Sub-50-fs laser retinal damage thresholds in primate eyes with group velocity dispersion, self-focusing and...

In vivo retinal injury studies using sub-50-femtosecond laser pulses in the near-infrared must consider nonlinear effects such as group velocity dispersion (GVD), self-focusing, laser-induced breakdown (LIB) and low-density plasmas (LDPs). In this paper we present the results of our theoretical calculations of nonlinear effects and our experimental measurements for the visible lesion thresholds in live eyes. We compare these values with the measured LIB and LDP thresholds in an artificial eye. All three thresholds were measured with and without pre-chirping the input pulse to compensate for GVD effects.

We recorded the minimum visible lesion (MVL) thresholds in vivo for sub-50-fs laser pulses, with and without pre-chirping the input pulses. In addition, we measured the LIB and LDP thresholds, with and without pre-chirping, within an artificial eye. Different degrees of pre-chirping were required to give optimal compensation for GVD in the live eye and the artificial eye. Probit analysis was used on all data, and comparisons among thresholds were made, to determine the effects on the three thresholds of chirp compensation for GVD.

Results of our nonlinear modeling and calculations for GVD compensation, self-focusing, LIB, and low-density plasmas were compared with our experimental results using live eyes and the artificial eye. The damage threshold in live eyes dropped in energy from 0.25 microJ, for the flat-phase input, to 0.17 microJ when optimally chirped pulses were used, while the LIB threshold was reduced from 0.29 microJ to 0.19 microJ with optimally chirped pulses. The LDP threshold dropped from 0.21 microJ to 0.14 microJ with the pre-chirped pulse. At 44 fs, these energies produced peak powers at least twice the calculated critical power that produces nonlinear self-focusing and beam collapse, for propagation of non-aberrated gaussian beams in a uniform medium.

Based on our measurements of the MVL thresholds, with and without GVD compensation, we conclude that the visible lesion thresholds produced by 44 fs pulses in rhesus eyes are increased in energy due to GVD. The MVL ED50 was reduced by one third when the pulse was pre-chirped to compensate for GVD in the eye. This reduction in amplitude also holds true in the artificial eye for the LIB ED50 bubble thresholds and the LDP ED50 plasma channels, when using pre-chirped pulses versus non-chirped pulses. We also conclude from the data presented that low-density plasmas, and not LIB cavitation bubbles, are the probable mediating factor at the visible lesion thresholds observed within live eyes, for pulse durations at and below 50 fs. Therefore, the plasma channel created by LDPs is the major damage mechanism, if not the only damage mechanism, at MVL threshold energies for these pulse durations.