Long-term impact of neonatal intensive care and surgery on somatosensory perception in children born extremely preterm

Abstract

Alterations in neural activity due to pain and injury in early development may produce long-term effects on sensory processing and future responses to pain. To investigate persistent alterations in sensory perception, we performed quantitative sensory testing (QST) in extremely preterm (EP) children (n=43) recruited from the UK EPICure cohort (born less than 26 weeks gestation in 1995) and in age and sex matched term-born controls (TC; n=44). EP children had a generalized decreased sensitivity to all thermal modalities, but no difference in mechanical sensitivity at the thenar eminence. EP children who also required neonatal surgery had more marked thermal hypoalgesia, but did not differ from non-surgical EP children in the measures of neonatal brain injury or current cognitive ability. Adjacent to neonatal thoracotomy scars there was a localized decrease in both thermal and mechanical sensitivity that differed from EP children with scars relating to less invasive procedural interventions or from those without scars. No relationship was found between sensory perception thresholds and current pain experience or pain coping styles in EP or TC children. Neonatal care and surgery in EP children are associated with persistent modality-specific changes in sensory processing. Decreases in mechanical and thermal sensitivity adjacent to scars may be related to localized tissue injury, whereas generalized decreases in thermal sensitivity but not in mechanical sensitivity suggest centrally mediated alterations in the modulation of C-fibre nociceptor pathways, which may impact on responses to future pain or surgery.

Interference of age and repetition of the same noxious stimulus on hyperalgesia

“…The amount of damaged tissue necessary to result in nervous long lasting pathways modification is controverse (Camozzato et al 2009, Walker et al 2009). Less intense stimuli may lead to long term activation of wide range neurons even during physiological conditions and this may be an induced afferent hyperalgesia mechanism and could justify the decrease in hyperalgesia threshold in group GF3 during subsequent sensitizations compared to previous ones (Rygh et al 1999, Johnston & Walker 2003.…”

“…Endogenous antinociceptive mechanisms may be activated by environmental stimuli such as battle fields, races, sexual acting or even by individual motivation when adapted do some condition (Sudhakar & Venkatesh 2003, Camozzato et al 2009, Walker et al 2009). Perhaps, inexperience to handling and the unknown conditions of the first stimulation may have evoked these antinociceptive mechanisms in GF3 animals, increasing their pain threshold as observed in T1-1h and T1-24h and in T-1h for GF6 ones.…”

“…Although pain perception is uniform among healthy individuals, affective fraction of pain varies largely. This suggests that previous knowledge as well as pain situation interferes with its affective response or tolerance (Ririe et al 2004, Walker et al 2009). …”

“…However, researches proved that newborns of several species are capable to identify noxious stimuli and that they interfere in maturation of sensitive pathways during central nervous system development (Ruda et al 2000, Johnston & Walker 2003. Apparently this occurs because during childhood central nervous system is prone to activity dependent modulation (Homaister et al 2009, Walker et al 2009). …”

“…Recently, several authors have purposed detailed theories of how nociceptive stimuli modify central nervous system (Zelter et al 1997, Al-Chaer et al 2000, Ruda et al 2000, Bhutta et al 2001, Melzak et al 2001. Although it's known that precocious stimuli modulates sensitive pathways and response to pain later, the amount of injured tissue necessary to modulate such alterations is to discuss (Walker et al 2009). …”