Effects of 1.32-μm Nd-YAG laser on brain thermal and histological experimental data

Considering that the 1.32-μm Nd-YAG laser should have physicothermal properties close to those of the CO₂ laser, a series of experiments were conducted on rat cortex (N = 51). Three laser wavelengths were compared: CO₂ laser (10.6 μm), 1.06-μm Nd-YAG, and 1.32-μm Nd-YAG lasers. For each shot, temperature measurements were recorded with an infrared thermographic videocamera. The digitized signals were figured as thermal profiles and temperature developments. Ninety-five shots were correctly studied and analyzed: CO₂, N = 29; 1.06-μm Nd-YAG, N = 20; 1.32-μm Nd-YAG, N = 46. The histological lesions produced by these three lasers were compared on animals killed 24 hours (N = 20), 8 days (N = 20), and 30 days (N = 5) after the laser impacts. For equivalent densities of energy, the depth of cortical necrosis was comparable for the CO₂ laser (200–250 μm) and the 1.32-μm Nd-YAG laser (210–260μm) whatever the date of death; the 1.06-μm Nd-YAG laser shots were responsible for much more important damage (400–550μm). Because of its important absorption in water and nervous tissue, the authors consider the 1.32-μm Nd-YAG laser most suitable for neurosurgery, particularly because it is conducted through optic fibers, and therefore is easy to handle during neurosurgical procedures.     

Development and experimental in vivo validation of mathematical modeling of laser coagulation

Most clinical procedures using the laser are based on thermal laser-tissue interactions. The treatment often consists of inducing damage of given degree and extent by heating the tissue. The aim of this study was to develop a model called HELIOS. The ability of HELIOS to predict thermal coagulation was evaluated by comparison with in vivo experimental results. Conversion of laser light in tissue was studied using the beam-broadening model. Temperature was described by the heat conduction equation solved using the finite difference method. The tissue dena-turation was modeled by the Henriques equation leading to the determination of the damage coefficient ω. For a given set of laser and tissue parameters, HELIOS makes a graphic representation of coagulation necrosis and temperature evolution in tissue. HELIOS was validated by experimental studies in vivo on rat liver using a CW Nd:YAG laser, a CO₂ laser, and an argon laser. For given sets of laser parameters, temperature measurements were performed using an infrared camera. Histological examinations were carried out on samples to quantify the depth of coagulation necrosis. Experimental data obtained in vivo were compared with those calculated using HELIOS and similar sets of parameters. The difference between the predicted temperature evolution on tissue surface and that measured by the infrared camera was < 5°C in all cases. The difference between the predicted coagulation necrosis depth and the corresponding experimental one was < 10%. In conclusion, HELIOS allows good prediction of tissue temperature and coagulation necrosis. © 1994 Wiley-Liss, inc.     

Localization of a gene for otosclerosis to chromosome 15q25-q26

Among white adults otosclerosis is the single most common cause of hearing impairment. Although the genetics of this disease are controversial, the majority of studies indicate autosomal dominant inheritance with reduced penetrance. We studied a large multi- generational family in which otosclerosis has been inherited in an autosomal dominant pattern. Five of16 affected persons have surgically confirmed otosclerosis; the remaining nine have a conductive hearing loss but have not undergone corrective surgery. To locate the disease- causing gene we completed genetic linkage analysis using short tandem repeat polymorphisms (STRPs) distributed over the entire genome. Multipoint linkage analysis showed that only one genomic region, on chromosome 15q, generated a lod score >2.0. Additional STRPs were typed in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis gene.