Appearance and modeling of bubble artifacts in intracranial magnetic resonance-guided laser interstitial thermal therapy (MRg-LITT) temperature images.

PURPOSE: To understand if unexplained signal artifacts in MRg-LITT proton resonance frequency- (PRF-) shift thermometry images are caused by air bubbles or hemorrhages, and to characterize their effects on temperature measurements. METHODS: Retrospective image data from an IRB-approved clinical trial of intracranial MRg-LITT were inspected for asymmetric distortions observed in phase data during ablations, which have been previously reported as likely hemorrhages. A total of eight patient cases were selected: seven with artifact occurrence and one without. Mathematical image models for air bubbles or hemorrhages were implemented to estimate the size of the air bubble or hemorrhage needed to explain the clinically observed phase artifacts. Correlations and Bland-Altman analyses were used to determine if an air bubble model or a hemorrhage model was better correlated to the clinical data. The model was used to inject bubbles into clean PRF phase data without artifacts to examine how temperature profile distortions change with slice orientation. The simulated air-bubble injected data were compared to clinical data containing artifacts to examine the bubbles' effects on temperature and thermal damage estimates. RESULTS: The model demonstrated that air bubbles up to approximately 1 cm in diameter could explain the clinically observed phase artifacts. The bubble model predicts that a hemorrhage would have to be 2.2 times as large as an air bubble in order to explain the same extent of phase distortion observed in clinical data. Air bubbles had 16% percent higher correlations to the clinical PRF phase data than hemorrhages, even after rescaling the hemorrhage phases to better match the data. The air bubble model also explains how the phase artifacts lead to both large positive and large negative temperature errors, up to ±100 °C, which could cascade to damage estimate errors of several millimeters. CONCLUSION: Results showed that the artifacts are likely caused by air bubbles rather than hemorrhages, which may be introduced before heating or appear during heating. Manufacturers and users of devices that rely upon PRF-shift thermometry should be aware these phase distortions from bubble artifacts can result in large temperature errors.

Trends in nanosecond melanosome microcavitation up to 1540 nm.

Thresholds for microcavitation of bovine and porcine melanosomes were previously reported, using single nanosecond (ns) laser pulses in the visible (532 nm) and the near-infrared (NIR) from 1000 to 1319 nm. Here, we report average radiant exposure thresholds for bovine melanosome microcavitation at additional NIR wavelengths up to 1540 nm, which range from ∼0.159 J∕cm2 at 800 nm to 4.5 J∕cm2 at 1540 nm. Melanosome absorption coefficients were also estimated, and decreased with increasing wavelength. These values were compared to retinal pigment epithelium coefficients, and to water absorption, over the same wavelength range. Corneal total intraocular energy retinal damage threshold values were estimated and compared to the previous (2007) and recently changed (2014) maximum permissible exposure (MPE) safe levels. Results provide additional data that support the recent changes to the MPE levels, as well as the first microcavitation data at 1540 nm, a wavelength for which melanosome microcavitation may be an ns-pulse skin damage mechanism.

Trends in melanosome microcavitation thresholds for nanosecond pulse exposures in the near infrared.

Thresholds for microcavitation of bovine and porcine melanosomes were determined using nanosecond laser pulses in the near-infrared (1000 to 1319 nm) wavelength regime. Isolated melanosomes were irradiated by single pulses (10 or 50 ns) using a Q-switched Spectra Physics Nd:YAG laser coupled with an optical parametric oscillator (1000 to 1200 nm) or a continuum laser at 1319 nm. Time-resolved nanosecond strobe photography after the arrival of the irradiation beam allowed imaging of microcavitation events. Average fluence thresholds for microcavitation increased nonlinearly with increasing wavelength from ∼0.5 J/cm2 at 1000 nm to 2.6 J/cm2 at 1319 nm. Fluence thresholds were also measured for 10-ns pulses at 532 nm and found to be comparable to visible nanosecond pulse values published in previous reports. Calculated melanosome absorption coefficients decreased from 925 cm-1 at 1000 nm to 176 cm-1 at 1319 nm. This trend was found to be comparable to the decrease in retinal pigmented epithelial layer absorption coefficients reported over the same wavelength region. Estimated corneal total intraocular energy retinal damage threshold values were determined in order to compare to current and proposed maximum permissible exposure (MPE) safe levels. Results from this study support recently proposed changes to the MPE levels.

Thresholds for phosphatidylserine externalization in Chinese hamster ovarian cells following exposure to nanosecond pulsed electrical fields (nsPEF).

High-amplitude, MV/m, nanosecond pulsed electric fields (nsPEF) have been hypothesized to cause nanoporation of the plasma membrane. Phosphatidylserine (PS) externalization has been observed on the outer leaflet of the membrane shortly after nsPEF exposure, suggesting local structural changes in the membrane. In this study, we utilized fluorescently-tagged Annexin V to observe the externalization of PS on the plasma membrane of isolated Chinese Hamster Ovary (CHO) cells following exposure to nsPEF. A series of experiments were performed to determine the dosimetric trends of PS expression caused by nsPEF as a function of pulse duration, τ, delivered field strength, ED, and pulse number, n. To accurately estimate dose thresholds for cellular response, data were reduced to a set of binary responses and ED50s were estimated using Probit analysis. Probit analysis results revealed that PS externalization followed the non-linear trend of (τ*ED (2))(-1) for high amplitudes, but failed to predict low amplitude responses. A second set of experiments was performed to determine the nsPEF parameters necessary to cause observable calcium uptake, using cells preloaded with calcium green (CaGr), and membrane permeability, using FM1-43 dye. Calcium influx and FM1-43 uptake were found to always be observed at lower nsPEF exposure parameters compared to PS externalization. These findings suggest that multiple, higher amplitude and longer pulse exposures may generate pores of larger diameter enabling lateral diffusion of PS; whereas, smaller pores induced by fewer, lower amplitude and short pulse width exposures may only allow extracellular calcium and FM1-43 uptake.

Trends in retinal damage thresholds from 100-millisecond near-infrared laser radiation exposures: a study at 1,110, 1,130, 1,150, and 1,319 nm.

BACKGROUND AND OBJECTIVES: Retinal damage thresholds from 100-millisecond exposures to laser radiation for wavelengths between 1,100 and 1,350 nm have never previously been established. We sought to determine the retinal damage threshold for 100-millisecond exposures of near-infrared (NIR) laser radiation wavelengths at 1,110, 1,130, 1,150, and 1,319 nm. These data were then used to create trends for retinal damage thresholds over the 1,100-1,350 nm NIR region based upon linear absorption of laser radiation in ocular media and chromatic dispersion of the eye. MATERIALS AND METHODS: The paramacula and macula areas of the retina in Macaca mulatta (rhesus) subjects were exposed for 100 milliseconds to NIR laser radiation wavelengths using a Coherent OPO laser for 1,110, 1,130, and 1,150 nm and a Lee laser for 1,319 nm. Probit analysis was used to establish the estimated damage threshold in the retina for 50% of exposures (ED(50)). Using trends of transmitted energy to the retina, refractive error of the eye and linear absorption of the retina, a scaling factor (SF) method was created to fit the experimental data, predicting retinal damage thresholds over the 1,100-1,350 nm region. RESULTS: The experimental retinal damage threshold, ED(50), for 100-millisecond exposures for laser radiation wavelengths at 1,110, 1,130, and 1,319 nm were determined to be 193, 270, and 13,713 mW of power delivered to the cornea, respectively. The retinal damage threshold for the 1,150 nm wavelength was statistically undetermined due to laser-power limitations, but was achieved in one out of three subjects tested. CONCLUSION: The SF predicts the experimental 100- millisecond NIR ED(50) value for wavelengths between 1,100 and 1,350 nm.

First-order model of thermal lensing in a virtual eye.

An ABCD beam-propagation method was used to build a first-order mathematical model of a thermal lens effect from a near-infrared laser beam in water and ocular media. The model was found to fit experimental z-scan data best when the thermo-optic coefficient dn/dT of liquid water at 292 K was -4.46x10(-5) K(-1). The physiological parameters of the human eye were simulated in a simple eye model using this fitted dn/dT value. Conservative model simulations for 1150 and 1318 nm laser radiation include parameter sets used in experimental ocular exposures performed by Zuclich et al. [Health Phys.92, 15 (2007)] to illustrate the transient response of the thermal lens approaching the limits of the retinal damage thresholds for equivalent laser radiation sources.

Thermal lensing in ocular media exposed to continuous-wave near-infrared radiation: the 1150-1350-nm region.

Ocular damage threshold data remain sparse in the continuous wave (CW), near-infrared (NIR) radiation region save for the 1300-nm area that has been investigated in the past several decades. The 1300-nm ocular damage data have yielded unusual characteristics where CW retinal damage was observed in rabbit models, but never in nonhuman primate models. This paper reviews the existing 1300-nm ocular damage threshold data in terms of the fundamental criteria of an action spectrum to assist in explaining laser-tissue effects from near-infrared radiation in the eye. Reviewing the action spectrum criteria and existing NIR retinal lesion data lend evidence toward the significant presence of thermal lensing in ocular media affecting damage, a relatively unexplored mechanism of laser-tissue interaction.