Abstract 233: Cortical Spread Depolarization: Monitoring Techniques and Clinical Applications

Introduction/Purpose Cortical spreading depolarization (CSD) describes a slow, sustained, synchronized depolarization within the cerebral gray matter that renders neurons unable to fire action potentials, resulting in widespread neuronal depression. CSD has been observed in stroke, subarachnoid hemorrhage, epilepsy, traumatic brain injury and migraines and is a potential indicator of imminent neuronal death. Therefore, the identification, monitoring and treatment of CSD are crucial in both neurointensive care and neurosurgical settings. Such measures are paramount for optimizing outcomes among patients with neurological injuries. However, this slow spreading depolarization at low amplitudes presents challenges to identify and monitor CSD in clinical settings. We aim to identify various current and potential techniques for monitoring CSD in neurocritical care and neurosurgical settings, alongside exploring available treatment modalities. We also analyze current limitations in the detection of CSD, including identification of potential biomarkers. Methods/Materials A comprehensive review of available literature utilizing search engines such as PubMed and Google Scholar was conducted using key search terms such as “cortical spreading depression”, “CSD”, “spreading depolarization” and “CSD monitoring”. Eligibility for this review was restricted to full‐text, english, peer‐reviewed literature articles. There were no restrictions on publication dates. Results 224 articles discussing CSD were reviewed and ultimately 93 articles were included in the analysis. Electrocorticography (ECoG) remains the primary modality to detect CSD, both in the neurological intensive care unit (nICU) and during neurosurgical procedures. However, there are other potential modalities for detection such as Electroencephalogram (EEG), pressure reactivity index (PRx), magnetoencephalography (MEG), MRI/fMRI and laser speckle imaging (LSI). These methods have been tested in animal models and/or in clinical practice but each has drawbacks that render these modalities not readily available or nonfunctional as independent detection methods in the nICU. Nevertheless, a multimodal monitoring approach utilizing a combination monitoring modalities such as ECoG in conjunction with tools that measure cerebral vascular response such as cerebral perfusion pressure, cerebral blood flow and PRx could provide timely measurements of CSD. There are potential biomarkers being studied for early detection of CSD which include adenosine, GFAP, lactate, IL‐6 or TNF‐alpha. Some treatment modalities have been studied that inhibit or halt CSD include: dizocilpine (NMDA‐R blocker), topiramate, valproate, propranolol, amitriptyline, methysergide, propofol and glutamate receptor inhibitors. Conclusion Although several methods have been studied, ECoG remains the gold standard for CSD detection. Nevertheless, a multimodal approach which utilizes ECoG in conjunction with different methods of monitoring, could prove a useful tool in nICU as well as neurosurgical procedures. Further research is needed to determine the utility and application of other monitoring methods in the clinical setting.