Stimulus Intensity Levels Research Articles

Enhanced sympathetic reactivity associates with insulin resistance in the young Zucker rat

Somatosympathetic reflexes were studied in young hyperinsulinemic, insulin-resistant (Zucker fatty) rats (ZFR) and a related control (Zucker lean) strain (ZLR). Glucose metabolism was characterized by minimal model analysis of intravenous glucose tolerance test data. Seven-week-old ZFR (n=18) and ZLR (n=17) were studied under pentobarbital anesthesia. Mean body weight and plasma glucose and insulin concentration were significantly greater (P<0.05) in ZFR than in ZLR, whereas basal values of mean arterial pressure (MAP) and heart rate (HR) were not significantly different. Increments of MAP (DeltaMAP) and HR (DeltaHR) elicited by electrical stimulation of the sciatic nerve (5-s trains of 100 pulses, 0.5-ms pulse duration, 100- to 400-microA pulse intensity) were significantly higher (ANOVA, P<0.05) in ZFR at each level of stimulus intensity. Regression analysis showed a linear increase in DeltaMAP and DeltaHR with increasing sciatic nerve stimulus intensity. Pressor responses to phenylephrine after ganglionic blockade demonstrated that vascular reactivity to adrenergic stimulation is not increased in ZFR compared with ZLR. Thus this factor does not contribute to enhancement of somatosympathetic reflexes observed in this strain. Insulin sensitivity in ZFR was one-fourth (P<0.05) that in ZLR. These results suggest that stronger sympathetic nervous reactivity in ZFR is associated with a severe insulin-resistant state before the onset of hypertension and support the hypothesis that insulin-mediated stimulation of the sympathetic nervous system is involved in the development of cardiovascular diseases related to alterations of glucose metabolism.

Lorazepam-induced effects on silent period and corticomotor excitability

TMS studies on the CNS effects of benzodiazepines have provided contradictory results. The objective of this study is to describe the effects of lorazepam on silent period (SP) and corticomotor excitability. Twelve healthy male subjects (median age 35 years) were studied at baseline, following i.v. lorazepam administration and after reversal of the benzodiazepine effects with i.v. flumazenil. Lorazepam was given at a low-dose in one subject (0.0225 mg/kg bolus + 2 microg/kg/h infusion) and at a high-dose (0.045 mg/kg bolus + 2.6 microg/kg/h infusion) in the rest. Threshold (Thr) was measured at 1% steps. SPs were investigated with two complementary methods. First, SPs were elicited using a wide range of stimulus intensities (SIs) (from 5 to 100% maximum SI at 5% increments). At each SI, four SPs were obtained and the average value of SP duration was used to construct a stimulus/response (S/R) curve of SI versus SP .The resulting S/R curves were then fitted to a Boltzman function, the best-fit values of which were statistically compared for each experimental condition (i.e., baseline vs. lorazepam vs. flumazenil). Second, a large number of SPs (n=100) was elicited during each of the three experimental conditions using blocks of four stimuli with an intensity alternating between MT and 200% MT. This method was employed so as to reveal the dynamic, time-varying effects of lorazepam and flumazenil on SP duration at two stimulus intensity (SI) levels. MEP recruitment curves were constructed at rest and during activation and fitted to a Boltzman function the best-fit values of which were statistically compared for each experimental condition. Lorazepam at a low dose did not affect Thr, SP, or the active MEP recruitment curves. The high dose also had no effect on Thr and the active MEPs whereas the resting MEP recruitment curves were depressed post-lorazepam at the higher range of stimulus intensities. With regard to SP, the Max value of the S/R curve decreased from 251+/-4.6 ms at baseline to 215.2+/-3.1 ms post-lorazepam (P<0.01). V50 also decreased significantly (from 47.92+/-0.9% to 43.73+/-0.81%, P<0.01) whereas there was no significant change regarding slope and SP Thr. The statistical analysis of the SP S/R curves as well as the study of SPs at two SI levels revealed that lorazepam reduced SP duration when high intensity stimuli were used (>60%). In contrast, at low SIs a small increase in SP duration was noted post-drug. Enhancement of GABAergic inhibition by lorazepam results in a reduction of SP duration when high SIs is used. At the lower range of SIs, a small but statistically significant increase in SP duration is observed. The kinetic behavior of this phenomenon as well as the possible underlying mechanisms are discussed.

Lorazepam effects on silent period and corticomotor excitability

Materials and methods Twelve healthy male subjects (median age 35 years) were studied at baseline, following i.v. lorazepam administration and after reversal of the benzodiazepine effects with i.v. flumazenil. Lorazepam was given at a low-dose in one subject (0.0225 mg/kg bolus + 2 μg/kg/h infusion) and at a high-dose (0.045 mg/kg bolus + 2.6 μg/kg/h infusion) in the rest. Threshold (Thr) was measured at 1% steps. SPs were investigated with two complementary methods. First, SPs were elicited using a wide range of stimulus intensities (SIs) (from 5 to 100% maximum SI at 5% increments). At each SI, 4 SPs were obtained and the average value of SP duration was used to construct a stimulus/ response (S/R) curve of SI vs. SP. The resulting S/R curves were then fitted to a Boltzman function, the best-fit values of which were statistically compared for each experimental condition (i.e., baseline vs. lorazepam vs. flumazenil). Second, a large number of SPs was elicited during the three experimental conditions using blocks of 4 stimuli with an intensity alternating between MT and 200% MT. This method was employed so as to reveal the dynamic, time-varying effects of lorazepam and flumazenil on SP duration at two stimulus intensity (SI) levels. Finally, active MEP recruitment curves were constructed and fitted to a Boltzman function the best-fit values of which were statistically compared for each experimental condition.

Tetanic Stimulation of the Peripheral Nerve before Transcranial Electrical Stimulation Can Enlarge Amplitudes of Myogenic Motor Evoked Potentials during General Anesthesia with Neuromuscular Blockade

Neuromuscular blockade can suppress myogenic motor evoked potentials (MEPs). The authors hypothesized that tetanic stimulation (TS) of the peripheral nerve before transcranial stimulation may enhance myogenic MEPs during neuromuscular blockade. In the current study, the authors evaluated MEP augmentations by TS at different levels of duration, posttetanic interval, neuromuscular blockade, and stimulus intensity. Thirty-two patients undergoing propofol-fentanyl-nitrous oxide anesthesia were examined. Train-of-five stimulation was delivered to C3-C4, and MEPs were recorded from the abductor hallucis muscle. In study 1, TS with a duration of 1, 3, or 5 s was delivered at 50 Hz to the tibial nerve 1, 3, or 5 s (interval) before transcranial stimulation, and the effects of TS on MEP amplitude were evaluated. In study 2, TS-induced MEP augmentations were evaluated at the neuromuscular blockade level (%T1) of 50% or 5%. In study 3, MEP augmentations by TS at stimulus intensities of 0, 5, 25, and 50 mA were evaluated. The application of TS significantly enlarged the amplitudes of MEPs at the combinations of duration (3, 5 s) and interval (1, 3, 5 s) compared with those without TS. TS-induced MEP augmentations were similarly observed at %T1 of both 50% and 5%. TS-induced MEP augmentations were observed at stimulus intensities of 25 and 50 mA. The results indicate that TS of the peripheral nerve before transcranial stimulation can enlarge the amplitude of MEPs during general anesthesia with neuromuscular blockade. TS of the peripheral nerve can be intraoperatively applied as a method to augment myogenic MEP responses.

Differential generators for N20m and P35m responses to median nerve stimulation

To study the spatial and behavioral dynamics of cortical sources for N20m and P35m at varying stimulus intensities, we measured neuromagnetic cortical responses to left electric median nerve stimulation at the wrist in 17 male healthy adults. The stimulus intensity levels were individually determined according to sensory threshold (ST) for perceiving electric pulses. Using equivalent current dipole (ECD) modeling, we analyzed the peak latencies, amplitudes, and locations of ECDs from 14 subjects for N20m and P35m elicited at 2 ST, 3 ST, and 4 ST. Compared with N20m, P35m was localized 3.3 ± 0.6 mm more superiorly at 2–4 ST, and 2.9 ± 1.2 mm more medially at 3–4 ST. Superimposed over subjects' own MR images, N20m ECDs were localized in the area of 3b contralateral to stimulus side in all 17 subjects at 3 ST, whereas P35m ECDs were localized either in the postcentral (in 14 subjects) or in the precentral areas (in 3 subjects). We found no clear correlation between N20m and P35m in terms of peak latencies as well as the corresponding growth of activation strengths along with stepwise increase in stimulus intensity. Our results imply that the two early SEF components, N20m and P35m, have differential cortical generators, with distinctive neurophysiological behaviors in response to varying stimulus intensity levels.

Detecting CA1 short-term plasticity variations associated with changes in stimulus intensity and extracellular medium composition

Changes in STP characteristics in the CA1 hippocampal region have been studied using the Volterra–Poisson modeling approach. Random impulse trains stimuli were applied to the Schaffer collaterals of the CA1 hippocampus in vitro and population spike responses were recorded at the pyramidal cell body layer. The computed Volterra–Poisson kernels captured the nonlinear dynamics associated with the mechanisms underlying STP by identifying quantitatively the magnitude and the duration of facilitatory and depressive behavior. The variations in STP characteristics secondary to changes in the stimulus intensity level and the addition of chemicals to the in vitro preparation were reflected in the differences of the calculated Volterra–Poisson kernels. Increasing the stimulus intensity caused an increase in the value of the first-order kernel (mean of the population spike amplitude) and decreased the peak facilitation of the second-order kernel. Picrotoxin caused an increase in the mean of PS amplitude, an increase in peak facilitation value, and an increase in the magnitude of the depressive phase of the second-order kernel. Decreasing the extracellular calcium concentration caused a decrease in the value of the first-order kernel and increased the peak facilitation value of the second-order kernel. Finally, the ability of the Volterra–Poisson modeling approach to track STP changes was confirmed through the low normalized mean square error associated with the prediction of in-sample and out-of-sample responses.

Automatic analysis of auditory nerve electrically evoked compound action potential with an artificial neural network

The auditory nerve’s electrically evoked compound action potential is recorded in deaf patients equipped with the Nucleus ® 24 cochlear implant using a reverse telemetry system (NRT™). Since the threshold of the NRT response (NRT-T) is thought to reflect the psychophysics needed for programming cochlear implants, efforts have been made by specialized management teams to develop its use. This study aimed at developing a valid tool, based on artificial neural networks (ANN) technology, for automatic estimation of NRT-T. The ANN used was a single layer perceptron, trained with 120 NRT traces. Learning traces differed from data used for the validation. A total of 550 NRT traces from 11 cochlear implant subjects were analyzed separately by the system and by a group of physicians with expertise in NRT analysis. Both worked to determine 37 NRT-T values, using the response amplitude growth function (AGF) (linear regression of response amplitudes obtained at decreasing stimulus intensity levels). The validity of the system was assessed by comparing the NRT-T values automatically determined by the system with those determined by the physicians. A strong correlation was found between automatic and physician-obtained NRT-T values (Pearson r correlation coefficient >0.9). ANOVA statistics confirmed that automatic NRT-Ts did not differ from physician-obtained values ( F=0.08999, P=0.03). Moreover, the average error between NRT-Ts predicted by the system and NRT-Ts measured by the physicians (3.6 stimulation units) did not differ significantly from the average error between NRT-Ts measured by each of the three physicians (4.2 stimulation units). In conclusion, the automatic system developed in this study was found to be as efficient as human experts for fitting the amplitude growth function and estimating NRT-T, with the advantage of considerable time-saving.

Surface EMG recording of heteronymous reflex excitation of semitendinosus motoneurones by group II afferents

Objective A potent stretch reflex originates in muscle spindle secondary endings and is mediated by group II muscle afferents. Electrical stimulation of peripheral nerve could also induce group II facilitation, as found in single motor unit recordings for various nerve–muscle combinations in man. The aim of the present investigation was to use surface electromyogram (EMG) to record and to quantify heteronymous excitation of semitendinosus (ST) motoneurones by group II afferents of the tibial nerve. Methods This study included 20 healthy subjects. The conditioning stimulation of the tibial nerve was delivered at the popliteal fossa at two intensity levels and for two levels of ST contraction. EMG activity was recorded by surface electrodes placed over the ST muscle, and the averaged and rectified ST EMG signal was analyzed. Results We observed 4 periods of interest: a first period of prestimulus background EMG activity; a second period of early reinforcement of ST EMG activity starting 30 ms poststimulus and lasting for 35–45 ms; a third period of relative inhibition of ST contraction; a fourth period of late reinforcement of poststimulus ST EMG activity. Conclusions We hypothesized that the early period of facilitation was mainly related to heteronymous excitation of ST motoneurones by group II afferents on the basis of the following observations: (i) the amount of facilitation increased for a high stimulus intensity level, which was suitable for group II recruitment; (ii) the onset latency of this facilitation was consistent with the theoretically calculated latency of a group II-mediated reflex. Significance Surface EMG recording offers various advantages compared to single motor unit recording to study group II facilitation in the ST muscle. This technique could be applied in the future to confirm that heteronymous reflex excitation by group II afferents is enhanced in spastics and plays an important role in the development of lower limb spasticity.

Silent functional magnetic resonance imaging (FMRI) of tonotopicity and stimulus intensity coding in human primary auditory cortex.

The aims of this study were to determine the feasibility of obtaining auditory cortex activation evoked by pure tones presented at threshold and suprathreshold hearing levels, to evaluate tonotopicity of the primary auditory cortex, and to determine the effect of stimulus intensity on auditory cortex activation using silent functional magnetic resonance imaging (fMRI). Sixteen subjects with normal hearing underwent silent fMRI. An audiometer was used to deliver pure tones of 1000, 2000, and 4000 Hz to the left ear. Two levels of acoustic stimulation were used: 1). threshold, hearing level determined in the scanner room and 2). suprathreshold, 70 dB hearing loss (HL). Tonotopicity and stimulus intensity coding was assessed on the basis of the location, extent, and amount of the auditory cortex activation. The localization of activation moved to more medial and posterior regions of the primary auditory cortex as the frequency of the pure tone increased. Compared with a threshold stimulus, a suprathreshold stimulus evoked the same regions with increased spatial extent. The average increase in the right auditory cortex activation in response to suprathreshold stimulus was 57% at 1000, 51% at 2000, and 45% at 4000 Hz compared with that activated by the threshold stimulus. Silent fMRI can be used to evaluate auditory cortex activation using low-intensity stimuli. The level of stimulus intensity increases the amount of auditory cortex activation and influences the fMRI mapping of the tonotopic organization of the primary auditory cortex.

Differential effects of stimulus intensity on peripheral and neuromagnetic cortical responses to median nerve stimulation

To study the differential effects of tactile stimulus intensity on cortical and peripheral responses, we measured neuromagnetic cortical responses, compound muscle action potentials (CMAP), sensory nerve action potentials (SNAP), and the subjective estimation of tactile magnitude to electric median nerve stimulation at the wrist in 13 male healthy adults. The sensory perception threshold (ST) for electric pulses at wrist skin was determined and then various levels of stimulus intensity (1 ∼ 6 ST) were given to each subject. At 1 ST, only the P50m components of the primary somatosensory (SI) cortical responses were recorded. The second somatosensory (SII) cortical responses were saturated at 2 ST, while the SI responses reached maximum at 3 ST equivalent to the subjective threshold intensity for “strong” tactility. The CMAP and SNAP were maximum at 4–5 ST. At 2 ST, >70% of maximum SI responses were produced, whereas only <40% of maximum CMAP or SNAP responses were obtained. We concluded that the stimulus intensities for activating or saturating somatosensory cortical responses were lower than those for CMAP and SNAP. The differential intensity effects on cortical and peripheral responses suggest a polysynaptic organization underlying the central amplification for somatosensory cortical activation. The optimal intensity levels for producing maximum SI and SII responses were 3 and 2 ST, respectively. Compared with the SII, the SI plays a crucial role in the coding of the tactile stimulus intensity.

Functional MRI determination of a dose-response relationship to lower extremity neuromuscular electrical stimulation in healthy subjects.

Although empirical evidence supports the use of neuromuscular electrical stimulation (NMES) to treat physical impairments associated with stroke, the mechanisms underlying the efficacy of this modality are poorly understood. Recent studies have employed functional imaging to investigations of brain responses to median nerve stimulation. These studies suggest a dose-response relationship may exist between selected stimulation parameters and hemodynamic responses in sensorimotor regions. However, substantial gaps exist in this literature. The present study was designed to address these deficiencies. Ten healthy subjects participated. In phase one, four stimulus intensity levels were established: (1). sensory threshold [Th], (2). (MM-Th)x0.333+Th [low-intermediate level, LI], (3). (MM-Th)x0.666+Th [high-intermediate level, HI], and (4). maximal motor (MM). In phase two, subjects were scanned using a spiral-echoplanar imaging technique at each stimulus level. Image sets were analyzed to determine hemodynamic responses at the highest Pearson correlation level ( r) ascertained for each of five areas of interest (AOI): (1). primary sensory, (2). primary motor, (3). cingulate gyrus, (4). thalamus, and (5). cerebellum. ANOVA demonstrated significant main effects for BOLD signal amplitude ( p<0.05) changes in all AOI. Similarly, ANOVA showed significant differences in the volume of activation ( p<0.05) with increasing stimulus intensity in four AOI. Secondary analyses of pooled data showed increasing probabilities of activation at higher stimulus intensities within each AOI. Collectively, these data indicate a dose-response relationship exists between lower extremity NMES and brain activation in specific neural regions. The current results, while limited in their generalizability, are foundational for future studies of interventions using NMES.

Regulation of oxygen transport during brain activation: stimulus-induced hemodynamic responses in human and animal cortices

BackgroundThe correlation between regional changes in neuronal activity and changes in hemodynamics is a major issue for noninvasive neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and near-infrared optical imaging (NIOI). A tight coupling of these changes has been assumed to elucidate brain function from data obtained with those techniques. In the present study, we investigated the relationship between neuronal activity and hemodynamic responses in the occipital cortex of humans during visual stimulation and in the somatosensory cortex of rats during peripheral nerve stimulation.MethodsThe temporal frequency dependence of macroscopic hemodynamic responses on visual stimuli was investigated in the occipital cortex of humans by simultaneous measurements made using fMRI and NIOI. The stimulus-intensity dependence of both microscopic hemodynamic changes and changes in neuronal activity in response to peripheral nerve stimulation was investigated in animal models by analyzing membrane potential (fluorescence), hemodynamic parameters (visible spectra and laser-Doppler flowmetry), and vessel diameter (image analyzer).ResultsAbove a certain level of stimulus-intensity, increases in regional cerebral blood flow (rCBF) were accompanied by a decrease in regional cerebral blood volume (rCBV), i.e., dissociation of rCBF and rCBV responses occurred in both the human and animal experiments. Furthermore, the animal experiments revealed that the distribution of increased rCBF and O2 spread well beyond the area of neuronal activation, and that the increases showed saturation in the activated area.ConclusionsThese results suggest that above a certain level of neuronal activity, a regulatory mechanism between regional cerebral blood flow (rCBF) and rCBV acts to prevent excess O2 inflow into the focally activated area.

The stimulus intensity modifies the blink reflex recovery cycle in healthy subjects and in blepharospasm

Objective: The excitability of human brainstem interneurons is measured by the blink reflex recovery cycle and is abnormal in blepharospasm. We wondered whether the results of this paradigm depend on the stimulus intensity. Methods: We investigated the blink reflex recovery cycle in 13 healthy control subjects and in 13 patients with blepharospasm (7 of them treated with botulinum toxin) using 4 levels of stimulus intensity (5, 12, 19 and 26 mA) and two interstimulus intervals (ISIs, 150 or 250 ms). Results: In all groups the inhibition of the second R2 response was reduced with strong stimulus intensities: In controls, the inhibition of the second R2 decreased significantly (e.g. young controls, ISI 150 ms, from 89.6±15.6% at 5 mA to 21.9±49.7% at 26 mA, mean±standard deviation). In patients the R2 inhibition found at 5 mA was converted in an R2 facilitation at 26 mA, irrespective of the status of treatment. In addition, the patients’ results at 5 mA did not differ significantly from the controls’ results at 26 mA. Conclusions: The R2 inhibition and its sensitivity to detect abnormal interneuronal excitability depend on the stimulus intensity, which may act by modifying the excitability of the R2 interneurons.

Effect of Stimulus Intensity Level on Auditory Middle Latency Response Brain Maps in Human Adults

Auditory middle latency response (AMLR) brain maps were obtained in 11 young adults with normal hearing. AMLR waveforms were elicited with monaural clicks presented at three stimulus intensity levels (50, 70, and 90 dB nHL). Recordings were made for right and left ear stimulus presentations. All recordings were obtained in an eyes open/awake status for each subject. Peak-to-peak amplitudes and absolute latencies of the AMLR Pa and Pb waveforms were measured at the Cz electrode site. Pa and Pb waveforms were present 100 percent of the time in response to the 90 dB nHL presentation. The prevalence of Pa and Pb to the 70 dB nHL presentation varied from 86 to 95 percent. The prevalence of Pa and Pb to the 50 dB nHL stimulus never reached 100 percent, ranging in prevalence from 77 to 68 percent. No significant ear effect was seen for amplitude or latency measures of Pa or Pb. AMLR brain maps of the voltage field distributions of Pa and Pb waveforms showed different topographic features. Scalp topography of the Pa waveform was altered by a reduction in stimulus intensity level. At 90 dB nHL, the Pa brain map showed a large positivity midline over the frontal and central scalp areas. At lower stimulus intensity levels, frontal positivity was reduced, and scalp negativity over occipital regions was increased. Pb scalp topography was also altered by a reduction in stimulus intensity level. Varying the stimulus intensity significantly altered Pa and Pb distributions of amplitude and latency measures. Pa and Pb distributions were skewed regardless of stimulus intensity.

Feasibility of establishing an early indicator for ototoxicity in children using otoacoustic emissions

AbstractThe present study aimed to investigate the feasibility of establishing an early indicator for ototoxicity in children using OAEs. The participants included an experimental group of four pediatric oncology patients (aged 4 to 7 years) undergoing chemotherapy. Participants were tested at least, twice (the first test being the baseline) using pure-tone audiometry, tympanometry, distortion product otoacoustic emissions (DPOAEs) (with stimulus intensity levels of 65/55 and 50/40 dB SPL), and transient evoked otoacoustic emissions (TEOAEs). The difference in OAE measures between two tests were recorded and compared with the results obtained from a control group of 10 normal hearing children (mean age = 7.7 years, SD = 3.3 years) using the same test battery, which provided the test–retest reliability data. A change in OAEs between two consecutive tests for the four pediatric oncology patients was considered significant if it exceeded the mean plus 2 SD of that of the control group. The results indicated ...

Phasic Pupil Dilation Response to Noxious Stimulation

Abstract The pupil dilation response (PDR) to a painful stimulus is a subtle, event-related increase in pupil diameter that occurs following brief noxious stimulation. It varies in amplitude with increasing stimulus intensity. Two competing hypotheses for the PDR are that (1) it reflects event-related cognitive efforts largely independent of pain, such as the task demand of discriminating intensity and readying a subjective report; and (2) like the pupillary light reflex, it is a simple reflexive response. In this study 21 subjects (11 male, 10 female) experienced painful stimuli matched in subjective intensity at two sites: finger tip and ear lobe, but they produced no subjective reports. If the PDR is a product of discriminating stimulus intensity levels and forming a report, then it should be minimal or nonexistent when subjects have no choices and make no overt judgments. On the other hand, if it is primarily a simple sympathetic reflex, then onset and peak latency should be longer for finger tip than for ear lobe stimulation because the conduction distance is longer. In addition to addressing these issues, we explored sex differences and the influence of age. Clear and similar PDRs appeared in response to stimulation of both sites despite an absence of subjective report requirements. PDR onset, peak amplitude and peak latency did not differ significantly across stimulation sites. Therefore, the PDR is neither an artifact of subjective report nor an uncomplicated sympathetic reflex. It appears to be an emotional arousal response, such as the defense response, the strength of which depends upon the magnitude of the noxious sensory input. Sex differences emerged, with women demonstrating a borderline larger PDR peak amplitude than men (P = .059) and a more rapid half recovery latency (P = .031). Age did not affect the PDR except at onset, with older subjects demonstrating a later onset latency (P = .003). The PDR may reflect preconscious processing associated with attention and perhaps other cognitive aspects of perception.

Dynamic brain topography of somatosensory evoked potentials and equivalent dipoles in response to graded painful skin and muscle stimulation.

The differential effects of painful stimulation of skin vs. muscle on the cerebral electrophysiology have been poorly described. This study examined the somatosensory evoked potentials (SEPs) and the associated dipole models of non-painful and graded painful electrical stimulation applied to the skin and muscle in 20 healthy subjects. With the psychophysical stimulus-response functions determined, the skin stimulation showed a steeper slope than muscle stimulation. For both types of stimulation, the SEPs indicated a similar temporo-spatial activation sequence: F4/N90-P4/P95, Fc2/N135, Cz/P250, Cz/P300, and Cz/N460. The SEP amplitudes increased significantly with the stimulus intensities in these components. The peak SEP latencies of skin stimulation were in general shorter than that of muscle stimulation. The SEP amplitudes to skin stimulation were significantly larger than those caused by muscle stimulation at every stimulus intensity level, except the early mid-latency component. In this case, muscle stimulation caused higher amplitudes over the contralateral parietal-frontal sites. For both types of stimulation, the topographic maps were quite similar. Equivalent dipole modeling revealed identical site parameters (<1.0 cm) between skin and muscle stimulation. However, the electrical skin stimulation did not correlate with the pain intensity. Pain intensity, in contrast, was uniquely associated with the Cz/P250 amplitudes for the muscle stimulation. It is concluded that non-nociceptive and nociceptive electrical stimuli applied to skin and muscle are processed in the common cerebral areas, but exhibit differential SEP effects.

Auditory associative cortex dysfunction in children with autism: evidence from late auditory evoked potentials (N1 wave–T complex)

Objectives: Auditory processing at the cortical level was investigated with late auditory evoked potentials (N1 wave–T complex) in 4–8-year-old autistic children with mental retardation and compared to both age-matched normal and mentally retarded children (16 children in each group).Methods: Two negative peaks which occurred in the 80–200 ms latency range were analyzed according to stimulus intensity level (50 to 80 dB SPL): the first culminated at fronto-central sites (N1b) and the second at bitemporal sites (N1c, equivalent to Tb of the T complex). The latter wave was the most prominent and reliable response in normal children at this age.Results: Our results in autistic children indicated abnormalities of this wave with markedly smaller amplitude at bitemporal sites and pronounced peak latency delay (around 20 ms). Moreover, in both reference groups the intensity effect was found on both sides whereas in autistic children it was absent on the left side but present on the right.Conclusion: These findings in autistic children showing very disturbed verbal communication argue for dysfunction in brain areas involved in N1c generation i.e., the auditory associative cortex in the lateral part of the superior temporal gyrus, with more specific left side defects when auditory stimulus have to be processed.

The effects of varying stimulus intensity on P300 during REM sleep.

Event-related potentials (ERPs) are often used to measure the extent of information processing during sleep. Previous studies have indicated that a late positive wave, P300, can be elicited during REM sleep if stimuli are very rare and/or very loud. The present study examined the role of stimulus intensity in eliciting a P300 during REM sleep. Eight subjects were presented with auditory tone pips with an intensity of either 0, 60, 80 or 100 dB SPL. Stimuli were delivered at random with equal probability. Trials were sorted by stage of sleep, stimulus intensity, and presence or absence of rapid eye movements in REM sleep. During the waking state, when subjects read a book, the loud 100 dB stimulus elicited short (P3a) and long latency (P300) positive waves (peaking at 293 and 373 ms respectively). In stage of 2 non-REM sleep, N1 decreased to baseline level while P2 increased in amplitude compared to the waking state. A P300 could not be observed in stage 2 sleep regardless of the level of stimulus intensity. During REM sleep, a late P300 (latency 363 ms) was elicited by the 100 dB stimulus. The earlier positive peak (i.e. P3a) was not apparent. The P300 was reduced in amplitude compared to the waking state. Its amplitude did not differ between phasic and tonic states of REM sleep. A late parietal negative slow wave (SW) was also apparent during REM. Although the SW was larger during phasic compared to tonic REM, the difference was not significant. These data suggest that stimuli which are sufficiently intrusive to elicit a P300 in the waking state continue to do so in REM sleep.

Monaural response properties of single neurons in the chinchilla inferior colliculus

The responses of 274 inferior colliculus (IC) central nucleus neurons from 20 chinchillas were studied. Characteristic frequency (CF) increased as the IC was traversed in the dorsal-ventral direction. Most units had little or no spontaneous activity, with a mean threshold for response of about 30 dB SPL across all units. Tuning curve width varied between units, with a significant increase in Q 20 with increasing CF. Peri-stimulus time histogram (PSTH) types were similar to those reported for cat inferior colliculus units. Transient, sustained, pauser, and buildup types were observed, with transient responses predominating. Response area (RA) types were also similar to those of cat IC units, with most units displaying stable best frequencies across a range of stimulus intensity levels. For a few units, excitatory RA regions were surrounded by inhibitory sidebands. Nonmonotonic discharge rate vs. stimulus intensity level functions were common in all CF ranges and for all PSTH and RA types. Mean first spike latencies, however, differed across PSTH groups, owing to the temporal definitions of these PSTH shapes. Latencies of sustained units were significantly longer than those of transient units, and buildup PSTHs showed significantly longer latencies than any other group.