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Biomedical subjects

J J Shea

Publications and source records attributed to J J Shea.

At least 37 records · Page 2Linked to original sources

Speech perception after multichannel cochlear implantation in the pediatric patient.

Clinical trials to evaluate multichannel cochlear implantation in children ages 2 to 17 years began in late 1986, with pre-market approval granted in 1990. To date, 870 children in the United States have received the Nucleus 22-channel device. Performance on measures of speech perception in 30 children who have used the Nucleus cochlear implant for a minimum of 6 months is presented and discussed in terms of the predictive value of patient biographic variables. Age at implantation and age to deafness onset were positively correlated with test performance for pre- and perilinguistically deafened subjects.

Adolescent↗

How I do primary and revision stapedectomy.

Localized anterior otosclerosis is found in about 80 percent of primary stapedectomy operations. For these patients, partial stapedectomy with vein graft is recommended. Obliterative otosclerosis is the pathology found in the remaining 20 percent of primary stapedectomy operations. In these cases, stapedectomy with lining membrane of the middle ear or vein graft is the procedure of choice. Revision stapedectomy may improve conductive hearing loss caused by (1) migration and/or dislocation of the prosthesis, (2) eversion of the lining membrane of the vestibule with resulting dislocation of the prosthesis and possible erosion of the lower incus, (3) bony closure of the oval window, or (4) epitympanic fixation of the incus and/or malleus. Successful operative techniques used in primary and revision stapedectomy are described.

Humans↗

Facial nerve stimulation after successful multichannel cochlear implantation.

Postoperative rehabilitation after cochlear implantation may be difficult and frustrating for both patient and audiologist. The occurrence of facial nerve stimulation with associated twitching and discomfort can interfere with the rehabilitative process and be a cause of great concern to the patient. Such stimulation can occur at the time of initial "tune-up" or can be delayed by months or years. The incidence of postoperative facial nerve stimulation 109 consecutive patients operated by the same surgeon over a period of 7 years is reviewed. Possible causes for immediate and delayed stimulation are discussed, and strategies at surgery are outlined. Rehabilitative techniques for dealing with facial nerve stimulation are reviewed.

Aged↗

Endolymphatic hydrops associated with otosclerosis.

Endolymphatic hydrops (EH) associated with otosclerosis has been noted for many years. However, the causal relationship of these two entities remains controversial. Having reviewed the records of patients with otosclerosis describing fluctuant hearing loss and vertiginous symptoms, the authors found the EH may coexist with otosclerosis preoperatively; they may be two separate diseases that exist coincidentally; or EH may be caused by the otosclerotic process. Secondly, EH may occur with a fistula after surgery. Occurring after stapedectomy, EH may be caused by fistulization of the bony labyrinth, which is effectively treated by surgery to seal the fistula, which may cause EH to subside and hearing to improve. Thirdly, delayed EH may occur months or years after stapedectomy, possibly as a result of otosclerotic foci or surgical insult to the labyrinth. Dexamethasone, diuretics, and a room air rebreather can be used in the treatment of delayed EH. Hearing may be maintained or may deteriorate, but there usually is no dizziness. The clinical manifestations of EH associated with otosclerosis include a conductive or mixed type of hearing loss; the presence of fullness, tinnitus, fluctuation of hearing, episodic vertigo, an elevated negative summating potential (SP), and an increased summating potential:action potential (SP:AP) ratio shown by ECoG. This report presents five cases of EH associated with otosclerosis.

Adult↗

Long-term results of low dose intramuscular streptomycin for Menière's disease.

The initial results of partial ablation of vestibular function are evident to control vertigo attacks and stabilize hearing as well as to reduce the severity of ataxia. The purpose of this study is to observe the long-term results of low dose intramuscular streptomycin in the treatment of bilateral Menière's disease. Eleven patients with disabling bilateral Menière's disease were treated with low doses of intramuscular streptomycin (20-40 g, mean = 25 g). Follow-up was 5-12 years (mean = 8 yr). All 11 patients achieved relief of their disabling vertigo. One patient had recurrent vertigo 1 year after treatment and streptomycin perfusion of the labyrinth was performed subsequently. Four patients reported feeling slightly off balance during follow-up. None experienced oscillopsia in this series. In the entire group of 11 patients (22 ears), hearing was unchanged in 17 ears, improved in two and worse in three. A hearing threshold of < 30 dB was found in two ears before and two after treatment; 30-60 dB was found in seven ears before and six after treatment; and > 60 dB was found in 13 ears before and 14 after treatment. The mean PTA of the 22 ears was 58 dB before and 65.5 dB after treatment. The mean speech discrimination scores were 61.4 percent before and 51.3 percent after treatment. The long-term results suggest that partial ablation of vestibular function by streptomycin has long-lasting effects of controlling vertigo attacks, stabilizing hearing, and reducing the severity of ataxia. Administration of low doses of intramuscular streptomycin is the treatment of choice for bilateral Menière's disease.

Adult↗

The classification and treatment of Menière's disease.

The classification and treatment of Menière's disease are especially difficult because the natural history of Menière's disease is so variable, and not possible to relate to the cochlear and vestibular pathology present, which is constantly changing and cannot be known during life. In the many new papers written each year on Menière's disease and the hundreds of older papers already in the medical literature, there is no good agreement about the definition of Menière's disease, the pathology and natural history, and the real benefit of the medical and surgical treatments given. Only recently, with transtympanic electrocochleography and three-dimensional CT scans of the external aperture of the vestibular aqueduct, have we significant information during life about the pathology present, from which to predict the likely natural history and the chances for successful treatment. This paper will define Menière's disease, will separate its pathology and natural history in five stages, and suggest reasonable methods of treatment for the stages for which treatment is possible.

Audiometry, Evoked Response↗

Factors influencing results with streptomycin perfusion of the labyrinth.

Streptomycin perfusion of the labyrinth is the logical choice of treatment for the third stage of Meniere's disease with intractable vertigo. The results of streptomycin perfusion of the labyrinth are comparable to those of other treatments, including endolymphatic shunt and vestibular nerve section. Refinements must be made in the process of selecting candidates for the operation. To study the factors influencing the results of streptomycin perfusion of the labyrinth, 144 patients who had streptomycin perfusion of the labyrinth and were followed for 1 year were studied using the 1972 AAOO classification of results. The findings of this study indicate that only a low dosage of streptomycin and a small volume of perfusate are required to obtain good results. Patients who have long lasting severe endolymphatic hydrops with poor hearing preoperatively are less likely to achieve good results.

Adult↗

Classification of Menière's disease.

To create a rational treatment system for Meniere's disease, it is helpful to divide Meniere's disease into five stages according to the signs, symptoms, pathology, and natural history by recalling what is known for certain and what is probably true about Meniere's disease. It is known that Meniere's disease is attributable to endolymphatic hydrops, caused by a small, malfunctioning endolymphatic sac, abnormally placed since birth, and Meniere's disease is therefore a congenital disorder of the endolymphatic sac. It is probably true that there is often an immune, viral, metabolic, or other insult to the inner ear, that disturbs the balance between the cochlea, where endolymph is produced, and the endolymphatic sac, where most of it is absorbed. Using this five-stage classification, it is possible to separate Meniere's disease into the first three stages, for which different but reasonable treatments are possible, and the last two stages, for which no treatments are effective.

Dexamethasone↗

Transtympanic electrocochleography in Menière's disease using clicks and tone-bursts.

Transtympanic electrocochleography (ECoG), using clicks and tone-bursts at 500, 1000, and 2000 Hz, was employed to study 80 patients with Meniere's disease and 25 non-Meniere's patients. The magnitude of the negative summating potential and the summating potential:action potential ratio (SP:AP) were examined in both groups. Groups were further divided based upon degree of hearing loss and audiometric configuration. An elevated SP:AP ratio was found in 83.7 percent of the Meniere's ears and 12 percent of the non-Meniere's. The likelihood of obtaining a positive ECoG in Meniere's patients was strongly related to degree of hearing loss but not audiometric configuration.

Audiometry, Evoked Response↗

Intramuscular streptomycin effect on dark cells of utricle in guinea pigs.

Streptomycin has been used in the treatment of Meniere's disease for almost half a century. Clinical studies showed that streptomycin may eliminate vertigo attacks and stabilize or improve hearing in the majority of patients. Animal experiments have demonstrated severe damage to the vestibular hair cells after streptomycin treatment. This study is to observe the effect of intramuscular streptomycin on dark cells of utricle. Guinea pigs that had received intramuscular injections of streptomycin sulfate 400 mg/kg per day for 1 and 2 weeks were studied. The dark cells of utricle were observed under transmission electron microscope. The pinocytotic vesicles and rough endoplasmic reticula markedly decreased and the plasmalemma infoldings in the lower part of the cell reduced in the 1-week group. The luminal membrane of the cells bulged out on the surface. After the cell membrane ruptured, the cytoplasmic organelle moved into the endolymphatic space and the cell dissolved. The morphologic changes indicated that streptomycin damaged the cytoplasmic granules and the plasma membrane infoldings of the dark cells. These cytologic characteristics are engaged in fluid secretion. The damage of secretory function of the dark cells may reduce the volume of endolymph.

Animals↗

Effect on endocochlear potential of streptomycin perfusion of the cochlea in guinea pigs.

Perilymphatic perfusion of the cochlea with streptomycin was performed on 17 guinea pigs. The first and second group, consisting of five animals each, received streptomycin 150 micrograms and 1500 micrograms respectively. In a control group, consisting of seven animals, the perilymph was perfused with artificial perilymph only. The endocochlear potential (EP) was recorded from the second turn of the cochlea in each animal. The results indicate that streptomycin in a low dosage that will destroy the vestibular receptors was not harmful to the function of either the stria vascularis or the hair cells in the cochlea, as measured by changes in the EP after streptomycin perfusion of the cochlea.

Animals↗

Streptomycin perfusion of the labyrinth.

The combination of fluctuant hearing loss, fullness, tinnitus and dizzy spells we call Meniere's disease is thought to be caused by endolymphatic hydrops. Most patients with the clinical picture of Meniere's disease do have endolymphatic hydrops but some patients with endolymphatic hydrops do not have the clinical picture of Meniere's disease. It would appear there is an, as yet unknown, immune-mediated, cause for Meniere's disease, in addition to endolymphatic hydrops, and this immune-mediated cause may aggravate those ears with endolymphatic hydrops. While medical treatment with a low-salt diet, diuretics and steroids are of value in some patients when given early in controlling dizzy spells and improving the hearing, there is usually no real, long-term benefit. Since none of these "shunts" of the sac could remain open for more than a few hours, they could have no more direct benefit than a one-time drainage of endolymph, while doing harm to the fluid absorption, immune response and phagocytosis roles of the endolymphatic sac. The various vestibular neurectomy operations, while usually stopping the dizzy attacks, are both difficult and potentially dangerous, but more important, do nothing for the hearing loss. The one direct attack on the problem, both easy to perform and certain to relieve the dizzy attacks, is to destroy the vestibular receptors with streptomycin. This destructive action on the stereocilia and sensory cells, without damage to the rest of the vestibular system and the cochlea, has been verified by two cat experiments with streptomycin by Norris et al. and Norris & Shea and two guinea pig experiments with gentamicin by Kimura.(ABSTRACT TRUNCATED AT 250 WORDS)

Ear, Inner↗

Medical and surgical treatment of Menière's disease.

To create a rational treatment system for Meniere's disease, it is helpful to recall what is known for sure and what is probably true about Meniere's disease, so as to recognise the stages through which the disease passes from beginning to end. Meniere's disease is a complex disorder of the inner ear, characterised by fullness, tinnitus, fluctuant hearing loss and dizzy spells. Meniere's disease is always associated with, and probably caused by endolymphatic hydrops, although all patients with endolymphatic hydrops do not have Meniere's disease. Meniere's disease is almost always associated with, and probably caused by a small, underdeveloped, abnormally-placed, malfunctioning endolymphatic sac. The first stage is entirely cochlear, where endolymphatic hydrops usually begins, with fullness, tinnitus and low-tone, sensorineural hearing loss, and is most amenable to medical treatment. In the second stage, the endolymphatic hydrops is more widespread, involving the vestibular labyrinth as well. There is fluctuant, low-tone sensorineural hearing loss, fullness and tinnitus, together with dizzy spells. In the third stage, the hearing loss is more severe and no longer fluctuates, with poor comprehension, but fullness, tinnitus, and dizzy spells are the chief complaints. In the fourth and final end-stage, the hearing is very bad, at 55 to 60 db, and no longer fluctuates, with very poor comprehension, fullness and tinnitus, but usually no more dizzy spells, although the patient is unsteady, especially in the dark. Most ears in Stage IV have reduced or absent response to rotation test.

Female↗