Concussionology® - Master The Complex
Research 40
Laser Therapy Within 4 Hours
Comment by Dr. Mladenoff
Low Level Laser Therapy within 4 hours of mild insult to the brain will provide a protective effect a secondary brain injury.
LLLT suppressed proinflammatory cytokine expression like (IL)-1β and IL-6. Stemming the neuroinflammatory cascade is critical in prevent the metabolic cascade of events that increases susceptability of a second brain injury but also helps minimize or prevent the triggering of apoptosis.
How many treatments?
wave length of LLLT ?
Low-level laser therapy effectively prevents secondary brain injury induced by immediate early responsive gene X-1 deficiency
Qi Zhang, Chang Zhou, Michael R Hamblin, Mei X Wu
Journal of Cerebral Blood Flow and Metabolism 2014, 34 (8): 1391-401
A mild insult to the brain can sometimes trigger secondary brain injury, causing severe postconcussion syndrome, but the underlying mechanism is ill understood. We show here that secondary brain injury occurs consistently in mice lacking immediate early responsive gene X-1 (IEX-1), after a gentle impact to the head, which closely simulates mild traumatic brain injury in humans. The pathologic lesion was characterized by extensive cell death, widespread leukocyte infiltrates, and severe tissue loss. On the contrary, a similar insult did not induce any secondary injury in wild-type mice. Strikingly, noninvasive exposure of the injured head to a low-level laser at 4 hours after injury almost completely prevented the secondary brain injury in IEX-1 knockout mice. The low-level laser therapy (LLLT) suppressed proinflammatory cytokine expression like interleukin (IL)-1β and IL-6 but upregulated TNF-α. Moreover, although lack of IEX-1 compromised ATP synthesis, LLLT elevated its production in injured brain. The protective effect of LLLT may be ascribed to enhanced ATP production and selective modulation of proinflammatory mediators. This new closed head injury model provides an excellent tool to investigate the pathogenesis of secondary brain injury as well as the mechanism underlying the beneficial effect of LLLT.
Qi Zhang, Chang Zhou, Michael R Hamblin, Mei X Wu
Journal of Cerebral Blood Flow and Metabolism 2014, 34 (8): 1391-401
A mild insult to the brain can sometimes trigger secondary brain injury, causing severe postconcussion syndrome, but the underlying mechanism is ill understood. We show here that secondary brain injury occurs consistently in mice lacking immediate early responsive gene X-1 (IEX-1), after a gentle impact to the head, which closely simulates mild traumatic brain injury in humans. The pathologic lesion was characterized by extensive cell death, widespread leukocyte infiltrates, and severe tissue loss. On the contrary, a similar insult did not induce any secondary injury in wild-type mice. Strikingly, noninvasive exposure of the injured head to a low-level laser at 4 hours after injury almost completely prevented the secondary brain injury in IEX-1 knockout mice. The low-level laser therapy (LLLT) suppressed proinflammatory cytokine expression like interleukin (IL)-1β and IL-6 but upregulated TNF-α. Moreover, although lack of IEX-1 compromised ATP synthesis, LLLT elevated its production in injured brain. The protective effect of LLLT may be ascribed to enhanced ATP production and selective modulation of proinflammatory mediators. This new closed head injury model provides an excellent tool to investigate the pathogenesis of secondary brain injury as well as the mechanism underlying the beneficial effect of LLLT.