Narrowed, uterine arterioles in the placental bed are the histologic hallmark of many, clinical obstetric syndromes including preeclampsia, IUGR, preterm labor, midtrimester loss, and, placental abruption. Early reports illustrate, but do not explain, accompanying "halos" of hyalinised cells around these narrowed arterioles that are consistent features of these lesions (Figure 1a). Similar, narrowed arterioles are common in many gynecologic syndromes where there are "halos" of regenerating, injured nerves around narrowed uterine arterioles in presentations of chronic pelvic pain, dysmenorrhea, endometriosis , dyspareunia, vulvodynia, irritative bladder, and, bowel syndromes (Figure 1b). The neurovascular injury is one, and the same, in both obstetric and gynecologic, clinical syndromes. It results from injuries to pelvic vasomotor nerves (the "neural" injury) that release neural cytokines and growth factors causing transmural hyperplasia and narrowing of denervated arterioles, that become susceptible to successive, hyaline and fibrinoid changes (the "vascular" injury). Their common origins have been difficult to recognise because during pregnancy the injured arterioles extend to the placental bed, but, the injured nerves do not, leaving one, or more, layers of hyalinised cells around the injured arteriole in the placental bed biopsy (Figures 1a-b). Injuries to pelvic nerves result from "difficult" first labors, physical efforts during defecation, complications of gynecologic surgical procedures, as well as hypertension. Injuries to arteriolar vasomotor nerves induce "new" and "novel" receptors including purinergic, P2X3 and VEGF receptors in arteriolar smooth muscle that may respond to "pain" and "stretch" , or, activate other autonomic reflexes. Recent evidence suggests that the unexpectedly diverse, and varying, consequences of these neurovascular injuries may contribute to the pathophysiology of different, obstetric and gynaecologic syndromes.