Acoustic startle reflex and pre-pulse inhibition in tinnitus patients

Gap induced pie-pulse inhibition(Gap-PPI) of acoustic startle reflex has been used as a measurement of tinnitus in animal models.However,whether this test is sensitive to detect tinnitus in humans is still unclear.Based on the testing procedure used in animal studies,a human subject testing method was formulated and conducted to investigate if a similar result could be found in tinnitus patients.Audiologic and tinnitus assessments and acoustic startle reflex measurements were performed on seven tinnitus subjects and nine age matched subjects without tinnitus.There was no significant difference found between the control and tinnitus group on the Gap-PPl across the frequencies evaluated.The amplitude of the startle response in the tinnitus group with normal hearing thresholds was significantly higher than the control group and those with tinnitus and hearing loss.This preliminary result suggests that hyperexcitability in the central auditory system may be involved in tinnitus.There was no correlation between hearing thresholds and the increased amplitude of startle response.

Differences in P50 and prepulse inhibition of the startle reflex between male smokers and non-smokers with first episode schizophrenia without medical treatment

Backgorund Nicotine may improve schizophrenia patient＇s cognitive deficit symptoms.This study was to explore the chronic effects of smoking on prepulse inhibition of the startle reflex （PPI） and P50 in the patients with first-episode schizophrenia （FES）.Methods The event-related potentials （ERP） recording and analysis instrument made by Brain Products,Germany,was used to detect PPI and P50 in 49 male FES patients （FES group,n=21 for smokers and n=28 for non-smokers） and 43 normal male controls （control group,n=19 for smokers and n=24 for non-smokers）.Results Compared with normal controls,the FES group had prolonged PPI latency when elicited by single stronger stimulus （P ＜0.05）; the FES group had prolonged PPI latency and increased PPI amplitude （P ＜0.05,0.01） when elicited by weak and strong stimuli.The FES group had lower PPI inhibition rate than normal controls （P ＜0.05）.Compared with normal controls,the FES group had increased P50-S2 amplitude and increased amplitude ratio S2/S1 （both P ＜0.05）.In the control group,the smokers had a tendency of increase in P50-S2 amplitude （P ＞0.05） and shorter P50-S2 latency （P ＜0.05） than the non-smokers.The smokers had higher PPI amplitude than the non-smokers （P ＜0.05）.In the FES group,the smokers had higher P50-S1 amplitude,shorter P50-S2 latency,and higher amplitude ratio S2/S1 than the non-smokers （P ＜0.05,0.01）.The smokers had higher PPI amplitude than the non-smokers （P ＜0.05）.Conclusions There is obvious PPI and P50 deficits in schizophrenic patients.However,these deficits are relatively preserved in the smokers compared with the non-smokers,which suggests that long-term smoking might partially improve the sensory gating in schizophrenic patients.Whether this conclusion can be deduced to female patients requires further follow-ups.

ACOUSTIC STARTLE RESPONSE AFFECTED BY AGING AND CHOLINERGIC NEUROTRANSMITTERS

The acoustic startle response has been used to evaluate tinnitus and hyperacusis in animal models. Gap induced prepulse in- hibition of the acoustic startle reflex （gap-PPI） is affected by tinnitus and loudness changes. Since tinnitus and reduced sound tolerance are commonly seen in elderly, we measured gap-PPI in Fischer 344 rats, an aging related hearing loss model, at dif- ferent agcs： 3-5 months, 9-12 months, and 15-17 months. The startle response was induced by three different intensity of sound： 105, 95 and 85 dB SPL. Gap-PPI was induced by different duration of silent gaps from 1 to 100 ms. When thc startle was induced by 105 dB SPL sound intensity, the gap-PPI induced by 50 ms silent gap was significantly lower than those in- duced by 25 or 100 ms duration, showing a ＂notch＂ in the gap-PPI function. The ＂notch＂ disappeared with the reduction of startle sound, suggesting the ＂notch＂ may be related with hyper-sensitivity to loud sound. As the intensity of the stimulus de- creased, the appearance of the hyperacusis-like effect decreased more quickly for the youngest group of rats. We also tested scopolamine, a muscarinic acetylcholine receptor antagonist, and mecamylamine, a nicotinic acetylcholine receptor antago- nist, on the effect of gap-PPI. When scopolamine was administered, the results indicated no addition effect on the hyperacu- sis-like phenomenon in the two older groups. Mecamylamine, the nicotinic antagonist also showed effects on the appearance of hyperacusis on rats in different ages. The information derived from the study will be fundamental for the further research in determining the cause and treatment for hyperacusis.

Acoustic trauma-induced auditory cortex enhancement and tinnitus

There is growing evidence suggests that noise-induced cochlear damage may lead to hyperexcitability in the central auditory system(CAS)which may give rise to tinnitus.However,the correlation between the onset of the neurophysiological changes in the CAS and the onset of tinnitus has not been well studied.To investigate this relationship,chronic electrodes were implanted into the auditory cortex(AC) and sound evoked activities were measured from awake rats before and after noise exposure.The auditory brainstem response(ABR) was used to assess the degree of noise-induced hearing loss.Tinnitus was evaluated by measuring gap-induced prepulse inhibition(gap-PPI).Rats were exposed monaurally to a high-intensity narrowband noise centered at 12 kHz at a level of 120 dB SPL for 1 h.After the noise exposure,all the rats developed either permanent(>2 weeks) or temporary(<3 days) hearing loss in the exposed ear(s).The AC amplitudes increased significantly 4 h after the noise exposure.Most of the exposed rats also showed decreased gap-PPI.The post-exposure AC enhancement showed a positive correlation with the amount of hearing loss.The onset of tinnitus-like behavior was happened after the onset of AC enhancement.

A Study on the Effect of Risperidone on PPI and P50 Deficit in FirstEpisode and Chronic Patients with Schizophrenia

Objective To investigate the effect of atypical antipsychotics risperidone on prepulse inhibition of the startle reflex(PPI) and P50 deficit in first-episode and chronic patients with schizophrenia. Methods PPI and P50 were tested and compared in 81 first-episode acute schizophrenia patients and 92 chronic schizophrenia patients before and after the risperidone. Results There was no significant difference in PPI and P50 indices between the two groups before treatment(P>0. 05); 2) there was no significant correlation between PPI & P50 inhibition indices and PANSS score, onset frequency and disease course(P>0.05); 3) Except the significant group main effect for S2 amplitude in P50(P=0. 02), there was no significant change for main effect and interaction of the other P50 and PPI inhibition ratio indices after treatment(P>0. 05). The effect of risperidone on PPI and P50 measurement index had nothing to do with the curative effect. Conclusion There exists a deficit in sensory gating inhibition in both first-episode schizophrenia and chronic schizophrenia, which is relatively independent from disease course. The risperidone is not effective in improving PPI and P50 inhibition deficit.