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Origin of Negative BOLD fMRI Signals. Norm Harel at al Presented by Hyunggoo Kim. History. 1930 Dia/paramagnetic property of Oxy/deoxyheamoglobin 1952 Discovered NMR 1971 nuclear magnetic relaxation times of tissues and tumors differed
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Origin of Negative BOLD fMRI Signals Norm Harel at al Presented by Hyunggoo Kim
History • 1930 Dia/paramagnetic property of Oxy/deoxyheamoglobin • 1952 Discovered NMR • 1971 nuclear magnetic relaxation times of tissues and tumors differed • 1982 blood oxygenation lead to decrease in T2, T2* NMR relaxation time of blood • 1989 in vivo imaging in rat • 1992, BOLD contrast by ogawa
TERM • CBF: cerebral blood flow • CBV: cerebral blood volumne • CMR: cerebral metabolic rate
MRI (1) • NMR(Nuclear magnetic resonance) Imaging technology • Proton, neutron spins along strong magnetic field • Spin frequency V = rB, r is specific for each atom • Using H (H2O is abundant in body) • High/low energy spin state • Emiting electomagnetic wave (High to low)
MRI (2) • Decaying time(T1,T2,T2*) varies along to environment (skeleton, tissue, etc) • Detecting signal using coil by electomagnetic Induction • Using constrast of signal strength for converting signal strength to visual graphic • Various technique about • How to evoke signal • How to detect signal • How to analyze data
fMRI • Functional <-> anatomical • Detect signal constrast between specific task • Spatio-temporal difference of signal • Correlate function achiving the task and the region of brain area
strength time BOLD fMRI (1) • Dia/Paramagnetic stuff change relaxation time • Oxygen + Fe (in Hb) : Diamagnetic • (Deoxy) + Fe (in Hb): Paramagnetic • Paramagnetic makes magnetic field inhomogeneous • Decay time prolonged in inhomogeneous M.F. • What cause deoxy ? • C6H12O6 + 6O2 -> 6CO2 + 6H20 (Glycolysis) • mainly in neurotransmitter metabolism • So, Neural activity is related • But much argument about precise mechanism • CBV, CBF, etc..
BOLD fMRI (2) • 1st phase • More deoxy -> more paramagnetic -> inhomogeneous magnetic field -> T2 time shortened -> signal- • 2st phase • CBF >> oxygen demand -> T2 prolonged -> signal+ • 3st phase • CBF return, oxygen demand return, signal return
Experiment Overview • Objective: Clarify BOLD mechanism • Question: Negative BOLD mean decreased neuroal activity ? • Input: square-wave grating stimulus • Output: BOLD constrast • Analysis: Cross-correlation method
Positive / Nagative BOLD • V1 positive, Higher area negative
BOLD – CBV relation • V1: TCBV < TBOLD • Higher: TBOLD < TCBV
Discussion (1) • V1 & Higher area are highly related • At lower PCO2, BOLD response faster and no initial dip
Discussion (2) • Common arterial branch share blood flow • More active region can ‘steel’ blood flow from relatively less active region • CBF may not explain all neuronal activation • Despite of Increased neuronal activity, these region may not escape ‘initial dip’ state • TCBV < TBOLD explains arterial expansion -> hemodynamic change
Conclusion • Caution should be taken when interpreting negative BOLD signal