Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, December 2, 2014

Augmentation of cognitive brain functions with transcranial lasers

No idea on this one, ask your doctor for guidance.

Augmentation of cognitive brain functions with transcranial lasers

Discovering that transcranial infrared laser stimulation produces beneficial effects on frontal cortex functions such as sustained attention, working memory, and affective state has been groundbreaking. Transcranial laser stimulation with low-power density (mW/cm2) and high-energy density (J/cm2) monochromatic light in the near-infrared wavelengths modulates brain functions and may produce neurotherapeutic effects in a nondestructive and non-thermal manner (Lampl, 2007; Hashmi et al., 2010). Barrett and Gonzalez-Lima (2013) provided the first controlled study showing that transcranial laser stimulation improves human cognitive and emotional brain functions. But for the field of low-level light/laser therapy (LLLT), development of a model of how luminous energy from red-to-near-infrared wavelengths modulates bioenergetics began with in vitro and in vivo discoveries in the last 40 years. Previous LLLT reviews have provided extensive background about historical developments, principles and applications (Rojas and Gonzalez-Lima, 2011, 2013; Chung et al., 2012). The purpose of this paper is to provide an update on LLLT's neurochemical mechanisms supporting transcranial laser stimulation for cognitive-enhancing applications. We will explain first LLLT's action on brain bioenergetics, briefly describe its bioavailability and dose-response, and finish with its beneficial effects on cognitive functions. Although our focus is on prefrontal-related cognitive functions, in principle LLLT should be able to modulate other brain functions. For example, stimulating different brain regions should affect different functions related to sensory and motor systems.

Brain bioenergetics

The way that near-infrared lasers and light-emitting diodes (LEDs) interact with brain function is based on bioenergetics, a mechanism that is fundamentally different than that of other brain stimulation methods such as electric and magnetic stimulation. LLLT has been found to modulate the function of neurons in cell cultures, brain function in animals, and cognitive and emotional functions in healthy persons and clinical conditions. Photoneuromodulation involves the absorption of photons by specific molecules in neurons that activate bioenergetic signaling pathways after exposure to red-to-near-infrared light. The 600–1150 nm wavelengths allow better tissue penetration by photons because light is scattered at lower wavelengths and absorbed by water at higher wavelengths (Hamblin and Demidova, 2006). Over 25 years ago, it was found that molecules that absorb LLLT wavelengths are part of the mitochondrial respiratory enzyme cytochrome oxidase in different oxidation states (Karu et al., 2005). Thus, for red-to-near-infrared light, the primary molecular photoacceptor of photon energy is cytochrome oxidase (also called cytochrome c oxidase or cytochrome a-a3) (Pastore et al., 2000).
Therefore, photon energy absorption by cytochrome oxidase is well-established as the primary neurochemical mechanism of action of LLLT in neurons (Wong-Riley et al., 2005). The more the enzymatic activity of cytochrome oxidase increases, the more metabolic energy that is produced via mitochondrial oxidative phosphorylation. LLLT supplies the brain with metabolic energy in a way analogous to the conversion of nutrients into metabolic energy, but with light instead of nutrients providing the source for ATP-based metabolic energy (Mochizuki-Oda et al., 2002). If an effective near-infrared light energy dose is supplied, it stimulates brain ATP production (Lapchak and De Taboada, 2010) and blood flow (Uozumi et al., 2010), thereby fueling ATP-dependent membrane ion pumps, leading to greater membrane stability and resistance to depolarization, which has been shown to transiently reduce neuronal excitability (Konstantinovic et al., 2013). On the other hand, electromagnetic stimulation directly changes the electrical excitability of neurons.
A long-lasting effect is achieved by LLLT's up-regulating the amount of cytochrome oxidase, which enhances neuronal capacity for metabolic energy production that may be used to support cognitive brain functions. In mice and rats, memory has been improved by LLLT (Michalikova et al., 2008; Rojas et al., 2012a) and by methylene blue, a drug that at low doses donates electrons to cytochrome oxidase (Rojas et al., 2012b). Near-infrared light stimulates mitochondrial respiration by donating photons to cytochrome oxidase, because cytochrome oxidase is the main acceptor of photons from red-to-near-infrared light in neurons. By persistently stimulating cytochrome oxidase activity, transcranial LLLT induces post-stimulation up-regulation of the amount of cytochrome oxidase in brain mitochondria (Rojas et al., 2012a). Therefore, LLLT may lead to the conversion of luminous energy into metabolic energy (during light exposure) and to the up-regulation of the mitochondrial enzymatic machinery to produce more energy (after light exposure).

Conclusions

Transcranial absorption of photon energy by cytochrome oxidase, the terminal enzyme in mitochondrial respiration, is proposed as the bioenergetic mechanism of action of LLLT in the brain. Transcranial LLLT up-regulates cortical cytochrome oxidase and enhances oxidative phosphorylation. LLLT improves prefrontal cortex-related cognitive functions, such as sustained attention, extinction memory, working memory, and affective state. Transcranial infrared stimulation may be used efficaciously to support neuronal mitochondrial respiration as a new non-invasive, cognition-improving intervention in animals and humans. This fascinating new approach should also be able to influence other brain functions depending on the neuroanatomical site stimulated and the stimulation parameters used.


Lots more at link including references for your doctor to verify this research.
 

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