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      Traumatic brain injury (TBI) is the leading cause of disability and death in children and adolescents in the U.S.; according to a report by the Centers for Disease Control and Prevention1,2.  Those aged 0 to 19 years, represent an average of 62,000 children annually who sustain brain injuries requiring hospitalization because of motor vehicle crashes, falls, sports injuries, and physical abuse while 564,000 children are seen in hospital emergency departments for TBI and released.
 
 
    Many times, these apparently normal children go on to develop learning disabilities and emotional problems leading to the disruption of family life.  Frequently, these symptoms are met with the standards of medical care with the child being placed on one or more mood-altering medications instead of having an investigation looking for the root causes. 
 
 
    Traumatic Brain injury (TBI) has an insidious component that drives the progression of brain loss in all ages; notably due to oxidative stress associated with inflammation.  Oxidative stress is another name for the damaged brain’s production of an excessive number of free radicals. These free radicals can lead to damage of brain cells (neurons) which can lead to alteration in our mental abilities and personality.  Medical journal articles are now associating brain inflammation with depression, schizophrenia, anxiety, and autism3,4.
 
 
    The Millennium-TBI Centers has been successfully treating adult patients for more than 13 years with a combination of hormonal replacement and the reduction of inflammatory chemistry5. Over the years, medical literature is supporting the position that brain inflammation can cause a number of mood and cognitive disorders. Therefore, the use of products that can reduce this inflammation may spare their damaging effects.
 
 

     We believe, based upon the overwhelming medical literature that the proactive treatment of a child who has sustained a TBI must be addressed. After a traditional medical work-up proves that there are no imminent and urgent problems, the use of TBI-Defense® can be considered as a supplementary treatment addressing the indolent but deleterious brain inflammation.

 
 

1. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths Langlois JA, Rutland-Brown W, Thomas KE.. Atlanta (GA): Centers for Disease Control and Prevention; 2004.

2. A population-based comparison of clinical and outcome characteristics of young children with serious inflicted and non-inflicted traumatic brain injury Keenan HT, Runyan DK, Marshall SW, Nocera MA, Merten DF.. Pediatrics. 2004 Sep;114(3):633-9. 

3. The role of markers of inflammation in traumatic brain injury.  Frontiers in Neurology, 2013. Thomas Woodcock, Maria Cristina Morganti-Kossmann. Australia Dept of Epidemiology and Preventive Medicine, Australian and New Zealand Intensive Care Research Centre, Monash University, Melbourne, VIC, Australia.


4. Understanding the neuro-inflammatory response following concussion to develop treatment strategies. Frontiers in cellular neuroscience, 2012. Zachary R. Patterson, Matthew R. Holahan Department of Neuroscience, Carleton University, Ottawa, ON, Canada

5. Pathophysiology of traumatic brain injury. British Journal of Anaesthesia 99 (1): 4–9 (2007)Werner, C, Engelhard, K. Klinik fur Anasthesiologie, der Johannes Gutenberg-Universitat Mainz, Langenbeckstrasse 1,D-55131 Mainz, Germany


6. The role of inflammation and microglial activation in the pathophysiology of psychiatric disorders. G. Z. REUS, G. R. FRIES,  L. STERTZ. Neuroscience (2015) Center for Translational Psychiatry, Dept of Psychiatry and Behavioral Sciences, U of Texas Medical School at Houston, Houston, TX, USA

 


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