Functional imaging of procedural motor learning: Relating cerebral blood flow with individual subject performance

1994 ◽  
Vol 1 (3) ◽  
pp. 221-234 ◽  
Author(s):  
Scot. T. Grafton ◽  
Roger P. Woods ◽  
Mike Tyszka
2003 ◽  
Vol 23 (7) ◽  
pp. 829-837 ◽  
Author(s):  
Gregory G. Brown ◽  
Lisa T. Eyler Zorrilla ◽  
Bassem Georgy ◽  
Sandra S. Kindermann ◽  
Eric C. Wong ◽  
...  

The authors studied the effects of altering global cerebral blood flow on both blood oxygen level–dependent (BOLD) response and perfusion response to finger-thumb apposition. A PICORE/QUIPSS II protocol was used to collect interleaved BOLD-weighted and perfusion-weighted images on eight finger-thumb apposition trials. Subjects were studied on a drug-free day and on a day when acetazolamide was administered between the second and third trials. After acetazolamide administration, resting cortical perfusion increased an average of 20% from preadministration levels, whereas the BOLD response to finger-thumb apposition decreased by an average of 35% in the S1M1 hand area. Contrary to predictions from the exhausted cerebrovascular reserve hypothesis and the oxygen limitation model, an effect of acetazolamide on cerebral blood flow response in the S1M1 hand area was not observed. Across the acetazolamide trials, BOLD response was inversely correlated with resting cortical perfusion for individual subject data. These results suggest that resting perfusion affects the magnitude of the BOLD response and is thus an important confounding factor in fMRI studies, and that the physiologic systems that increase cerebral blood flow in response to acetazolamide administration and systems that increase cerebral blood flow in response to altered neural activity appear to have additive effects.


RADIOISOTOPES ◽  
1977 ◽  
Vol 26 (4) ◽  
pp. 221-227
Author(s):  
Hisato MAEDA ◽  
Tsuyoshi NAKAGAWA ◽  
Nobuo YAMAGUCHI ◽  
Mitsuo TAGUCHI ◽  
Gisuke YAMAMOTO

Neuroglia ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 36-47
Author(s):  
G. Campbell Teskey ◽  
Cam Ha T. Tran

Neurovascular coupling is a key control mechanism in cerebral blood flow (CBF) regulation. Importantly, this process was demonstrated to be affected in several neurological disorders, including epilepsy. Neurovascular coupling (NVC) is the basis for functional brain imaging, such as PET, SPECT, fMRI, and fNIRS, to assess and map neuronal activity, thus understanding NVC is critical to properly interpret functional imaging signals. However, hemodynamics, as assessed by these functional imaging techniques, continue to be used as a surrogate to map seizure activity; studies of NVC and cerebral blood flow control during and following seizures are rare. Recent studies have provided conflicting results, with some studies showing focal increases in CBF at the onset of a seizure while others show decreases. In this brief review article, we provide an overview of the current knowledge state of neurovascular coupling and discuss seizure-related alterations in neurovascular coupling and CBF control.


NeuroImage ◽  
1996 ◽  
Vol 3 (3) ◽  
pp. 175-184 ◽  
Author(s):  
Stephan Arndt ◽  
Ted Cizadlo ◽  
Daniel O'Leary ◽  
Sherri Gold ◽  
Nancy C. Andreasen

2019 ◽  
Author(s):  
Aleksandra Bortel ◽  
Roland Pilgram ◽  
Ze Shan Yao ◽  
Amir Shmuel

ABSTRACTFunctional MRI (fMRI) utilizes changes in metabolic and hemodynamic signals to indirectly infer the underlying local changes in neuronal activity. To investigate the mechanisms of fMRI responses, spontaneous fluctuations, and functional connectivity in the resting-state, it is important to pursue fMRI in animal models. Animal studies commonly use dexmedetomidine sedation. It has been demonstrated that potent sensory stimuli administered under dexmedetomidine are prone to inducing seizures in Sprague-Dawley (SD) rats.Here we combined optical imaging of intrinsic signals and cerebral blood flow with neurophysiological recordings to measure responses in rat area S1FL to electrical forepaw stimulation administered at 8 Hz. We show that the increased susceptibility to seizures starts no later than 1 hour and ends no sooner than 3 hours after initiating a continuous administration of dexmedetomidine. By administering different combinations of anesthetic and sedative agents, we demonstrate that dexmedetomidine is the sole agent necessary for the increased susceptibility to seizures. The increased susceptibility to seizures prevails under a combination of 0.3%-0.5% isoflurane and dexmedetomidine anesthesia. The blood-oxygenation and cerebral blood flow responses to seizures induced by forepaw stimulation have a higher amplitude and a larger spatial extent relative to physiological responses to the same stimuli. The epileptic activity and the associated blood oxygenation and cerebral blood flow responses stretched beyond the stimulation period. We observed seizures in response to forepaw stimulation with 1-2 mA pulses administered at 8 Hz. In contrast, responses to stimuli administered at 4 Hz were seizure-free. We demonstrate that such seizures are generated not only in SD rats but also in Long-Evans rats, but not in C57BL6 mice stimulated with similar potent stimuli under dexmedetomidine sedation.We conclude that high-amplitude hemodynamic functional imaging responses evoked by peripheral stimulation in rats sedated with dexmedetomidine are possibly due to the induction of epileptic activity. Therefore, caution should be practiced in experiments that combine the administration of potent stimuli with dexmedetomidine sedation. We propose stimulation paradigms that elicit seizure-free, well detectable neurophysiological and hemodynamic responses in rats. We further conclude that the increased susceptibility to seizures under dexmedetomidine sedation is species dependent.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Lucas M. Hart ◽  
Danica Jakovcevic ◽  
David Harder

RADIOISOTOPES ◽  
1977 ◽  
Vol 26 (9) ◽  
pp. 624-629
Author(s):  
Hisato MAEDA ◽  
Tsuyoshi NAKAGAWA ◽  
Nobuo YAMAGUCHI ◽  
Mitsuo TAGUCHI ◽  
Gisuke YAMAMOTO

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