Background: Cerebral hyperperfusion syndrome (CHS) occurs after the restoration of blood flow to a previously low-flow, low-pressure region of the cerebral vasculature, which subsequently responds with chronic compensatory vasodilation, leading to a dysregulated state. Sudden restoration of normal blood flow can overwhelm the vasculature leading to intracranial hemorrhage (ICH). Separately, the Windkessel phenomenon describes the capacity for elastic vessels to expand with systolic pressure and decompress with diastole, thereby suppressing distal pulse pressure. We encountered a case involving giant basilar aneurysms in which we believe the Windkessel phenomenon precipitated a catastrophic manifestation of CHS at treatment.
Observation: We present a 60-year-old female found to have marked dolichoectasia of the right cervical internal carotid, vertebral, and basilar arteries concurrent with two large vertebrobasilar dissecting-type fusiform aneurysms. Managed conservatively for ten years before developing gait ataxia, new imaging revealed dramatic interval growth of the larger aneurysm. Flow diversion with partial coiling of the aneurysms was pursued. The patient suffered intra-procedural catastrophic thalamic and midbrain hemorrhage with intraventricular extension. A meticulous review of the case data was undertaken. Our findings suggest that giant aneurysms can act as a Windkessel reservoir, depressing the distal pulse pressure. Flow diversion bypasses the reservoir, increasing the distal pulse pressure beyond the autoregulatory capacity, resulting in ICH analogous to CHS.
Lessons: CHS and Windkessel phenomenon can contribute to catastrophic sequelae in the treatment of giant intracranial aneurysms with flow diversion. Awareness of this mechanism can protect future patients from harm.
Keywords: Giant vertebrobasilar aneurysm; Windkessel phenomenon; cerebral hyperperfusion syndrome; flow diversion.