Electroencephalographic evidence for a respiratory-related cortical activity specific of the preparation of prephonatory breaths.

Speech is a major disturbance to automatic breathing control. Speech occurs during exhalation, involving controlled inhibition of automatic inspiration. Additionally, utterances are preceded by prephonatory inspirations that must be prepared to account for prosody and loudness. We hypothesized that the speech-related breathing control activities shaping prephonatory breaths originate in cortical pre-motor areas and should be associated with corresponding EEG evidence. We studied 10 normal subjects (4 men, age 23-27) during spontaneous breathing, sniff manoeuvres, and while reading out loud. Fronto-median inspiratory potentials (Cz EEG derivation) were consistently present before voluntary inspirations and large prephonatory breaths, while these potentials were generally absent during resting breathing or small prephonatory breaths. We conclude that the preparation of prephonatory breaths during speech has a cortical substrate, involving the cortical sources of premotor potentials. These results have important implications to validate whether co-modulation of the pre-motor cortex and breathing during speech are incidental or whether these cortical modulations are necessary for initiation of "speech breathing".

Does the supplementary motor area keep patients with Ondine's curse syndrome breathing while awake?

BACKGROUND: Congenital central hypoventilation syndrome (CCHS) is a rare neuro-respiratory disorder associated with mutations of the PHOX2B gene. Patients with this disease experience severe hypoventilation during sleep and are consequently ventilator-dependent. However, they breathe almost normally while awake, indicating the existence of cortical mechanisms compensating for the deficient brainstem generation of automatic breathing. Current evidence indicates that the supplementary motor area plays an important role in modulating ventilation in awake normal humans. We hypothesized that the wake-related maintenance of spontaneous breathing in patients with CCHS could involve supplementary motor area. METHODS: We studied 7 CCHS patients (5 women; age: 20-30; BMI: 22.1 ± 4 kg.m(-2)) during resting breathing and during exposure to carbon dioxide and inspiratory mechanical constraints. They were compared with 8 healthy individuals. Segments of electroencephalographic tracings were selected according to ventilatory flow signal, from 2.5 seconds to 1.5 seconds after the onset of inspiration. After artefact rejection, 80 or more such segments were ensemble averaged. A slow upward shift of the EEG signal starting between 2 and 0.5 s before inspiration (pre-inspiratory potential) was considered suggestive of supplementary motor area activation. RESULTS: In the control group, pre-inspiratory potentials were generally absent during resting breathing and carbon dioxide stimulation, and consistently identified in the presence of inspiratory constraints (expected). In CCHS patients, pre-inspiratory potentials were systematically identified in all study conditions, including resting breathing. They were therefore significantly more frequent than in controls. CONCLUSIONS: This study provides a neurophysiological substrate to the wakefulness drive to breathe that is characteristic of CCHS and suggests that the supplementary motor area contributes to this phenomenon. Whether or not this "cortical breathing" can be taken advantage of therapeutically, or has clinical consequences (like competition with attentional resources) remains to be determined.

Simplified recording technique for the identification of inspiratory premotor potentials in humans.

Inspiratory premotor potentials reflect the involvement of premotor cortical networks in the compensation of mechanical respiratory loading. Electromagnetic pollution and movement artefacts make them difficult to record, particularly in clinical environment. In 7 healthy subjects, we tested a simplified recording setup (single vs. linked earlobe reference, bandwidth restriction from 0.05-500 to 0.1-500 Hz) to identify premotor potentials during volitional inspiratory manoeuvres. Pre-triggered ensemble averaging of Cz EEG epochs starting 2.5 s before the onset of inspiration was used to identify the potentials. The simplified setup reliably detected the potentials identified by the conventional setup (Cohen's Kappa score of 1). It slightly underestimated the slope of the potentials (P=0.0156). In conclusion, using a single earlobe reference and a restricted filtering bandwidth does not impair the detection of inspiratory premotor potentials. This could make the study of respiratory premotor potentials easier in difficult clinical environments.

Sustained preinspiratory cortical potentials during prolonged inspiratory threshold loading in humans.

Humans can program and control movements, including breathing-related movements. On the electroencephalogram (EEG), this preparation is accompanied by a low-amplitude negativity starting approximately 2.5 s before inspiration that is best known as a Bereitschaftspotential (BP). The presence of BPs has been described during the compensation of mechanical inspiratory loading, thus identifying a cortical involvement in the corresponding ventilatory behavior. The pathophysiological interpretation of this cortical involvement depends on its transient or enduring nature. This study addressed this issue by looking for BPs during sustained inspiratory loading (1 h). Nine healthy male volunteers were studied during unloaded quiet breathing and inspiratory threshold loading (with unloaded expiration). Analyses of EEG signal and ventilatory variables were used to compare beginning and end of sessions. Inspiratory threshold loading caused ventilatory modifications that persisted, unchanged, for an hour. The presence of a BP at the beginning and end of a session was the most frequent occurrence (6 of 9 cases with a 17-cmH2O threshold load; 8 of 9 cases with a 23-cmH2O load). These observations support the hypothesis that the cerebral cortex is involved in the compensation of sustained experimental inspiratory loading. How this translates to respiratory disease involving acute changes in respiratory mechanics remains to be determined.