Acute brain injury (ABI) encompassing traumatic brain injury, ischemic stroke, and intracranial hemorrhage remains a leading cause of morbidity and long-term neurological disability worldwide. While traditional paradigms emphasize mechanical and vascular injury, recent advances in neurofluid research have redefined ABI as a multifactorial disorder involving failure of the glymphatic and meningeal lymphatic systems. These systems facilitate cerebrospinal fluid (CSF) and interstitial solute transport and depend on tightly regulated mechanisms, including aquaporin-4 (AQP4) water channel polarization, vascular pulsatility, and intact lymphatic drainage through the meninges. Disruption of these processes through AQP4 mislocalization, sleep–wake cycle disturbances, neuroinflammation, and hemodynamic instability contributes to impaired waste clearance, immune dysregulation, and progressive neurodegeneration following injury. Despite the development of advanced imaging techniques such as ultrafast MRI and computational waveform analyses that enable visualization of glymphatic and meningeal lymphatic transport, integrated clinical frameworks and standardized metrics remain absent. These knowledge gaps underscore the need for translational models that connect molecular alterations with physiological dysfunction and functional recovery.
This Research Topic aims to bridge mechanistic insights in glymphatic and meningeal lymphatic failure with translational and clinical implications for ABI. The central goal is to establish validated, measurable indicators of neurofluid transport that can inform diagnosis, monitoring, and therapeutic intervention. It invites investigations defining how AQP4 polarity, inflammatory cascades, autonomic regulation, and sleep architecture influence post-injury glymphatic and meningeal lymphatic function, and how these relationships can be leveraged to improve patient outcomes. By integrating physiology, imaging, and neurotechnological innovation, this initiative encourages exploration of targeted therapies to restore solute clearance, mitigate chronic inflammation, and prevent long-term neurodegenerative complications. Ultimately, it seeks to reposition neurofluid dysfunction as both a mechanistic framework and a therapeutic avenue for acute brain injury care.
To gather further insights into the mechanisms and clinical relevance of glymphatic and meningeal lymphatic impairment, we welcome contributions spanning computational, translational, and clinical domains. We invite submissions addressing, but not limited to, the following themes:
• Quantitative and imaging-based measurement of glymphatic and meningeal lymphatic transport (ultrafast MRI, ultrasound, TCD, ICP waveform analysis) • Mechanistic evaluation of AQP4 localization, astrocyte polarity, and blood–brain interface integrity after neurotrauma • Roles of sleep disruption, circadian rhythm, and autonomic dysregulation in impaired clearance and recovery • Neuroinflammatory and immune signaling pathways linking glymphatic dysfunction to secondary injury and neurodegeneration • Pharmacologic or physiologic modulation of neurofluid transport via sedation, vasopressors, or hemodynamic interventions • Multimodal neuromonitoring and data integration for real-time assessment of neurofluid and meningeal lymphatic function • Non-invasive and device-based therapeutic strategies such as ultrasound or photobiomodulation to enhance clearance • Advanced data analytics and artificial intelligence approaches for automated quantification, prediction, and outcome modeling • Translational frameworks connecting glymphatic and meningeal lymphatic biomarkers to neurocognitive recovery, neuroprotection, and rehabilitation outcomes
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