Acute and longitudinal changes in motor cortex function following mild traumatic brain injury

Miller, Nick R.; Yasen, Alia L.; Maynard, L.; Chou, Li-Shan; Howell, David R.; Christie, Anita

doi:10.3109/02699052.2014.915987

Cited by 46 publications

(71 citation statements)

References 36 publications

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“…TBI may vary in severity, but Ͼ75% of all TBI is classified as mild Elder and Cristian 2009;Langlois et al 2005;Miniño et al 2006). In this study, we sought to determine how rmTBI affects the pediatric brain.…”

Section: Discussionmentioning

confidence: 98%

“…In humans, the use of transcranial magnetic stimulation from 72 h to 2 mo after mTBI has shown increases in intracortical inhibition (Miller et al 2014). Young athletes who have sustained multiple concussions have also been reported to have abnormal intracortical inhibition (De Beaumont et al 2007, 2011Tremblay et al 2011).…”

Section: Discussionmentioning

confidence: 99%

“…In general, TBI is categorized into mild, moderate, and severe. Mild TBI (mTBI), including concussions, accounts for nearly 75% of all TBI cases Elder and Cristian 2009;Langlois et al 2005Langlois et al , 2006Miniño et al 2006). mTBI is often called an "invisible wound," as it results in a minimal loss of consciousness (Ͻ30 min) and minimal acute neuropathological findings Morey et al 2013;Smith et al 2013).…”

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confidence: 99%

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Repetitive mild traumatic brain injury induces ventriculomegaly and cortical thinning in juvenile rats

Goddeyne

Nichols

et al. 2015

Journal of Neurophysiology

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Goddeyne C, Nichols J, Wu C, Anderson T. Repetitive mild traumatic brain injury induces ventriculomegaly and cortical thinning in juvenile rats. J Neurophysiol 113: 3268 -3280, 2015. First published February 18, 2015 doi:10.1152/jn.00970.2014.-Traumatic brain injury (TBI) most frequently occurs in pediatric patients and remains a leading cause of childhood death and disability. Mild TBI (mTBI) accounts for nearly 75% of all TBI cases, yet its neuropathophysiology is still poorly understood. While even a single mTBI injury can lead to persistent deficits, repeat injuries increase the severity and duration of both acute symptoms and long-term deficits. In this study, to model pediatric repetitive mTBI (rmTBI) we subjected unrestrained juvenile animals (postnatal day 20) to repeat weight-drop impacts. Animals were anesthetized and subjected to sham injury or rmTBI once per day for 5 days. Magnetic resonance imaging (MRI) performed 14 days after injury revealed marked cortical atrophy and ventriculomegaly in rmTBI animals. Specifically, beneath the impact zone the thickness of the cortex was reduced by up to 46% and the area of the ventricles increased by up to 970%. Immunostaining with the neuron-specific marker NeuN revealed an overall loss of neurons within the motor cortex but no change in neuronal density. Examination of intrinsic and synaptic properties of layer II/III pyramidal neurons revealed no significant difference between sham-injured and rmTBI animals at rest or under convulsant challenge with the potassium channel blocker 4-aminopyridine. Overall, our findings indicate that the neuropathological changes reported after pediatric rmTBI can be effectively modeled by repeat weight drop in juvenile animals. Developing a better understanding of how rmTBI alters the pediatric brain may help improve patient care and direct "return to game" decision making in adolescents.concussion; electrophysiology; MRI; pediatrics; traumatic brain injury

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Repetitive mild traumatic brain injury induces ventriculomegaly and cortical thinning in juvenile rats

Goddeyne

Nichols

et al. 2015

Journal of Neurophysiology

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“…TMS has been used extensively in the investigation of neurological disorders such as stroke, Parkinson's disease and multiple sclerosis 10 , as well as those with long-term cognitive and motor impairments with concussion sustained in early adulthood. 11,12 Specifically brain injury, Christyakov et al 13 and Miller et al 14 showed increased intracortical inhibition in mild to severe TBI patients two weeks following injury. Similarly, De Beaumont et al 9 showed increased intracortical inhibition in previously concussed collegiate athletes with repeated concussions.…”

Section: Introductionmentioning

confidence: 99%

Acute motor, neurocognitive and neurophysiological change following concussion injury in Australian amateur football. A prospective multimodal investigation

Pearce

Hoy

Rogers

et al. 2015

Journal of Science and Medicine in Sport

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“…Static comparisons of the inhibitory marker short-interval intracortical inhibition (SICI), a GABA A mediated form of inhibition, have largely failed to differentiate between concussion and control groups at the acute (Bashir et al, 2012; Powers et al, 2014; Pearce et al, 2015) and chronic (De Beaumont et al, 2007, 2009; Tremblay et al, 2011) stages post-injury, however, there has been a report of reduced SICI in retired Australian football players (Pearce et al, 2014). Of all the TMS measures of motor cortex excitability, the most consistent finding in concussed individuals is an enhanced cortical silent period duration, a GABA B mediated form of intracortical inhibition (Tremblay et al, 2011; De Beaumont et al, 2012; Miller et al, 2014; Pearce et al, 2014, 2015) that appears to persist (De Beaumont et al, 2007) or is even enhanced (De Beaumont et al, 2009) as time from injury increases. However, even though cortical silent period is enhanced in younger active Australian football players with a history of concussion (Pearce et al, 2015) in a cohort of older retired players the silent period was decreased (Pearce et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Changes in Cortical Plasticity in Relation to a History of Concussion during Adolescence

Meehan

Mirdamadi

Martini

et al. 2017

Front. Hum. Neurosci.

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Adolescence and early adulthood is a critical period for neurophysiological development potentially characterized by an increased susceptibility to the long-term effects of traumatic brain injury. The current study investigated differences in motor cortical physiology and neuroplastic potential across a cohort of young adults with adolescent concussion history and those without. Transcranial magnetic stimulation (TMS) was used to assess motor evoked potential (MEP) amplitude, short-interval cortical inhibition (SICI) and intracortical facilitation (ICF) before and after intermittent theta burst stimulation (iTBS). Pre-iTBS, MEP amplitude, but not SICI or ICF, was greater in the concussion history group. Post-iTBS, the expected increase in MEP amplitude and ICF was tempered in the concussion history group. Change in SICI was variable within the concussion history group. Post hoc assessment revealed that SICI was significantly lower in individuals whose concussion was not diagnosed at the time of injury compared to both those without a concussion history or whose concussion was medically diagnosed. Concussive impacts during adolescence appear to result in a persistent reduction of the ability to modulate facilitatory motor networks. Failure to report/identify concussive impacts close to injury during adolescence also appears to produce persistent change in inhibitory networks. These findings highlight the potential long-term impact of adolescent concussion upon motor cortical physiology.

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Acute and longitudinal changes in motor cortex function following mild traumatic brain injury

Abstract: mTBI appeared to have little effect on cortical excitability, but an acute and long-lasting effect on intra-cortical inhibition.

Cited by 46 publications

References 36 publications

Repetitive mild traumatic brain injury induces ventriculomegaly and cortical thinning in juvenile rats

Repetitive mild traumatic brain injury induces ventriculomegaly and cortical thinning in juvenile rats

Acute motor, neurocognitive and neurophysiological change following concussion injury in Australian amateur football. A prospective multimodal investigation

Changes in Cortical Plasticity in Relation to a History of Concussion during Adolescence

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