Most patients who die after traumatic brain injury (TBI) show evidence of ischemic brain damage. Nevertheless, it has proven difficult to demonstrate cerebral ischemia in TBI patients. After TBI, both global and localized changes in cerebral blood flow (CBF) are observed, depending on the extent of diffuse brain swelling and the size and location of contusions and hematoma. These changes vary considerably over time, with most TBI patients showing reduced CBF during the first 12 hours after injury, then hyperperfusion, and in some patients vasospasms before CBF eventually normalizes. This apparent neurovascular uncoupling has been ascribed to mitochondrial dysfunction, hindered oxygen diffusion into tissue, or microthrombosis. Capillary compression by astrocytic endfeet swelling is observed in biopsies acquired from TBI patients. In animal models, elevated intracranial pressure compresses capillaries, causing redistribution of capillary flows into patterns argued to cause functional shunting of oxygenated blood through the capillary bed. We used a biophysical model of oxygen transport in tissue to examine how capillary flow disturbances may contribute to the profound changes in CBF after TBI. The analysis suggests that elevated capillary transit time heterogeneity can cause critical reductions in oxygen availability in the absence of ‘classic' ischemia. We discuss diagnostic and therapeutic consequences of these predictions.

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Purpose Repeat imaging in patients with non-aneurysmal subarachnoid hemorrhage (NASAH) remains controversial. We aim to report our experience with NASAH with different hemorrhage patterns, and to investigate the need for further diagnostic workup to determine the underlying cause of hemorrhage. Method We conducted a retrospective analysis of all spontaneous SAH with an initial negative computed tomography (CT) with angiography (CTA) and/or digital subtraction angiography (DSA) from October 2011 through May 2017. According to the bleeding pattern on the admission CT scan, NASAH was divided into two subgroups: (1) perimesencephalic SAH (PMSAH) and (2) non-perimesencephalic SAH (nPMSAH). Radiological data included the admission CT, CTA, DSA, and magnetic resonance imaging (MRI) with angiography (MRA). Results Seventy-four patients met the inclusion criteria. Thirty-nine (52.7%) patients had PMSAH on the initial CT scan, and 35 (47.3%) had nPMSAH. All underwent CTA and/or DSA revealing no vascular abnormalities. Forty-seven (63.5%) patients underwent subsequent diagnostic workup. DSA was performed in all patients at least once. No abnormalities were found on the repeat DSA or other radiological follow-up studies except in one (1.4%) patient with nPMSAH, in whom a follow-up DSA revealed a small saccular anterior choroidal artery aneurysm, considered to be the source of hemorrhage. Conclusion A repeat DSA may not be needed in case of PMSAH, if the initial negative DSA is technically adequate with absence of hematoma and vasospasm. In contrast, a follow-up DSA should be mandatory for confirming or excluding vascular pathology in case of nPMSAH in order to prevent rebleeding.

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