Search PubMed⌕ Search

Biomedical subjects

J P Carey

Publications and source records attributed to J P Carey.

At least 19 recordsLinked to original sources

Superior canal dehiscence: mechanisms of pressure sensitivity in a chinchilla model.

BACKGROUND: Patients with superior canal dehiscence syndrome may experience vertigo and nystagmus when pressure changes occur in the external auditory canal, the middle ear, or the intracranial space. The cause is a defect in the bone of the superior canal. OBJECTIVE: To study the mechanisms of pressure sensitivity of the labyrinth in superior canal dehiscence syndrome and its surgical repair in a chinchilla model. METHODS: We investigated the changes in firing rates of vestibular nerve afferents in the chinchilla in response to changes in external auditory canal pressure before and after fenestration of the superior canal, and after repair of the fenestra. RESULTS: Before superior canal fenestration, external auditory canal pressure changes caused no responses in horizontal canal or otolith afferents, and only 1 of 9 superior canal afferents responded to pressure. After fenestration, all superior canal afferents were excited by positive pressure and inhibited by negative pressure. Half of 18 otolith and most (21 of 33) horizontal canal afferents were unaffected by pressure. The superior canal afferents had higher pressure gain than the horizontal canal afferents (P =.03). Pressure responses could be abolished only by applying a rigid seal to the fenestra. CONCLUSIONS: Fenestration of the superior canal rendered all superior canal afferents sensitive to pressure, whereas less than half of the other afferents became pressure sensitive. The direction of the superior canal afferent responses agreed with the predictions of our model of endolymph flow within the superior canal. A rigid seal applied to the fenestra abolished pressure sensitivity while maintaining physiologic rotational sensitivity.

Animals↗

Vestibular-evoked myogenic potentials in the diagnosis of superior canal dehiscence syndrome.

Patients with superior canal dehiscence (SCD) syndrome have vertigo and oscillopsia induced by loud noises and by stimuli that result in changes in middle ear or intracranial pressure. We recorded vestibular-evoked myogenic potentials (VEMP responses) in 10 patients with SCD syndrome. The diagnosis had been confirmed in each case by evoked eye movements and by high-resolution CT scans of the temporal bones that showed a dehiscence overlying the affected superior canal. For the 8 patients without prior middle ear disease, the VEMP threshold from the dehiscent ears measured 72 +/- 8 dB NHL (normal hearing level) whereas the threshold from normal control subjects was 96 +/- 5 dB NHL (p < 0.0001). The VEMP threshold measured from the contralateral ear in patients with unilateral dehiscence was 98 +/- 4 dB NHL (p > 0.9 with respect to normal controls). Two patients with apparent conductive hearing loss from middle ear disease, and SCD, had VEMP responses from the affected ears. In the absence of dehiscence, VEMP responses would not have been expected in the setting of conductive hearing loss. These findings confirm earlier studies demonstrating that patients with SCD syndrome have lowered VEMP thresholds. Conditions other than SCD syndrome may also lead to lowered VEMP thresholds. Rather than being based upon a single test, the diagnosis of SCD syndrome is best established when the characteristic symptoms, signs, VEMP response, and CT imaging all indicate SCD.

Adult↗

Symptoms and signs in superior canal dehiscence syndrome.

Patients with superior canal dehiscence (SCD) syndrome experience vertigo and oscillopsia in response to loud sounds and to stimuli that result in changes in middle ear or intracranial pressure. They may also experience hyperacusis to bone-conducted sounds. The evoked eye movements in this syndrome align with the plane of the dehiscent superior canal. The symptoms and signs can be understood in terms of the effect of the dehiscence in creation of a third mobile window into the inner ear. The SCD syndrome has been diagnosed in 28 patients who were examined in the neuro-otology clinics at the Johns Hopkins Medical Institutions from May 1995 through January 2001. The diagnosis is best established based upon the symptoms that are characteristic for the syndrome, the vertical-torsional eye movements evoked by sound or pressure stimuli noted on examination performed with Frenzel goggles, the lowered thresholds for responses to vestibular-evoked myogenic potentials, and CT imaging of the temporal bones.

Adult↗

Eye movements in patients with superior canal dehiscence syndrome align with the abnormal canal.

BACKGROUND: The superior canal dehiscence (SCD) syndrome consists of sound- or pressure-induced nystagmus and vertigo caused by a defect in bone overlying the superior semicircular canal. The SCD syndrome is diagnosed based upon characteristic symptoms, signs, and findings on CT imaging of the temoral bones. However, SCD syndrome is often misdiagnosed as perilymphatic fistula (PLF), and the symptoms of sound- and pressure-induced vertigo are more commonly attributed to the vestibular utricle, rather than to the superior semicircular canal. This study explored the role of the superior canal and the utricle in the pathophysiology of SCD syndrome. METHODS: Three-dimensional scleral search coils were used to record eye movements in 11 patients with SCD syndrome. RESULTS: Ten patients developed nystagmus with upward torsional slow phases characteristic of superior canal activation when loud tones were presented to the affected ear or when the patients performed a Valsalva maneuver. Visual fixation led to a suppression of the nystagmus and the appearance of a sustained torsional deviation of the eyes. Two patients also had sound-evoked head movements in the same direction as the ocular slow phases. The response of the affected superior canal to rapid head rotations was tested in nine patients. The response was diminished in those with large (>/=5 mm) defects in the bone overlying the superior canal. CONCLUSIONS: The evoked eye movements in patients with SCD syndrome arise from the superior canal, not the utricle. The syndrome is recognized by the characteristic nystagmus evoked by tones or maneuvers that change middle ear or intracranial pressure. Examination for this nystagmus should be performed under conditions that prevent visual fixation.

Adult↗

Dehiscence or thinning of bone overlying the superior semicircular canal in a temporal bone survey.

OBJECTIVE: To determine the incidence and etiology of dehiscences of bone overlying the superior semicircular canal in a temporal bone archive. DESIGN: A microscopic study was performed of 1000 temporal bones from 596 adults in a university hospital registry. Specimens were sectioned vertically in the plane of the superior semicircular canal. Measurements of minimum bone thickness over the superior canal were made in a subset of 108 randomly chosen specimens. All bones were examined for thinning or dehiscence relative to these norms. Clinical histories, when available, were reviewed. RESULTS: Complete dehiscence of the superior canal was identified in 5 specimens (0.5%), at the middle fossa floor (n = 1) and where the superior petrosal sinus was in contact with the canal (n = 4). In 14 other specimens (1.4%), the bone at the middle fossa floor (n = 8) or superior petrosal sinus (n = 6) was no thicker than 0.1 mm, significantly less than values measured in the control specimens (P<.001). Abnormalities were typically bilateral. Specimens from infants demonstrated uniformly thin bone over the superior canal in the middle fossa at birth, with gradual thickening until 3 years of age. CONCLUSIONS: Dehiscence of bone overlying the superior canal occurred in approximately 0.5% of temporal bone specimens (0.7% of individuals). In an additional 1.4% of specimens (1.3% of individuals), the bone was markedly thin (< or =0.1 mm), such that it might appear dehiscent even on ultra-high-resolution computed tomography of the temporal bone. Sites affected were in the middle fossa floor or a deep groove for the superior petrosal sinus, often bilaterally. These abnormalities may arise from failure of postnatal bone development. Thin areas of bone over the superior canal may be predisposed to disruption by trauma.

Adult↗

Recovery of the vestibulocolic reflex after aminoglycoside ototoxicity in domestic chickens.

Avian auditory and vestibular hair cells regenerate after damage by ototoxic drugs, but until recently there was little evidence that regenerated vestibular hair cells function normally. In an earlier study we showed that the vestibuloocular reflex (VOR) is eliminated with aminoglycoside antibiotic treatment and recovers as hair cells regenerate. The VOR, which stabilizes the eye in the head, is an open-loop system that is thought to depend largely on regularly firing afferents. Recovery of the VOR is highly correlated with the regeneration of type I hair cells. In contrast, the vestibulocolic reflex (VCR), which stabilizes the head in space, is a closed-loop, negative-feedback system that seems to depend more on irregularly firing afferent input and is thought to be subserved by different circuitry than the VOR. We examined whether this different reflex also of vestibular origin would show similar recovery after hair cell regeneration. Lesions of the vestibular hair cells of 10-day-old chicks were created by a 5-day course of streptomycin sulfate. One day after completion of streptomycin treatment there was no measurable VCR gain, and total hair cell density was approximately 35% of that in untreated, age-matched controls. At 2 wk postlesion there was significant recovery of the VCR; at this time two subjects showed VCR gains within the range of control chicks. At 3 wk postlesion all subjects showed VCR gains and phase shifts within the normal range. These data show that the VCR recovers before the VOR. Unlike VOR gain, recovering VCR gain correlates equally well with the density of regenerating type I and type II vestibular hair cells, except at high frequencies. Several factors other than hair cell regeneration, such as length of stereocilia, reafferentation of hair cells, and compensation involving central neural pathways, may be involved in behavioral recovery. Our data suggest that one or more of these factors differentially affect the recovery of these two vestibular reflexes.

Aminoglycosides↗

Differential central projections of physiologically characterized horizontal semicircular canal vestibular nerve afferents in the toadfish, Opsanus tau.

Anatomical and neurophysiological studies were undertaken to examine the central projection pattern of physiologically characterized horizontal semicircular canal vestibular nerve afferents in the toadfish, Opsanus tau. The variations in individual response characteristics of vestibular nerve afferents to rotational stimulus provided a means of typing the afferents into descriptive classes; the afferents fell into a broad continuum across the spectrum from low-gain, velocity-sensitive to high-gain, acceleration-sensitive responses (Boyle and Highstein [1990b] J. Neurosci. 10:1557-1569; Boyle and Highstein [1990a] J. Neurosci. 10:1570-1582). In the present study, each afferent was typed as a low-gain, high-gain, or acceleration fiber during rotational or mechanical stimulation (Rabbitt et al. [1995] J. Neurophysiol. 73:2237-2260) and was then intracellularly injected with biocytin. The axons were reconstructed, and the morphology, synaptic boutons, and projection pattern of each axon were determined. The results indicated that the three descriptive classes of vestibular nerve afferents have unique as well as overlapping central projection patterns and destinations in the vestibular nuclei, with intranuclear parcellation in the anterior octavus, magnocellularis, tangentialis, posterior octavus, and descending octavus nuclei. In general, increased sensitivity and faster response dynamics were correlated with both a more extensive central projection and a progressive increase in morphological complexity. Low-gain, velocity-sensitive fibers were the simplest morphologically, with the fewest number of branches (n = 17) and shortest length (4,282 microm), and projections were confined to the middle portions of the vestibular nuclei. High-gain, velocity-sensitive fibers were morphologically more diverse than low-gain fibers, with a greater number of branches (n = 26), longer length (6,059 microm), 29% greater volume, and a more widespread projection pattern with projections to both the anterior and the middle portions of the vestibular nuclei. Acceleration fibers were morphologically distinct from low- and high-gain fibers, with more elaborate branching (n = 41), greatest overall length (17,370 microm) and volume (16% greater than high gains), and displayed the most extensive central projection pattern, innervating all vestibular nuclei except tangentialis. Thus, there are anatomically demonstrable differential central projections of canal afferents with different response dynamics within the vestibular complex of the fish.

Animals↗

Paradoxical vocal cord motion presenting as acute stridor.

We report the cases of two patients who presented with acute-onset stridor that did not respond to standard medical therapy. Both were eventually found to have paradoxical vocal cord motion (PVCM). The ED management of these patients is reviewed.

Acute Disease↗

Hair cell regeneration and recovery of the vestibuloocular reflex in the avian vestibular system.

1. Although auditory and vestibular hair cells are known to regenerate after aminoglycoside intoxication in birds, there is only sparse evidence that the regenerated hair cells are functional. To address this issue, we examined the relation of hair cell regeneration to recovery of the vestibuloocular reflex (VOR), whose afferent signal originates at hair cells in the vestibular epithelium. Hair cell damage was produced by treating white Leghorn chicks (Gallus domesticus, 4-8 days posthatch) with streptomycin sulfate in normal saline (1,200 mg.kg-1.day-1 im) for 5 days. 2. In the 1st wk after treatment, the VOR gain was essentially 0, and hair cell density as assessed by light microscopy was approximately 40% of normal. Between the 1st and 3rd wk after treatment, the VOR was present. Although VOR gain varied considerably from one chick to another, it increased, on average, between the 1st and 3rd wk, as did the average hair cell density. At the end of 8-9 wk, the gain and phase of the VOR had returned to normal values, as had the average density of hair cells. 3. Therefore, despite the catastrophic initial effect of hair cell loss on the VOR, recovered hair cells appeared to restore the VOR completely. Average hair cell density increased with average VOR gain. VOR gain correlated better with recovery of type 1 hair cells than with recovery of type II hair cells. 4. In contrast to hair cell density, the appearance of the vestibular epithelia as assessed by hair cell stereocilia in scanning electron micrographs was a poor indicator of VOR gain. In both treated and control birds, epithelia with the same appearance could have quite different VOR gains, suggesting a variation in the functional viability of the hair cells. 5. This observation suggests that several factors, such as the repair of stereocilia, the efficacy of hair cell synapses on afferent fibers, and the extent of compensation by central vestibular pathways, may affect the recovery of VOR gain. However, our data suggest that hair cell regeneration plays an important role in this recovery.

Animals↗

Morphological correlates of response dynamics and efferent stimulation in horizontal semicircular canal afferents of the toadfish, Opsanus tau.

1. We used the intraaxonal labeling technique to study correlations between the terminal dendritic morphology of horizontal semicircular canal primary afferents and their response dynamics to sinusoidal head rotation and combined electrical stimulation of central efferent vestibular neurons. Thirty-eight canal afferents were identified by their sensitivity and phase of response to rotation between 0.1 and 1.0 Hz (+/- 10 degrees/s) and were subsequently labeled with horseradish peroxidase or biocytin. The afferent's dendritic field and synaptic specializations in the neuroepithelium of the crista were examined under light microscopy. 2. Rate and regularity of background discharge of the afferent were not correlated with its axon diameter or relative location of its dendritic field in the crista. 3. Response sensitivity of the afferent to rotation was correlated both with the relative location of its dendritic field in the crista and with the number of terminal endings it possesses. Afferents having low sensitivities, slow dynamics, and few terminal endings supply the peripheral portions of the crista; afferents with higher sensitivities, faster dynamics, and greater number of terminal endings supply the more central portions. It is suggested that the differences in sensitivity among the afferents reflect principally the variations in both the cupular dynamics along the crista and the number of possible hair cell contact sites in the neuroepithelium. 4. Response phase of the afferent was correlated only with the extent of its dendritic processes along the transverse axis of the crista. Afferents having transversely oriented dendritic fields had less phase lags relative to acceleration than did those having a more longitudinally oriented dendritic field. 5. Efferent stimulation produced a change in both the afferent's discharge rate and its response sensitivity to rotation. Afferents discharge rate and its response sensitivity to rotation. Afferents having a centrally located dendritic field and acceleration afferents, defined by their response to rotation, were the most affected by efferent stimulation. These results suggest that efferent innervation is either directed toward, or most efficacious in, the central regions of the crista and that it may select specific hair cell-afferent complexes.

Animals↗

Complications of controlled tissue expansion in the pediatric burn patient.

All patients at the Burn Institute reconstructed with tissue expanders between June of 1984 and June of 1987 were included in this review. There were 122 expanders used in 77 patients. Complications were defined as "absolute" (23 of 122 expanders, 20 percent) if they resulted in loss of expanders or additional surgery or none of preoperative plan was satisfied or "relative" (14 of 122 expanders, 11 percent) if they included spotty alopecia or alopecia greater than 50 percent or the operative plan only partially satisfied, reflecting poor judgment. The most common absolute complication was prosthetic exposure secondary to wound dehiscence occurring in the scalp area. Complications relative to specific anatomic areas were neck and face, 2 of 20 (10 percent); lower extremity, 1 of 4 (25 percent); trunk, 0 of 6 (0 percent); and scalp, 20 of 92 (22 percent). We feel that this high complication rate in the use of tissue expanders may be unique to the pediatric burn patient. Knowledge of indications for use and potential complications is essential to add this entity to the armamentarium of the burn reconstructive surgeon.

Adolescent↗

The latissimus dorsi flap for reconstruction of the brachium and shoulder.

The latissimus dorsi was transferred on its neurovascular pedicle to reconstruct the shoulder or brachium in nineteen patients. Group I consisted of seven patients in whom transfer of the latissimus dorsi was used only to obtain active flexion of the elbow. Although there was complete necrosis of the transferred muscle in one patient, six patients achieved an average of 111 degrees of active flexion and full extension of the elbow. There was only a modest gain in active supination because of pre-existing pronation contractures. The three patients in Group II had sustained loss of the flexor muscles of the elbow and the overlying soft tissue as a result of trauma. After the latissimus dorsi musculocutaneous flexorplasty, an average of 135 degrees of active flexion of the elbow was restored, but there was an average loss of 12 degrees of extension. The three patients in Group III had a large, noninfected defect of the soft tissue over the shoulder or brachium; the bone, shoulder joint, or neurovascular structures were exposed in each patient. Transfer of the latissimus dorsi with the overlying skin provided satisfactory coverage of the defect. The six patients in Group IV had chronic osteomyelitis or septic arthritis of the glenohumeral joint. Treatment consisted of radical débridement of the infected soft tissue and bone followed by transfer of the latissimus dorsi. This provided satisfactory coverage for subsequent osteosynthesis of the humerus or arthrodesis of the shoulder when one of these procedures was indicated. At the time of writing, an average of 2.3 years after the latissimus dorsi transfer, none of the patients in this group (including one who died nine months post-operatively of unrelated causes) had drainage.

Adult↗

Reconstruction following head and neck burns.

Burn reconstruction of the head and neck must first start with special care to this anatomic area in the early acute phase, with appropriate early débridement and coverage with sheet grafts of medium thickness into unit facial orientation. Postoperative garment and mask splinting, will help lessen the hypertrophic scar formation that frequently follows facial burns and skin coverage. Carefully planned reconstruction of these areas is indicated, with priority given first to the neck, then to the periorbital area, and then to perioral areas. Principles of scalp, ear, nasal, and cheek reconstruction following burns of the face are carefully outlined. The unit concept of burn scar resurfacing of the face has been the mainstay of our treatment. We have emphasized skin coverage of the face from similar donor site areas. The emotional and psychological effects of facial scarring secondary to severe burns are crippling to patients. Although numerous reconstructive surgical procedures may lessen the deformity, ultimately burn patients realize that their burn scars are permanent and no surgeon can give them back their original facial appearance. These patients need strong and continued support and reassurance from their physicians and nursing professional staff to maintain their self-identity and confidence.

Adolescent↗

Fatal complications of tracheotomy.

Thirty-six of 403 deaths after tracheotomy were direct complications of that procedure. Arterial hemorrhage caused three deaths, venous bleeding, seven. Airway obstruction resulted in six fatalities. Tracheoesophageal fistula caused five deaths. Eight deaths were due to infection and sepsis. Tension pneumothorax developed in one patient and the remaining six deaths were due to cardiopulmonary collapse. Many of the complications of tracheotomy can be avoided with accurate knowledge of anatomic variations, ideal operating conditions, proper technic, careful arterial and venous hemostasis, routine postoperative chest x-ray films, sterile suction technic, proper use of soft cuffed tracheotomy tubes, adequate humidification, and careful postoperative blood gas monitoring.

Airway Obstruction↗