Repeat mild traumatic brain injury: how to adjust return to play guidelines.
ABSTRACT Determining when it is safe for an athlete to return to play (RTP) after concussion is one of the most difficult decisions facing the team physician. There is significant variability in the evaluation and management of mild traumatic brain injury (mTBI). In the past decade, a tremendous amount of sport-specific research has improved our understanding of mTBI. The advent of neuro-psychologic (NP) testing batteries designed to assess concussive injury has improved the assessment of cognitive dysfunction that occurs in the absence of structural brain abnormalities. The severity of injury is determined by the nature, burden, and duration of symptoms. Athletes must be asymptomatic and have a normal neurologic and cognitive evaluation prior to RTP. Several factors aid in making the RTP decision, including age, the severity of injury, and history of prior mTBIs. Given the potential complications of mTBI, the RTP decision must be made using a thoughtful, individualized process.
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- "While MTBI is seen frequently in athletes, severity grading and management remain controversial (Gebke, 2002). Evaluation of the concussed athlete is essential before a recommendation to return to play can be made (Putukian, 2006). Often these decisions are made by the certifi ed athletic trainer either on the fi eld or sideline during the game or at post-game follow-up. "
ABSTRACT: This chapter has two goals: to provide the reader with a general awareness of traumatic brain injury (TBI), mild in particular, and the multiple complex issues involved in this area, and to offer a detailed understanding of the role of quantitative electroencephalography (qEEG) in the assessment and treatment of the cognitive defi cits of the TBI patient. Sections I–IV address the fi rst goal. Section I discusses defi nitions, sports, vulnerable groups, the concept of spontaneous cure, and roles of loss of consciousness and post-traumatic amnesia criteria. Section II addresses the biomechanics of a TBI. Section III discusses the physical damage to the brain caused by the TBI as measured by modern medical imaging. Section IV reviews the neuropsychological and emotional results of a TBI that may be clinically manifested in a patient. The second goal is addressed in section V, which discusses the scientifi c basics of qEEG technology, development of the technology over the past two decades, and its application in the assessment of the TBI patient. The coordinated allocation of resources (CAR) model of brain functioning, which employs a cognitive challenge or activation method, is discussed in the context of how a TBI specifi cally affects brain and cognitive functioning. An example of the differences between the normative and the TBI response patterns are presented in detail for the cognitive task of auditory memory. We review the results of rehabilitation efforts employing the CAR model, which have proved to be dramatically superior to the minimalHandbook of Integrative Clinical Psychology, Psychiatry and Behavioral Medicine: Perspectives, Practices And Research, 2010 edited by R. Carlstedt (Ed, 01/2010: pages 463-508; Springer, New York.
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ABSTRACT: In the present study, we investigate the existence of a temporal window of brain vulnerability in rats undergoing repeat mild traumatic brain injury (mTBI) delivered at increasing time intervals. Rats were subjected to two diffuse mTBIs (450 g/1 m height) with the second mTBI delivered after 1 (n = 6), 2 (n = 6), 3 (n = 6), 4 (n = 6), and 5 days (n = 6) and sacrificed 48 hours after the last impact. Sham-operated animals were used as controls (n = 6). Two further groups of six rats each received a second mTBI after 3 days and were sacrificed at 120 and 168 hours postinjury. Concentrations of adenine nucleotides, N-acetylated amino acids, oxypurines, nucleosides, free coenzyme A, acetyl CoA, and oxidized and reduced nicotinamide adenine dinucleotides, oxidized nicotinamide adenine dinucleotide phosphate, and reduced nicotinamide adenine dinucleotide, reduced nicotinamide adenine dinucleotide phosphate nicotinic coenzymes were measured in deproteinized cerebral tissue extracts (three right and three left hemispheres), whereas the gene expression of N-acetylaspartate acylase, the enzyme responsible for N-acetylaspartate (NAA) degradation, was evaluated in extracts of three left and three right hemispheres. A decrease of adenosine triphosphate, adenosine triphosphate/adenosine diphosphate ratio, NAA, N-acetylaspartylglutamate, oxidized and reduced nicotinamide adenine dinucleotide, reduced nicotinamide adenine dinucleotide, and acetyl CoA and increase of N-acetylaspartate acylase expression were related to the interval between impacts with maximal changes recorded when mTBIs were spaced by 3 days. In these animals, protracting the time of sacrifice after the second mTBI up to 1 week failed to show cerebral metabolic recovery, indicating that this type of damage is difficult to reverse. A metabolic pattern similar to controls was observed only in animals receiving mTBIs 5 days apart. This study shows the existence of a temporal window of brain vulnerability after mTBI. A second concussive event falling within this time range had profound consequences on mitochondrial-related metabolism. Furthermore, because NAA recovery coincided with normalization of all other metabolites, it is conceivable to hypothesize that NAA measurement by 1H-NMR spectroscopy might be a valid tool in assessing full cerebral metabolic recovery in the clinical setting and with particular reference to sports medicine in establishing when to return mTBI-affected athletes to play. This study also shows, for the first time, the influence of TBI on acetyl-CoA, N-acetylaspartate acylase gene expression, and N-acetylaspartylglutamate, thus providing novel data on cerebral biochemical changes occurring in head injury.Neurosurgery 09/2007; 61(2):379-88; discussion 388-9. DOI:10.1227/01.NEU.0000280002.41696.D8 · 3.03 Impact Factor
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ABSTRACT: In the present study, we investigated the occurrence of oxidative and nitrosative stresses in rats undergoing repeat mild traumatic brain injury (mTBI) delivered with increasing time intervals. Rats were subjected to two diffuse mTBIs (450 g/1 m height), with the second mTBI delivered after 1 (n = 6), 2 (n = 6), 3 (n = 6), 4 (n = 6), or 5 days (n = 6). The rats were sacrificed 48 hours after the last mTBI. Sham-operated animals were used as controls (n = 6). Concentrations of biochemical indices of oxidative stress (malondialdehyde, ascorbic acid, reduced and oxidized glutathione) and nitrosative stress (nitrite, nitrate) were synchronously measured by high-performance liquid chromatography in deproteinized tissue extracts (three right + three left hemispheres for each group of animals). Increase of malondialdehyde, reduced/oxidized glutathione ratio, nitrite, nitrate, and decrease of ascorbic acid and glutathione were dependent on the interval between impacts with maximal changes recorded when mTBIs were spaced by 3 days. Biochemical markers of oxidative and nitrosative stresses were near control levels only in animals receiving mTBIs 5 days apart. This study shows the remarkable negative contribution of reactive oxygen species overproduction and activation of inducible nitric oxide synthase in repeat mTBI. Because these effects were maximal when mTBIs were spaced by 3 days, it can be inferred that occurrence of a second mTBI within the temporal window of brain vulnerability not only causes profound derangement of mitochondrial functions, but also induces sustained oxidative and nitrosative stresses. Both phenomena certainly play a major role in the overall brain tissue damage occurring under these pathological conditions.Neurosurgery 09/2007; 61(2):390-5; discussion 395-6. DOI:10.1227/01.NEU.0000255525.34956.3F · 3.03 Impact Factor