Authors
Stephanie Alice Treichl, Ruth Steiger, Johanna Schönherr, Philipp Geiger, Christian Preuss-Hernández, Verena Rass, Ronny Beer, Markus Luger, Lukas Lenhart, Astrid Ellen Grams, Elke Gizewski, Claudius Thomé, Ondra Petr
Published in
Neurocritical care. Jul 14, 2026. Epub Jul 14, 2026.
Abstract
Aneurysmal subarachnoid hemorrhage (aSAH) is followed by a high‑risk subacute phase in which secondary brain injury is a major determinant of outcome, yet in vivo characterization of cerebral bioenergetics during this critical time period is limited.
In this prospective single‑center pilot study, adult patients with aSAH (N = 21) underwent 3 T magnetic resonance imaging and whole‑brain phosphorus‑31 magnetic resonance spectroscopy (31P‑MRS) between days 6 and 14 after hemorrhage. Metabolite ratios reflecting adenosine triphosphate (ATP) resynthesis (PCr/ATP), ATP hydrolysis (Pi/ATP), energetic reserve (PCr/Pi), and membrane turnover (PME/PDE) were quantified in territories of the anterior, middle, and posterior cerebral arteries and the basal ganglia and compared with those of age‑ and sex‑matched healthy controls (N = 21). Patients were stratified according to the presence or absence of both, the clinical signs of delayed cerebral ischemia, and symptomatic imaging-confirmed cerebral vasospasm.
Compared with controls, patients with aSAH exhibited significantly reduced PCr/ATP and Pi/ATP, increased PCr/Pi, and marked alterations in PME/PDE across all analyzed regions (all P < 0.01), indicating impaired ATP turnover, altered energetic reserve, and disturbed phospholipid membrane metabolism. These abnormalities were consistently more pronounced in patients with cerebral vasospasm than in those without, suggesting that cerebral vasospasm amplifies a preexisting global bioenergetic crisis.
The subacute phase after aSAH is characterized by a brain‑wide disturbance of energy and membrane metabolism that extends beyond structurally overt lesions and is modulated by cerebral vasospasm. 31P‑MRS captures these changes noninvasively and emerges as a promising tool for mechanistic insight, risk stratification, and the development of metabolism‑oriented therapeutic strategies in aSAH.
PMID:
42449089
Bibliographic data and abstract were imported from PubMed on 15 Jul 2026.
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