Improving clinical treatments for hydrocephalus
For nearly 30 years my lab has maintained a comprehensive interdisciplinary translationalresearch program whose ultimate goal is to improve clinical treatments for hydrocephalus, aprevalent form of traumatic brain injury caused by failure to absorb cerebrospinal fluid (CSF).This program continues to explore the cellular and physiological neuropathology associated withneonatal, infantile and adult hydrocephalus and focuses on neuroinflammation, non-invasiveneuroimaging (MRI, diffusion tensor imaging, and MR elastography), pharmacological strategiesfor neuroprotection and recovery of function, and clinical evaluations of patient outcome andnew treatment applications. Our multidisciplinary approach also includes biomedical engineeringimprovements in the design of CSF drainage systems (shunts), development of implantablesensors, and the biocompatibility of neural prostheses. Based on the recognition that treatmentimprovements for hydrocephalus have not progressed because of our lack of knowledge aboutthe pathophysiology of this frequent disorder, I recently moved from the University of Utah tocollaborate with David D. Limbrick, MD, PhD, a pediatric neurosurgeon at WashingtonUniversity and a member of the Hope Center. We are expanding Dr. Limbrick’s clinical researchprogram to include several animal models of hydrocephalus: a porcine model to test the efficacyof a new neurosurgical procedure, combined endoscopic third ventriculostomy and choroidplexectomy; an infant ferret model to measure biomechanical changes during progressivehydrocephalus; a neonatal rat model of communicating hydrocephalus to explore all aspects ofpathophysiology, and finally a congenital rat model of aqueductal stenosis to identifypathogenetic mechanisms and neurodevelopmental outcomes. All of these approaches willinvolve advanced neuroimaging, protein analyses of CSF, immunohistochemistry of braintissue, and disease modulation with anti-inflammation agents and chemokines.