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Dovepress Low-level light therapy sham embolized group and in an absolute increase in ATP content of 22.5% compared to naive rabbits. This effect was maximized when a higher LLLT energy was delivered as a pulse. When five and 35 times more energy was delivered, the amount of cortical ATP increased 157% and 221% compared to the sham embolized group, respectively.93 Encouraging results from a recent clinical study suggest that LLLT is safe and might be effective in the treatment of ischemic stroke in humans.94 The NeuroThera Effectiveness and Safety Trial-1 tested the safety and effectiveness of LLLT at 808 nm to improve the 90-day outcomes in ischemic stroke given within 24 hours from stroke onset. This study included 120 patients with National Institutes of Health Stroke Scale (NIHSS) scores of 7–22. Patients receiving thrombolytic therapy were excluded. The primary outcome measure was a complete recovery at day 90 (NIHSS 0–1) or a decrease in NIHSS score of at least nine points. Median time to treatment was 18 hours. Among the 79 treated patients, 38% achieved both a final NIHSS score of 0–1 and improved by more than nine points, 20% had only a more than nine-point improve- ment, 11% obtained a final score of 0–1 without improving by more than nine, and 30% achieved neither end point. Among the 41 control patients the corresponding proportions were 29%, 7%, 15%, and 49%. The mortality rates and adverse effects were similar in the treated and control groups.94 However, a larger follow-up multicenter double-blind study that randomized 660 patients to LLLT or sham showed no significant difference in favorable outcomes, although favorable trends were observed in the LLLT group for less disability at 90 days. In this second study, LLLT seemed to benefit patients with lower NIHSS scores at baseline.95 Together, these experiments provide in vivo evidence that the effects of LLLT on cytochrome oxidase and nitric oxide play a major role in the neuroprotective action of LLLT against ischemia and possibly other metabolic insults, such as the LLLT benefits found after traumatic brain injury in ani- mals96 and humans.97 Current clinical trials are investigating the beneficial effects of transcranial LLLT in the rehabilita- tion of hemiplegic patients after ischemic stroke.98 Further clinical research is expected to improve the understanding of LLLT effects in stroke and neurotrauma patients. Parkinson’s disease The protective effects of LLLT have also been demonstrated in paradigms of neurodegeneration. Shaw et al99 showed that LLLT has a potential application in the treatment of Parkinson’s disease. This group tested the neuroprotective effects if LLLT in a mouse in vivo model of dopaminergic Eye and Brain 2011:3 degeneration induced by the neurotoxin 1-methyl-4- phenyl-1,2,3,6-tetrahydropyridine (MPTP). LLLT was given 15 minutes after MPTP intraperitoneal injection at 670 nm and 40 mW/cm2. A total dose of 2 J/cm2 was delivered in four fractions of 9 seconds evenly spaced over 30 hours. Approximately 10% of the power density reaching the skull reached the brain. Two days after MPTP injection, there was a 45% reduction in the number of dopaminergic cells in the substantia nigra compared to saline-treated controls. LLLT completely prevented the loss of dopaminergic cells in the substantia nigra. When the dose of MPTP was doubled, there was an even more profound decrease in dopaminergic cells of 60%. However, LLLT limited the neurodegeneration induced by this higher MPTP dose to only 30% compared to control. This study not only offered evidence that LLLT induces neuroprotective effects against dopaminergic toxins in vivo, but that its effects reach structures deep in the brain. Cognition and emotional states Among the most fascinating experimental applications of LLLT are those related to enhancement of normal brain func- tion and the treatment of memory loss and mood disorders. Cognitive impairment and neurodegeneration associated with dementia have been shown to have regional brain metabolic deficits in early stages of the neurodegenerative process. For example, early decreases in brain metabolic activity can be detected in patients at risk of developing Alzheimer’s disease, especially reductions in cytochrome oxidase activity.100,101 Similarly, the phenotypic expression of mood disorders such as major depression and post-traumatic stress disorder have been shown to be associated with decreased meta- bolic capacity in prefrontal brain regions,102 and electrical stimulation of prefrontal cortex has antidepressant effects.103 LLLT is expected to enhance the metabolic capacity in those regions showing functional deficits, thus increasing the functional connectivity of the networks involved in the expression of a particular phenotype. This is in addition to the potential neuroprotective effects that LLLT may have in tissue susceptible to neurodegeneration. Michalikova et al104 demonstrated improvement in working memory using LLLT in middle-aged mice tested in an appetitive spatial navigation task. Such memory improvements occurred in the absence of nonspecific effects on exploratory activity or anxiety responses. This study used LLLT at 1072 nm that was given in 10 fractions, one fraction per day. However, no other LLLT dose parameters such as power density or energy density were reported. Mice treated with LLLT showed higher latencies to make a choice, but with improved correct choice rates. Indeed submit your manuscript | www.dovepress.com Dovepress 63PDF Image | Low-level light therapy of the eye and brain
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