Samuel A. Reyes

The functional anatomy of gaze-evoked tinnitus and sustained lateral gaze

Objective: To identify neural sites associated with gaze-evoked tinnitus (GET), an unusual condition that may follow cerebellar–pontine angle surgery. Methods: The authors examined eight patients with GET and used PET to map the neural sites activated by lateral gaze in them and seven age- and sex-matched control subjects. Results: In patients with GET, tinnitus loudness and pitch increased with lateral gaze and, to a lesser extent, up and down gaze. Evidence for neural activity related to GET was seen in the auditory lateral pontine tegmentum or auditory cortex. GET-associated nystagmus appears to activate the cuneus and cerebellar vermis. These sites were found in addition to an extensive network that included frontal eye fields and other sites in frontal, parietal, and temporal cortex that were activated by lateral gaze in seven control subjects and the patients. The unilateral deafness in patients with GET was associated with expansion of auditory cortical areas responsive to tones delivered to the good ear. In addition to GET, unilateral deafness, end-gaze nystagmus, and facial nerve dysfunction were common. Conclusions: Patients with GET have plastic changes in multiple neural systems that allow neural activity associated with eye movement, including those associated with the neural integrator, to stimulate the auditory system. Anomalous auditory activation is enhanced by the failure of cross-modal inhibition to suppress auditory cortical activity. The time course for the development of GET suggests that it may be due to multiple mechanisms.

Brain imaging of the effects of lidocaine on tinnitus

Using a single-blind placebo-controlled design, we mapped lidocaine related changes in neural activity, measured by regional cerebral blood flow (rCBF) with (15)O-H(2)O positron emission tomography. Intravenous lidocaine produced both increases and decreases in the loudness of tinnitus. The change in tinnitus loudness was associated with a statistically significant change in neural activity in the right temporal lobe in auditory association cortex. Decreases in tinnitus loudness resulted in larger changes in rCBF than increases. The unilateral activation pattern associated with tinnitus, in contrast with the bilateral activation produced by a real sound, suggests that tinnitus originates in the central auditory system rather than the cochlea. In addition, generalized lidocaine effects were found in the basal ganglia, thalamus, and a region spanning the Rolandic fissure.

Mapping the 40-Hz auditory steady-state response using current density reconstructions

We mapped the 40-Hz aSSR from nine normal subjects using PET-independent low-resolution electroencephalographic tomography (LORETA) as well as PET-weighted LORETA and minimum norm (MinNorm) current density reconstructions. In grand mean data, PET-independent LORETA identified seven sites with peaks in current density in right temporal lobe, right brainstem/cerebellum, right parietal lobe, left cerebellum/temporal lobe, and right frontal lobe. PET-weighted LORETA found six of the same sites as the PET-independent LORETA: the right brainstem source was eliminated and two right-frontal sources were added. Both LORETA analyses revealed considerable phase dispersion across identified sources. In both LORETA analyses, the relative time course of activation measured from an arbitrary starting phase progressed from right temporal lobe to right mid-frontal lobe to right parietal-frontal to right inferior parietal and finally to left cerebellum and left temporal lobe. MinNorm analysis incorporating PET information identified sources in the same locations as specified in the PET data. These sources were synchronized, with their amplitudes peaking almost simultaneously. Both PET-independent and PET-weighted LORETA results suggest that the aSSR is: (1) the result of a reverberating network with two or more groups of sources that recurrently excite each other or (2) the result of sequential auditory processing through various levels of a hierarchical network. In contrast, the PET-weighted MinNorm results suggest that the 40-Hz response represents simultaneous activation over widely spaced areas of the brain, perhaps due to synchronization of gamma-band activity to a common neural clock.

PET imaging of the 40 Hz auditory steady state response.

The auditory steady state response (aSSR) is an oscillatory electrical potential recorded from the scalp induced by amplitude-modulated (AM) or click/tone burst stimuli. Its clinical utility has been limited by uncertainty regarding the specific areas of the brain involved in its generation. To identify the generators of the aSSR, 15O-water PET imaging was used to locate the regions of the brain activated by a steady 1 kHz pure tone, the same tone amplitude modulated (AM) at 40 Hz and the specific regions of the brain responsive to the AM component of the stimulus relative to the continuous tone. The continuous tone produced four clusters of activation. The boundaries of these activated clusters extended to include regions in left primary auditory cortex, right non-primary auditory cortex, left thalamus, and left cingulate. The AM tone produced three clusters of activation. The boundaries of these activated clusters extended to include primary auditory cortex bilaterally, left medial geniculate and right middle frontal gyrus. Two regions were specifically responsive to the AM component of the stimulus. These activated clusters extended to include the right anterior cingulate near frontal cortex and right auditory cortex. We conclude that cortical sites, including areas outside primary auditory cortex, are involved in generating the aSSR. There was an unexpected difference between morning and afternoon session scans that may reflect a pre- versus post-prandial state. These results support the hypothesis that a distributed resonating circuit mediates the generation of the aSSR.

Creation of a 3D printed temporal bone model from clinical CT data

PURPOSE Generate and describe the process of creating a 3D printed, rapid prototype temporal bone model from clinical quality CT images. MATERIALS AND METHODS We describe a technique to create an accurate, alterable, and reproducible rapid prototype temporal bone model using freely available software to segment clinical CT data and generate three different 3D models composed of ABS plastic. Each model was evaluated based on the appearance and size of anatomical structures and response to surgical drilling. RESULTS Mastoid air cells had retained scaffolding material in the initial versions. This required modifying the model to allow drainage of the scaffolding material. External auditory canal dimensions were similar to those measured from the clinical data. Malleus, incus, oval window, round window, promontory, horizontal semicircular canal, and mastoid segment of the facial nerve canal were identified in all models. The stapes was only partially formed in two models and absent in the third. Qualitative feel of the ABS plastic was softer than bone. The pate produced by drilling was similar to bone dust when appropriate irrigation was used. CONCLUSION We present a rapid prototype temporal bone model made based on clinical CT data using 3D printing technology. The model can be made quickly and inexpensively enough to have potential applications for educational training.

Effect of inner and outer hair cell lesions on electrically evoked otoacoustic emissions

When the cochlea is stimulated by a sinusoidal current, the inner ear emits an acoustic signal at the stimulus frequency, termed the electrically evoked otoacoustic emission (EEOAE). Recent studies have found EEOAEs in birds lacking outer hair cells (OHCs), raising the possibility that other types of hair cells, including inner hair cells (IHCs), may generate EEOAEs. To determine the relative contribution of IHCs and OHCs to the generation of the EEOAE, we measured the amplitude of EEOAEs, distortion product otoacoustic emissions (DPOAEs), the cochlear microphonic (CM) and the compound action potential (CAP) in normal chinchillas and chinchillas with IHC lesions or IHC plus OHC lesions induced by carboplatin. Selective IHC loss had little or no effect on CM amplitude and caused a slight reduction in mean DPOAE amplitude. However, IHC loss resulted in a massive reduction in CAP amplitude. Importantly, selective IHC lesions did not reduce EEOAE amplitude, but instead, EEOAE amplitude increased at high frequencies. When both IHCs and OHCs were destroyed, the amplitude of the CM, DPOAE and EEOAE all decreased. The increase in EEOAE amplitude seen with IHC loss may be due to (1) loss of tonic efferent activity to the OHCs, (2) change in the mechanical properties of the cochlea or (3) elimination of EEOAEs produced by IHCs in phase opposition to those from OHCs.

Analysis of an Online Match Discussion Board: Improving the Otolaryngology–Head and Neck Surgery Match

Objective “The Match” has become the accepted selection process for graduate medical education. Otomatch.com has provided an online forum for Otolaryngology–Head and Neck Surgery (OHNS) Match-related questions for over a decade. Herein, we aim to delineate the type of posts on Otomatch to better understand the perspective of medical students applying for OHNS residency. Study Design Retrospective review of an OHNS Match-related online forum. Subjects and Methods Subjects were contributors to an OHNS Match-related online forum. Posts on Otomatch between December 2001 and April 2014 were reviewed. The title of each thread and number of views were recorded for quantitative analysis. Each thread was organized into 1 of 6 major categories and 1 of 18 subcategories. National Resident Matching Program (NRMP) data were utilized for comparison. Results We identified 1921 threads corresponding to over 2 million page views. Over 40% of threads were related to questions about specific programs, and 27% were discussions about interviews. Views, a surrogate measure for popularity, reflected different trends. The majority of individuals viewed posts on interviews (42%), program-specific questions (20%), and how to rank programs (11%). There was an increase in viewership tracked with a rise in applicant numbers based on NRMP data. Conclusion Our study provides an in-depth analysis of a popular discussion forum for medical students interested in the OHNS Match process. The most viewed posts are about interview dates and questions regarding specific programs. We provide suggestions to address unmet needs for medical students and potentially improve the Match process.

The functional anatomy of tinnitus

We have used positron emission tomography to map the neural systems that mediate subjective tinnitus. In two studies, subjects altered their tinnitus by voluntary jaw muscle contraction or sustained lateral gaze. In the third, tinnitus was altered by intravenous lidocaine. These experiments all linked the loudness of tinnitus with unilateral spontaneous neural activity in auditory cortex. This unilaterality contrasts with the bilaterality of cortical responses during acoustic stimulation, evidence for a noncochlear central origin for tinnitus. Plasticity in the central auditory system, thought to be associated with deafferentation, was demonstrated in hearing‐impaired or unilaterally deaf patients by the greater extent of auditory cortex activation by tonal stimuli when compared to normals. Other sensory and motor systems may interact with these aberrant pathways, further upsetting the balance of auditory system activity. This is manifested by patients’ reports of transient voluntary loudness and/or pitch control. In controls, lateral gaze suppressed auditory cortical activity: this cross‐modal inhibition was absent in the patients. Subjective tinnitus appears to be due to spontaneous neural activity in aberrant central auditory pathways that have abnormal interactions with other sensory and motor systems. This complexity may explain the unresponsiveness of tinnitus to pharmacological interventions.