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Biomedical subjects

D B Quine

Publications and source records attributed to D B Quine.

8 recordsLinked to original sources
PubMed1985

Amino-oxyacetic acid as a palliative in tinnitus.

Amino-oxyacetic acid, previously shown to cause a reversible loss of hearing sensitivity and a reduction in endocochlear potential, was tried as a palliative in human tinnitus. Because the drug seemed to have a cochlear site of action, patients were selected for the study if their audiograms were indicative of cochlear lesions and if there was a reduction in tinnitus following intravenous lidocaine (lidocaine positive). Ten such patients received either 50 or 75 mg of amino-oxyacetic acid four times a day orally for one week or placebo administered in a random, crossover, double-blind design. Of these ten, three reported subjective lessening of tinnitus. One of those three and two others not reporting subjective lessening of tinnitus showed a substantial improvement in speech discrimination scores while receiving amino-oxyacetic acid but not placebo. One additional patient who did not receive lidocaine also reported a subjective lessening of tinnitus. Four patients who were lidocaine negative showed neither subjective nor objective improvement in tinnitus after treatment with amino-oxyacetic acid.

Acetates↗
PubMed1985

Computer analysis of vestibular responses to putative neurotransmitters.

An inexpensive microcomputer (Commodore 64K) based system was developed for the analysis of neural spike trains. The trains were recorded from single ampullary units in response to mechanical stimulation of the isolated semicircular canal of the bullfrog (Rana catesbeiana). A BASIC program provided a number of options while machine language subroutines generated interstimulus interval (ISI) and peristimulus time (PST) histograms. Up to thirty 5-s spike trains could be combined for analysis (0.1 ms resolution ISI, 100 ms bin width PST). Histograms and summary statistics were saved on floppy disks. The cost of adding this computer system to an existing neurophysiology laboratory is less than US $600 (printed, tape, and disk versions of these programs are available). The system was used to measure vestibular responses to putative vestibular neurotransmitters such as carbachol (an acetylcholine mimic) (Rossi et al., 1980) and gamma-aminobutyric acid (GABA) (Flock and Lam, 1974).

Animals↗
PubMed1984

Patients with multiple sclerosis experience hearing loss specifically for shifts of tone frequency.

After exposure to a prolonged tone of changing intensity but constant frequency, controls, patients with peripheral hearing loss, and patients with multiple sclerosis (MS) demonstrated a reduced sensitivity to shifts in intensity; sensitivity to frequency shifts was unaffected. After exposure to a prolonged tone of changing frequency but constant intensity, control and patients with peripheral hearing loss demonstrated reduced sensitivity to shifts in frequency; sensitivity to intensity shifts was unaffected. Some patients with MS showed no loss of sensitivity to shifts in frequency. Our findings suggest that some patients with MS have abnormal mechanisms for processing changes of frequency. If such processing of frequency change is important for understanding speech, then this observation of a specific central hearing defect may help to explain poor speech discrimination in some patients with MS who have normal audiograms.

Adolescent↗
PubMed1984

The potentiation of ototoxicity when aminooxyacetic acid and kanamycin are co-administered.

Aminooxyacetic acid (AOAA) has been shown to confer protection against noise-induced cochlear trauma [3]. We, therefore, decided to study the possible protective effect of AOAA against kanamycin (KM) ototoxicity and found, instead, that AOAA potentiated the toxicity. To produce ototoxicity in guinea pigs, KM is usually given in 10-14 daily doses of 400 mg/kg s.c. However, when combined with a single dose of AOAA (8, 11, 15, or 25 mg/kg) a single 400 mg/kg dose of KM is sufficient to cause cochlear damage. Such animals show a negative Preyer's reflex between 1 to 3 days post injection. 21 days later hearing thresholds as detected electrocochleographically at 2, 4, 8, 12 and 16 kHz have changed drastically sometimes to the point of being undetectable. The damage seen histologically at this time is destruction of both inner and outer hair cells. A pharmacokinetic analysis of this potentiation revealed a slight prolongation of KM's sojourn in the inner ear. The possible mechanisms of this unexpected, marked potentiation are discussed but remain unknown.

Acetates↗
PubMed1984

Degraded discrimination between speech-like sounds by patients with multiple sclerosis and Friedreich's ataxia.

We previously found that some patients with multiple sclerosis are selectively 'deaf' to changes in the pitch of a tone, even when audiometric sensitivity to pure tones is unimpaired. This subtle form of deafness is not experienced by patients with noise-induced hearing loss of exclusively peripheral origin. It was suggested that this auditory defect may be one possible cause for difficulties in discriminating speech, on the grounds that frequency changes in the speech waveform are known to be important for intelligibility. This implication is not self-evident; our earlier studies tested hearing with a single pure tone that was either frequency-modulated or amplitude-modulated, while even a simple approximation to speech sounds involves not one, but three narrow bands of noise (formants) whose frequencies and intensities change from instant to instant. The present study has investigated the ability of subjects to discriminate between speech-like sounds. These consisted of three formant frequencies generated by computer. The only difference between the sounds was that the lowest-frequency formant rose or fell in pitch by different amounts. In order to ensure that subjects used frequency (pitch) cues rather than any associated loudness cues were mixed different loudness shifts with the frequency shifts. Nineteen control subjects, 25 patients with multiple sclerosis (MS) and 4 patients with Friedreich's ataxia (FA) were tested. Nine of the patients with MS and all 4 patients with FA gave results that fell outside the range of the control subjects. A possible pathophysiological basis for this observation is the finding that some neurons in the auditory pathway of animals respond preferentially to changes in tone frequency: homologues of these neurons might be functionally impaired in some patients with MS and FA.

Adolescent↗
PubMed1983

Delayed auditory tone perception in multiple sclerosis.

Delays of auditory perception at three frequencies were measured in 30 multiple sclerosis patients using a psychophysical technique. Nineteen patients had abnormal delays at one or more tone frequencies, though 15 had normal audiograms at those frequencies. In addition, auditory acuity for left-right asynchrony was abnormally poor in 13 patients, 9 of whom had normal audiograms. Such delays of auditory perception within a restricted frequency band may provide a partial explanation for degraded speech comprehension in some multiple sclerosis patients.

Adult↗
PubMedDate not supplied

Cholinomimetics mimic efferent effects on semicircular canal afferent activity in the frog.

Acetylcholine (Ach) has received strong support as the neurotransmitter at vestibular efferent nerve endings. Ach, cholinomimetics and cholinergic antagonists were therefore applied to frog isolated whole labyrinths and isolated semicircular canals. Both spontaneous and evoked single unit and multiple unit activities were recorded from the decentralized posterior semicircular canal afferent nerve. In a manner analogous to efferent nerve stimulation, Ach produced both facilitatory and inhibitory changes in afferent firing rates. The facilitatory effect is likely mediated by muscarinic receptors (i.e. atropine antagonizes it at low concentrations). The facilitatory effect can also be elicited by muscarine and carbachol and it is likely produced presynaptically on the vestibular sensory cell. That is, the effects of Ach are not changed by removal of the efferent neurons but they are absent when afferent transmitter release is blocked. The inhibitory effect is not as well characterized as is the facilitatory effect but it can be blocked by strychnine. The results are consistent with the hypothesis that Ach is the transmitter responsible for both the facilitatory and the inhibitory effects of efferent vestibular nerve stimulation.

Acetylcholine↗