TY - JOUR
T1 - Dysfunction of neurovascular/metabolic coupling in chronic focal epilepsy
AU - Song, Yinchen
AU - Torres, Rafael A.
AU - Garcia, Sarahy
AU - Frometa, Yisel
AU - Bae, Jihye
AU - Deshmukh, Abhay
AU - Lin, Wei Chiang
AU - Zheng, Ying
AU - Riera, Jorge J.
N1 - Publisher Copyright:
© 2015 IEEE.
PY - 2016/1
Y1 - 2016/1
N2 - We aim to evaluate the mechanisms underlying the neurovascular/metabolic coupling in the epileptogenic cortices of rats with chronic focal epilepsy. Methods: We performed and analyzed intracranial recordings obtained from the seizureonset zones during ictal periods on epileptic rats, and then, used these data to fit a metabolically coupled balloon model. Normal rats undergoing forepaw stimulation were used as control. Results: We found a significant higher contribution from high local field potential frequency bands to the cerebral blood flow (CBF) responses in the epileptogenic cortices during ictal neuronal activities. The hemodynamic responses associated with ictal activities were distance-dependent with regard to the seizure focus, though varied in profiles from those obtained from acute seizure models. Parameters linking the CBF and relative concentration of deoxyhemoglobin to neuronal activity in the biophysical model were significantly different between epileptic and normal rats. Conclusion: We found that the coefficient associated with the strength of the functional hyperemic response was significantly larger in the epileptogenic cortices, and changes in hemoglobin concentration associated with ictal activity reflected the existence of a significantly higher baseline for oxygen metabolism in the epileptogenic cortices. Significance: Introducing methods to estimate these physiological parameters would enhance our understanding of the neurovascular/metabolic coupling in epileptic brains and improve the localization accuracy on irritative zones and seizure-onset zones through neuroimaging techniques.
AB - We aim to evaluate the mechanisms underlying the neurovascular/metabolic coupling in the epileptogenic cortices of rats with chronic focal epilepsy. Methods: We performed and analyzed intracranial recordings obtained from the seizureonset zones during ictal periods on epileptic rats, and then, used these data to fit a metabolically coupled balloon model. Normal rats undergoing forepaw stimulation were used as control. Results: We found a significant higher contribution from high local field potential frequency bands to the cerebral blood flow (CBF) responses in the epileptogenic cortices during ictal neuronal activities. The hemodynamic responses associated with ictal activities were distance-dependent with regard to the seizure focus, though varied in profiles from those obtained from acute seizure models. Parameters linking the CBF and relative concentration of deoxyhemoglobin to neuronal activity in the biophysical model were significantly different between epileptic and normal rats. Conclusion: We found that the coefficient associated with the strength of the functional hyperemic response was significantly larger in the epileptogenic cortices, and changes in hemoglobin concentration associated with ictal activity reflected the existence of a significantly higher baseline for oxygen metabolism in the epileptogenic cortices. Significance: Introducing methods to estimate these physiological parameters would enhance our understanding of the neurovascular/metabolic coupling in epileptic brains and improve the localization accuracy on irritative zones and seizure-onset zones through neuroimaging techniques.
KW - Cerebral blood flow
KW - Chronic focal epilepsy
KW - Metabolically coupled balloon model
KW - Neurovascular/metabolic coupling
KW - Oxygen consumption
KW - Preclinical model
UR - https://www.scopus.com/pages/publications/84959333428
UR - https://www.scopus.com/inward/citedby.url?scp=84959333428&partnerID=8YFLogxK
U2 - 10.1109/TBME.2015.2461496
DO - 10.1109/TBME.2015.2461496
M3 - Article
C2 - 26241965
AN - SCOPUS:84959333428
SN - 0018-9294
VL - 63
SP - 97
EP - 110
JO - IEEE Transactions on Biomedical Engineering
JF - IEEE Transactions on Biomedical Engineering
IS - 1
M1 - 2461496
ER -