Christopher Pawela, PhD
Associate Professor, Joint Department of Biomedical Engineering; Anesthesiology; Biophysics
MS, Chemistry, University of Wisconsin
BS, Bacteriology, University of Wisconsin
Upon receipt of his PhD in 2008, Dr. Pawela joined the MCW faculty as an assistant professor of plastic surgery with a secondary appointment in biophysics. He joined the Department of Anesthesiology in 2015 and the Department of Biomedical Engineering in 2017. In 2019, he was promoted to associate professor, and in 2021, he accepted a primary appointment to the Joint Department of Biomedical Engineering, maintaining a secondary appointment in anesthesiology.
Honors and Awards
- Brain connectivity
- Neural plasticity
- Cerebrovascular structure and function
- Neurovascular coupling
(Saber M, Schwabe D, Park HJ, Tessmer J, Khan Z, Ding Y, Robinson M, Hogan QH, Pawela CP.) Neuromodulation. 2022 01;25(1):53-63 PMID: 35041588 01/19/2022
(Mecca CM, Chao D, Yu G, Feng Y, Segel I, Zhang Z, Rodriguez-Garcia DM, Pawela CP, Hillard CJ, Hogan QH, Pan B.) J Neurosci. 2021 09 01;41(35):7492-7508 PMID: 34244365 PMCID: PMC8412994 SCOPUS ID: 2-s2.0-85114152937 07/11/2021
(Saber M, Schwabe D, Park HJ, Tessmer J, Khan Z, Ding Y, Robinson M, Hogan QH, Pawela CP.) Neuromodulation. 2021 Jun 02 PMID: 34076938 06/03/2021
(Feng Y, Li K, Roth E, Chao D, Mecca CM, Hogan QH, Pawela C, Kwok WM, Camara AKS, Pan B.) Front Cell Neurosci. 2021;15:689334 PMID: 34447298 PMCID: PMC8383341 SCOPUS ID: 2-s2.0-85113358817 08/28/2021
(Pawela C, Brunsdon RK, Williams TA, Porter M, Dale RC, Mohammad SS.) Dev Med Child Neurol. 2017 04;59(4):445-448 PMID: 27991656 12/20/2016
(Pawela CP, Kramer JM, Hogan QH.) Neuroimage. 2017 02 15;147:10-18 PMID: 27876655 11/24/2016
(Pawela C, DeYoe E, Pashaie R.) Methods Mol Biol. 2016;1408:227-41 PMID: 26965126 SCOPUS ID: 2-s2.0-84961285244 03/12/2016
(Biswal B, Pawela C, Grist T, Meyerand ME, Nencka AS, DeYoe EA, Li SJ, Rowe DB, Kiviniemi V, Cox RW, Bodurka J, Ogawa S, Koretsky A, Hu X, Kim SG.) Brain Connect. 2014 Nov;4(9):631-5 PMID: 25415836 PMCID: PMC4238237 SCOPUS ID: 2-s2.0-84937197534 11/22/2014
(Li C, Li Z, Ward BD, Dwinell MR, Lombard JH, Hudetz AG, Pawela CP.) Brain Connect. 2014 Nov;4(9):760-8 PMID: 25387238 PMCID: PMC4238242 SCOPUS ID: 2-s2.0-84937199899 11/12/2014
(Li Z, Ward BD, Dwinell MR, Lombard JH, Pawela CP.) Neuroimage. 2014 Apr 15;90:403-12 PMID: 24084065 SCOPUS ID: 2-s2.0-84893717855 10/03/2013
(Li R, Hettinger PC, Machol JA, Liu X, Stephenson JB, Pawela CP, Yan JG, Matloub HS, Hyde JS.) J Brachial Plex Peripher Nerve Inj. 2013 May 09;8(1):4 PMID: 23659705 PMCID: PMC3659007 05/11/2013
(Hettinger PC, Li R, Yan JG, Cho YR, Sanger J, Dzwierzynski W, Pawela CP, Hyde JS, Matloub HS.) Hand (N Y). 2011 Jun;6(2):194-201 PMID: 22654704 PMCID: PMC3092895 06/02/2012
My laboratory focuses on identifying reorganizational changes in brain associated with injury and disease. Our expertise is in magnetic resonance imaging (MRI) methodologies. However, we also use other modalities such as electrophysiology, optical coherence tomography (OCT), laser Doppler, animal behavior testing, and optogenetics to complement our MRI results. Our projects are generally initiated in a preclinical animal model with possible concurrent studies in human subjects. I am the founding co-editor-in-chief of the scientific journal, Brain Connectivity, and I am also on the executive committee for the Society for Brain Connectivity which organizes a biennial scientific conference. There are three ongoing projects in my laboratory.
Hypertension and Neurovascular Coupling
My laboratory is funded through an NIH grant titled: “FMRI studies of cerebrovascular structure and function in low-renin hypertension.” Chronic hypertension causes reduced vascular function, reduced blood flow, damaged cerebral autoregulation, and is a known risk factor for ischemic stroke and vascular-associated cognitive decline. Blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) is sensitive to changes in cerebrovascular hemodynamic function. Preliminary rodent fMRI data demonstrate a diminished cerebrovascular BOLD hyperemic response to sensory stimulation in salt-induced hypertensive Dahl Salt-Sensitive (SS) rats, a widely-used animal model of low-renin hypertension. Clinically, salt-induced low-renin hypertension accounts for 25% of all essential hypertensive patients, but 75% in African Americans.
Our data suggests that neurovascular coupling is impaired in low-renin salt-induced hypertension. Mechanistically, we hypothesize that salt-sensitive hypertension leads to vessel endothelium dysfunction through damage by oxidative stress. Free radicals reduce the bioavailability of nitric oxide, a key factor in neurovascular coupling. Our research has three goals: 1) Characterize the neurovascular uncoupling in salt-induced hypertension. 2) Define the sensitivity and selectivity of the brain BOLD fMRI signal to chronic hypertension. 3) Determine the influence of the SS Renin gene allele on phenotypic differences in the BOLD signal in salt-induced hypertension. This collaborative project includes investigators in the MCW Physiology Department.
Brain Reorganization following Peripheral Nerve Injury
This project is funded through a VA grant titled: “Persisting functional CNS changes following peripheral nerve repair” and is a cooperative effort with my MCW Anesthesiology colleague, Dr. Quinn Hogan MD. Peripheral nerve injuries are a common consequence of trauma and often result in a poor prognosis with complications such as abnormal sensation, motor function loss, pain, and depression. Our laboratory and others have shown that brain reorganization occurs immediately after a nerve is damaged or transected.
The reorganizational process (or neuroplasticity) post-injury/repair is dynamic and persists even after surgical repair and a subsequent recovery period. We hypothesize that a portion of the neuroplasticity following injury is maladaptive and accounts for some of the individual variability in outcomes post-repair within the same nerve(s)/level of injury. Our laboratory is developing methods to track brain reorganization post-injury/repair and strategies to target this process therapeutically. Our overall goal is to improve outcomes for these debilitating injuries where few new treatment strategies have been introduced clinically in the last 40 years.
Brain Connectivity Mechanisms
The biological mechanism(s) that generate the BOLD fMRI signal and drive BOLD signal low-frequency fluctuations leading to correlations between brain regions is unclear after many years of scholarship. FMRI methodologies are being explored as biomarkers of neurological and psychiatric diseases and the number of studies using these techniques is growing exponentially. Understanding the nature of these signals is key to the utility of these imaging methods as potential biomarkers. My laboratory is carrying out fundamental studies in preclinical animal models using multi-modal imaging techniques to explore the BOLD fMRI signal mechanism. We are using evolving methods such as optogenetics and concurrent MR/electrophysiology experiments to study neurovascular coupling at high spatial and temporal resolution. Our goal is to discover essential knowledge about the BOLD fMRI signal which will lead to further refinement of the imaging methodology and enhance stability with clinical application of fMRI as a potential biomarker for neurological and psychiatric diseases.