Late Cortical Responses Research Articles

Neuronal mechanisms of auditory backward recognition masking in macaque auditory cortex.

The sensation of a single sound event can be altered by subsequent sounds. This study searched for neural mechanisms of such retroactive effects in macaque auditory cortex by comparing neural responses to single tones with responses to two consecutive tones. Retroactive influences were found to affect late parts of the response to a tone, which comprised 53/134 of the recordings of action potentials and 88/131 of the recordings of field potentials performed in primary, caudal, and medial auditory fields. If before or during the occurrence of the late response to the first tone a second tone was presented the late response was suppressed. Suppression of late cortical responses parallels perceptual phenomena like backward recognition masking, suggesting that suppression of late responses provides a neural correlate of auditory backward effects.

Midazolam and flumazenil in neuroanaesthesia

Of the numerous benzodiazepines currently available, only a few are used in anaesthetic practice. Midazolam is utilised as a premedicant, sedative, and an induction agent and produces minimal depression of ventilation or of the cardiovascular system. The anticonvulsant activity is similar to that of diazepam. In neuroanaesthesia midazolam may be an acceptable alternative to other intravenous induction agents like barbiturates or etomidate in patients with compromised intracranial compliance. Midazolam produces dose-related reductions in cerebral blood flow and cerebral oxygen consumption. However, midazolam does not necessarily prevent increases in intracranial pressure during induction of anaesthesia. In the electroencephalogram (EEG) midazolam produces a reduction in alpha-activity, an increase in theta-delta-activity and low-voltage beta-activity. Midazolam like other benzodiazepines does not affect early components of auditory and somatosensory evoked responses, whereas late cortical responses may be suppressed. Flumazenil, a specific benzodiazepine antagonist, has been demonstrated to be effective in reversing benzodiazepine-induced sedation. In the EEG midazolam-induced changes vanish almost instantaneously. Flumazenil is also effective in restoring the amplitudes of cortical auditory and somatosensory evoked responses. However, as has been demonstrated in head-injured patients and animal experiments after incomplete cerebral ischaemia, increases in cerebral blood flow and intracranial pressure cannot be excluded after flumazenil administration. When utilising flumazenil for wake-up procedures in midazolam-sedated patients with pathological intracranial compliance, flumazenil has to be titrated very carefully in low doses over prolonged periods.

The effects of signal/masker phase conditions on the late cortical response

Previous investigations have produced indirect evidence of a coherent relationship between the presence and magnitude of the binaural masking level difference (MLD) and the pattern of monaural early auditory brainstem potentials exhibited by the same subjects. This investigation sought electrophysiologic changes corresponding to the presence or absence of behavioral MLD by monitoring via surface electrodes the late cortical potentials (P1, N1, P2, N2) aroused by signal/masker configurations known to produce an MLD. Tonal stimuli of 500 and 2000 Hz were presented binaurally along with binaural narrow-band noise centered at the test frequency under SoNo and SπNo signal/masker phase conditions. Twenty-five young (X̄ age: 24.6 yrs) normal-hearing subjects with normal ABR for 2000- and 4000-Hz tone pips and normal 500-Hz behavioral MLD were tested. A consistent and statistically significant increase in the amplitude and/or reduction in the latency of onset of the cortical potentials was evidenced for 500-Hz stimuli for the SπNo condition when compared to the SoNo condition. Such changes did not occur in response to 2000-Hz stimuli. [Work supported by NIH.]

Precentral unit activity following torque pulse injections into elbow movements

(1) Precentral neural activity was studied in relation to transient load changes on self-paced elbow movements. Four Cebus monkeys were trained to turn a freely moving handle back and forth between two targets by alternating self-paced elbow flexions and extensions. Torque pulses (of 10 or 100 msec) injected randomly to load or unload the movements stretched or slackened the appropriate prime movers: biceps or triceps. Perturbed movements oscillated at about 5.5 Hz but were completed successfully in about the same time as unperturbed movements. (2) Torque pulses evoked distinct ‘early’ responses with latencies of 20–40 msec in 134 out of 153 precentral neurons. Oppositely directed torque pulses evoked reciprocal ( i.e. increased or decreased) early responses in 61 neurons, and uniform responses in 27 neurons. (3) Early responses were followed by ‘late’ responses with peaks succeeding one another at about 5.5 Hz in 111 neurons, but another 16 exhibited late responses only. (4) Timing of both early and late cortical responses was tightly coupled to peripheral changes. Early responses were timed by the initial torque-induced passive elbow jerk. Timing of late responses was best related to subsequent peak decelerations or accelerations. Intensity of the early but not of all late precentral responses was tightly coupled to peripheral events. (5) Torque pulses that impeded flexions or extensions evoked spinal stretch reflexes in biceps or triceps with EMG latencies of about 15 msec, leading to an acceleration peak about 25 msec later. A second EMG burst followed the first in about 30 msec. The second burst occured about 20 msec after onset of the early precentral response, which is thought to have caused it, as well as a second acceleration peak that was seen about 60 msec after precentral response (for flexion load pulses). Peaks of late precentral responses were followed by acceleration peaks within about 70 msec. (5) An interaction akin to the spinal stretch reflex is thus revealed between elbow perturbations, early responses of precentral neurons and subsequent elbow movements: discharges of neurons that usually fire in relation to an intended movement can be altered by sudden load changes so that the neurons tend to reduce mismatch between intended and actual movements (cortical load compensation), created by the perturbation. An analogous interaction may also occur with late cortical responses.