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We recorded auditory evoked magnetic responses with a whole-scalp 122-channel SQUID neuromagnetometer in 14 patients with Bell's palsy (9 with left-sided and 5 with right-sided) and in 10 controls. The stimuli were 50-ms 1-kHz tone bursts, delivered first to the left and then to the right ear at interstimulus intervals (ISIs) of 1, 2 and 4 s. In patients, the N100m, the 100-ms response originating in the auditory cortices peaked, on average, 8 ms earlier and the response strengths were, on average, 7 nAm stronger over the contralateral than ipsilateral hemisphere. The response latencies and strengths did not differ significantly from those of controls and there were no significant differences in response latencies and strengths between the stimulation of the affected and healthy side. On average, the response latencies and strengths increased as a function of ISI over both hemispheres both in patients and in controls. These findings suggest that Bell's palsy is an isolated peripheral neuropathy that does not affect the function of the auditory pathways.

We recorded auditory evoked magnetic fields from five patients with profound unilateral sensorineural hearing loss from early childhood, using a 122-channel whole-scalp neuromagnetometer. The stimuli were 50-ms 1-kHz tone bursts delivered to the healthy ear at interstimulus intervals (ISI) of 1, 2, and 4 s. As the normal-hearing controls, four patients had shorter latencies of N100m, the 100-ms response, over the hemisphere contralateral to the stimulation than over the ipsilateral hemisphere. With 1-s ISI, three patients had, instead of N100m, a deflection of opposite polarity at about 100 ms (P100m) after the stimulus onset. A 10-year-old patient had a prominent P100m response, did not produce a clear N100m at any ISI, but had a clear N50m at the 4-s ISI. Four patients had bilateral N200m deflections peaking about 200 ms after the stimulus onset; the fifth patient showed N200m over the right hemisphere. N200m was also observed in the three youngest controls in both hemispheres. The ISI dependence of N100m amplitude and latency was similar in controls and patients. The amplitudes and latencies of N200m did not show any ISI dependence. In patients, the appearance of P100m-N200m deflections of auditory evoked fields, normally present in children, is more pronounced than in controls. The defect apparently delays the development of N100m, possibly by interfering with function of callosal connections.

Cortical signals associated with infrequent tone omissions were recorded from 9 healthy adults with a whole-head 122 channel neuromagnetometer. The stimulus sequence consisted of monaural (left or right) 50-ms 1-kHz tones repeated every 0.2 or 0.5 s, with 7% of the tones randomly omitted. Tones elicited typical responses in the supratemporal auditory cortices. Omissions evoked strong responses over temporal and frontal areas, independently of the side of stimulation, with peak amplitudes at 145-195 ms. Response amplitudes were 60% weaker when the subject was not attending to the stimuli. Omission responses originated in supratemporal auditory cortices bilaterally, indicating that auditory cortex plays an important role in the brain's modelling of temporal characteristics of the auditory environment. Additional activity was observed in the posterolateral frontal cortex and in the superior temporal sulcus, more often in the right than in the left hemisphere.

Auditory motion can be simulated by presenting binaural sounds with time-varying interaural intensity differences. We studied the human cortical response to both the direction and the rate of illusory motion by recording the auditory evoked magnetic fields with a 122-channel whole-head neuromagnetometer. The illusion of motion from left to right, right to left, and towards and away from the subject was produced by varying a 6-dB intensity difference between the two ears in the middle of a 600-ms tone. Both the onset and the intensity transition within the stimulus elicited clear responses in auditory cortices of both hemispheres, with the strongest responses occurring about 100 ms after the stimulus and transition onsets. The transition responses were significantly earlier and larger for fast than slow shifts and larger in the hemisphere contralateral to the increase in stimulus intensity for azimuthal shifts. Transition response amplitude varied with the direction of the simulated motion, suggesting that these responses are mediated by directionally selective cells in auditory cortex.

Neuromagnetic responses were recorded over the whole head with a 122-channel gradiometer. A pair of 150-ms 1-kHz tones separated by an interval of 150 ms was presented to one ear every 2 s. The other ear received either no input, an identical pair simultaneous to the first, an identical pair alternating with the first or a continuous 600-ms tone. The 'monaural shift' condition in which stimuli alternated between ears produced a clear perception of changing lateralisation, but the evoked response could be explained as merely the sum of simple monaural onset and offset responses; thus we found no evidence for a separate response to interaural intensity difference in this condition. The 'binaural shift' condition, in which intensity changed in one ear while the other received a continuous tone, evoked a transient response (N130m) at a latency of about 130 ms. N130m was larger over the hemisphere contralateral to the direction of shift, and larger than the corresponding monaural response, whether to an onset or an offset. We concluded that N130m also was not a separate directional response, but was analogous to a simple monaural response, the prolonged latency being due to masking and the enhanced amplitude to facilitation by the sustained response to the continuous tone.

To determine if interaural time differences (ITDs) in binaural stimuli affect the middle-latency auditory evoked fields (AEFs) in the same manner as they affect the N100m deflection, neuromagnetic responses were recorded over the whole head using a 122-channel SQUID magnetometer. Binaural stimuli were lateralized to three positions, left, midline, and right, on the basis of ITDs. The N100m was significantly larger to stimuli with contralaterally-leading ITDs than to stimuli with no, or with ipsilaterally-leading ITDs. Neither the P30m nor the P50m deflections of the middle-latency response were significantly affected by ITD, although the P30m showed a tendency, similar to but smaller than that of N100m, to be larger to stimuli with contralaterally-leading ITDs. In some subjects, the source location of the P50m was anterior and inferior to the sources of the P30m and N100m, which are generated in the superior surface of the temporal lobe. Sound-related muscular artifacts were seen in the posterior recording channels of one subject, and the contribution of this activity to the signals over the temporal area was determined.

We recorded auditory evoked magnetic fields from 6 patients with congenital unilateral conductive hearing disorder with a 122-channel whole-head neuromagnetometer. The stimuli were 50-ms 1-kHz tones delivered to the better ear at interstimulus intervals (ISIs) of 2 and 8 s at two different intensities (50 and 70 dB HL). As in normal-hearing subjects, the amplitudes of N100m, the 100-ms response, were larger in 5 patients and the latencies were shorter in 3 patients over the hemisphere contralateral to stimulation. However, in one patient N100m peaked already at 61 ms over the contralateral hemisphere and amplitudes were larger over the ipsilateral hemisphere, possibly reflecting reorganization of the auditory pathways. In 3 patients the latencies were shorter over the ipsilateral hemisphere. The effects of ISI and intensity were similar over both hemispheres and did not differ from those in controls. It seems that congenital unilateral conductive hearing loss does not necessarily lead to any gross disturbances in the human auditory cortex.

We recorded neuromagnetic evoked responses from the right auditory cortex of 7 healthy adults with a 24-channel planar SQUID gradiometer. The stimuli were 200-ms click trains presented at rates of 40, 80, 160 and 320 Hz, with interstimulus intervals (ISIs) of 1 and 4 s. The transient N100m response to the train onset depended on the click rate: the peak latency shortened to the same extent as the interval between successive clicks decreased in trains with rates from 40 Hz to 320 Hz. The N100m amplitude increased simultaneously, saturating at rates of 160-320 Hz. The mean N100m latency was slightly longer with the 1-s than with the 4-s ISI for all click rates. The systematic changes of the N100m amplitude and latency according to click rate demonstrate the importance of temporal integration for N100m generation, and imply an integration time of 20-25 ms. The 20- and 40-Hz click trains also elicited oscillatory 40-Hz responses 80-250 ms after the train onset. The 40-Hz responses were more resistant than N100m to changes of the ISI, and their sources slightly differed from those of N100m. These two responses evidently reflect different aspects of auditory processing.

Auditory evoked magnetic fields to noise/square-wave sequences, presented once every 2.2 seconds, were recorded in 8 patients who had ischemic lesions in the auditory cortex or in its vicinity. In 2 patients with large temporoparietal lesions, the magnetic 100-msec deflection (N100m) was absent over the damaged side. In 1 patient with a large but less deep frontotemporal lesion, a small N100m could be discerned on the defective side. Frontal lesions or small lesions in the vicinity of the supratemporal plane had no effect on N100m. Auditory evoked magnetic field recordings may be useful in clinical studies of auditory cortical functions.

Responses to 350 ms trains of clicks with 10-100 Hz repetition rate were recorded from the auditory cortices of six cats. Click trains of 30-50 and 90-100 Hz elicited a clear steady-state response (SSR) in awake state. SSRs were small or absent below 30 Hz and in 60-70 Hz stimulus range. In slow wave sleep the optimal rate to elicit SSR shifted towards lower frequencies. 90 Hz SSR was largest in paradoxical sleep. SSRs were strongly suppressed by barbiturate anesthesia. The amplitude of the SSR from the medial geniculate body (MGB) in two cats gradually decreased from 20 to 100 Hz and was more resilient to barbiturate anesthesia than the cortical SSRs. Only low amplitude or no SSRs could be recorded from vertex, visual and association cortices and from the hippocampus in control recordings. The results suggest different generation mechanisms for SSRs recorded from cat auditory cortex and MGB. Human auditory SSRs resemble cat auditory cortical SSRs more than those recorded from cat MGB. The results imply that auditory SSRs in humans are generated in the cortex.

We have studied the effect of selective listening on the neuromagnetic evoked activity of the human auditory cortex. In the word categorization experiment the stimuli were 5-letter words, each beginning with (k). Half of them were targets, i.e., names of animals or plants, and half other meaningful Finnish words. In the duration discrimination experiment equiprobable tones of 425 ms (targets) or 600 ms duration were presented. In both experiments the interstimulus interval (ISI) was 2.3 s and the stimuli of the two classes were presented randomly. Subjects either ignored the stimuli (reading condition) or counted the number of targets (listening condition). The magnetic field over the head was measured with a 7-channel 1st-order SQUID-gradiometer. The stimuli evoked a transient response followed by a sustained field. The transient response did not differ between the two conditions but the sustained field was significantly larger in the listening than reading condition; the increase began 120-200 ms after stimulus onset and continued for several hundred milliseconds. The equivalent source locations of both transient and sustained responses agreed with activation of the supratemporal auditory cortex. In the dichotic listening experiment 25-ms square-wave stimuli were presented randomly and equiprobably either to the left or to the right ear at an ISI of 0.8-1 s, either alone or in presence of a speech masker. Counting the stimuli of either ear resulted in differences between responses to relevant and irrelevant sounds. The difference began 140-150 ms after stimulus onset and peaked at 200-240 ms. During monaural speech masking, N100m was larger for attended than ignored stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

We have measured auditory evoked magnetic fields to intermittent frequency and amplitude modulations (FMs and AMs) of a continuous tone in 6 healthy humans. The stimuli were presented in pairs separated by 500 ms in four different combinations (FM-AM, FM-FM, AM-FM and AM-AM). Both modulations elicited neuromagnetic responses of similar waveforms: the largest deflection, N100m (magnetic counterpart of the electric N100), was preceded by a low amplitude P60m and followed by P200m. For stimuli of different types, the decrease of N100m from the first to the second response was less than expected from the recovery cycle of the responses, estimated from the pairs of similar stimuli. We interpret these results as evidence for different processing of amplitude and frequency modulations in the auditory pathways up to the level of supratemporal auditory cortex.

Cortical sources of neuromagnetic responses to noise bursts were compared in 7 healthy humans. The earliest response, P40m, peaking about 40 ms after the stimulus onset, was followed by a prominent deflection in the opposite direction at about 100 ms (N100m) and by another peak at 200 ms (P200m). A sustained field, seen near the end of the 400- to 550-ms stimuli, ended with an off-response of the same polarity as N100m. All deflections could be explained by cortical activity within the Sylvian fissure. The source of P200m was anterior to other sources of the on-response, except P40m. When noise bursts, or pauses of equal duration in a continuous noise were presented to the subject, striking similarities were found between the 100-ms deflections of the on- and off-responses: both peaked at about the same latency; their estimated sources were closed to each other in the supratemporal plane and their amplitudes depended in a similar way on the interstimulus interval (1.1-8.8 s). However, only the on-response was preceded by P40m, suggesting that P40m and N100m are not causally linked. N100m seems to reflect cortical activity related to any abrupt change in the auditory environment.

We have recorded cerebral electric and magnetic responses to electric stimulation of the auditory nerve in a deaf patient with multichannel cochlear prosthesis. The electric response peaked with a vertex-negative deflection at 65 ms. Clear magnetic responses, coinciding with the vertex potential, were obtained only over the hemisphere ipsilateral to the stimulation; the field pattern indicated activation of the auditory cortex within the Sylvian fissure. The results suggest modification of the central auditory pathways in this patient deaf from early childhood.

We recorded evoked magnetic fields from the human auditory cortex to noise/square wave sequences. Two prominent deflections were observed: one 100 msec after the noise onset (N100m) and another 100 msec after the noise/square wave transition (N100m'). The amplitude of N100m' increased with decrease in square wave frequency from 2 kHz to 0.125 kHz and with increase in square wave duration from 4 msec to 200 msec. The latency of N100m' was on the average 23 msec longer for noise durations of 60 msec than 310 msec, whereas the amplitude of N100m' did not change. Increase in interstimulus interval from 1.1 to 8.8 sec enhanced the amplitude of N100m significantly more than that of N100m'. The small interaction between N100m and N100m' and their different recovery cycles suggest that different activation patterns underlie these two 100 msec responses at the auditory cortex.

We have recorded middle-latency magnetic evoked responses to 50-ms noise bursts, presented once every 0.9 s, over the right hemisphere of healthy humans. The measurements were carried out with a sensitive 7-channel SQUID gradiometer with a passband of 0.5-2000 Hz. The response consisted of peaks at about 30, 50 and 65 ms. The location of the equivalent source of the 30-ms deflection agrees with activation of the supratemporal auditory cortex, slightly anterior to the source area of the well-known 100-ms deflection.

Auditory evoked magnetic fields were recorded over the right hemisphere of healthy humans. The stimuli were noise bursts presented either to the contra- (C) or ipsilateral (I) ear in different combinations. The largest deflection of the responses, N100m (magnetic counterpart of electric N100), showed a field pattern which suggests activation of the supratemporal auditory cortex. In an oddball paradigm, where the standards (90%) were 400-ms noise bursts presented to the contralateral ear, and the deviants (10%) similar stimuli to the ipsilateral ear, the deviants elicited on the average 130% stronger equivalent dipoles for N100m than standards. Contralateral standards did not substantially decrease the response amplitude of ipsilateral deviants as compared with the response amplitude to ipsilateral stimuli alone presented at the interstimulus interval of the deviants. When two 50 ms noise bursts, separated by 310 ms, were presented once every 2 s, N100m evoked by the second stimulus of the pair was smaller when the stimuli were presented monaurally (C-C or I-I) than to different ears (I-C or C-I). The results suggest that contra- and ipsilateral auditory stimuli are analyzed, at least in part, in different neural networks at the human auditory cortex.

We have recorded electric potentials and neuromagnetic fields evoked by electric stimulation of the auditory nerve in a totally deaf patient with an implanted multichannel prosthesis. The evoked electric responses were a vertex-negative deflection at about 70 ms after stimulus onset and a vertex-positive deflection at about 180 ms. Evoked magnetic responses coinciding with the vertex potential were found in the right hemisphere, ipsilateral to the stimulated ear. The equivalent source of these responses corresponds to activation of the right auditory cortex. In the left hemisphere, the magnetic responses were considerably smaller and less reliable. These results suggest an abnormality of the central auditory pathways in this patient. In the future, neuromagnetic recordings might be used preoperatively to forecast the effectiveness of the possible implantation.

We have studied the effects of masking sounds on auditory evoked magnetic fields (AEFs) of healthy humans. The AEFs were elicited by 25-ms tones presented randomly to the left or to the right ear, and the responses were recorded over the right auditory cortex. Without masking, the 100-ms deflection (N100m) was of somewhat higher amplitude and of shorter latency for contra- than ipsilateral stimuli. Continuous speech, music, or intermittent noise, delivered to the left ear, dampened N100m to stimulation of both ears without correlated changes in sensation. Intermittent noise had a weaker effect on N100m than speech or music. Continuous noise fed to the left ear dampened both the sensation of and the responses to the left-ear stimuli, with no significant effect on the responses to the right-ear stimuli. The results suggest that the masking effects of continuous noise, seen at the auditory cortex, derive mainly from the periphery whereas the effects of sounds with intensity and frequency modulations take place at more central auditory pathways.

Auditory evoked magnetic fields were recorded over the right hemisphere of healthy humans The stimuli were noise bursts presented either to the contra- (C) or ipsilateral (I) ear in different combinations. The largest deflection of the responses, N100m (magnetic counterpart of electric N100), showed a field pattern which suggests activation of the supratemporal auditory cortex. In an oddball paradigm, where the standards (90%) were 400-ms noise bursts presented to the contralateral ear, and the deviants (10%) similar stimuli to the ipsilateral ear, the deviants elicited on the average 130% stronger equivalent dipoles for N100m than standards. Contralateral standards did not substantially decrease the response amplitude of ipsilateral deviants as compared with the response amplitude to ipsilateral stimuli alone presented at the interstimulus interval of the deviants. When two 50 ms noise bursts, separated by 310 ms, were presented once every 2 s, N100m evoked by the second stimulus of the pair was smaller when the stimuli were presented monaurally (C-C, or I-I) than to different ears (I-C or C-I). The results suggest that contra- and ipsilateral auditory stimuli are analyzed, at least in part, in different neural networks at the human auditory cortex. [ABSTRACT FROM AUTHOR]