Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ACOUSTICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,567 records · Page 87Linked to original sources
PubMed2002

Effects of corticotropin-releasing factor on prepulse inhibition of the acoustic startle response in two rat strains.

RATIONALE: Prepulse inhibition (PPI) of the acoustic startle response is altered by manipulations that affect brain monoamine neurotransmission. Corticotropin-releasing factor (CRF), a neurotransmitter that is released during stress, and CRF receptors are expressed in areas of the brain which contribute to PPI, and central administration of CRF changes extracellular concentrations of the monoamines. Therefore, CRF is in a position to alter PPI, either by causing the release of other neurotransmitters, or by direct effects at CRF receptors. OBJECTIVES: The present experiments were conducted to test the hypothesis that intracerebroventricular (ICV) administration of CRF would decrease PPI in rats. Additionally, these experiments were used to examine whether CRF results in differential changes in PPI in rat strains that show high and low basal PPI, and whether CRF-induced grooming behavior and increased startle amplitude are also strain-dependent. METHODS: Male Wistar-Kyoto (WKY) rats inbred in our colony in La Jolla, WKY rats obtained from Charles River, and Brown Norway (BN) rats from Harlan, Sprague-Dawley were tested for grooming behavior, PPI and startle amplitude following ICV infusion of either CRF (1.0-3.0 microg) or saline. RESULTS: CRF significantly decreased PPI in both BN rats, which show relatively little PPI in the basal condition and, in WKY rats. The amplitude of the acoustic startle response was increased in WKY rats only and, only by the 3.0 microg dose of CRF. CRF increased grooming behavior in the La Jolla colony WKY and BN rats. However, within the time frame during which the rats were being observed, CRF failed to significantly increase grooming in Charles River WKY rats. CONCLUSIONS: CRF diminished PPI of the acoustic startle response in rats that show high (WKY) and low (BN) basal PPI. This effect does not appear to be dependant on CRF-induced changes in startle amplitude. The results suggest the possibility that stress-induced exacerbation of symptoms in schizophrenia, which is characterized by deficient PPI, may be CRF-dependent.

Acoustic Stimulation↗
PubMed2003

Topiramate attenuates exaggerated acoustic startle in an animal model of PTSD.

RATIONALE: Exaggerated acoustic startle is a prominent symptom of post-traumatic stress disorder (PTSD); however, its physiological basis is not well understood, and there are few available treatments. Neurobiological research has suggested that anti-kindling agents and/or glutamate antagonists can attenuate the acoustic startle response (ASR) in animal models. The anticonvulsant topiramate is an AMPA antagonist that also demonstrates potent anti-kindling effects and may, therefore, have promise in treating trauma-enhanced ASR. OBJECTIVE: To evaluate the ability of topiramate to attenuate stress-induced increases in ASR in a previously validated animal model of PTSD. METHODS: Male Sprague-Dawley rats ( n=36) served as controls or received single prolonged stress (SPS). SPS consisted of 2 h restraint, forced swim and ether anesthesia, then a 7-day "undisturbed" period. Animals then received vehicle, 10 mg/kg or 30 mg/kg of topiramate orally, twice daily for 7 days. ASR was assessed for all animals before and after the study, in light and dark environments. RESULTS: SPS produced a sustained increase in the ASR in both environments, an effect that was significantly reduced by topiramate. Meanwhile the ASR of control animals remained unaffected by topiramate. CONCLUSIONS: The current results provide one of the few demonstrations of a single stress episode producing sustained enhancement of ASR. In addition, topiramate demonstrates promise in treating exaggerated acoustic startle symptoms in PTSD or other stress-related disorders.

Acoustic Stimulation↗
PubMed2004

Effects of combined cortical and acoustic stimuli on muscle activity.

Hitherto, it has proven difficult to investigate interactions between cerebral and brainstem motor systems in the human. We hypothesised that transcranial magnetic stimulation (TMS) centred over the dorsal premotor and primary motor cortices might elicit net facilitatory cortico-reticular effects that could interact at the level of the brainstem with a habituated startle to give a reticulospinal discharge and electromyographic (EMG) response with a longer latency than the direct corticospinal response. Conversely, any reticulo-cortical activity evoked by a habituated startle should influence the size of the direct response to cortical TMS. EMG was recorded from active left deltoid muscle in nine healthy volunteers. Acoustic stimulation was delivered binaurally through headphones and repeated until the startle response was habituated. When TMS was centred over the right dorsal premotor or primary motor cortices and delivered 50 ms after the habituated acoustic stimulus, the contralateral direct motor evoked potential was inhibited, compared with the response elicited by TMS alone. The contralateral silent period was shortened and associated with less of a decrease in EMG levels relative to TMS alone. Indeed, an actual increase in EMG over baseline levels occurred in the later half of the silent period in all subjects. We conclude that both cortico-reticular and reticular-cortical effects could be elicited in deltoid through the combination of acoustic stimulation and TMS at short interstimulus intervals. Effects were similar with TMS over premotor and primary motor cortex.

Acoustic Stimulation↗
PubMed1997

The size of acoustic neuromas: CT and MRI.

The growth rate of acoustic neuromas is very variable: some tumours grow rapidly, some do not grow and some even get smaller. When making treatment decisions, it may be important to have an idea of the growth rate of the individual tumour, and this is only possible when there are comparable examinations. We performed both CT and MRI on 15 patients. Two radiologists estimated the size of their acoustic neuromas. There was a significant difference between the two examiners' calculations of tumour volumes on CT and between the first examiner's CT and MRI volume calculations. No difference was found between the two MRI volume estimations or the second examiner's estimation of volumes on CT and MRI. Measurements of the maximal tumour diameter along the pyramid showed good concordance. We conclude that measurement the size of acoustic neuromas is reproducible with MRI and the measurement of the maximal tumour diameter is in practice a better parameter for comparison than calculation of real volume.

Adult↗
PubMed2002

Objective acoustic and aerodynamic measures of breathiness in paralytic dysphonia.

This study was designed to determine which objective acoustic or aerodynamic parameters allowed a homogeneous group of patients with unilateral vocal fold paralysis (UVFP) to be distinguished from an age-matched and smoking-matched control group and to search for linear correlations between the objective parameters and the subjective breathiness ratings. Eight patients with recent-onset UVFP and 12 controls were prospectively studied. The acoustic parameters measured for the vowel /a/ at a comfortable frequency and intensity were: jitter, shimmer, harmonics-to-noise ratio, cepstral peak prominence, the difference between the levels of the first two harmonics and the relative energy above 6 kHz. Aerodynamic parameters included the mean flow rate during a sustained /a/ and intraoral pressure during the production of the phoneme /pi/. The long-term average spectrum was calculated for 40 s of text, and the relative average energies in four frequency bands were compared. Six judges rated a mid-/a/ sample using a five-parameter scale with four levels of severity. Nonparametric statistical analysis revealed significant differences ( P<.05) between the UVFP group and the control group for 14 of the 19 parameters studied. Correlations between the objective parameters and perceived breathiness differed in the two groups. Correlations were not always as expected as based on previous literature reports. These measurements provided an objective qualification of voice in patients with UVFP and successfully distinguished them from the normal controls. The objective acoustic and aerodynamic measurements had generally low linear correlations with breathiness ratings in the control group. Higher correlations were seen in the UVFP group, in which breathiness was best correlated with airflow measurements.

Aged↗
PubMed1999

Small acoustic neuromas: monitoring the growth rate by MRI.

In a proportion of small acoustic neuroma patients, monitoring with magnetic resonance imaging shows no volumetric increase of tumour size over the years. The object of the study was to identify some indications for the clinical choice between immediate surgery (with the related risks) and watchful waiting. We performed a retrospective study of 47 non-surgically-treated patients affected by acoustic neuroma and monitored by gadolinium-enhanced MRI between January 1990 and February 1999. Six clinical variables (tumour size, sex, age, initial symptoms, ABR pattern and duration of the symptoms) were examined by univariate analysis. Chi-square test and variance analysis were performed to evaluate the statistical significance. In 30/47 (63.8%) cases, no growth was observed during the entire period of follow-up. In the remaining 17/47 (36.2%) patients, a volumetric increase was detected, most often within the first year of observation. The clinical factors examined did not significantly correlate with growth. Despite the relatively short period of observation, we believe that immediate surgery does not need to be considered mandatory for small acoustic neuromas, even in young patients. However the irregular behaviour of the tumour underlines the importance of monitoring with MRI at least once a year.

Adult↗
PubMed2005

Acoustic aspects of the formation of speech in children in the third year of life.

This study covers the third year of life as part of a longitudinal investigation of the establishment of speech in Russian children performed on the basis of listener, phonetic, and instrumented acoustical analysis. The present report addresses the establishment of those additional acoustic and phonetic characteristics in children's speech which allow speech recognition. This is the first instrumented analysis in Russian children with statistical assessment of the dynamics of vowel formants in children's words, of the establishment of characteristics (stress, lack of stress), opposition (palatalization, lack of palatalization of consonants), and voice onset time for plosive consonants. The results showed that recognition of children's words by listeners with a high probability of success resulted from the formation of a system of acoustically stable properties in the children's speech which together provide informational adequacy for verbal communication.

Adult↗
PubMed1987

External vibratory acoustic stimulation near term: fetal heart rate and heart rate variability responses.

Twenty-five pregnant women between 36 and 40 weeks' gestational age were studied to examine effects of a 5-second external vibratory acoustic stimulus on the fetal heart rate and fetal heart rate variability. There was an immediate significant increase in the basal heart rate, which persisted for 1 hour after the stimulus, compared to that of the control subjects. There was also a significant increase in the total time during which accelerations occurred for the first 20 minutes after the stimulus. There were no changes in computer-derived indices of fetal heart rate variability. Maternal blood pressure and heart rate were not altered following vibratory acoustic stimulus. We hypothesize that external vibratory acoustic stimulus causes a change from a state of sleep to a state of wakefulness in near term healthy fetuses.

Acoustic Stimulation↗
PubMed1988

Auscultated fetal heart rate accelerations. III. Use of vibratory acoustic stimulation.

The auscultated acceleration test has been proposed as a simple, inexpensive screening test for fetal health; previous studies of the auscultated acceleration test used external stimulation to elicit fetal movement. This study was conducted to explore the ability of the auscultated acceleration test to predict nonstress test results when vibratory acoustic stimulation is used to elicit fetal reactivity. After antepartum nonstress testing on 100 gravid women between 28 and 43 weeks' gestation, a 6-minute auscultated acceleration test protocol was performed with two vibratory acoustic stimulations to the maternal abdomen if no spontaneous fetal heart rate acceleration occurred. The ability of the auscultated acceleration test to predict nonstress test results after selected variables were controlled for was as follows: sensitivity, 75%; specificity, 97.6%; false-positive results, 14.3%; and false-negative results, 4.7%. Logistic regression analysis indicated that, in addition to the auscultated acceleration test, gestational age and race contributed significantly to the prediction of nonstress test results. Although specificity and the false-positive rate were improved, the use of vibratory acoustic stimulations to elicit fetal movement did not improve the validity of the auscultated acceleration test in terms of sensitivity and false-negative results over previous studies. However, the auscultated acceleration test continues to show potential as an initial screening test for fetal assessment. In addition to recommendations for further research, methodologic issues related to sampling techniques are identified.

Acoustic Stimulation↗
PubMed1988

Fetal acoustic stimulation in early labor in patients screened with the admission test.

Fetal heart rate reactions to the fetal acoustic stimulation test were investigated in 952 women in early labor. All had cephalic presentations (greater than 33 weeks of gestation) and were screened with a 15-minute fetal heart rate recording (admission test) before the sound stimulation was applied. Three different types of responses were observed: type I, an accelerative response; type II, a biphasic response with acceleration(s) followed by a deceleration; type III, no response or a prolonged deceleration (greater than 60 beats/min and greater than 60 seconds). A type I response was recorded in 98.0% of the women after a reactive admission test result, in 90.2% after an equivocal admission test result, and in 42.9% after an ominous admission test result. Fetal distress in labor occurred in these three groups in 2.0%, 22.2%, and 35.7% of cases, respectively. The risk for fetal distress was high after an ominous admission test and a type III response on the fetal acoustic stimulation test (75.0%). The fetal acoustic stimulation test might be of value in labor and give additional information about fetal well-being in patients previously screened by the admission test. Testing time can be shortened after an equivocal admission test.

Acoustic Stimulation↗
PubMed1989

Preterm and term fetal cardiac and movement responses to vibratory acoustic stimulation.

To assess fetal response to vibratory acoustic stimulation, 24 preterm (group A; less than 36 weeks' gestation) and 30 term (group B; greater than or equal to 36 weeks' gestation) pregnancies were studied. Study variables were perceived fetal movement, fetal heart rate, and fetal heart rate pattern. Observer- and patient-perceived fetal movement responses were noted in most cases but were slightly more common in term patients (group A: + fetal movement, patient 87.5%/observer 87.5%) group B: + fetal movement, patient 96.7%/observer 90%). Baseline changes in fetal heart rate (greater than or equal to 10 beats/min) were observed in 46% of preterm fetuses and 70% of term fetuses. Tachycardia (fetal heart rate greater than 160 beats/min) was a common finding in both groups. In group A, tachycardia after vibratory acoustic stimulation persisted more than 1 minute in 29.2% and more than 5 minutes in 12.5% of patients. In group B tachycardia beyond 1 and 5 minutes was noted in 73.3% and 50% of patients, respectively. A significant shift to "awake" fetal heart rate patterns occurred in both groups; 29% to 79% was noted in group A (p less than 0.001) and 46.7% to 90% in group B (p less than 0.001). When vibratory acoustic stimulation was used, the high occurrence of increased baseline, tachycardia, and emergence of unusual fetal heart rate patterns must be recognized to adequately interpret fetal heart rate tracings.

Acoustic Stimulation↗
PubMedDate not supplied

Concurrent assessment of acoustic startle and auditory P50 evoked potential measures of sensory inhibition.

The acoustic startle response (ASR) and midlatency auditory evoked potentials (AEP) have been utilized in the measurement of sensory inhibition. Using these different paradigms, abnormalities suggesting a lack of normal inhibition have been noted in a number of psychiatric syndromes. To date, the most commonly used sensory inhibition paradigms have not been studied in the same individuals, making generalizations across studies tenuous. In this report, reduction of ASR over multiple trials (habituation), prepulse inhibition (PPI) of ASR (decrease in ASR caused by low intensity prepulses) and P50 suppression (P50 AEP amplitude reduction in a paired-click paradigm) were measured in the same individuals. Relationships between these measures of acoustic startle and AEP inhibition were then assessed. Twenty subjects with no personal history of psychiatric disorder were tested and exhibited significant habituation and PPI of ASR as well as P50 suppression. Habituation of ASR was significantly and positively correlated with P50 suppression early, but not late, in AEP testing. Only a modest trend for a positive association between PPI and P50 suppression was noted. Habituation and PPI of startle were both highly correlated (positively) with P50 AEP amplitude. Habituation of startle remained significantly predictive of P50 suppression after controlling for P50 amplitude, whereas the modest association between PPI and P50 suppression was removed when P50 amplitude was factored out. Results indicate that habituation of acoustic startle, but not PPI, is highly associated with P50 suppression in control subjects. An unexpected finding was a robust positive correlation between P50 amplitude and both measures of startle inhibition. These findings and methodologic issues are discussed in terms of possible neural substrates involved in different measures of sensory inhibition.

Acoustic Stimulation↗
PubMed1981

Acoustically driven thermal-identified neurons in the preoptic area of unanesthetized rabbits.

The convergence of acoustically stimulated neural activity onto central and peripheral thermal-stimulated neurons in the preoptic/anterior hypothalamus (POAH) was studied in the unanesthetized rabbit. POAH single units were either directly thermally stimulated with a water-perfused thermode, or indirectly stimulated by warming the ears with an infrared lamp. There was no statistical distinction in the way central thermal-stimulated neurons responded to an 89 dB, 510 Hz sound pulse. There was a significant interaction in the response of neurons inhibited by skin heating (cold-responsive) to acoustic stimulation with 52% facilitated, 33% inhibited and 15% unaffected. It is possible that some neurons in the POAH are part of a common pathway leading to an activation of thermal- and acoustically-induced changes in motor activity.

Acoustic Stimulation↗
PubMed1988

Binaural acoustic stimulation exercises protective effects at the cochlea that mimic the effects of electrical stimulation of an auditory efferent pathway.

Low-level acoustic stimulation of one (contralateral) ear reduced the neural desensitization caused by a simultaneous loud sound exposure in the other (ipsilateral) ear in a loss-related manner. Greatest reductions in the temporary threshold shifts (TTS) in the exposed ear were obtained when the exposure would have caused large amounts of TTS. Low-level exposures (reduced intensity or duration of exposure) which caused low levels of TTS, from which the cochlea could recover relatively quickly, were not affected by the contralateral stimulus. Intermediate levels of TTS showed intermediate levels of reduction for the same contralateral acoustic stimulus. These effects were similar to effects previously demonstrated with electrical stimulation of an efferent pathway to the cochlea, the crossed olivocochlear bundle (COCB); lesioning the COCB prevented the contralateral stimulus from having any effect on TTS due to an ipsilateral exposure. Like COCB stimulation, the contralateral acoustic stimulus had tonic effects, so that reductions in ipsilateral TTS could be obtained even when the contralateral stimulus was presented 5 min before the ipsilateral exposure. With 10 min delay no effect on TTS occurred. The contralateral stimulus did not appear to cause any changes in responses in the ipsilateral cochlea prior to the loud sound exposure. These results are discussed as indicating an interaction between the two inputs at a central locus, leading to activation of the COCB fibres to the cochlea exposed to the loud sound.

Acoustic Stimulation↗
PubMed1988

Excitatory amino acid antagonists depress acoustic startle after infusion into the ventral nucleus of the lateral lemniscus or paralemniscal zone.

Rats were implanted with bilateral cannulas in an area just medial to the ventral nucleus of the lateral lemniscus, an obligatory relay along the acoustic startle pathway. Bilateral infusions of excitatory amino acid transmitter antagonists into this region (10, 25 or 50 nmol per side) produced a rapid, dose-dependent depression of acoustic startle. gamma-D-Glutamylglycine, gamma-D-glutamylaminomethyl sulfonate and 2-amino-5-phosphonovalerate were equally effective in depressing the startle response over this dose range. These results indicate that excitatory amino acid transmitters play an important role in the expression of acoustic startle at this part of the startle pathway.

2-Amino-5-phosphonovalerate↗
PubMed1990

Gastrin, cholecystokinin and their precursors in acoustic neuromas.

Using sequence-specific radioimmunoassays the occurrence of 4 neuropeptides (cholecystokinin (CCK), gastrin, somatostatin, substance P and some of their precursors) was examined in 19 human acoustic nerve tumors and corresponding normal tissue. The normal acoustic nerve tissue obtained by autopsy contained traces of CCK, somatostatin, and substance P (less than or equal to 0.5 pmol/g), but neither proCCK, gastrin nor progastrin. In contrast 8 tumors expressed proCCK (range 0.2-4.5 pmol/g), 3 tumors gastrin (0.1-7.3 pmol/g) and 14 tumors progastrin (0.6-2.2 pmol/g). Traces of somatostatin were present in two and substance P in one tumor. The results show that acoustic neuromas often express the homologous CCK and gastrin genes, but process their propeptides poorly to transmitter-active peptides. The tumor synthesis of gastrin/progastrin contrasts to the rare, sporadic expression of the gastrin gene in normal nerve tissue.

Adult↗
PubMed1990

Lesions producing REM sleep without atonia disinhibit the acoustic startle reflex without affecting prepulse inhibition.

This study determined whether the brainstem motor inhibition system that mediates muscle atonia during rapid eye movement (REM) sleep is involved in the elicitation and prepulse inhibition of the acoustic startle reflex. Electrolytic or neurotoxic (glutamate) lesions were made in the dorsolateral pontine tegmentum or the medial medulla, respectively, to produce the syndrome of REM sleep without atonia. Startle responses were released during REM sleep following the lesions. However, the amount of startle suppression produced by auditory prepulse after the lesion did not differ from that seen in intact controls. We conclude that REM sleep suppression of the acoustic startle responses is mediated by the system responsible for tonic motor inhibition, but auditory prepulse inhibition of the acoustic startle is not.

Animals↗
PubMed1990

Differential blockade of early and late components of acoustic startle following intrathecal infusion of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or D,L-2-amino-5-phosphonovaleric acid (AP-5).

The present study investigated the individual contributions of spinal cord N-methyl-D-aspartate (NMDA) and non-NMDA receptors to the acoustic startle reflex in rats. The first experiment measured whole body acoustic startle before and after intrathecal infusion of various doses of either the NMDA receptor antagonist, D,L-2-amino-5-phosphonovaleric acid (AP-5), or the non-NMDA antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Both compounds depressed startle in a dose-dependent fashion with similar potencies. A second experiment measured startle electromyographically (EMG) in the quadriceps femoris muscle complex in the hindlimbs during auditory stimulation to characterized the effects of these two compounds on the early (approximately 8 ms) or late (approximately 15 ms) EMG components of the startle response. CNQX preferentially blocked the early EMG component of startle, whereas AP-5 preferentially blocked the late component. These results suggest that the acoustic startle reflex involves an early EMG component mediated by spinal non-NMDA receptors, and a late EMG component mediated by spinal NMDA receptors.

2-Amino-5-phosphonovalerate↗