Near-infrared light (NIR) has been investigated for its ability to modulate intracellular mechanisms related to healing. The application of NIR by low-power laser or by light-emitting diode (LED) is also known as laser phototherapy or near-infrared photobiomodulation. NIR can facilitate wound healing, promote muscle repair, and stimulate angiogenesis. NIR phototherapy has been studied and applied clinically in a wide array of ailments, including skin ulcers, osteoarthritis, peripheral nerve injury, low back pain, myocardial infarction, and stem cell induction.
The finding that NIR passes relatively efficiently through bone has spurred interest in its application to treating disorders of the brain. Over the past decade, transcranial near-infrared light therapy (NILT) has been studied in animal models to understand its ability to repair damaged or dysfunctional brain tissue resulting from stroke and TBI. The first published study of NILT for TBI in humans described two cases of chronic mTBI with significant disability. Each patient was treated with an LED device delivering low level (red and near infrared) light therapy (LLLT) for 6-10 minutes per area daily for several months. Both patients had marked neuropsychological improvement after a minimum of 7-9 months of LLLT treatment.
The precise mechanisms underlying photobiomodulation and its therapeutic benefits are not fully understood. Purportedly, light in the wavelength range of 600 – 1,200 nm has significant photobiomodulation capability. Current data most strongly support that absorption of NIR photons by cytochrome-c-oxidase in the mitochondrial respiratory chain is the key initiating event in photobiomodulation. This induces an increase in cytochrome-c-oxidase activity which in turn increases adenosine triphosphate (ATP) production. Such an increase in ATP in wounded or underperfused cells may be sufficient to activate cells in areas of injury or metabolic derangement. Data from numerous tissue culture and animal studies point to the importance of several secondary molecular and cellular events. For example, NIR can modulate reactive oxygen species, activate mitochondrial DNA replication, increase early-response genes, increase growth factor expression, induce cell proliferation, and alter nitric oxide (NO) levels.
When examined in the specific model of neural tissue injury, NILT can lead to demonstrable neural repair and recovery. For example, LLLT of a power density of 0.9 – 36 J/cm2 applied at 24 hours post-stroke in a rodent model yielded a 32% reduction in neurological deficits, as well as histochemical evidence of neuron proliferation and migration. LLLT had similar benefits in a rodent model of TBI. Interestingly, these cellular changes evolved over a period of days after light exposure and persisted for considerably longer than the interval of actual NIR exposure. These findings are consistent with a progressive regeneration cascade set in motion by the NIR exposure.
