Transcranial Near-infrared Laser Therapy Research Articles

Transcranial Near-infrared Laser Therapy in Improving Cognitive Recovery of Function Following Traumatic Brain Injury.

: Traumatic brain injury (TBI) has turned into a major health and socioeconomic problem affecting young people and military personnel. Numerous TBI patients experienced the sequela of brain injury called cognitive impairment, which re-duced functions in attention, working memory, motivation, and execution. In recent years, transcranial near-infrared laser therapy (tNiRLT) as a possible therapy has been gradually applied in treating cognitive impairment post-TBI. In the present review, the biological mechanisms of transcranial tNiRLT for TBI are synthesized mainly based on the photonic impact of chronic mild TBI. Various exciting molecular events possibly occur during the procedure, such as stimulation of ATP pro-duction, regional cerebral blood flow, acupoint, neurogenesis and synaptogenesis, as well as a reduction in anti-inflammatory effect. Some animal experiments and clinical studies of tNiRLT for TBI are outlined. Several labs have displayed that tNiRLT is effective not only in improving neurological functions but also in increasing memory and learning capacity in ro-dent animals’ model of TBI. In a 2 patients case report and a 11-case series, cognitive functions were ameliorated. Efficacy on cognitive and emotional effects was also observed in a double-blind, controlled clinical study. Several Randomized, paral-lel, double blind, sham-controlled trials are underway, aiming to evaluate the efficacy of tLED on cognitive functions and neuropsychiatric status in participants post-TBI. Therefore, tNiRLT is a promising method applied to cognitive impairment following TBI.

Thermal effects of transcranial near-infrared laser irradiation on rabbit cortex

Transcranial near-infrared laser therapy (TLT) improves stroke outcome in animal models. Adequate laser doses are necessary to exert therapeutic effects. However, applying higher laser energy may cause cortical tissue heating and exacerbate stroke injury. The objective of this study is to examine the thermal effect and safety of transcranial near-infrared laser therapy. Diode laser with a wavelength of 808nm was used to deliver different power densities to the brain cortex of rabbits. Cortical temperature was monitored and measured using a thermal probe during the 2min transcranial laser irradiation. Neuro-pathological changes were examined with histological staining 24h after laser treatment. Transcranial laser irradiation for 2min at cortical power densities of 22.2 and 55.6mW/cm2 with continuous wave (CW) did not increase cortical temperature in rabbits. With the same treatment regime, cortical power density at 111.1mW/cm2 increased brain temperature gradually by 0.5°C over the 2min exposure and returned to baseline values within 1–2min post-irradiation. Separately, histological staining was evaluated after triple laser exposure of 22.2mW/cm2 CW and 111.1mW/cm2 pulse wave (PW) and showed normal neural cell morphology. The present study demonstrated that the TLT powers currently utilized in animal stroke studies do not cause cortical tissue heating and histopathological damage.

Incremental treatments with laser therapy augments good behavioral outcome in the rabbit small clot embolic stroke model

Transcranial near-infrared laser therapy (TLT) improves behavioral outcome in animal stroke models when applied as single treatment within the 24h of the stroke onset. It is unknown if the multiple TLT treatments have an added beneficial effect. We aim to determine whether multiple irradiations with TLT would have further improvement in behavioral outcomes in the rabbit small clot embolic stroke model (RSCEM). Using the RSCEM, two and three TLT treatments (7.5-20mW/cm(2)) were compared against single laser treatment alone (7.5-10.8mW/cm(2)). Two sham irradiation groups were added for the control curves. The double treatment group received TLT at 3 and 5h and the triple treatment group at 2, 3, and 4h after embolization. Behavioral analysis was conducted 24h after embolization using a dichotomized behavioral score. The determination of the effective clot amount (milligrams) that produces neurological deficits in 50% of the rabbits (P 50) was used to compare TLT treatments with the sham. The P 50 for double treatment was 5.47 ± 0.90, with n = 39; the corresponding P 50 value for a single treatment was 3.87 ± 0.73, with n = 38; and the corresponding control curve was 3.25 ± 0.4, n = 32. The P 50 for triple treatment was 5.91 ± 0.49, with n = 23; the corresponding P 50 value for a single treatment was 3.09 ± 0.59, with n = 15, and the corresponding control curve was 1.71 ± 0.26, with n = 17. The triple treatment had 91% improvement when compared with the single treatment and 245% improvement when compared with the sham. The present study suggests that the additional TLT treatments provide further behavioral improvement when given during the acute ischemic stroke phase.

Transcranial near-infrared laser therapy applied to promote clinical recovery in acute and chronic neurodegenerative diseases

One of the most promising methods to treat neurodegeneration is noninvasive transcranial near-infrared laser therapy (NILT), which appears to promote acute neuroprotection by stimulating mitochondrial function, thereby increasing cellular energy production. NILT may also promote chronic neuronal function restoration via trophic factor-mediated plasticity changes or possibly neurogenesis. Clearly, NILT is a treatment that confers neuroprotection or neurorestoration using pleiotropic mechanisms. The most advanced application of NILT is for acute ischemic stroke based upon extensive preclinical and clinical studies. In laboratory settings, NILT is also being developed to treat traumatic brain injury, Alzheimer’s disease and Parkinson’s disease. There is some intriguing data in the literature that suggests that NILT may be a method to promote clinical improvement in neurodegenerative diseases where there is a common mechanistic component, mitochondrial dysfunction and energy impairment. This article will analyze and review data supporting the continued development of NILT to treat neurodegenerative diseases.

Potential for Transcranial Laser or LED Therapy to Treat Stroke, Traumatic Brain Injury, and Neurodegenerative Disease

Near-infrared (NIR) light passes readily through the scalp and skull and a small percentage of incident power density can arrive at the cortical surface in humans.1 The primary photoreceptors for red and NIR light are mitochondria, and cortical neurons are exceptionally rich in mitochondria. It is likely that brain cells are ideally set up to respond to light therapy. The basic biochemical pathways activated by NIR light, e.g., increased adenosine-5′-triphosphate (ATP) production, and signaling pathways activated by reactive oxygen species, nitric oxide release, and increased cyclic adenosine monophosphate (AMP) all work together to produce beneficial effects in brains whose function has been compromised by ischemia, traumatic injury, or neurodegeneration. One of the main mechanisms of action of transcranial light therapy (TLT) is to prevent neurons from dying, when they have been subjected to some sort of hypoxic, traumatic, or toxic insult. This is probably because of light-mediated upregulation of cytoprotective gene products such as anti-oxidant enzymes, heat shock proteins, and anti-apoptotic proteins. Light therapy in vitro has been shown to protect neurons from death caused by methanol,2 cyanide or tetrodotoxin,3 and amyloid beta peptide.4 There is also probably a second mechanism operating in TLT; increased neurogenesis. Neurogenesis is the generation of neuronal precursors and birth of new neural cells.5 Two key sites for adult neurogenesis include the subventricular zone (SVZ) of the lateral ventricles, and the subgranular layer (SGL) of the dentate gyrus in the hippocampus.6 Neurogenesis can be stimulated by physiological factors, such as growth factors and environmental enrichment, and by pathological processes, including ischemia and neurodegeneration.7 Adult neurogenesis (in the hippocampus particularly) is now recognized as a major determinant of brain function both in experimental animals and in humans. Neural progenitor cells in their niche in the SGL of the dentate gyrus give birth to newly formed neurons that are thought to play a role in brain function, particularly in olfaction and in hippocampal-dependent learning and memory.8 In small animal models neurogenesis can be readily detected by incorporation of bromodeoxyuridine (BrdU), injected before euthanasia, into proliferating brain cells. Increased neurogenesis after TLT, has been demonstrated in a rat model of stroke,9 and in the Hamblin laboratory after TLT for acute traumatic brain injury (TBI) in mice (W. Xuan, T. Ando, et al., unpublished data). These two mechanisms of action of TLT in ameliorating brain damage (prevention of neuronal death and increased neurogenesis) have motivated studies in both animals and humans for diverse brain disorders and diseases. TLT for acute stroke is the most developed,10 but acute TBI has also been shown to benefit from TLT.11 These areas are reviewed further.

Laser-Induced ATP Formation: Mechanism and Consequences

Photomedicine and Laser SurgeryVol. 28, No. 4 Letters to the EditorLaser-Induced ATP Formation: Mechanism and ConsequencesGabi DrochioiuGabi DrochioiuSearch for more papers by this authorPublished Online:12 Aug 2010https://doi.org/10.1089/pho.2009.2651AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"Laser-Induced ATP Formation: Mechanism and Consequences." , 28(4), pp. 573–574FiguresReferencesRelatedDetailsCited byPhotobiomodulation Therapy Improves Spermatogenesis in Busulfan-Induced Infertile Mouse6 April 2021 | Reproductive Sciences, Vol. 28, No. 10Photobiomodulation restores spermatogenesis in the transient scrotal hyperthermia-induced miceLife Sciences, Vol. 254Unusual ferrite induced photohydrolysis of dinitrophenols to nonaromatic and nontoxic derivativesJournal of Photochemistry and Photobiology A: Chemistry, Vol. 394The challenge of effectively translating transcranial near-infrared laser therapy to treat acute ischemic strokePhotobiomodulation improved stereological parameters and sperm analysis factors in streptozotocin-induced type 1 diabetes mellitusJournal of Photochemistry and Photobiology B: Biology, Vol. 186Banned dinitrophenols still trigger both legal and forensic issues22 March 2016 | Environmental Forensics, Vol. 17, No. 1Morphological and Biochemical Answer of the Wheat Seeds at Treatment with 2,4-Dinitrophenol and Potassium IodateBrazilian Archives of Biology and Technology, Vol. 59, No. 0Transcranial Near-Infrared Laser Therapy for Stroke: How to Recover from Futility in the NEST-3 Clinical TrialMeasuring the dynamics of cyclic adenosine monophosphate level in living cells induced by low-level laser irradiation using bioluminescence resonance energy transferJournal of Biomedical Optics, Vol. 20, No. 5Letter: Study on the Mechanism of Ferrite-Induced Dinitrophenol Photodegradation1 April 2014 | European Journal of Mass Spectrometry, Vol. 20, No. 2Genetic expression of adipose derived stem cell and smooth muscle cell markers to monitor differentiation potential following low intensity laser irradiationBone marrow aspirate combined with low-level laser therapy: A new therapeutic approach to enhance bone healingJournal of Photochemistry and Photobiology B: Biology, Vol. 121Quenching of Tryptophan Fluorescence in the Presence of 2,4-DNP, 2,6-DNP, 2,4-DNA and DNOC and Their Mechanism of Toxicity18 February 2013 | Molecules, Vol. 18, No. 2Regenerative Medicine, Stem Cells, and Low-Level Laser Therapy: Future Directives Heidi Abrahamse26 November 2012 | Photomedicine and Laser Surgery, Vol. 30, No. 12Nah-Infrarot-Lasertherapie beim akuten Schlaganfall18 July 2012 | Der Nervenarzt, Vol. 83, No. 8Transcranial near-infrared laser therapy applied to promote clinical recovery in acute and chronic neurodegenerative diseases9 January 2014 | Expert Review of Medical Devices, Vol. 9, No. 1Taking a light approach to treating acute ischemic stroke patients: Transcranial near-infrared laser therapy translational science1 November 2010 | Annals of Medicine, Vol. 42, No. 8 Volume 28Issue 4Aug 2010 InformationCopyright 2010, Mary Ann Liebert, Inc.To cite this article:Gabi Drochioiu.Laser-Induced ATP Formation: Mechanism and Consequences.Photomedicine and Laser Surgery.Aug 2010.573-574.http://doi.org/10.1089/pho.2009.2651Published in Volume: 28 Issue 4: August 12, 2010PDF download

Safety Profile of Transcranial Near-Infrared Laser Therapy Administered in Combination With Thrombolytic Therapy to Embolized Rabbits

Transcranial near-infrared laser therapy (TLT) is currently under investigation in a pivotal clinical trial that excludes thrombolytic therapy. To determine if combining tissue plasminogen activator (tPA; Alteplase) and TLT is safe, this study assessed the safety profile of TLT administered alone and in combination with Alteplase. The purpose for this study is to determine if the combination of TLT and thrombolysis should be investigated further in a human clinical trial. We determined whether postembolization treatment with TLT in the absence or presence of tPA would affect measures of hemorrhage or survival after large clot embolism-induced strokes in New Zealand white rabbits. TLT did not significantly alter hemorrhage incidence after embolization, but there was a trend for a modest reduction of hemorrhage volume (by 65%) in the TLT-treated group compared with controls. Intravenous administration of tPA, using an optimized dosing regimen, significantly increased hemorrhage incidence by 160%. The tPA-induced increase in hemorrhage incidence was not significantly affected by TLT, although there was a 30% decrease in hemorrhage incidence in combination-treated rabbits. There was no effect of TLT on hemorrhage volume measured in tPA-treated rabbits and no effect of any treatment on 24-hour survival rate. In the embolism model, TLT administration did not affect the tPA-induced increase in hemorrhage incidence. TLT may be administered safely either alone or in combination with tPA because neither treatment affected hemorrhage incidence or volume. Our results support the study of TLT in combination with Alteplase in patients with stroke.