No abstract

We investigate the relationship between the laser beam at the retina (spot size) and the extent of retinal injury from single ultrashort laser pulses. From previous studies it is believed that the retinal effect of single 3-ps laser pulses should vary in extent and location, depending on the occurrence of laser-induced breakdown (LIB) at the site of laser delivery. Single 3-ps pulses of 580-nm laser energy are delivered over a range of spot sizes to the retina of Macaca mulatta. The retinal response is captured sequentially with optical coherence tomography (OCT). The in vivo OCT images and the extent of pathology on final microscopic sections of the laser site are compared. With delivery of a laser pulse with peak irradiance greater than that required for LIB, OCT and light micrographs demonstrate inner retinal injury with many intraretinal and/or vitreous hemorrhages. In contrast, broad outer retinal injury with minimal to no choriocapillaris effect is seen after delivery of laser pulses to a larger retinal area (60 to 300 microm diam) when peak irradiance is less than that required for LIB. The broader lesions extend into the inner retina when higher energy delivery produces intraretinal injury. Microscopic examination of stained fixed tissues provide better resolution of retinal morphology than OCT. OCT provides less resolution but could be guided over an in vivo, visible retinal lesion for repeated sampling over time during the evolution of the lesion formation. For 3-ps visible wavelength laser pulses, varying the spot size and laser energy directly affects the extent of retinal injury. This again is believed to be partly due to the onset of LIB, as seen in previous studies. Spot-size dependence should be considered when comparing studies of retinal effects or when pursuing a specific retinal effect from ultrashort laser pulses.

Recent studies ofretinal damage due to ultrashort laser pulses' have shown interesting behavior. Laser induced retinal damage for ultrashort (i.e. less than ins) laser pulses is produced at lower energies than in the nanosecond to microsecond laser pulse regime and the energy required for hemorrhagic lesions is much greater times greater than for the nanosecond regime. We investigated the tissue effects exhibited in histopathology ofretinal tissues exposed to ultrashort laser pulses.

Purpose: To assess the early in vivo evolution of tissue response and wound healing from ultrashort pulsed laser retinal lesions by correlating the cross sectional morphology from sequential optical coherence tomography with histopathologic sectioning. Methods: Single ultrashort laser pulses (20-40 1.tJ, 580 nm 3 picosecond) were placed in the Macacca mulatta retina and evaluated by cross-section optical coherence tomography (OCT). These images were compared at selected time-points with corresponding histological sections. Results: OCT was able to detect the acute tissue injury from laser delivery and the evolution of the healing response over 8 days after laser delivery. These OCT images correlated well with histopathologic findings. Conclusion: Analysis of the extent of initial laser lesions and the type of healing response can be performed in serial sequence with OCT providing new insight into the healing response from laser injury. This information correlates well with light microscopic data.

CTuS4 Fig. 3 Measured electrical impulse response of the waveguide on sampling oscilloscope. The waveguide was illuminated by 150-fs optical pulses at 80 MHz repetition rate. The FWHM of the electrical pulses is -400 ps.vices can respond at rates suitable for optical network applications.In conclusion, our results reveal the strong pulsewidth dependence of the photocurrent as well as the subnanosecond electrical response time of TPA waveguide photodetectors. With improvements in packaging, these devices can approximate the ultrafast optical thresholding function important for CDMA and other ultrafast network applications.We gratefully acknowledge stimulating discussions with J. S. Aitchison. Z. Zheng and A. M. Weiner were supported by AFOSR under contract F49620-95-1-0533.