Conduction velocity of the human phrenic nerve in the neck.

PURPOSE: To measure phrenic nerve conduction velocity in the neck in humans. SCOPE: We studied 15 healthy subjects (9 men, 32.4+/-6.7). We performed bipolar electrical phrenic stimulation in the neck, from a distal and a proximal stimulation site, and recorded diaphragm electromyographic responses on the surface of the chest. The ratio of the between-site distance to the latency difference provided phrenic velocities. Ulnar motor velocity was assessed similarly. In addition, five homogeneous patients with Charcot-Marie-Tooth disease type 1A (CMT1A) were studied for validation purposes. We obtained diaphragmatic responses from the two stimulation sites in all cases. The distal latencies (anterior axillary line recording) were 6.51+/-0.63ms (right) and 6.13+/-0.64ms (left). The minimal between site distance was 39mm. Phrenic motor velocity was 55.2+/-6.3ms(-1) (right) and 56.3+/-7.2ms(-1) (left). In CMT1A, phrenic velocities were 17.1+/-8.1ms(-1) (from 7 to 32ms(-1)) and were similar to ulnar and median velocities. CONCLUSIONS: Phrenic nerve velocities can be estimated in humans and compare with upper limb motor conduction velocities. This should refine the investigation of phrenic function in peripheral neuropathies.

Impaired cortical processing of inspiratory loads in children with chronic respiratory defects.

BACKGROUND: Inspiratory occlusion evoked cortical potentials (the respiratory related-evoked potentials, RREPs) bear witness of the processing of changes in respiratory mechanics by the brain. Their impairment in children having suffered near-fatal asthma supports the hypothesis that relates asthma severity with the ability of the patients to perceive respiratory changes. It is not known whether or not chronic respiratory defects are associated with an alteration in brain processing of inspiratory loads. The aim of the present study was to compare the presence, the latencies and the amplitudes of the P1, N1, P2, and N2 components of the RREPs in children with chronic lung or neuromuscular disease. METHODS: RREPs were recorded in patients with stable asthma (n = 21), cystic fibrosis (n = 32), and neuromuscular disease (n = 16) and in healthy controls (n = 11). RESULTS: The 4 RREP components were significantly less frequently observed in the 3 groups of patients than in the controls. Within the patient groups, the N1 and the P2 components were significantly less frequently observed in the patients with asthma (16/21 for both components) and cystic fibrosis (20/32 and 14/32) than in the patients with neuromuscular disease (15/16 and 16/16). When present, the latencies and amplitudes of the 4 components were similar in the patients and controls. CONCLUSION: Chronic ventilatory defects in children are associated with an impaired cortical processing of afferent respiratory signals.

Upper airway afferents are sufficient to evoke the early components of respiratory-related cortical potentials in humans.

Repeated inspiratory occlusions in humans elicit respiratory-related cortical potentials, the respiratory counterpart of somatosensory-evoked potentials. These potentials comprise early components (stimulus detection) and late components (cognitive processing). They are considered as the summation of several afferent activities from various part of the respiratory system. This study assesses the role of the upper airway as a determinant of the early and late components of the potentials, taking advantage of the presence of a tracheotomy in patients totally or partially deafferented. Eight patients who could breathe either through the mouth or through a tracheotomy orifice (whole upper airway bypassed) were studied (4 quadriplegic patients with phrenic pacing, 4 patients with various sources of inspiratory pump dysfunction). Respiratory-related evoked potentials were recorded in CZ-C3 and CZ-C4. They were consistently present after mouth occlusions, with a first positive P1 and a first negative N1 components of normal latencies (P1: 40.4 +/- 6.1 ms in CZ-C3 and 47.6 +/- 7.6 ms in CZ-C4; N1: 84.4 +/- 27.1 ms in CZ-C3 and 90.2 +/- 17.4 ms in CZ-C4) and amplitudes. Tracheal occlusions did not evoke any cortical activity. Therefore, in patients with inspiratory pump dysfunction, the activation of upper airway afferents is sufficient to produce the early components of the respiratory-related evoked cortical potentials. Per contra, in this setting, pulmonary afferents do not suffice to evoke these components.

Abnormal respiratory-related evoked potentials in untreated awake patients with severe obstructive sleep apnoea syndrome.

AIM: Obstructive sleep apnoeas generate an intense afferent traffic leading to arousal and apnoea termination. Yet a decrease in the sensitivity of the afferents has been described in patients with obstructive sleep apnoea, and could be a determinant of disease severity. How mechanical changes within the respiratory system are processed in the brain can be studied through the analysis of airway occlusion-related respiratory-related evoked potentials. Respiratory-related evoked potentials have been found altered during sleep in mild and moderate obstructive sleep apnoea syndrome, with contradictory results during wake. We hypothesized that respiratory-related evoked potentials' alterations during wake, if indeed a feature of the obstructive sleep apnoea syndrome, should be present in untreated severe patients. METHODS: Ten untreated patients with severe obstructive sleep apnoea syndrome and eight matched controls were studied. Respiratory-related evoked potentials were recorded in Cz-C3 and Cz-C4, and described in terms of the amplitudes and latencies of their components P1, N1, P2 and N2. RESULTS: Components amplitudes were similar in both groups. There was no significant difference in P1 latencies. This was also the case for N1 in Cz-C3. In contrast, N1 latencies in Cz-C4 were significantly longer in patients with obstructive sleep apnoea syndrome [median 98 ms (interquartile range 16.00) versus 79.5 ms (5.98), P = 0.015]. P2 and N2 were also significantly delayed, on both sides. CONCLUSIONS: The cortical processing of airway occlusion-related afferents seems abnormal in untreated patients with severe obstructive sleep apnoea syndrome. This could be either a severity marker and/or an aggravating factor.