The effects of experimental knee pain on lower limb corticospinal and motor cortex excitability.

INTRODUCTION: Notable weakness of the quadriceps muscles is typically observed as a consequence of knee joint arthritis, knee surgery and knee injury. This is partly due to ongoing neural inhibition that prevents the central nervous system from fully activating the quadriceps, a process known as arthrogenic muscle inhibition (AMI). To investigate the mechanisms underlying AMI, this study explored the effects of experimental knee pain on lower limb corticospinal and motor cortex excitability. METHODS: Twenty-four healthy volunteers participated in this study. In experiment 1, experimental knee pain was induced by the injection of hypertonic saline into the infrapatellar fat pad (n = 18). In experiment 2, isotonic saline was injected into the fat pad as a non-painful control (n = 8). Pain intensity was measured on a 10-cm electronic visual analogue scale. Transcranial magnetic stimulation and electromyography were used to measure lower limb motor-evoked potential amplitude and short-interval intracortical inhibition before and after the injection. RESULTS: The peak VAS score following hypertonic saline (5.0 ± 0.5 cm) was higher than after isotonic saline (p <0.001). Compared with baseline, there was a significant increase in vastus lateralis (p = 0.02) and vastus medialis motor-evoked potential amplitude (p = 0.02) during experimental knee pain that was not apparent during the control condition. Biceps femoris and tibialis anterior motor-evoked potential amplitude did not change following injection (all p >0.05). There was no change in short-interval intracortical inhibition measured from vastus lateralis following injection (both p >0.05). CONCLUSIONS: Quadriceps corticospinal excitability increases during experimental knee pain, providing no evidence for a supraspinal contribution to quadriceps AMI.

Quadriceps arthrogenic muscle inhibition: the effects of experimental knee joint effusion on motor cortex excitability.

INTRODUCTION: Marked weakness of the quadriceps muscles is typically observed following injury, surgery or pathology affecting the knee joint. This is partly due to ongoing neural inhibition that prevents the central nervous system from fully activating the quadriceps, a process known as arthrogenic muscle inhibition (AMI). This study aimed to further investigate the mechanisms underlying AMI by exploring the effects of experimental knee joint effusion on quadriceps corticomotor and intracortical excitability. METHODS: Seventeen healthy volunteers participated in this study. Transcranial magnetic stimulation was used to measure quadriceps motor evoked potential area, short-interval intracortical inhibition, intracortical facilitation and cortical silent period duration before and after experimental knee joint effusion. Joint effusion was induced by the intraarticular infusion of dextrose saline into the knee. RESULTS: There was a significant increase in quadriceps motor evoked potential area following joint infusion, both at rest (P = 0.01) and during voluntary muscle contraction (P = 0.02). Cortical silent period duration was significantly reduced following joint infusion (P = 0.02). There were no changes in short interval intracortical inhibition or intracortical facilitation over time (all P > 0.05). CONCLUSIONS: The results of this study provide no evidence for a supraspinal contribution to quadriceps AMI. Paradoxically, but consistent with previous observations in patients with chronic knee joint pathology, quadriceps corticomotor excitability increased after experimental knee joint effusion. The increase in quadriceps corticomotor excitability may be at least partly mediated by a decrease in gamma-aminobutyric acid (GABA)-ergic inhibition within the motor cortex.

Quadriceps arthrogenic muscle inhibition: neural mechanisms and treatment perspectives.

OBJECTIVES: Arthritis, surgery, and traumatic injury of the knee joint are associated with long-lasting inability to fully activate the quadriceps muscle, a process known as arthrogenic muscle inhibition (AMI). The goal of this review is to provide a contemporary view of the neural mechanisms responsible for AMI as well as to highlight therapeutic interventions that may help clinicians overcome AMI. METHODS: An extensive literature search of electronic databases was conducted including AMED, CINAHL, MEDLINE, OVID, SPORTDiscus, and Scopus. RESULTS: While AMI is ubiquitous across knee joint pathologies, its severity may vary according to the degree of joint damage, time since injury, and knee joint angle. AMI is caused by a change in the discharge of articular sensory receptors due to factors such as swelling, inflammation, joint laxity, and damage to joint afferents. Spinal reflex pathways that likely contribute to AMI include the group I nonreciprocal (Ib) inhibitory pathway, the flexion reflex, and the gamma-loop. Preliminary evidence suggests that supraspinal pathways may also play an important role. Some of the most promising interventions to counter the effects of AMI include cryotherapy, transcutaneous electrical nerve stimulation, and neuromuscular electrical stimulation. Nonsteroidal anti-inflammatory drugs and intra-articular corticosteroids may also be effective when a strong inflammatory component is present with articular pathology. CONCLUSIONS: AMI remains a significant barrier to effective rehabilitation in patients with arthritis and following knee injury and surgery. Gaining a better understanding of AMI's underlying mechanisms will allow the development of improved therapeutic strategies, enhancing the rehabilitation of patients with knee joint pathology.