“…Suggested mechanisms include increased energy requirements and metabolic disturbances from emotional arousal, Valsalva induced hippocampal venous congestion, arterial watershed compromise in hippocampal Sommer sectors 1,9 . The exact mechanism responsible for the underlying relationship between TGA and RCVS remains unknown; however, triggering factors, such as migraine attacks, emotional/physical stress, medications or vasoactive drugs may lead to sympathetic dysregulation and/or hyperresponsiveness causing sudden and prolonged vascular constriction resulting in hypoxic injury to vulnerable parenchyma 1,6 . As neuroimaging continues to improve, radiologic parallels between RCVS and posterior reversible encephalopathy syndrome (PRES) have been observed, suggesting the two are a continuum of disease rather than two independent disease entities, as PRES can present with similar radiologic findings and is associated with dysregulation of cerebral arterial tone; however, despite the shared clinical prodrome and radiologic features, the exact pathophysiology also remains elusive 10 .…”