Steady-state responses to tone amplitude-modulated at 75 to 110 Hz can be used for frequency-specific objective audiometry. The multiple-stimulus technique allows thresholds to be estimated for eight different stimuli at the same time.

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The ocular artifacts that contaminate the EEG derive from the potential difference between the cornea and the fundus of the eye. This corneofundal or corneoretinal potential can be considered as an equivalent dipole with its positive pole directed toward the cornea. The cornea shows a steady DC potential of approximately +13 mV relative to the forehead. Blink potentials are caused by the eyelids sliding down over the positively charged cornea. The artifacts from eye-movements result from changes in orientation of the corneo-fundal potential. The scalp-distribution of the ocular artifacts can be described in terms of propagation factors--the fraction of the EOG signal at periocular electrodes that is recorded at a particular scalp location. These factors vary with the location of the scalp electrode. Propagation factors for blinks and upward eye-movements are significantly different.

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Objective To describe the clinical, radiological, and electromyographic features in a series of children with joint contractures (arthrogryposis) associated with congenital infection presumably caused by Zika virus.Design Retrospective case series study.Setting Association for Assistance of Disabled Children, Pernambuco state, Brazil.Participants Seven children with arthrogryposis and a diagnosis of congenital infection presumably caused by Zika virus during the Brazilian microcephaly epidemic.Main outcome measures Main clinical, radiological, and electromyographic findings, and likely correlation between clinical and primary neurological abnormalities.Results The brain images of all seven children were characteristic of congenital infection and arthrogryposis. Two children tested positive for IgM to Zika virus in the cerebrospinal fluid. Arthrogryposis was present in the arms and legs of six children (86%) and the legs of one child (14%). Hip radiographs showed bilateral dislocation in seven children, subluxation of the knee associated with genu valgus in three children (43%), which was bilateral in two (29%). All the children underwent high definition ultrasonography of the joints, and there was no evidence of abnormalities. Moderate signs of remodeling of the motor units and a reduced recruitment pattern were found on needle electromyography (monopolar). Five of the children underwent brain computed tomography (CT) and magnetic resonance imaging (MRI) and the remaining two CT only. All presented malformations of cortical development, calcifications predominantly in the cortex and subcortical white matter (especially in the junction between the cortex and white matter), reduction in brain volume, ventriculomegaly, and hypoplasia of the brainstem and cerebellum. MRI of the spine in four children showed apparent thinning of the cord and reduced ventral roots.Conclusions Congenital Zika syndrome should be added to the differential diagnosis of congenital infections and arthrogryposis. The arthrogryposis was unrelated to the abnormalities of the joints themselves, but was possibly of neurogenic origin, with chronic involvement of central and peripheral motor neurones leading to deformities as a result of fixed postures in utero. Based on the neurophysiological observations, we suggest two possible mechanisms: tropism of neurones, with involvement of peripheral and central motor neurones, or a relation with vascular disorders.

The objective of this study was to localize the intracerebral generators for auditory steady-state responses. The stimulus was a continuous 1000-Hz tone presented to the right or left ear at 70 dBSPL. The tone was sinusoidally amplitude-modulated to a depth of 100% at 12, 39, or 88 Hz. Responses recorded from 47 electrodes on the head were transformed into the frequency domain. Brain electrical source analysis treated the real and imaginary components of the response in the frequency domain as independent samples. The latency of the source activity was estimated from the phase of the source waveform. The main source model contained a midline brainstem generator with two components (one vertical and lateral) and cortical sources in the left and right supratemporal plane, each containing tangential and radial components. At 88 Hz, the largest activity occurred in the brainstem and subsequent cortical activity was minor. At 39 Hz, the initial brainstem component remained and significant activity also occurred in the cortical sources, with the tangential activity being larger than the radial. The 12-Hz responses were small, but suggested combined activation of both brainstem and cortical sources. Estimated latencies decreased for all source waveforms as modulation frequency increased and were shorter for the brainstem compared to cortical sources. These results suggest that the whole auditory nervous system is activated by modulated tones, with the cortex being more sensitive to slower modulation frequencies.

The source dipoles for blinks point radially whereas the source dipoles for saccades point tangentially, in the direction of the eye movement. This indicates that blink potentials are not generated by eye movements but by the eyelid sliding down over the positively charged cornea. Dipole source dipole analysis shows that the "rider artifact" at the onset of upward and lateral saccades is caused by the eyelid as it lags a little behind the eyes at the beginning of the movement. Dipole source analysis allows both the EEG and the EOG to be modeled simultaneously and EOG generators to be distinguished from nearby EEG generators. Ocular source components can be calculated from a principal component analysis of EEG and EOG recordings during blinks and saccades. The effectiveness of propagation factors, source dipoles and source components in removing ocular artifacts from EEG samples was assessed. The most effective correction procedure uses source components.

Steady-state responses can be recorded from the human scalp in response to tones that are sinusoidally modulated in amplitude at rates between 60 and 120 Hz. For 60 dB SPL 1000-Hz tones the maximum baseline-to-peak amplitude of about 0.06 microV occurs for modulation rates between 80 and 95 Hz. The phase of the response does not change with modulation depths greater than 25% and the amplitude saturates at modulation depths greater than 50%. The presence or absence of a response can be accurately determined by frequency-domain statistics and the response becomes clearly recognizable at intensities that are 16 +/- 8 dB above behavioral thresholds. With increasing intensity the response increases in amplitude at 1.9 nV/dB until an intensity of 70 dB SPL. As the intensity increases above 70 dB SPL the response increases in amplitude more rapidly at 7.8 nV/dB (at 1000 Hz) and contains significant energy at harmonics of the modulation frequency. This second stage of the intensity function is more prominent for stimuli with lower carrier frequencies (500 more than 1000 more than 2000 Hz) and is attenuated by high-pass masking. These steady-state responses should be helpful in evaluating human auditory physiology and in objective audiometry.