The present review summarizes findings in our continuing study of the use of low-power laser irradiation (LPLI) in the treatment of severely injured peripheral (PNS) and central nervous systems (CNS). The radiation method was proposed by Rochkind and has been modified over the last 13 years. LPLI in specific wavelengths and energy density maintains the electrophysiological activity of severely injured peripheral nerve in rats, preventing scar formation (at injury site) as well as degenerative changes in the corresponding motor neurons of the spinal cord, thus accelerating regeneration of the injured nerve. Laser irradiation applied to the spinal cord of dogs following severe spinal cord injury and implantation of a segment of the peripheral nerve into the injured area diminished glial scar formation, induced axonal sprouting in the injured area and restoration of locomotor function. The use of laser irradiation in mammalian CNS transplantation shows that laser therapy prevents extensive glial scar formation (a limiting factor in CNS regeneration) between a neural transplant and the host brain or spinal cord. Abundant capillaries developed in the laser-irradiated transplants, and was of crucial importance in their survival. Intraoperative clinical use of laser therapy following surgical treatment of the tethered spinal cord (resulting from myelomeningocele, lipomyelomeningocele, thickened filum terminale or fibrous scar) increases functional activity of the irradiated spinal cord. In a previous experimental work, we showed that direct laser treatment on nerve tissue promotes restoration of the electrophysiological activity of the severely injured peripheral nerve, prevents degenerative changes in neurons of the spinal cord and induces proliferation of astrocytes and oligodendrocytes. This suggested a higher metabolism in neurons and improved ability for myelin production under the influence of laser treatment. The tethering of the spinal cord causes mechanical damage to neuronal cell membranes leading to metabolic disturbances in the neurons. For this reason, we believe that using LPLI may improve neuronal metabolism, prevent neuronal degeneration and promote improved spinal cord function and repair. The possible mechanism of LPLI is investigated. Using electron paramagnetic resonance in cell culture models, we found that at low radiation doses, singlet oxygen is produced by energy transfer from porphyrin (not cytochrome as commonly assumed) which is known to be present in the cell. At low concentration, singlet oxygen can modulate biochemical processes taking place in the cell and trigger accelerated cell division. On the other hand, at high concentration, singlet oxygen damages the cell. We show that when irradiating NIH fibroblastic cells with 632 nm wavelength, accelerated cell mitosis occurs at low energy doses, and cell destruction at high energy doses. 360 nm is much more effective than 632 nm. This concurs with the fact that porphyrins have an intense absorption band in the 360 nm region and five additional absorption bands decreasing in intensity at 502, 540, 560 and 630 nm. Previous experimental findings both supplement and substantiate the clinical results, which showed that LPLI has a 'preventive' and therapeutic effect which can be used in different neurosurgical situations associated with peripheral and central nervous system injuries and disorders.