T1? MRI CONTRAST IN THE HUMAN BRAIN ADIABATIC RF PULSE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. T1¿ MRI Contrast in the Human Brain: Modulation of the Longitudinal Rotating Frame Relaxation Shutter-Speed During an Adiabatic RF Pulse In this work, we developed a method to access T1¿ relaxation during adiabatic pulses. We demonstrated that T1¿ is the dominant relaxation mechanism during a train of AFP pulses (with no interpulse time intervals) place prior the excitation, and showed how AFP pulses constructed using different modulation functions can be exploited to generate tissue contrast in human brain images. We demonstrated that dipolar relaxation channels contribute to the T1¿ relaxation. For the dipolar interaction between two identical spins, the dependence of the T1¿ time constant on the AFP pulse modulation functions is insignificant for the rotational correlation times ¿c < 1 ns. We also show that the adiabatic R1¿ rate constant differences obtained using different modulation functions (HS1 and HS4) can be quite well described by a two-site-exchange (2SX) model. This can provide intrinsic relaxation parameters in-vivo of the specific site A (or B) undergoing equilibrium exchange. An important feature of the adiabatic T1¿ and T2¿ methods is the following: Because adiabatic 1H2O T1¿ contrast originates predominantly from dipolar relaxation pathways, while adiabatic T2¿ contrast appears to originate mainly from the averaging of exchange and diffusion, these two measurements are likely to provide complementary contrasts, and thus, improved non-invasive tissue characterization.