Ramon Diaz-Arrastia
Born
United States
NationalityAmerican
Occupation(s)Neurologist and clinical investigator
Academic background
EducationBA in Biochemistry
PhD in Biochemistry
Doctor of Medicine
Alma materRice University
Baylor College of Medicine
Academic work
InstitutionsUniversity of Pennsylvania Perelman School of Medicine, Philadelphia
Penn Presbyterian Medical Center
Hospital of the University of Pennsylvania

Ramon Diaz-Arrastia is an American neurologist and clinical investigator. He is the John McCrae Dickson, MD Presidential professor of Neurology at the University of Pennsylvania Perelman School of Medicine in Philadelphia,[1] Director of Clinical Traumatic Brain Injury Research, and Attending Neurologist at the Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center.

Diaz-Arrastia is most known for his research on the molecular and cellular mechanisms involved in neuronal injury and neurodegeneration. He has received the 1992 American Academy of Neurology Neuropharmacology Research Award and is a Zenith Fellow of the Alzheimers Association.[2] His primary areas of research interest are focused on traumatic brain injury, epilepsy, and neurodegenerative disease.[3]

Education

In 1979, Diaz-Arrastia received a Bachelor of Arts degree in biochemistry from Rice University in Houston, Texas. He went on to earn a PhD in Biochemistry from the Baylor College of Medicine in 1986, followed by a Doctor of Medicine degree from the same institution in 1988.[4]

Career

Diaz-Arrastia began his academic career in 1993 by joining the University of Texas Southwestern Medical Center in Dallas, where he held various academic appointments, including assistant professor, associate professor, and professor in the Department of Neurology. In 2004, he became an adjunct professor at the School of Behavioral and Brain Sciences at the University of Texas at Dallas. He worked at UT Southwestern until 2011, when he took on concurrent appointments as the professor of neurology at the Uniformed Services University of Health Sciences and an investigator at the National Institute of Neurological Disorders and Stroke in Bethesda, which he held until 2016. As of 2016, he is serving as the Presidential Professor of Neurology at the University of Pennsylvania Perelman School of Medicine in Philadelphia.[4]

Diaz-Arrastia previously served as director of clinical research at the Center for Neuroscience and Regenerative Medicine and currently holds the position of director of clinical TBI research at the University of Pennsylvania Perelman School of Medicine in Philadelphia as of 2016.[5]

As of July 2016, he has been holding concurrent appointments as an attending neurologist at the Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center.[1]

Research

Diaz-Arrastia has authored numerous publications, including, articles in peer-reviewed journals and is most known for his research in internal medicine, specifically for his contributions towards advancing contemporary understanding of traumatic brain injury.[6] His research work spans the fields of neurodegeneration, traumatic brain injury, and post-traumatic epilepsy.[3]

Traumatic brain injury

Diaz-Arrastia's early research work focuses on the role of traumatic cerebral vascular injury (TCVI) in the development of functional deficits and chronic disability following traumatic brain injury, concluding that TCVI is a frequent occurrence and endorsed the use of non-invasive imaging techniques such as MRI-ASL, TCD, and NIRS to assess microvascular function post-traumatic brain injury.[7] His group was the first group to show that phosphodiesterase 5 (PDE5) inhibition reverses part of the deficit in cerebrovascular reactivity after TBI, and constitutes a promising therapy for traumatic cerebrovascular injury.[8]

Diaz-Arrastia's group was among the first to use diffusion tensor imaging (DTI) MRI to study traumatic axonal injury during the acute, subacute, and chronic period after traumatic brain injury. In a series of publications, they showed that DTI measures of fractional anisotropy (FA) and mean diffusivity (MD) are altered in patients with TBI within 24 hours of injury, and change dynamically over the subsequent weeks. Their group was also the first to use functional MRI (resting state functional connectivity) to identify functional disruption of white matter tracts in the acute and chronic stage after TBI.[9]

Post traumatic epilepsy

Diaz-Arrastia's research on post-traumatic epilepsy explores the prevalence, risk factors, clinical features, and management options of epilepsy that arise as a result of a traumatic brain injury. His research on surgical outcomes in Post-Traumatic Epilepsy revealed that surgery could be a viable option for reducing seizure frequency or severity, even in cases where other treatments have been unsuccessful. His work has focused on establishing the electrophysiologic and neuroimaging endophenotypes of TBI. His group showed that mesial temporal sclerosis was a common finding in post-traumatic epilepsy of adult onset.[10] He published a study of post-traumatic epilepsy evaluated with MRI and video-EEG monitoring over 10 years at a single epilepsy center.[11]

Biomarkers for traumatic brain injury

In his exploration of new ways to diagnose mild traumatic brain injuries by testing for certain proteins in both the blood and small particles released by brain cells, also known as extracellular vesicles, his work revealed that these two sources of protein information i.e. (plasma and brain-derived extracellular vesicles) provide independent diagnostic information and when combined, accurately diagnose mild traumatic brain injuries.[12] Evaluating the effects of time and age on traumatic brain injury, he demonstrated that glial fibrillary acidic protein has good to excellent performance in discriminating TBI from other diagnostic groups across all age categories up to at least 3 days post-injury and suggested that the addition of a blood-based diagnostic to the evaluation of traumatic brain injury has the potential to improve diagnosis.[13]

Awards and honors

  • 2006 – Zenith Fellow, Alzheimer's Association[2]
  • 2006 – Teaching Award for Neurology Clerkship, UT Southwestern Medical Center
  • 2008 – Distinguished Alumnus Award, Baylor College of Medicine

Selected articles

  • Levin, H. S., & Diaz-Arrastia, R. R. (2015). Diagnosis, prognosis, and clinical management of mild traumatic brain injury. The Lancet Neurology, 14(5), 506–517.
  • Iturria-Medina, Y., Sotero, R. C., Toussaint, P. J., Mateos-Pérez, J. M., & Evans, A. C. (2016). Early role of vascular dysregulation on late-onset Alzheimer's disease based on multifactorial data-driven analysis. Nature communications, 7(1), 11934.
  • Sandsmark DK, Bashir A, Wellington CL, Diaz-Arrastia R. Cerebral Microvascular Injury: A Potentially Treatable Endophenotype of Traumatic Brain Injury-Induced Neurodegeneration. Neuron. 2019 Aug 7;103(3):367–379. Review. PubMed PMID 31394062; PubMed Central PMCID: PMC6688649.
  • Maas AIR, Menon DK, ...Diaz-Arrastia R, et al. Traumatic brain injury: Progress and challenges in prevention, clinical care, and research. Lancet Neurol. 2022;doi.org/10.1016/S1474-4422(22)00337-4.

References

  1. 1 2 "Ramon R. Diaz-Arrastia, MD, PhD profile | PennMedicine.org". www.pennmedicine.org.
  2. 1 2 "Zenith Fellows | Alzheimer's Association". Zenith.
  3. 1 2 "Ramon Diaz-Arrastia". scholar.google.com.
  4. 1 2 "Ramon Diaz-arrastia | Institute for Translational Medicine and Therapeutics | Perelman School of Medicine at the University of Pennsylvania". www.med.upenn.edu.
  5. ↑ "Ramon Diaz-Arrastia, MD, PhD | NeuroNEXT". neuronext.org.
  6. ↑ "Ramon Diaz-Arrastia – Implications for the Next Generation of Clinical Trials" (PDF).
  7. ↑ Kenney, Kimbra; Amyot, Franck; Haber, Margalit; Pronger, Angela; Bogoslovsky, Tanya; Moore, Carol; Diaz-Arrastia, Ramon (January 27, 2016). "Cerebral Vascular Injury in Traumatic Brain Injury". Experimental Neurology. 275 Pt 3: 353–366. doi:10.1016/j.expneurol.2015.05.019. PMID 26048614. S2CID 5388184 – via PubMed.
  8. ↑ Kenney, Kimbra; Amyot, Franck; Moore, Carol; Haber, Margalit; Turtzo, L. Christine; Shenouda, Christian; Silverman, Erika; Gong, Yunhua; Qu, Bao-Xi; Harburg, Leah; Wassermann, Eric M.; Lu, Hanzhang; Diaz-Arrastia, Ramon (April 27, 2018). "Phosphodiesterase-5 inhibition potentiates cerebrovascular reactivity in chronic traumatic brain injury". Annals of Clinical and Translational Neurology. 5 (4): 418–428. doi:10.1002/acn3.541. PMC 5899908. PMID 29687019.
  9. ↑ Wang, J. Y.; Bakhadirov, K.; Abdi, H.; Devous, M. D.; Marquez de la Plata, C. D.; Moore, C.; Madden, C. J.; Diaz-Arrastia, R. (August 30, 2011). "Longitudinal changes of structural connectivity in traumatic axonal injury". Neurology. 77 (9): 818–826. doi:10.1212/WNL.0b013e31822c61d7. PMC 3162636. PMID 21813787.
  10. ↑ Diaz-Arrastia, R.; Agostini, M. A.; Frol, A. B.; Mickey, B.; Fleckenstein, J.; Bigio, E.; Van Ness, P. C. (November 27, 2000). "Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults". Archives of Neurology. 57 (11): 1611–1616. doi:10.1001/archneur.57.11.1611. PMID 11074793 – via PubMed.
  11. ↑ Gupta, Puneet K.; Sayed, Nasreen; Ding, Kan; Agostini, Mark A.; Van Ness, Paul C.; Yablon, Stuart; Madden, Christopher; Mickey, Bruce; D'Ambrosio, Raimondo; Diaz-Arrastia, Ramon (August 15, 2014). "Subtypes of post-traumatic epilepsy: clinical, electrophysiological, and imaging features". Journal of Neurotrauma. 31 (16): 1439–1443. doi:10.1089/neu.2013.3221. PMC 4132580. PMID 24693960.
  12. ↑ "Extracellular vesicles as distinct biomarker reservoirs for mild traumatic brain injury diagnosis – Brain Communications".
  13. ↑ "Effects of age and time since injury on traumatic brain injury blood biomarkers: a TRACK-TBI study – Brain Communications".
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