Question: 

Diffuse noxious inhibitory control (DNIC) can be induced by strong nociceptive input and has been shown to reduce spinal excitability by recruitment of descending inhibitory systems. Here we tested whether DNIC inhibits synaptic plasticity in a human surrogate model of spinal nociceptive long-term potentiation (LTP; Klein et al. 2004).

Methods: 

The non-dominant hand of 21 males (age 24.6±5.04) was immersed either in cold (0°C; DNIC condition) or warm water (32°C; control) for 180s in a two-way cross-over design. Pain-LTP was induced by high-frequency stimulation (HFS; 5x1s at 100Hz at 10x detection threshold via 10 circular arranged electrodes) immediately after DNIC induction followed by determination of pressure pain thresholds (PPT). Hyperalgesia to single electrical test stimuli applied via the conditioning electrode (homotopic pain-LTP) as well as to mechanical pinprick stimuli (8–512mN) adjacent to the conditioned area (heterotopic pain-LTP) were estimated by means of a numerical rating scale (0–100).

Results: 

PPT was increased by 11% (55 kPa vs. 60 kPa; p<0.05) and pain to HFS was reduced by 24% (47/100 vs. 61/100; p=0.001) under DNIC condition. Pain increase to pinprick after HFS was reduced by 42% (heterotopic pain-LTP, +76% vs. +131% at control condition, p<0.05 both), whereas hyperalgesia to electrical stimuli (–40%; homotopic pain-LTP, +41% vs. +70% at control condition; p=0.07) showed a trend towards reduction.

Conclusions: 

Analgesia to pressure pain as well as to HFS by painful cold water suggests sufficient DNIC activation. The reduction of neurogenic hyperalgesia during DNIC indicates that activating the descending inhibitory system interferes with the induction of spinal hypersensitivity in humans.