ArticleNeurocritical care2026
Cerebral Energy Crisis in the Subacute Phase of Aneurysmal Subarachnoid Hemorrhage: A 31P-MRS Pilot Study on Cerebral Vasospasm and Delayed Cerebral Ischemia.
Article in Neurocritical care, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAneurysmal 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.
methodsIn 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.
resultsCompared 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.
conclusionsThe 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.
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