Neurovascular coupling is altered in women who have a history of brain injury from intimate partner violence: a preliminary study.

Introduction: Intimate partner violence (IPV) is a global health crisis with 30% of women over the age of 15 experiencing at least one event in their lifetime. Brain injury (BI) due to head impacts and/or strangulation is a common but understudied part of this experience. Previous research has shown BI from other injury mechanisms can disrupt neurovascular coupling (NVC). To gain further insight into whether similar changes occur in this population, we assessed NVC responses in women with a history of IPV-BI. Methods: NVC responses were measured for the middle and posterior cerebral arteries (MCA, PCA) using transcranial Doppler ultrasound while participants performed a complex visual search task. The lifetime history of previous exposure to IPV-BI was captured using the Brain Injury Severity Assessment (BISA) along with measures of post-traumatic stress disorder (PTSD), anxiety, depression, substance use, and demographic information. Initial analyses of NVC metrics were completed comparing participants who scored low vs. high on the BISA or did or did not experience non-fatal strangulation followed by a stepwise multiple regression to examine the impact of PTSD, anxiety, and depression on the relationship between the NVC metrics and IPV-BI. Results: Baseline and peak cerebral blood velocity were higher and the percentage increase was lower in the PCA in the low compared to the high BISA group whereas no differences between the groups were apparent in the MCA. In addition, those participants who had been strangled had a lower initial slope and area under the curve in the PCA than those who had not experienced strangulation. Finally, the stepwise multiple regression demonstrated the percentage increase in the PCA was significantly related to the BISA score and both depression and anxiety significantly contributed to different components of the NVC response. Conclusions: This preliminary study demonstrated that a lifetime history of IPV-BI leads to subtle but significant disruptions to NVC responses which are modulated by comorbid depression and anxiety. Future studies should examine cerebrovascular function at the acute and subacute stages after IPV episodes to shed additional light on this experience and its outcomes.