Flow kinetics of endolymph in rotational stimulation

In this paper, experimental and mathematical results are presented, indicating rotatory nystagmus to be caused by endolymph flow in the ampulla of the horizontal semicircular canal. During positive or negative acceleration circular flows may develop within the endolymph system, especially in the ampulla of the horizontal semicircular canal. While being independent of the position of the axis of the horizontally rotating system, the velocity of the flow depends on the radius of the establishing "whirl" in the ampulla. It is demonstrated that, close to the corresponding angular acceleration threshold, the velocity of the tangential flow along the cupula is in the same range as that calculated for a caloric stimulus. Like in our model of calorisation also in rotation there is strong evidence that an endolymph flow directed from crista to cupula in the lateral part of the ampulla causes a nystagmus towards the corresponding side, whereas a flow from cupula to crista causes a nystagmus in the opposite direction. Our results suggest that endolymph flows, evoked either by calorisation or rotation, represent adequate stimuli for vestibular excitability.     

Relationship between Inner-Ear Fluid Pressure and Semicircular Canal Afferent Nerve Discharge

The present study was designed to determine (1) the transcupular fluid pressure (P) generated across the semicircular canal cupula in response to sinusoidal head rotation, (2) the translabyrinthine dilational pressure (P₀) generated across the membranous labyrinth in response to an increase in endolymph fluid volume (hydrops), (3) afferent nerve discharge patterns generated by these distinct pressure stimuli and, (4) threshold values of P and P₀ required to elicit afferent neural responses. The experimental model was the oyster toadfish, Opsanus tau. Micromechanical indentation of the horizontal canal (HC) duct and utricular vestibule was used to simulate sinusoidal head rotation and fluid volume injection. Single-unit neural spike trains and endolymph pressure within the ampulla, on both sides of the cupula, were recorded simultaneously. P averaged 0.013 Pa per 1°/s of sinusoidal angular head velocity and P₀ averaged 0.2 Pa per 1 nL of endolymph volume injection. The most responsive afferents had a threshold sensitivity to P of 10^-3 Pa and to P₀ of 5 × 10^-2 Pa based on a discharge modulation criterion of 1 impulse/s per cycle for 2 Hz pressure stimuli. Neural sensitivity to P was expected on the basis of transverse cupular and hair bundle deflections. Analysis of mechanics of the end organ, neuronal projections into the crista, and individual neural firing patterns indicates that P₀ sensitivity resulted from pressure-induced distension of the ampulla that led to a nonuniform cupular deformation pattern and hair bundle deflections. This explanation is consistent with predictions of a finite element model of the end organ. Results have implications regarding the role of P in angular motion transduction and the role of P₀ under transient hydropic conditions. Abbreviations: 1 Pa = 1 N/m² = 10 dyn/cm² 102 µm H₂O 0.0075 mm Hg. nL = nanoliter     

Valproic acid-associated sialadenosis of the parotid and submandibular glands: diagnostic and therapeutic aspects

It has taken many decades to arrive at today's concept of cupula mechanics in the stimulation of endolymphatic flows on the hair cells in the ampullae of the semicircular canal. While Steinhausen assumed free swing-door movement of the cupula in the 1930s, Hillman was the first to demonstrate firm cupula attachment to the ampulla wall as a physiological necessity in the 1970s. In contrast to the present clinical concepts of acute peripheral vestibular functional disorders (circulatory disturbances, viral or bacterial infection, altered electrolytes in the endolymph), this study examines the extent to which an impaired attachment mechanism can trigger peripheral vestibular disorders. For this purpose, we used a pigeon model ( n = 8), in which mechanical detachment of the cupula from the ampulla wall was achieved by means of a targeted pressure increase in the ampulla of the lateral semicircular canal. In two additional animals the labyrinth was completely destroyed on one side in order to directly compare partial and complete vestibular disorders. In this way partial damage to the lateral semicircular canal ampulla presents a clinical picture whose symptoms are very similar to those of an idiopathic vestibular disorder in humans. Their intensity and course of compensation differ markedly from the symptoms of complete vestibular destruction. Subsequent histological examination revealed that the hair cells remained intact during the experimental detachment of the cupula. Our results thus show that only altered cupula mechanics seem to trigger the clinical picture of a peripheral vestibular disorder. This may result in completely new approaches to differential diagnosis and the therapy of vestibular neuronitis.     

Mechanism of posterior semicircular canal stimulation in patients with benign paroxysmal positional vertigo

A quantitative study of the stimuli and vestibulo-ocular response associated with benign paroxysmal positional vertigo (BPPV) was made to test and further develop the canalithiasis theory of BPPV. The angular velocities of the head in the planes of the semicircular canals during the Dix-Hallpike test were measured in four healthy subjects using electromagnetic sensors to record the position of the head in a six degrees of freedom paradigm. Next, the nystagmus reactions in seven patients diagnosed with idiopathic BPPV were recorded with video-oculography. The characteristics of the vestibulo-ocular reflex (VOR) response were analyzed using three-dimensional vector techniques. The angular velocity of the head was primarily, but not exclusively, in the plane of the posterior semicircular canal (PSC) in question. Both the anterior and horizontal canals were also stimulated by a lesser degree. The duration of the motion stimulus in the PSC was < 1.3 s with peak angular velocities of 150 deg/s. The eye response in BPPV patients began 4 s after the test and had a duration of 15-20 s. Peak slow-component eye velocities of about 42 deg/s were reached 3-5 s after onset of nystagmus. The motion of the eye, as predicted by the cupulolithiasis theory, is disconjugated and has torsional, vertical, and horizontal components. In the eye ipsilateral to the tested ear it is primarily torsional (0.80, 0.54, 0.16) and in the contralateral eye it is mainly vertical (0.57, 0.73, 0.08). These results suggest that particles, initially resting on the floor of the cupula dome in the PSC, are perturbed by the Dix-Hallpike test and disperse freely into the endolymph where they are propelled by gravity into the canal lumen. This creates abnormal pressure on the cupula and the specific VOR activation of the ipsilateral superior oblique and the contralateral inferior rectus muscles, whose force vectors are indistinguishable from the measured eye motion vectors. The estimated pressure exerted on the crista is approximately 10(-2) dyn/cm2.     

Ecological Aspects of Auditory Rehabilitation

A quantitative study of the stimuli and vestibulo-ocular response associated with benign paroxysmal positional vertigo (BPPV) was made to test and further develop the canalithiasis theory of BPPV. The angular velocities of the head in the planes of the semicircular canals during the Dix-Hallpike test were measured in four healthy subjects using electromagnetic sensors to record the position of the head in a six degrees of freedom paradigm. Next, the nystagmus reactions in seven patients diagnosed with idiopathic BPPV were recorded with video-oculography. The characteristics of the vestibulo-ocular reflex (VOR) response were analyzed using three-dimensional vector techniques. The angular velocity of the head was primarily, but not exclusively, in the plane of the posterior semicircular canal (PSC) in question. Both the anterior and horizontal canals were also stimulated by a lesser degree. The duration of the motion stimulus in the PSC was &;lt;1.3 s with peak angular velocities of 150 deg/s. The eye response in BPPV patients began 4 s after the test and had a duration of 15-20 s. Peak slow-component eye velocities of about 42 deg/s were reached 3-5 s after onset of nystagmus. The motion of the eye, as predicted by the cupulolithiasis theory, is disconjugated and has torsional, vertical, and horizontal components. In the eye ipsilateral to the tested ear it is primarily torsional (0.80, 0.54, 0.16) and in the contralateral eye it is mainly vertical (0.57, 0.73, 0.08). These results suggest that particles, initially resting on the floor of the cupula dome in the PSC, are perturbed by the Dix-Hallpike test and disperse freely into the endolymph where they are propelled by gravity into the canal lumen. This creates abnormal pressure on the cupula and the specific VOR activation of the ipsilateral superior oblique and the contralateral inferior rectus muscles, whose force vectors are indistinguishable from the measured eye motion vectors. The estimated pressure exerted on the crista is approximately 10^-2 dyn/cm².     

Altered cupular mechanics: a cause of peripheral vestibular disorders?

It has taken many decades to arrive at today's concept of cupula mechanics in the stimulation of endolymphatic flows on the hair cells in the ampullae of the semicircular canal. While Steinhausen assumed free swing-door movement of the cupula in the 1930s, Hillman was the first to demonstrate firm cupula attachment to the ampulla wall as a physiological necessity in the 1970s. In contrast to the present clinical concepts of acute peripheral vestibular functional disorders (circulatory disturbances, viral or bacterial infection, altered electrolytes in the endolymph), this study examines the extent to which an impaired attachment mechanism can trigger peripheral vestibular disorders. For this purpose, we used a pigeon model (n = 8), in which mechanical detachment of the cupula from the ampulla wall was achieved by means of a targeted pressure increase in the ampulla of the lateral semicircular canal. In two additional animals the labyrinth was completely destroyed on one side in order to directly compare partial and complete vestibular disorders. In this way partial damage to the lateral semicircular canal ampulla presents a clinical picture whose symptoms are very similar to those of an idiopathic vestibular disorder in humans. Their intensity and course of compensation differ markedly from the symptoms of complete vestibular destruction. Subsequent histological examination revealed that the hair cells remained intact during the experimental detachment of the cupula. Our results thus show that only altered cupula mechanics seem to trigger the clinical picture of a peripheral vestibular disorder. This may result in completely new approaches to differential diagnosis and the therapy of vestibular neuronitis.     

Directional Plasticity Rapidly Improves 3D Vestibulo-Ocular Reflex Alignment in Monkeys Using a Multichannel Vestibular Prosthesis

Bilateral loss of vestibular sensation can be disabling. We have shown that a multichannel vestibular prosthesis (MVP) can partly restore vestibular sensation as evidenced by improvements in the 3-dimensional angular vestibulo-ocular reflex (3D VOR). However, a key challenge is to minimize misalignment between the axes of eye and head rotation, which is apparently caused by current spread beyond each electrode’s targeted nerve branch. We recently reported that rodents wearing a MVP markedly improve 3D VOR alignment during the first week after MVP activation, probably through the same central nervous system adaptive mechanisms that mediate cross-axis adaptation over time in normal individuals wearing prisms that cause visual scene movement about an axis different than the axis of head rotation. We hypothesized that rhesus monkeys would exhibit similar improvements with continuous prosthetic stimulation over time. We created bilateral vestibular deficiency in four rhesus monkeys via intratympanic injection of gentamicin. A MVP was mounted to the cranium, and eye movements in response to whole-body passive rotation in darkness were measured repeatedly over 1 week of continuous head motion-modulated prosthetic electrical stimulation. 3D VOR responses to whole-body rotations about each semicircular canal axis were measured on days 1, 3, and 7 of chronic stimulation. Horizontal VOR gain during 1 Hz, 50 °/s peak whole-body rotations before the prosthesis was turned on was <0.1, which is profoundly below normal (0.94 ± 0.12). On stimulation day 1, VOR gain was 0.4–0.8, but the axis of observed eye movements aligned poorly with head rotation (misalignment range ∼30–40 °). Substantial improvement of axis misalignment was observed after 7 days of continuous motion-modulated prosthetic stimulation under normal diurnal lighting. Similar improvements were noted for all animals, all three axes of rotation tested, for all sinusoidal frequencies tested (0.05–5 Hz), and for high-acceleration transient rotations. VOR asymmetry changes did not reach statistical significance, although they did trend toward slight improvement over time. Prior studies had already shown that directional plasticity reduces misalignment when a subject with normal labyrinths views abnormal visual scene movement. Our results show that the converse is also true: individuals receiving misoriented vestibular sensation under normal viewing conditions rapidly adapt to restore a well-aligned 3D VOR. Considering the similarity of VOR physiology across primate species, similar effects are likely to occur in humans using a MVP to treat bilateral vestibular deficiency.     

Benign paroxysmal positional vertigo: diagnosis and treatment

Benign paroxysmal positional vertigo is a common disorder in Neurotology. This vestibular syndrome is characterized by transient attacks of vertigo, caused by change in head position, and associated with paroxysmal characteristic nystagmus. The symptoms result from movement of the free floating otoconia particles in the endolymph or their attachment to the cupulae of the semicircular canal. The diagnosis is essentially clinical and should be confirmed by performing diagnostic maneuvers. Treatment is based on the identification of the affected semicircular canal and performance of liberatory maneuvers or repositioning of free floating particles of otoliths. The effectiveness varies from 70 to 100%.     

Positional nystagmus showing neutral points

We encountered patients who had their static direction-changing positional nystagmus canceled at about 20-30 degrees yaw head rotation from the supine position. This nystagmus was also canceled when the head was rotated 180 degrees from this position. We call these head positions neutral points. At the neutral points, the cupula of the horizontal semicircular canal of the affected ear is positioned vertical to the gravitational plane and no deflection of the cupula occurs. The positional nystagmus observed (except the neutral points) was thought to occur due to a "heavy cupula" or "light cupula", which may be determined by the specific gravity of its endolymph.     

Free-Floating endolymph particles: A new operative finding during posterior semicircular canal occlusion

Most clinicians accept cupulolithiasis as the pathophysiological mechanism underlying benign paroxysmal positional vertigo (BPPV.) According to this theory, a cupular deposit induces a gravitational effect on the posterior canal crista. Posterior semicircular canal occlusion is a new operative procedure for treating incapacitating BPPV. It is postulated that canal occlusion abolishes endolymph movement within the canal, effectively fixing the cupula and rendering it unresponsive to both angular and linear acceleration (gravity). During two recent canal occlusions, abundant “free-floating particles” were identified within the posterior canal endolymph. When changing the position of the canal in the earth vertical plane, these free-floating particles would move under the influence of gravity. The hydrodynamic drag of the particles would induce endolymph movement with cupular displacement leading to the typical response. This finding supports an alternate explanation to cupulolithiasis as the pathophysiological mechanism underlying BPPV.     

Gentamicin is Primarily Localized in Vestibular Type I Hair Cells after Intratympanic Administration

Intratympanic (IT) gentamicin injections are effective in the control of episodic vertigo due to Ménière’s disease. Histological studies in animals have found that the loss of type I vestibular hair cells far exceeds that of type II cells after IT gentamicin treatment. The objective of this study was to determine whether this selective toxicity for type I hair cells might be due to selective concentration of the drug by these cells. Gentamicin was localized within the vestibular epithelium by both direct and indirect methods. Gentamicin conjugated to Texas Red® was used as a direct tracer, and anti-gentamicin antibody provided an indirect means of localization. Conjugated or unconjugated gentamicin was injected into the left tympanic space of chinchillas. The animals were killed and fixed 1 or 3 weeks post-treatment. Confocal fluorescence microscopy was used to determine the localization of gentamicin in semicircular canal cristae. Results from the animals killed within 1 week of administration showed that numerous type I hair cells still remained throughout the epithelium. The mean intensity in grayscale units (0–255) of anti-gentamicin labeling for type I hair cells was 28.14 (95% CI 24.60–31.69), for type II hair cells was 17.09 (14.99–19.20), and for support cells was 5.35 (5.34–5.46; p < 0.001, ANOVA). Anti-gentamicin antibody labeling appeared in the majority of type I hair cells throughout their cytoplasm, but with greater intensity at the apex (p < 0.001). Intensity of fluorescence with Texas-Red conjugated gentamicin was 25.38 (22.83–27.94) in type I hair cells, 15.60 (14.73–16.48) in type II cells, and 12.62 (12.06–13.17) in support cells (p < 0.001, ANOVA). These results suggest that type I hair cells are more susceptible to gentamicin because they more avidly take up or retain the drug in the early period after administration.     

The mechanics of benign paroxysmal vertigo.

Benign paroxysmal vertigo (BPV) is a disorder of the vestibular labyrinth. The clinical features can be explained by an abnormality in the posterior semicircular canal. Under the influence of gravity, a density differential between the endolymph and the cupula will cause displacement of the cupula when changes in head position occur. The presence or absence of fatiguability is a useful test as it helps define etiology, prognosis, and therapy. At the risk of adding yet another classification of nystagmus to the literature, we submit that division of BPV into two types (fatiguable and nonfatiguable) will simplify and rationalize the management of this common complaint.     

Persistent geotropic nystagmus—a different kind of cupular pathology and its localizing signs

Abstract

Conclusion. A persistent geotropic positional nystagmus indicates a dysfunction in the lateral semicircular canal with a cupula of less specific weight than the surrounding endolymph. It is possible to determine the side of the affected cupula by recording the nystagmus pattern in yaw and pitch plane. Objectives. To identify the clinical features in patients with a persistent geotropic positional nystagmus, establish lateralizing signs and relate the findings to a pathophysiologic mechanism. Patients and methods. Six patients with acute onset vertigo of a peripheral origin and persistent geotropic nystagmus were examined with videonystagmoscopy and the nystagmus characteristics in different positions of the head in yaw and pitch plane were studied. Results. Besides the persistent geotropic nystagmus, a zero zone was found with no nystagmus, beyond which the nystagmus changed direction when the head of the patient in supine position was gradually rotated from side to side. The zero zone was present when the head was turned slightly towards one side and is thought to represent a position where the affected cupula is aligned with the gravitational vertical. With the head bent forwards the nystagmus direction was to the non-affected side and when the head was bent backwards to the affected side.     

Three-Dimensional Vibration-Induced Vestibulo-ocular Reflex Identifies Vertical Semicircular Canal Dehiscence

Vertical semicircular canal dehiscence (VSCD) due to superior canal dehiscence (SCD) or posterior canal dehiscence (PCD) of the temporal bone causes vestibular and cochlear hypersensitivity to sound. This study aimed to characterize the vibration-induced vestibulo-ocular reflex (ViVOR) in VSCD. ViVORs in one PCD and 17 SCD patients, confirmed by CT imaging reformatted in semicircular canal planes, were measured with dual-search coils as binocular three-dimensional eye rotations induced by skull vibrations from a bone oscillator (B71—10 ohms) at 7 ms, 500 Hz, 135-dB peak-force level (re: 1 μN). The ViVOR eye rotation axes were computed by vector analysis and referenced to known semicircular canal planes. Onset latency of the ViVOR was 11 ms. ViVOR from VSCD was up to nine times greater than normal. The ViVOR’s torsional rotation was always contraversive-torsional (the eye’s upper pole rotated away from the stimulated ear), i.e. its direction was clockwise from a left and counterclockwise from a right VSCD, thereby lateralizing the side of the VSCD. The ViVORs vertical component distinguishes PCD from SCD, being downwards in PCD and upwards in SCD. In unilateral VSCD, the ViVOR eye rotation axis aligned closest to the dehiscent vertical semicircular canal axis from either ipsilateral or contralateral mastoid vibrations. However, in bilateral VSCDs, the ViVOR eye rotation axis lateralized to the ipsilateral dehiscent vertical semicircular canal axis. ViVOR was evoked in ossicular chain dysfunction, even when air-conducted click vestibulo-ocular reflex (VOR) was absent or markedly reduced. Hence, ViVOR could be a useful measurement to identify unilateral or bilateral VSCD even in the presence of ossicular chain dysfunction.     

Persistent geotropic nystagmus--a different kind of cupular pathology and its localizing signs

CONCLUSION: A persistent geotropic positional nystagmus indicates a dysfunction in the lateral semicircular canal with a cupula of less specific weight than the surrounding endolymph. It is possible to determine the side of the affected cupula by recording the nystagmus pattern in yaw and pitch plane. OBJECTIVES: To identify the clinical features in patients with a persistent geotropic positional nystagmus, establish lateralizing signs and relate the findings to a pathophysiologic mechanism. PATIENTS AND METHODS: Six patients with acute onset vertigo of a peripheral origin and persistent geotropic nystagmus were examined with videonystagmoscopy and the nystagmus characteristics in different positions of the head in yaw and pitch plane were studied. RESULTS: Besides the persistent geotropic nystagmus, a zero zone was found with no nystagmus, beyond which the nystagmus changed direction when the head of the patient in supine position was gradually rotated from side to side. The zero zone was present when the head was turned slightly towards one side and is thought to represent a position where the affected cupula is aligned with the gravitational vertical. With the head bent forwards the nystagmus direction was to the non-affected side and when the head was bent backwards to the affected side.     

Hyperpolarization-Activated Current (I h) in Vestibular Calyx Terminals: Characterization and Role in Shaping Postsynaptic Events

Calyx afferent terminals engulf the basolateral region of type I vestibular hair cells, and synaptic transmission across the vestibular type I hair cell/calyx is not well understood. Calyces express several ionic conductances, which may shape postsynaptic potentials. These include previously described tetrodotoxin-sensitive inward Na⁺ currents, voltage-dependent outward K⁺ currents and a K(Ca) current. Here, we characterize an inwardly rectifying conductance in gerbil semicircular canal calyx terminals (postnatal days 3–45), sensitive to voltage and to cyclic nucleotides. Using whole-cell patch clamp, we recorded from isolated calyx terminals still attached to their type I hair cells. A slowly activating, noninactivating current (I_h) was seen with hyperpolarizing voltage steps negative to the resting potential. External Cs⁺ (1–5 mM) and ZD7288 (100 μM) blocked the inward current by 97 and 83 %, respectively, confirming that I_h was carried by hyperpolarization-activated, cyclic nucleotide gated channels. Mean half-activation voltage of I_h was −123 mV, which shifted to −114 mV in the presence of cAMP. Activation of I_h was well described with a third order exponential fit to the current (mean time constant of activation, τ, was 190 ms at −139 mV). Activation speeded up significantly (τ = 136 and 127 ms, respectively) when intracellular cAMP and cGMP were present, suggesting that in vivo I_h could be subject to efferent modulation via cyclic nucleotide-dependent mechanisms. In current clamp, hyperpolarizing current steps produced a time-dependent depolarizing sag followed by either a rebound afterdepolarization or an action potential. Spontaneous excitatory postsynaptic potentials (EPSPs) became larger and wider when I_h was blocked with ZD7288. In a three-dimensional mathematical model of the calyx terminal based on Hodgkin–Huxley type ionic conductances, removal of I_h similarly increased the EPSP, whereas cAMP slightly decreased simulated EPSP size and width.     

Benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is characterized by positional vertigo (brief attacks of rotatory vertigo triggered by head position changes in the direction of gravity) and is the most common peripheral cause of vertigo. There are two types of BPPV pathophysiology: canalolithiasis and cupulolithiasis. In canalolithiasis, otoconial debris is detached from the otolithic membrane and floats freely within the endolymph of the canal. In cupulolithiasis, the otoconial debris released from the otolithic membrane settles on the cupula of the semicircular canal and the specific gravity of the cupula is increased. Consensus has been reached regarding three subtypes of BPPV: posterior-canal-type BPPV (canalolithiasis), lateral-canal-type BPPV (canalolithiasis) and lateral-canal-type BPPV (cupulolithiasis). In the interview-based medical examination of BPPV, questions regarding the characteristics of vertigo, triggered movement of vertigo, duration of vertigo and cochlear symptoms during vertigo attacks are important for the diagnosis of BPPV. The Dix–Hallpike test is a positioning nystagmus test used for diagnosis of posterior-canal-type BPPV. The head roll test is a positional nystagmus test used for diagnosis of lateral-canal-type BPPV. When the Dix–Hallpike test is repeated, positional nystagmus and the feeling of vertigo typically become weaker. This phenomenon is called BPPV fatigue. The effect of BPPV fatigue typically disappears within 30 min, at which point the Dix–Hallpike test again induces clear positional nystagmus even though BPPV fatigue had previously caused the positional nystagmus to disappear. For the treatment of BPPV, sequential head movements of patients can cause the otoconial debris in the semicircular canal to move to the utricle. This series of head movements is called the canalith repositioning procedure (CRP). The appropriate type of CRP depends on the semicircular canal in which the otoconial debris is located. The CRP for posterior-canal-type BPPV is called the Epley maneuver, and the CRP for lateral-canal-type BPPV is called the Gufoni maneuver. Including a time interval between each head position in the Epley maneuver reduces the immediate effect of the maneuver. This finding can inform the development of methods for reducing the effort exerted by doctors and the discomfort experienced by patients with posterior-canal-type BPPV during the Epley maneuver.     

Human Yaw Rotation Aftereffects with Brief Duration Rotations Are Inconsistent with Velocity Storage

In many sensory systems, perception of stimuli is influenced by previous stimulus exposure such that subsequent stimuli may be perceived as more neutral. This phenomenon is known as an aftereffect and has been studied for vision, audition, and some vestibular stimuli including roll and translation. Previous data on yaw rotation perception has focused on low-frequency stimuli on the order of a minute which may not be directly applicable to frequencies during ambulation. The aim of the current study is to look at the influence of yaw rotation on subsequent perception near 1 Hz, the predominant frequency of yaw rotation during human ambulation. Humans were rotated with 12 ° whole body adapting stimulus over 1 or 1.5 s. After an interstimulus interval (ISI) of 0.5, 1.0, 1.5, or 3 s, a test stimulus the same duration as the adapting stimulus was presented, and subjects pushed a button to identify the direction of the test stimulus as right or left. The direction and magnitude of the test stimulus was adjusted based on prior responses to find the stimulus at which no rotation was perceived. Experiments were conducted both in darkness and with a visual fixation point. The presence of a fixation point did not influence the aftereffect which was largest at 0.5 s with an average size of 0.78 ± 0.18 °/s (mean ± SE). The aftereffect diminished with a time constant of ~1 s. Thresholds were elevated after the adapting stimulus and also decreased with a time constant of ~1 s. These findings demonstrate that short adapting stimuli can induce significant aftereffects in yaw rotation perception and that these aftereffects are independent from the previously described velocity storage.