding increased central damage (3.3 per cent of class A, 35 per cent of class B and 100 per cent of class C subjects). In contrast, the incidence of peripheral vestibular disorders remained almost the same, comparing the three categories (33.3 per cent in class A and 50 per cent in classes B and C subjects). Moreover, a higher number of human immunodeficiency virus positive subjects showed abnormal otoneurological findings, compared with the dizzy, human immunodeficiency virus negative subjects. In our opinion, a vestibular disorder may occur in human immunodeficiency virus positive patients as a result of direct viral damage, even in the early phase of infection. Central vestibular damage may be established later on, and may be linked to different causes (e.g. superinfections, vascular causes and drug toxicity).

Otolith dysfunction in vestibular neuritis

To prospectively follow patients with vestibular neuritis (VN), to compare the recovery pattern of canal and otolith dysfunction, and to determine which tests best predict symptom recovery. Between March 2006 and December 2006, 51 consecutive patients with unilateral VN were enrolled within 7 days of onset (average 3 days). Otolith function tests included ocular torsion (OT), subjective visual vertical (SVV), and vestibular evoked myogenic potential (VEMP), and canal function tests included head-shaking nystagmus (HSN), caloric stimulation, and head-thrust testing. Patients returned for two follow-up evaluations at approximately 1 week and 6 weeks after the initial evaluation. On the first examination, all patients had abnormal HSN, caloric, and head-thrust test results, and at least one otolith-related test abnormality: abnormal tilt of SVV (48/51, 94%), abnormal OT (42/51, 82%), or abnormal VEMPs (25/51, 49%). The degree of SVV tilts correlated with the degree of OT for one or both eyes (p < 0.05). Skew deviation was observed in 7 patients (14%), and a complete ocular tilt reaction was detected in only 2 patients. On follow-up, otolith test results returned to normal more rapidly than canal test results. The head-thrust test was the best predictor of symptom recovery. Eighty percent of patients who continued to report dizziness at the last follow-up visit had a positive head-thrust test result, whereas only 10% of patients who were not dizzy had a positive head-thrust test result. Otolith-related test abnormalities improve more rapidly than canal-related test abnormalities after vestibular neuritis. If patients have a positive head-thrust test result on follow-up, they are more likely to be dizzy.

Vestibular Neuritis and Bilateral Vestibulopathy

Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. The key signs and symptoms are the acute onset of sustained rotatory vertigo without hearing loss, postural imbalance with Romberg's sign, and peripheral type nystagmus. Head thrust and caloric tests show ipsilateral hyporesponsiveness, but hearing test shows normal. Either an inflammation of the vestibular nerve or labyrinthine ischemia was proposed as a cause of vestibular neuritis. Recovery after vestibular neuritis is usually incomplete. Despite the assumed viral cause, the effects of corticosteroids, antiviral agents, or the two in combination are uncertain. Bilateral vestibulopathy is a rare disorder of the peripheral labyrinth or the eighth nerve. The most frequent etiologies include ototoxicity, autoimmune disorders, meningitis, neuropathies, sequential vestibular neuritis, cerebellar degeneration, tumors, and miscellaneous otological diseases. The two key symptoms are unsteadiness of gait and oscillopsia associated with head movements or when walking. The diagnosis is made with the simple bedside tests for defective vestibulo-ocular reflex (head thrust and dynamic visual acuity tests). Bilateral vestibulopathy is confirmed by the absence of nystagmus reaction to both caloric and rotatory chair tests. The spontaneous recovery is relatively rare and incomplete. Vestibular rehabilitation is supportive of the improvement, but the efficacy of physical therapy is limited.

Vertigo due to Stroke

Episodic vertigo frequently occurs in patients suffering from transient ischemia in the distribution of the vertebrobasilar circulation (i.e., vertebrobasilar insufficiency). It may occur in isolation, with other symptoms of vertebrobasilar insufficiency or with persisting symptoms and signs of the infarction of the brain stem and/or cerebellum. Typical attacks of ischemic vertigo are abrupt in onset and last minutes. Ischemic stroke in the distribution of posterior circulation commonly develops acute onset of spontaneous prolonged vertigo and imbalance. As many as 25% of patients with risk factors for stroke who present to an emergency medical setting with isolated, severe vertigo, nystagmus, and postural instability have an infarction of the caudal cerebellum (i.e., pseudo-vestibular neuritis). Since the head thrust test can be performed at the bedside with no requirement of special equipments, it is invaluable for separating 'pseudo-vestibular neuritis' from true vestibular neuritis. Physicians who evaluate stroke patients should be trained to perform and interpret the result of the head impulse test. Since the inner ear is supplied by the vertebrobasilar circulation, inner ear symptoms are common with ischemia in the distribution. We briefly reviewed the clinical symptoms and neurological examinations of stroke presenting with vertigo, especially focusing on ischemic stroke of the vertebrobasilar territory.

The High-Frequency/Acceleration Head Heave Test in Detecting Otolith Diseases

OBJECTIVE:: To investigate whether transient, high-acceleration interaural head heaves (translational vestibulo-ocular reflex [tVOR]) could aid in the diagnosis of otolith diseases. STUDY DESIGN:: Prospective cohort study. SETTING:: Tertiary referral center. PATIENTS:: Thirteen patients with symptoms suggestive of otolith diseases and 10 age-matched controls. INTERVENTIONS:: Patients underwent a clinical otoneurologic examination and standard laboratory audiovestibular evaluation, including audiometry, electronystagmography with bithermal caloric, Halmagyi-Curthoys head thrust test with search coils, and vestibular-evoked myogenic potential. All subjects underwent subjective visual vertical (SVV) and tVOR testings. MAIN OUTCOME MEASURES:: Sensitivity (ratio of peak eye to peak head velocities) and velocity gain (ratio of actual to ideal peak eye velocities). RESULTS:: Five of 13 patients showed no abnormality in any tests. Of the remaining 8, 3 (38%) had reduced tVOR responses, whereas 1 (13%) had abnormal SVV. Sensitivity and velocity gains were symmetrically reduced in 2 patients, who had symptoms for 8 and 24 months. A third patient, symptomatic for 7 weeks, had asymmetric reduction of tVOR responses and a deviated SVV. CONCLUSION:: Both head heave and SVV tests detect acute, asymmetric otolith diseases. Subjective visual vertical test relies on imbalance of utricular tone and may not detect bilateral symmetric diseases or partial diseases with central compensation. Our preliminary data in a small group of patients show that measuring the tVOR in a higher and more physiologic range of frequencies may serve as useful adjunct to detect acute and chronic otolith dysfunction and seems to be superior to the SVV in detecting bilateral symmetric or asymmetric otolith diseases.

Recovery of Vestibular Imbalances After Vestibular Neuritis

To determine chronological characteristics of vestibular recovery after vestibular neuritis (VN) by using various clinical parameters. Prospective clinical study. Twenty of 22 consecutive patients with acute VN underwent serial follow-ups of static (spontaneous nystagmus, subjective visual vertical, and ocular torsion) and dynamic (head-shaking nystagmus [HSN], vibration-induced nystagmus [VIN], head thrust test, and caloric test) vestibular imbalances for 1 year after symptom onset. Static vestibular imbalances improved more rapidly than dynamic imbalances. Among the dynamic imbalances, a trend of higher recovery rate was found in head thrust sign, HSN, and VIN than in caloric asymmetry. HSN tended to be more sensitive in detecting vestibular asymmetry than VIN and head thrust sign. Some patients showed direction reversal of HSN (n = 5, 25.0%) or VIN (n = 5, 25.0%) during follow-up. Direction of VIN changed according to the stimulation sites in four (20.0%) patients. In view of more rapid resolution of static vestibular imbalance after VN, evaluation of the dynamic vestibular imbalances may provide more useful information for underlying vestibulopathy, especially in the compensated phase. The different temporal profiles ofdynamic vestibular recovery may reflect different chronological characteristics of vestibular compensation according to stimulus frequency. Direction reversal of HSN and VIN during follow-up suggests that lateralization of VNbased on the direction of these nystagmus should be considered in the context of disease phase.