Short-latency inhibitory reflex responses to inspiratory loading of the scalene muscles are impaired in spinal cord injury.

Abstract

What is the central question of this study? The aim was to determine whether the reflex inhibition in the electromyographic activity of scalene muscles in response to inspiratory muscle loading is present in individuals with cervical spinal cord injury and to examine whether the intercostal muscle afferents are critical for genesis of the reflex. What is the main finding and its importance? The lack of reflex inhibition in response to inspiratory loading in individuals with complete cervical spinal cord injury suggests that the reflex critically requires input from intercostal afferents and/or an intact intersegmental neural network. In healthy individuals, transient loading of inspiratory muscles with a brief inspiratory occlusion produces a short-latency inhibitory response (IR) in the electromyographic activity of scalene muscles at ∼40 ms, followed by an excitatory response (ER). It has been argued that this reflex plays a protective role in neuromuscular control of the inspiratory muscles and that it is co-ordinated by spinal segmental or supraspinal circuits. In this study, the reflex response to airway occlusion was recorded bilaterally from scalene muscles in 14 subjects and from the right costal diaphragm in seven subjects with spinal cord injury [SCI, C4-C6; American Spinal Injury Association (ASIA) Impairment Scale (AIS) A]. The incidence, latency and size of the reflex were compared with previously published data from able-bodied subjects. Only two subjects with SCI showed an IR, and six subjects had an ER. Latencies to the onset and peak of the IR and ER were 5-50 ms longer than in able-bodied subjects. However, when reflexes were identified, their size in individuals with SCI was similar to that of control subjects. We conclude that afferents from the scalene muscles and diaphragm are insufficient in most subjects with SCI to evoke the usual inhibition to airway occlusion and that input from chest wall afferents below the spinal cord lesion may be important for genesis of the short-latency inhibition in the able-bodied subjects.