There has recently been a shift towards understanding how early life experiences alter neuropathological mechanisms, thereby priming individuals to be more susceptible to the chronification of pain. Specifically, adverse early life experiences, including those that begin in utero, such as intimate partner violence (IPV) have to potential to reorganize the brain. IPV is an unfortunately common form of abuse that affects women, daily, on a global scale and frequently arises or escalates in severity during pregnancy. Adverse outcomes investigated in infants exposed to IPV while in utero have focused on short term outcomes and include low birth weight, preterm labour, and perinatal death. The long-term implications of intergenerational trauma have been established in the offspring of genocide survivors, war veterans, and famine sufferers. However, an important gap in the literature still exists within the context of IPV-induced neuroplastic changes in the developing fetus. Unfortunately, while it is well understood that modification to the corticolimbic and mesocorticolimbic systems underpin chronic pain pathology, how this translates into altered nociceptive input is still poorly understood. I will explore some of the the underlying intergenerational mechanisms that regulate changes in plasticity and neural connectivity to produce the large-scale cortical reorganisation observed in chronic pain patients.