Abstract
Background: The most common cause of death and disability after severe trauma in childhood is traumatic brain injury (TBI). Of all trauma deaths, 25% are caused by head injury. Objectives: The complex pathobiology of traumatic brain injury (TBI) offers numerous targets for potential neuroprotective agents. We evaluate the clinical benefit after creatine administration in children and adolescents. Methods: A prospective, randomized, comparative, open – labeled pilot study of the possible neuroprotective effect of creatine was carried out on 39 children and adolescents, aged between one to eighteen years old, with (TBI). The creatine was administered for 6 months at a dose of 0.4gr/kg in an oral suspension form every day. For categorical variables, we used the χ² test (Chi-square test) to identify differences between controls and cases . Statistical significance was defined as a p-value 0.1. Results: The administration of creatine to children and adolescents with TBI improved results in several parameters, including duration of post-traumatic amnesia (PTA), duration of intubation, intensive care unit stay. Significant improvement was recorded in the categories of dysarthria (p<0.001) and lingual problems of understanding (p<0.001) aspects in all patients. No side effects were seen due to creatine administration. Conclusions: More specific examinations for in vivo evaluation of creatine must be performed, in order to draw conclusions for the optimal duration and manner of creatine supply, as well as its possible role for the prevention of TBI complications, in double blind studies.
Highlights
The most common cause of death and disability after severe trauma in childhood is traumatic brain injury (TBI)
Significant improvement was recorded in the categories of dysarthria (p
The secondary injury, defined as cellular damage not immediately apparent after the trauma but developing within minutes, hours, or even days, seems to be related to mitochondria dysfunction associated with the disruption in cellular calcium homeostasis that is known to occur after TBI
Summary
The most common cause of death and disability after severe trauma in childhood is traumatic brain injury (TBI). The secondary injury, defined as cellular damage not immediately apparent after the trauma but developing within minutes, hours, or even days, seems to be related to mitochondria dysfunction associated with the disruption in cellular calcium homeostasis that is known to occur after TBI. Creatine supplementation increases intramuscular and cerebral stores with both creatine, and its phosphorylated form, phosphocreatine [PCr] [3] The increase of these stores may offer therapeutic benefits by stimulating protein synthesis or reducing protein degradation, stabilizing biological membranes, and preventing ATP depletion, which occurs in patients with traumatic brain injury [4].
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