Perceptual direction detection thresholds for yaw rotation about an earth-vertical axis were measured at seven frequencies (0.05, 0.1, 0.2, 0.5, 1, 2, and 5 Hz) in seven subjects in the dark. Motion stimuli consisted of single cycles of sinusoidal acceleration and were generated by a motion platform. An adaptive two-alternative categorical forced-choice procedure was used. The subjects had to indicate by button presses whether they perceived yaw rotation to the left or to the right. Thresholds were measured using a 3-down, 1-up staircase paradigm. Mean yaw rotation velocity thresholds were 2.8 deg s(-1) for 0.05 Hz, 2.5 deg s(-1) for 0.1 Hz, 1.7 deg s(-1) for 0.2 Hz, 0.7 deg s(-1) for 0.5 Hz, 0.6 deg s(-1) for 1 Hz, 0.4 deg s(-1) for 2 Hz, and 0.6 deg s(-1) for 5 Hz. The results show that motion thresholds increase at 0.2 Hz and below and plateau at 0.5 Hz and above. Increasing velocity thresholds at lower frequencies qualitatively mimic the high-pass characteristics of the semicircular canals, since the increase at 0.2 Hz and below would be consistent with decreased gain/sensitivity observed in the VOR at lower frequencies. In fact, the measured dynamics are consistent with a high pass filter having a threshold plateau of 0.71 deg s(-1) and a cut-off frequency of 0.23 Hz, which corresponds to a time constant of approximately 0.70 s. These findings provide no evidence for an influence of velocity storage on perceptual yaw rotation thresholds.

No abstract

Third arch anomalies are more common than previously reported. They appear to be best treated by complete excision of the cyst, sinus, or fistula during a quiescent period. Repeated incision and drainage yields high rates of recurrence and should be avoided. Complications might be minimized by first initiating antibiotic treatment, delaying surgical treatment until the inflammatory process is maximally resolved, and by using endoscopic cauterization.

Surgery for a large vestibular schwannoma has a significant impact on the patient's QOL. To improve QOL postoperatively, the patient should be prepared and well informed of the consequences of such a surgery on QOL. Clinicians must be aware that early involvement of a clinical psychologist may be very helpful.

When making perceptual decisions, humans have been shown to optimally integrate independent noisy multisensory information, matching maximum-likelihood (ML) limits. Such ML estimators provide a theoretic limit to perceptual precision (i.e., minimal thresholds). However, how the brain combines two interacting (i.e., not independent) sensory cues remains an open question. To study the precision achieved when combining interacting sensory signals, we measured perceptual roll tilt and roll rotation thresholds between 0 and 5 Hz in six normal human subjects. Primary results show that roll tilt thresholds between 0.2 and 0.5 Hz were significantly lower than predicted by a ML estimator that includes only vestibular contributions that do not interact. In this paper, we show how other cues (e.g., somatosensation) and an internal representation of sensory and body dynamics might independently contribute to the observed performance enhancement. In short, a Kalman filter was combined with an ML estimator to match human performance, whereas the potential contribution of nonvestibular cues was assessed using published bilateral loss patient data. Our results show that a Kalman filter model including previously proven canal-otolith interactions alone (without nonvestibular cues) can explain the observed performance enhancements as can a model that includes nonvestibular contributions. We found that human whole body self-motion direction-recognition thresholds measured during dynamic roll tilts were significantly lower than those predicted by a conventional maximum-likelihood weighting of the roll angular velocity and quasistatic roll tilt cues. Here, we show that two models can each match this "apparent" better-than-optimal performance: ) inclusion of a somatosensory contribution and) inclusion of a dynamic sensory interaction between canal and otolith cues via a Kalman filter model.

No abstract

Vestibular symptoms caused by migraine, referred to as vestibular migraine, are a frequently diagnosed but poorly understood entity. Based on recent evidence that normal subjects generate vestibular-mediated percepts of head motion and reflexive eye movements using different mechanisms, we hypothesized that percepts of head motion may be abnormal in vestibular migraine. We therefore measured motion detection thresholds in patients with vestibular migraine, migraine patients with no history of vestibular symptoms, and normal subjects using the following paradigms: roll rotation while supine (dynamically activating the semicircular canals); quasi-static roll tilt (statically activating the otolith organs); and dynamic roll tilt (dynamically activating the canals and otoliths). Thresholds were determined while patients were asymptomatic using a staircase paradigm, whereby the peak acceleration of the motion was decreased or increased based on correct or incorrect reports of movement direction. We found a dramatic reduction in motion thresholds in vestibular migraine compared to normal and migraine subjects in the dynamic roll tilt paradigm, but normal thresholds in the roll rotation and quasi-static roll tilt paradigms. These results suggest that patients with vestibular migraine may have enhanced perceptual sensitivity (e.g. increased signal-to-noise ratio) for head motions that dynamically modulate canal and otolith inputs together.

In this study, we have found that dipeptidylpeptidase IV (DPPIV) plays in vivo an active role in the modulation of the inflammatory response of chronic rhinosinusitis. Human nasal mucosa expresses DPPIV-like immunoreactivity in submucosal seromucus glands, leukocytes, and endothelial cells of blood vessels. DPPIV enzymatic activity in nasal tissue biopsies taken from patients suffering from chronic rhinosinusitis was correlated inversely with the density of inflammatory cells in the nasal mucosa, and the DPPIV activity rose when chronic rhinosinusitis was treated. By using a pig animal model, we have shown that the intranasal administration of recombinant DPPIV decreased the vasodilatation induced by exogenous substance P (SP), a proinflammatory peptide released by sensory nerves. In contrast, an inhibitor of DPPIV enhanced the vasodilatatory effect at low doses of SP. SP5-11 was 100- to 1000-fold less potent than SP as a vasodilator of the nasal mucosa. The vasodilatatory effect of SP was abolished by a NK1 receptor antagonist. In conclusion, these results suggest a new pathophysiological pathway for rhinitis based on clinical observations in humans, indicating the involvement of an enzyme to modulate non-adrenergic and non-cholinergic substrate that occurred during nasal dysfunctions.