Infrared Laser Therapy: Hope For Stroke Victims?

Infrared laser therapy is a promising treatment for stroke victims, with studies showing that it can aid neuroprotection and repair of the damaged brain. Transcranial near-infrared laser therapy (NILT) is a non-invasive method that uses laser light at a specific wavelength to pass through the skull and activate biochemical processes that protect brain cells from damage and promote the repair of damaged neurons.

Research has shown that infrared laser therapy can increase the production of energy molecules in brain tissue, improving the chances of survival for cells that would normally die after a stroke. It can also increase brain blood flow, leading to improved behavioural and motor function.

However, there are challenges to using infrared laser therapy effectively to treat human stroke victims due to the thickness of the human skull, which can limit light penetration. Further research and funding are needed to optimise treatment parameters and improve the efficacy of infrared laser therapy for stroke.

Transcranial near-infrared laser therapy (NILT) can increase the production of energy molecules in brain tissue

Transcranial near-infrared laser therapy (NILT) is a powerful, non-invasive method to promote neuroprotection and repair of the damaged brain. Research has shown that laser light at a specific wavelength (808nm) can pass through the skull and activate biochemical processes that aid in protecting brain cells from damage and promote the repair of damaged neurons.

NILT works by increasing the production of energy molecules in brain tissue. Specifically, it increases the production of adenosine-5′-triphosphate (ATP) by activating mitochondrial function, the energy producers in cells. By increasing the energy molecules, some of the cells that would normally die after a stroke stand a better chance of surviving.

In a study by Paul A. Lapchak, it was found that laser light penetrating the skull can increase the production of ATP. The study also showed that when ATP was increased, laser therapy significantly improved behavioral function, particularly motor function, following a stroke.

Another study by Lapchak and colleagues found that NILT increases cortical ATP content by 41% when applied with continuous wave (CW) laser delivery. However, when NILT was delivered using a pulse wave (PW) mode, it increased cortical ATP content by 157% and 221%, depending on the specific PW settings.

Overall, NILT has been shown to be a promising treatment for stroke, with potential benefits including neuroprotection, increased cerebral blood flow, and improved behavioral and neurological function.

Laser therapy can help prevent the spread of brain cell death after injury

LLLT can increase the production of energy molecules in brain tissue by activating mitochondrial function, which produces energy for cells. By increasing the number of energy molecules, some of the cells that would normally die after a stroke have a better chance of surviving. LLLT can also increase brain blood flow, which provides oxygen and nutrients to the damaged brain.

The use of LLLT as a treatment for stroke is based on the idea that it can realign homeostatic mechanisms to promote neuronal survival within the "at-risk" area, increasing the function of neuronal circuits and improving clinical presentation. LLLT may also decrease apoptosis and enhance recovery of function through neurogenesis and the production of endogenous neurotrophic factors.

The effectiveness of LLLT depends on finding the optimal parameters, including the total energy delivered, irradiance, power density, and wavelength of the laser. The optimal treatment regimen is also important, as there is a biphasic dose-response relationship, meaning that too much or too little light may be ineffective or even harmful.

Overall, LLLT is a promising treatment for stroke, and further research is needed to optimize its effectiveness and better understand its mechanisms of action.

Low-level laser therapy (LLLT) can reduce inflammation and provide neuroprotection

LLLT can also increase blood flow to the brain, which improves oxygenation in damaged areas. This is achieved by breaking nitric oxide (NO) from cytochrome c oxidase (CCO), which prevents NO from inhibiting CCO and decreasing cellular respiration and ATP production.

LLLT can also reduce inflammation by decreasing the expression of pro-inflammatory cytokines and increasing the expression of anti-inflammatory mediators.

Transcranial low-level laser therapy (tLLLT) can improve cognitive function

TLLLT can also increase brain blood flow and improve behavioural and motor function following a stroke. It can increase adenosine triphosphate (ATP) levels and blood flow by preventing the inhibition of cytochrome c oxidase (CCO) by nitric oxide (NO). This can lead to improved oxygenation in damaged areas of the brain.

Several clinical and preclinical studies have shown that tLLLT can lead to improved recovery from stroke. For example, a study on rats and rabbits showed that intervention by tLLLT within 24 hours of a stroke could have meaningful beneficial effects. Another study on mice with controlled cortical impact (CCI) showed that tLLLT could improve cognitive function, with significant improvements in response time to a hidden platform and probe trial performance.

TLLLT can also increase neurogenesis and synaptogenesis, which may lead to its application as a treatment modality for neurodegenerative diseases.

Infrared laser therapy can be used in combination with a thrombolytic to enhance cerebral reperfusion

Transcranial near-infrared laser therapy (NILT) is a non-invasive method that can be used to promote neuroprotection and repair of the brain after a stroke. NILT works by using laser light at a specific wavelength (808 nm) to pass through the skull and activate biochemical processes that aid in protecting brain cells from damage and promote the repair of damaged neurons. This can be combined with a thrombolytic, such as tissue plasminogen activator (tPA), which is a biological protein that can break down blood clots. When used together, NILT and tPA can enhance cerebral reperfusion and improve the quality of life of stroke victims.

The combination of NILT and tPA has been studied in both animal models and human clinical trials. In animal models, NILT has been shown to reduce brain damage and recovery times in stroke models when applied within 24 hours of the stroke. Clinical trials have also shown that NILT can improve clinical recovery in stroke patients when applied within 24 hours of the stroke.

The benefits of combining NILT and tPA are thought to be due to the ability of NILT to stimulate mitochondrial function and increase the production of energy molecules such as adenosine-5'-triphosphate (ATP). This can help protect brain cells from damage and improve behavioral and motor function following a stroke. The combination of NILT and tPA has been shown to be safe and well-tolerated in both animal models and human clinical trials.

However, there are some challenges and limitations to the use of NILT in stroke treatment. One challenge is the thick human skull, which can attenuate the penetration of light energy and reduce the effectiveness of NILT. Additionally, the optimal parameters for NILT treatment, such as the power density and wavelength, are still being studied and optimized. Furthermore, the current clinical trials of NILT have focused on acute stroke treatment within a narrow time window, and the long-term effects of NILT are still unknown.

Overall, the combination of NILT and a thrombolytic, such as tPA, shows promise as a neuroprotective therapy for stroke victims. However, further research is needed to optimize the treatment parameters and evaluate the long-term effects of NILT.

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