Experimental investigation of the impact of a high-load working memory task on the development of secondary hyperalgesia : a pilot study

Central sensitization, a key factor of chronic pain, operates in the dorsal horn of the spinal cord following high levels of activity in peripheral nociceptive afferents (Harte et al., 2018). In particular, it is manifested by an increased sensitivity extending outside the site of injury, called secondary hyperalgesia. It is increasingly recognized that attentional factors play a role in the modulation of the pain experience, particularly via descending pathways to the spinal cord (Filbrich et al., 2020). According to the attentional load theory (Lavie et al., 2004), if a high attentional load is allocated to non-painful stimuli, then the processing of nociceptive stimuli should be reduced (Legrain, Van Damme, et al., 2009). Thus, it could be hypothesized that a greater engagement of attentional resources in a non-painful task would protect against the development of central sensitization, by decreasing the attentional resources committed to the perception of nociceptive stimuli (Torta et al., 2020). The present study aimed to investigate the involvement of attentional load in the development of central sensitization. Twenty-four healthy subjects were tested to examine whether attentional load could modulate central sensitization through the experimental induction of secondary mechanical hyperalgesia. Participants were assigned to two experimental conditions. The first included a low load working memory task while the second consisted of a high load working memory task. Simultaneously with task performance, secondary hyperalgesia was induced on the subject’s non-dominant arm using high-frequency electrical stimulation (HFS) of the skin. Mechanical secondary hyperalgesia was measured using mechanical pinprick stimuli. The intensity of sensitivity to pinprick stimuli was measured before HFS (T0), 20 minutes after HFS (T1), and 40 minutes after HFS (T2), respectively. In addition, the area extension of pinprick sensitivity was measured at T1 and T2. The results indicate that HFS induced hypersensitivity to pinprick stimuli on the stimulated arm that was maintained up to 40 minutes after its placement, confirming the successful induction of secondary hyperalgesia. In contrast, the findings do not support the hypothesis that attentional load would modulate the subsequent development of mechanical secondary hyperalgesia, and, consequently, of central sensitization. Further studies remain necessary to elucidate the involvement of this cognitive process in central sensitization.