Here is a snippet of some helpful research that I do to help those with concussion, post concussion or suspected traumatic brain injury. it is far more common than you think!
This article here is eye opening:
Pop in and I can help.
Nutr Neurosci. 2018 Feb;21(2):79-91. doi: 10.1080/1028415X.2016.1236174. Epub 2016 Oct 5.
Supplements, nutrition, and alternative therapies for the treatment of traumatic brain injury.
Lucke-Wold BP1,2, Logsdon AF2, Nguyen L2, Eltanahay A3, Turner RC1, Bonasso P2, Knotts C1, Moeck A4, Maroon JC5, Bailes JE6, Rosen CL1.
Studies using traditional treatment strategies for mild traumatic brain injury (TBI) have produced limited clinical success. Interest in treatment for mild TBI is at an all time high due to its association with the development of chronic traumatic encephalopathy and other neurodegenerative diseases, yet therapeutic options remain limited. Traditional pharmaceutical interventions have failed to transition to the clinic for the treatment of mild TBI. As such, many pre-clinical studies are now implementing non-pharmaceutical therapies for TBI. These studies have demonstrated promise, particularly those that modulate secondary injury cascades activated after injury. Because no TBI therapy has been discovered for mild injury, researchers now look to pharmaceutical supplementation in an attempt to foster success in human clinical trials. Non-traditional therapies, such as acupuncture and even music therapy are being considered to combat the neuropsychiatric symptoms of TBI. In this review, we highlight alternative approaches that have been studied in clinical and pre-clinical studies of TBI, and other related forms of neural injury. The purpose of this review is to stimulate further investigation into novel and innovative approaches that can be used to treat the mechanisms and symptoms of mild TBI.
Alternative therapies; Chronic symptoms; Mild traumatic brain injury; Secondary injury cascades; Supplementation
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Neuropharmacology. 2019 Feb;145(Pt B):160-176. doi: 10.1016/j.neuropharm.2018.06.021. Epub 2018 Jun 20.
Novel therapies for combating chronic neuropathological sequelae of TBI.
Ikonomovic MD1, Abrahamson EE2, Carlson SW3, Graham SH2, Dixon CE3.
Traumatic brain injury (TBI) is a risk factor for development of chronic neurodegenerative disorders later in life. This review summarizes the current knowledge and concepts regarding the connection between long-term consequences of TBI and aging-associated neurodegenerative disorders including Alzheimer’s disease (AD), chronic traumatic encephalopathy (CTE), and Parkinsonism, with implications for novel therapy targets. Several aggregation-prone proteins such as the amyloid-beta (Aβ) peptides, tau proteins, and α-synuclein protein are involved in secondary pathogenic cascades initiated by a TBI and are also major building blocks of the hallmark pathological lesions in chronic human neurodegenerative diseases with dementia. Impaired metabolism and degradation pathways of aggregation-prone proteins are discussed as potentially critical links between the long-term aftermath of TBI and chronic neurodegeneration. Utility and limitations of previous and current preclinical TBI models designed to study the link between TBI and chronic neurodegeneration, and promising intervention pharmacotherapies and non-pharmacologic strategies to break this link, are also summarized. Complexity of long-term neuropathological consequences of TBI is discussed, with a goal of guiding future preclinical studies and accelerating implementation of promising therapeutics into clinical trials. This article is part of the Special Issue entitled “Novel Treatments for Traumatic Brain Injury”.
Alpha synuclein; Alzheimer’s disease; Amyloid; Brain trauma; Chronic traumatic encephalopathy; Tau
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Neurotherapeutics. 2010 Jan; 7(1): 91–99.
Use of magnesium in traumatic brain injury
Ananda P. Sencorresponding author1 and Anil Gulati2
Depletion of magnesium is observed in animal brain and in human blood after brain injury. Treatment with magnesium attenuates the pathological and behavioral changes in rats with brain injury; however, the therapeutic effect of magnesium has not been consistently observed in humans with traumatic brain injury (TBI). Secondary brain insults are observed in patients with brain injury, which adversely affect clinical outcome. Systemic administration studies in rats have shown that magnesium enters the brain; however, inducing hypermagnesemia in humans did not concomitantly increase magnesium levels in the CSF. We hypothesize that the neuroprotective effects of magnesium in TBI patients could be observed by increasing its brain bioavailability with mannitol. Here, we review the role of magnesium in brain injury, preclinical studies in brain injury, clinical safety and efficacy studies in TBI patients, brain bioavailability studies in rat, and pharmacokinetic studies in humans with brain injury. Neurodegeneration after brain injury involves multiple biochemical pathways. Treatment with a single agent has often resulted in poor efficacy at a safe dose or toxicity at a therapeutic dose. A successful neuroprotective therapy needs to be aimed at homeostatic control of these pathways with multiple agents. Other pharmacological agents, such as dexanabinol and progesterone, and physiological interventions, with hypothermia and hyperoxia, have been studied for the treatment of brain injury. Treatment with magnesium and hypothermia has shown favorable outcome in rats with cerebral ischemia. We conclude that coadministration of magnesium and mannitol with pharmacological and physiological agents could be an effective neuroprotective regimen for the treatment of TBI.
Key Words: Traumatic brain injury, magnesium, neuroprotection, hyperoxia, hypothermia
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so you get the idea, there is a heap of research on supporting traumatic brain injury and post concussion and this is what I read to bring you practical strategies.
If I can help please ask.
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