Relationship between significant perinatal events and migraine severity.

OBJECTIVE Nociceptive neuronal circuits are formed during embryonic and postnatal times, so insult during these periods may result in long-term alterations to pain circuitry via synaptic plasticity. One possible long-term result of plasticity is central hyperexcitability, which is suspected to be involved in chronic headache. This study aimed to establish whether there is an association between early pain experiences and the experience of migraines in later childhood. METHODS In a retrospective study, we examined the charts of 280 pediatric migraineurs at the Division of Pediatric Neurology at Robert Wood Johnson Medical School and documented their perinatal history and migraine characteristics. RESULTS Analysis revealed that there was a significant relationship between patients who had been in the NICU at birth and the type of pain medication prescribed when compared with patients who had not been in the NICU (chi2 test, chi2(2) = 23.304; N = 30250). Findings also suggested that pediatric migraine patients who had been in the NICU at birth had a significantly earlier age of onset of their migraines (chi2 +/- SD = 7.83 +/- 3.23; N = 30) when compared with patients who did not remain in the NICU (chi2 +/- SD = 9.68 +/- 3.57; N = 250; Kolmogorov-Smirnov Test, chi2 = 10.699). CONCLUSION On the basis of these findings, we speculate that pain experience as a neonate, through neuronal plasticity and resulting central hyperexcitability, can alter the later experience of pain. However, this observational study cannot validate these links. Other potential explanations that work either synergistically or alone include other forms of stimulation and greater parental vigilance that may occur when neonates spend time in the NICU. This study would prompt additional development of a larger prospective study to establish a link between early pain experience and subsequent pain syndromes and also future investigation into the treatment of pain in neonates as a preventive measure for avoiding long-lasting neuronal alterations.