Red Light Therapy Brain Injury

Cognition is the higher neural function of the brain to acquire knowledge and understanding through thought, experience and the senses. A variety of pathologies or disease conditions can lead to cognitive dysfunction and may impair learning and memory with aphasia, dyscalculia, prosopagnosia or dyslexia.

Near-infrared light at 1050 wavelengths penetrates the scalp and skull (approximately 1 cm). Exposure of cells to red and near-infrared light wavelengths induces two physiological changes: 1) an increase in mitochondrial adenosine triphosphate (ATP) production; and 2) an increase in vasodilation/local cerebral blood flow (rCBF). The last enzyme complex of the electron transport chain in the mitochondrial membrane (cytochrome c oxidase) is a photoreceptor for red and near-infrared light. Mitochondrial damage and dysfunction occur after traumatic brain injury ( TBI). Increased mitochondrial ATP production improves cellular respiration, oxygenation and function. Furthermore, in hypoxic/damaged cells, noncovalently bound nitric oxide inhibits cytochrome c oxidase. When mitochondria are exposed to red/near-infrared photons, nitric oxide is released and diffuses outside the cell wall, promoting local vasodilation and increased blood flow.

What the advantages of C320 red light therapy brain injury?

1. Suitable for professionals and home use

2.COZING-C320 is good for brain health

3.320 high power LEDs covering the entire scalp for optimal photon transmission

4.1050 nm light penetrates deep into tissues

The 1050 nm wavelength is located within the near-infrared spectrum, allowing it to reach deeper brain tissue.

5. Frequency adjustable: 1-20,000 Hz can be adjusted

6. For drug therapy, the device is safe and has no side effects.

This pilot, open-protocol study examined whether scalp application of red and near-infrared (NIR) light-emitting diodes (LED) could improve cognition in patients with chronic, mild traumatic brain injury (mTBI). Application of red/NIR light improves mitochondrial function (especially in hypoxic/compromised cells) promoting increased adenosine triphosphate (ATP) important for cellular metabolism. Nitric oxide is released locally, increasing regional cerebral blood flow. LED therapy is noninvasive, painless, and non-thermal (cleared by the United States Food and Drug Administration [FDA], an insignificant risk device).

Eleven chronic, mTBI participants (26–62 years of age, 6 males) with nonpenetrating brain injury and persistent cognitive dysfunction were treated for 18 outpatient sessions (Monday, Wednesday, Friday, for 6 weeks), starting at 10 months to 8 years post- mTBI (motor vehicle accident [MVA] or sports-related; and one participant, improvised explosive device [IED] blast injury). Four had a history of multiple concussions. Each LED cluster head (5.35 cm diameter, 500 mW, 22.2 mW/cm2) was applied for 10 min to each of 11 scalp placements (13 J/cm2). LEDs were placed on the midline from front-to-back hairline; and bilaterally on frontal, parietal, and temporal areas. Neuropsychological testing was performed pre-LED, and at 1 week, and 1 and 2 months after the 18th treatment.

A significant linear trend was observed for the effect of LED treatment over time for the Stroop test for Executive Function, Trial 3 inhibition (p=0.004); Stroop, Trial 4 inhibition switching (p=0.003); California Verbal Learning Test (CVLT)-II, Total Trials 1–5 (p=0.003); and CVLT-II, Long Delay Free Recall (p=0.006). Participants reported improved sleep, and fewer post-traumatic stress disorder (PTSD) symptoms, if present. Participants and family reported better ability to perform social, interpersonal, and occupational functions. These open-protocol data suggest that placebo-controlled studies are warranted.

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