We studied six adult male dogs to determine whether free patellar tendon grafts show evidence of reinnervation when used for anterior cruciate ligament reconstruction. Histologic return of neural elements and return of a somatosensory-evoked potential defined evidence of reinnervation. Before removal, the native anterior cruciate ligament was electrically stimulated with a bipolar electrode and a somatosensory-evoked potential was recorded from a scalp electrode. The ligament was excised and reconstructed using an autogenous patellar tendon graft. Somatosensory-evoked potential was attempted immediately after reconstruction. Histology for nerve endings was performed on the native ligaments. Each animal underwent repeat arthrotomy 6 months later. The grafts were isolated and somatosensory-evoked potentials were attempted. An evoked potential was seen in all six dogs before reconstruction. No graft demonstrated a somatosensory-evoked potential acutely; however, 6 months postoperatively, the somatosensory-evoked potential returned in two cases. Histology of native ligaments showed that 25% of the 100 sections evaluated contained neural elements. Of the receptors present, 89% were mechanoreceptors and 11% were free nerve endings. Histologic examination of the graft tissue 6 months postoperatively revealed that all six grafts also contained neural elements. Mechanoreceptors and free nerve endings were present in approximately equal numbers in the grafts. The results of histology and somatosensory-evoked potential demonstrate that in at least some cases, free patellar tendon grafts show evidence of reinnervation when used for anterior cruciate ligament reconstruction.

An electrophysiological study was carried out in sixteen decerebrate and paralyzed New Zealand rabbits to determine how a bolus injection of a nociceptor stimulant (hypertonic saline, 5%) into the masseter muscle influences the activity of the trigeminal motor circuitry during fictive jaw movements. Hypodermic needles connected to a syringe held in a computer-controlled infusion pump were inserted into the anterior deep layer of either the right or the left masseter. Twenty-three infusions of 50, 70 or 80 microl saline were made in fourteen animals at constant rates over 1 min. Eight control infusions of normal saline (0.9%) were made in a subpopulation of five animals in an identical manner. Fictive jaw movements were evoked before and after the infusions by repetitive electrical stimulation of the corticobulbar tract. Effects were assessed by extracellular microelectrode recordings made from the digastric motoneuron pool and from putative last-order interneurons in the oral subnucleus of the spinal trigeminal tract and adjacent structures. In comparison with pre-infusion control cycles, nociceptor stimulation caused significant slowing of the rhythm and a reduction of the area of the digastric motoneuron bursts in the majority of the animals (12/14). The decrease in cycle frequency was due almost entirely to a lengthening of the time between the digastric bursts. Changes usually began 1-2 min after the infusion and returned to pre-infusion values within 10-15 min. No significant effects were seen when isotonic saline was applied. Recordings were obtained from nine interneurons, eight of which had low threshold mechanosensitive receptive fields. One neuron was, in addition, excited by pinch. Eight were not active in the absence of motor activity and this did not change when hypertonic saline was applied. However, once fictive movements began, all started to fire rhythmic bursts of spikes. In five cases, there was a significant post-infusion increase in spike frequency, and three showed decreases. Seven showed significant post-infusion changes in mean phase and/or concentration of their firing within the movement cycle. Changes in the preferred phase of interneuronal firing were significantly correlated to changes in the phase of offset of the digastric burst. The present results provide evidence that the stimulation of nociceptors in a muscle slows the frequency of rhythmical movements in the absence of sensory feedback. They confirm that infusions into one muscle affect the output of its antagonist. The results also suggest that neurons in the oral subnucleus of the spinal trigeminal tract and adjacent reticular formation appear to participate in programming these changes in motor output.

No abstract