Previous studies from these laboratories have shown that airway occlusion applied from the onset of inspiration or during midinspiration is associated with cerebral evoked potentials in human subjects. The hypothesis tested in the present study was that the more abrupt decrease in mouth pressure produced by midinspiratory occlusion will be associated with evoked potentials that have shorter peak latencies and greater peak amplitudes than those produced by occlusions from the onset of inspiration. The second objective of the present study was to determine whether there is bilateral projection of inputs from the respiratory system to the somatosensory cortex. Random presentation of 64 midinspiratory occlusions and 64 occlusions from the onset of inspiration was performed in eight subjects. The inspirations preceding the occlusions served as control. Evoked potentials were recorded from the scalp with electrode pairs Cz-C3 and Cz-C4. Reaction time to each type of occlusion was measured from the burst in electromyogram activity produced by contraction of the muscles encircling the eye. Each type of inspiratory occlusion was associated with evoked potentials that could be recorded bilaterally. The peak amplitudes of the evoked potentials recorded over the right cerebral hemisphere were significantly greater than those recorded from the left side. The peak amplitude was greater and the peak latency shorter for the evoked potentials produced by the midinspiratory occlusions. The results are consistent with the hypothesis that afferents mediating these potentials are stimulated by added loads to breathing and project bilaterally to the somatosensory cortex in humans.

Short latency phrenic motor responses to phrenic nerve stimulation were studied in anesthetized, paralyzed cats. Electrical stimulation (0.2 ms, 0.01-10 mA, 2 Hz) of the right C5 phrenic rootlet during inspiration consistently elicited a transient reduction in the phrenic motor discharge. This attenuation occurred bilaterally with an onset latency of 8-12 ms and a duration of 8-30 ms. Section of the ipsilateral C4-C6 dorsal roots abolished the response to stimulation, thereby confirming the involvement of phrenic nerve afferent activity. Stimulation of the left C5 phrenic rootlet or the right thoracic phrenic nerve usually elicited similar inhibitory responses. The difference in onset latency of responses to cervical vs. thoracic phrenic nerve stimulation indicates activation of group III afferents with a peripheral conduction velocity of approximately 10 m/s. A much shorter latency response (5 ms) was evoked ipsilaterally by thoracic phrenic nerve stimulation. Section of either the C5 or C6 dorsal root altered the ipsilateral response so that it resembled the longer latency contralateral response. The low-stimulus threshold and short latency for the ipsilateral response to thoracic phrenic nerve stimulation suggest that it involves larger diameter fibers. Decerebration, decerebellation, and transection of the dorsal columns at C2 do not abolish the inhibitory phrenic-to-phrenic reflex.

The projections of phrenic nerve afferents to neurons in the dorsal (DRG) and ventral (VRG) respiratory group were studied in anesthetized, paralyzed, and vagotomized cats. Extracellular recordings of neuronal responses to vagal nerve and cervical phrenic nerve stimulation (CPNS) indicated that about one-fourth of the DRG respiratory-modulated neurons were excited by phrenic nerve afferents with an onset latency of approximately 20 ms. In addition, non-respiratory-modulated neurons within the DRG were recruited by CPNS. Although some convergence of vagal and phrenic afferent input was observed, most neurons were affected by only one type of afferent. In contrast to the DRG, only 3 out of 28 VRG respiratory-modulated neurons responded to CPNS. A second study determined that most of these neuronal responses were due to activation of diaphragmatic afferents since 90% of the DRG units activated by CPNS were also excited at a longer latency by thoracic phrenic nerve stimulation. The difference in onset latency of neuronal excitation indicates an afferent peripheral conduction velocity of about 10 m/s, which suggests that they are predominately small myelinated fibers (group III) making paucisynaptic connections with DRG neurons. Decerebration, decerebellation, and bilateral transection of the dorsal columns at C2 do not abolish the neuronal responses to cervical PNS.

PFM significantly reduced pediatric asthma morbidity in this sample.

A long-held belief is that respiratory-related reflexes mediated by afferents in the diaphragm are weak or absent. However, recent data suggest that diaphragmatic afferents are capable of altering ventilatory motor drive as well as influencing perception of added inspiratory loads in humans. This review describes the sensory elements of the diaphragm, their central projections, and their functional significance in the control of respiratory muscle activation. The reflexes elicited by electrical stimulation of phrenic nerve afferents and the contribution of diaphragmatic afferents in respiratory load compensation and perception are considered. There is growing evidence that phrenic nerve afferents are activated under a variety of conditions. However, the significance of this input to the central nervous system is yet to be discerned.