Dependence of the negative BOLD response on somatosensory stimulus intensity

Klingner, Carsten M.; Hasler, Caroline; Brodoehl, Stefan; Witte, Otto W.

doi:10.1016/j.neuroimage.2010.05.087

Cited by 58 publications

(67 citation statements)

References 43 publications

(89 reference statements)

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“…The SI exhibited an NBR ipsilateral to the somatosensory stimulus. This result is also consistent with recent reports on somatosensory processing (Hlushchuk and Hari, 2006;Kastrup et al, 2008;Klingner et al, 2010). The physiological basis of the NBR has not been fully characterized.…”

Section: Discussionsupporting

confidence: 90%

“…Animal experiments have revealed a tight coupling between NBRs and reduced neuronal activity (Boorman et al, 2010;Shmuel et al, 2006) or enhanced inhibition within sensory systems (Devor et al, 2007). Furthermore, a correlation between the NBR in the ipsilateral SI and changes of the sensory threshold has been shown in humans (Kastrup et al, 2008;Klingner et al, 2010). These studies demonstrate that it is beneficial to consider NBRs in addition to PBRs for a more complete understanding of brain functions.…”

Section: Introductionmentioning

confidence: 89%

“…More recently, negative deflections of the BOLD response (negative bold response, NBR) have also been described. These were found, for instance, in the primary motor cortex in response to an ipsilateral motor task (Hamzei et al, 2002;Stefanovic et al, 2004) and in the primary somatosensory cortex (SI) in response to an ipsilateral somatosensory stimulus (Hlushchuk and Hari, 2006;Kastrup et al, 2008;Klingner et al, 2010Klingner et al, , 2011. Animal experiments have revealed a tight coupling between NBRs and reduced neuronal activity (Boorman et al, 2010;Shmuel et al, 2006) or enhanced inhibition within sensory systems (Devor et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Influences of negative BOLD responses on positive BOLD responses

et al. 2011

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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Influences of negative BOLD responses on positive BOLD responses

et al. 2011

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“…The local sensorimotor neuronal population activity increases with stimulus intensity/duration, thus increasing the magnitude of both the primary positive and negative BOLD responses (21,49). However, the constant amplitude stimuli delivered here results in an increase in the amplitude of the positive primary BOLD response and a decrease in the amplitude of the negative primary BOLD response in trials with high PERS mu power (Fig.…”

Section: Are the Davis And Baseline Assumptions Correct For Poststimulusmentioning

confidence: 73%

Poststimulus undershoots in cerebral blood flow and BOLD fMRI responses are modulated by poststimulus neuronal activity

Mullinger

Mayhew

Bagshaw

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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fMRI is the foremost technique for noninvasive measurement of human brain function. However, its utility is limited by an incomplete understanding of the relationship between neuronal activity and the hemodynamic response. Though the primary peak of the hemodynamic response is modulated by neuronal activity, the origin of the typically negative poststimulus signal is poorly understood and its amplitude assumed to covary with the primary response. We use simultaneous recordings of EEG with blood oxygenation level-dependent (BOLD) and cerebral blood flow (CBF) fMRI during unilateral median nerve stimulation to show that the poststimulus fMRI signal is neuronally modulated. We observe high spatial agreement between concurrent BOLD and CBF responses to median nerve stimulation, with primary signal increases in contralateral sensorimotor cortex and primary signal decreases in ipsilateral sensorimotor cortex. During the poststimulus period, the amplitude and directionality (positive/negative) of the BOLD signal in both contralateral and ipsilateral sensorimotor cortex depends on the poststimulus synchrony of 8-13 Hz EEG neuronal activity, which is often considered to reflect cortical inhibition, along with concordant changes in CBF and metabolism. Therefore we present conclusive evidence that the fMRI time course represents a hemodynamic signature of at least two distinct temporal phases of neuronal activity, substantially improving understanding of the origin of the BOLD response and increasing the potential measurements of brain function provided by fMRI. We suggest that the poststimulus EEG and fMRI responses may be required for the resetting of the entire sensory network to enable a return to resting-state activity levels.simultaneous EEG-fMRI | event-related synchronization | rebound | alpha power | neurovascular-coupling

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“…One popular hypothesis has been the vascular steal hypothesis, stating that since the positive BOLD response reroutes an increased amount of blood into one area, that blood must be taken from somewhere, and therefore there will be areas with a lower signal caused by the active areas "stealing" the blood from their surroundings [39][40] [41]. However, there are also studies showing a consistent negative BOLD response in areas which are ipsilateral to activated areas, and therefore unlikely to be explained by hemodynamic steal [42] [43]. Another hypothesis is that an uncoupling of the oxygen metabolism and the regulation of CBF and CBV can cause a negative BOLD if the oxygen metabolism increases in response to increased neuronal activity while the CBF and CBV remain the same [44] [45].…”

Section: The Negative Bold Responsementioning

confidence: 99%

Mechanistic modelling - a BOLD response to the fMRI information loss problem

Lundengård

2017

Linköping University Medical Dissertations

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To everyone who let me take a look at their brain, particularly the pilots; the test participants get all the credit, even though you are the ones spending all that extra time in the scanner to sort out the messes we make.Without you, none of our experiments would be running at all.i Populärvetenskaplig sammanfattningNär vi studerar hur människans hjärna fungerarär det viktigt att använda en teknik somär säker för försökspersonerna och samtidigt ger relevant information om hjärnan. Funktionell Magnetresonanstomografi (fMRI) kan snabbt avbilda hela hjärnan om och om igen på samma person. Från bildserien kan man använda fMRI-signalen för att mäta lokala förändringar i syrehalt i olika delar av hjärnan. Syrehaltenändras på grund av att nervcellerna använder mer syre när de arbetar mer. Men för att cellerna inte ska få brist på syre och glukos vidgas blodkärlen för att skicka dit mer blod, och detändrar också fMRI-signalen.Även om nerverna bara tar några millisekunder på sig att skicka signaler så kan syreförändringen vi mäter pågå upp till 20 sekunder. Den stora tidsskillnaden gör det svårt att lista ut hur nervaktiviteten ser ut genom att bara titta på fMRI-signalen. Hur hjärncellerna påverkar blodkärlenär vi inte helt säkra på, men det finns flera olika hypoteser. Den hypotes som vi har undersökt beskriver hur när nerverna i hjärnan startar en signalkedja som får andra typer av hjärnceller att skicka ut signalsubstanser som i sin tur styr hur blodkärlen vidgar sig eller drar ihop sig när nervaktivitetenökar. I det här projektetöversätter vi hypotesen till matematiska ekvationer i en datormodell som efterliknar kommunikationen mellan hjärncellerna och blodkärlen. Först en datormodell. Sedan visar jag att modellen kan simulera data som vi har tränat den på. Den kanäven korrekt förutsäga hur hjärnaktiviteten borde se ut i nya experiment där stimulit varierar på ett sätt som modellen inte har sett innan. Efter det visar vi att modellen kan se skillnad på när det finns hjärnaktivitet i signalen och när det bara finns brus, samt bedöma hur starkt stimulitär. Detta gör vi genom att använda oss av en inre egenskap i modellen, nämligen hur mycket hjärncellerna säger till blodkärlen att vidga sig, istället för att bara titta på fMRI-signalen. I dessa tester använder vi simulerade data för att vara säker på vad det rätta svaretär, eftersom vi inte alltid vet hur aktiva hjärncellernä ar i verkligheten.Modellen kan också simulera inhibering, vilket innebär att något område i hjärnan förhindras från att aktiveras. Inhiberingär en viktig egenskap eftersom den reglerar de olika nätverken av hjärnområden så att de inte stör ut varandra när de utför olika uppgifter. Den sista egenskapen vi undersöker med modellenär att simulera vad som händer när man tillför det lugnandeämnet diazepam. Det finns ett område i hjärnan som blir inhiberat när man får diazepam. Med modellen kan vi visa att detär för att en viss receptor blir känsligare förämnen som dämpar hjärnaktivitet när man har fått diazepam. Förhoppningsvis kommer vår modell och m...

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Dependence of the negative BOLD response on somatosensory stimulus intensity

Cited by 58 publications

References 43 publications

Influences of negative BOLD responses on positive BOLD responses

Influences of negative BOLD responses on positive BOLD responses

Poststimulus undershoots in cerebral blood flow and BOLD fMRI responses are modulated by poststimulus neuronal activity

Mechanistic modelling - a BOLD response to the fMRI information loss problem

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