ArticleJournal of personalized medicine2022
Spreading Depolarization as a Therapeutic Target in Severe Ischemic Stroke: Physiological and Pharmacological Strategies.
Article in Journal of personalized medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cortical spreading depolarizations in stroke: Mechanisms, neuroprotective interventions, and monitoring techniques.GeroScience · 2026Review
- The Role of TNF-α in Ischemic Stroke.International journal of molecular sciences · 2026Review
- Oxygen-Based Autoregulation Indices Associated with Clinical Outcomes and Spreading Depolarization in Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2025Observational
- Behavioral and Cognitive Consequences of Spreading Depolarizations: A Translational Scoping Review.Journal of neurotrauma · 2025Article
- Cerebral autoregulation, spreading depolarization, and implications for targeted therapy in brain injury and ischemia.Reviews in the neurosciences · 2024Review
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- Cellular Mechanisms of Electromagnetic Field in Traumatic Brain Injury.Journal of biotechnology and biomedicine · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundSpreading depolarization (SD) occurs nearly ubiquitously in malignant hemispheric stroke (MHS) and is strongly implicated in edema progression and lesion expansion. Due to this high burden of SD after infarct, it is of great interest whether SD in MHS patients can be mitigated by physiologic or pharmacologic means and whether this intervention improves clinical outcomes. Here we describe the association between physiological variables and risk of SD in MHS patients who had undergone decompressive craniectomy and present an initial case of using ketamine to target SD in MHS.
methodsWe recorded SD using subdural electrodes and time-linked with continuous physiological recordings in five subjects. We assessed physiologic variables in time bins preceding SD compared to those with no SD.
resultsUsing multivariable logistic regression, we found that increased ETCO2 (OR 0.772, 95% CI 0.655-0.910) and DBP (OR 0.958, 95% CI 0.941-0.991) were protective against SD, while elevated temperature (OR 2.048, 95% CI 1.442-2.909) and WBC (OR 1.113, 95% CI 1.081-1.922) were associated with increased risk of SD. In a subject with recurrent SD, ketamine at a dose of 2 mg/kg/h was found to completely inhibit SD.
conclusionFluctuations in physiological variables can be associated with risk of SD after MHS. Ketamine was also found to completely inhibit SD in one subject. These data suggest that use of physiological optimization strategies and/or pharmacologic therapy could inhibit SD in MHS patients, and thereby limit edema and infarct progression. Clinical trials using individualized approaches to target this novel mechanism are warranted.
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