Disruption of cortical synaptic homeostasis in individuals with chronic low back pain

OBJECTIVE: Homeostatic plasticity mechanisms regulate synaptic plasticity in the human brain. Impaired homeostatic plasticity may contribute to maladaptive synaptic plasticity and symptom persistence in chronic musculoskeletal pain.

METHODS: We examined homeostatic plasticity in fifty individuals with chronic low back pain (cLBP) and twenty-five pain-free controls. A single block (7-min) of anodal transcranial direct current stimulation ('single tDCS'), or two subsequent blocks (7-min and 5-min separated by 3-min rest; 'double tDCS'), were randomised across two experimental sessions to confirm an excitatory response to tDCS applied alone, and evaluate homeostatic plasticity, respectively. Corticomotor excitability was assessed in the corticomotor representation of the first dorsal interosseous muscle by transcranial magnetic stimulation-induced motor evoked potentials (MEPs) recorded before and 0, 10, 20, and 30-min following each tDCS protocol.

RESULTS: Compared with baseline, MEP amplitudes increased at all time points in both groups following the single tDCS protocol (P < 0.003). Following the double tDCS protocol, MEP amplitudes decreased in pain-free controls at all time points compared with baseline (P < 0.01), and were unchanged in the cLBP group.

CONCLUSION: These data indicate impaired homeostatic plasticity in the primary motor cortex of individuals with cLBP.

SIGNIFICANCE: Impaired homeostatic plasticity could explain maladaptive synaptic plasticity and symptom persistence in cLBP.