Development of a hybrid broadband NIRS/diffusion correlation spectroscopy system to monitor preterm brain injury (Conference Presentation)

Author(s):  
Ajay Rajaram ◽  
Keith St. Lawrence ◽  
Mamadou Diop
2021 ◽  
Vol 11 (8) ◽  
pp. 1093
Author(s):  
Chien-Sing Poon ◽  
Benjamin Rinehart ◽  
Dharminder S. Langri ◽  
Timothy M. Rambo ◽  
Aaron J. Miller ◽  
...  

Survivors of severe brain injury may require care in a neurointensive care unit (neuro-ICU), where the brain is vulnerable to secondary brain injury. Thus, there is a need for noninvasive, bedside, continuous cerebral blood flow monitoring approaches in the neuro-ICU. Our goal is to address this need through combined measurements of EEG and functional optical spectroscopy (EEG-Optical) instrumentation and analysis to provide a complementary fusion of data about brain activity and function. We utilized the diffuse correlation spectroscopy method for assessing cerebral blood flow at the neuro-ICU in a patient with traumatic brain injury. The present case demonstrates the feasibility of continuous recording of noninvasive cerebral blood flow transients that correlated well with the gold-standard invasive measurements and with the frequency content changes in the EEG data.


2017 ◽  
Vol 38 (2) ◽  
pp. 230-240 ◽  
Author(s):  
Ashwin B Parthasarathy ◽  
Kimberly P Gannon ◽  
Wesley B Baker ◽  
Christopher G Favilla ◽  
Ramani Balu ◽  
...  

Cerebral autoregulation (CA) maintains cerebral blood flow (CBF) in the presence of systemic blood pressure changes. Brain injury can cause loss of CA and resulting dysregulation of CBF, and the degree of CA impairment is a functional indicator of cerebral tissue health. Here, we demonstrate a new approach to noninvasively estimate cerebral autoregulation in healthy adult volunteers. The approach employs pulsatile CBF measurements obtained using high-speed diffuse correlation spectroscopy (DCS). Rapid thigh-cuff deflation initiates a chain of responses that permits estimation of rates of dynamic autoregulation in the cerebral microvasculature. The regulation rate estimated with DCS in the microvasculature (median: 0.26 s−1, inter quartile range: 0.19 s−1) agrees well (R = 0.81, slope = 0.9) with regulation rates measured by transcranial Doppler ultrasound (TCD) in the proximal vasculature (median: 0.28 s−1, inter quartile range: 0.10 s−1). We also obtained an index of systemic autoregulation in concurrently measured scalp microvasculature. Systemic autoregulation begins later than cerebral autoregulation and exhibited a different rate (0.55 s−1, inter quartile range: 0.72 s−1). Our work demonstrates the potential of diffuse correlation spectroscopy for bedside monitoring of cerebral autoregulation in the microvasculature of patients with brain injury.


2003 ◽  
Vol 23 (2) ◽  
pp. 219-231 ◽  
Author(s):  
Jonathan Lifshitz ◽  
Hans Friberg ◽  
Robert W. Neumar ◽  
Ramesh Raghupathi ◽  
Frank A. Welsh ◽  
...  

The cellular and molecular pathways initiated by traumatic brain injury (TBI) may compromise the function and structural integrity of mitochondria, thereby contributing to cerebral metabolic dysfunction and cell death. The extent to which TBI affects regional mitochondrial populations with respect to structure, function, and swelling was assessed 3 hours and 24 hours after lateral fluid—percussion brain injury in the rat. Significantly less mitochondrial protein was isolated from the injured compared with uninjured parietotemporal cortex, whereas comparable yields were obtained from the hippocampus. After injury, cortical and hippocampal tissue ATP concentrations declined significantly to 60% and 40% of control, respectively, in the absence of respiratory deficits in isolated mitochondria. Mitochondria with ultrastructural morphologic damage comprised a significantly greater percent of the population isolated from injured than uninjured brain. As determined by photon correlation spectroscopy, the mean mitochondrial radius decreased significantly in injured cortical populations (361 ± 40 nm at 24 hours) and increased significantly in injured hippocampal populations (442 ± 36 at 3 hours) compared with uninjured populations (Ctx: 418 ± 44; Hipp: 393 ± 24). Calcium-induced deenergized swelling rates of isolated mitochondrial populations were significantly slower in injured compared with uninjured samples, suggesting that injury alters the kinetics of mitochondrial permeability transition (MPT) pore activation. Cyclosporin A (CsA)-insensitive swelling was reduced in the cortex, and CsA-sensitive and CsA-insensitive swelling both were reduced in the hippocampus, demonstrating that regulated MPT pores remain in mitochondria isolated from injured brain. A proposed mitochondrial population model synthesizes these data and suggests that cortical mitochondria may be depleted after TBI, with a physically smaller, MPT-regulated population remaining. Hippocampal mitochondria may sustain damage associated with ballooned membranes and reduced MPT pore calcium sensitivity. The heterogeneous mitochondrial response to TBI may underlie posttraumatic metabolic dysfunction and contribute to the pathophysiology of TBI.


2016 ◽  
Vol 7 (2) ◽  
pp. 481 ◽  
Author(s):  
Johannes D. Johansson ◽  
Miguel Mireles ◽  
Jordi Morales-Dalmau ◽  
Parisa Farzam ◽  
Mar Martínez-Lozano ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document