Cortical hypoexcitability persists beyond the symptomatic phase of a concussion

Abstract

Taken together, these findings suggest a state of hypoexcitability that persists beyond the immediate acute phase of a concussion and may result in neuromuscular impairments that would call to question the athlete's readiness to return to sport.

What is the physiological time to recovery after concussion? A systematic review

“…Three of these examined cortical excitability after concussion and found increased inhibition. One reported increased inhibition in the corticospinal tract at 2–4 days after concussion with normalisation by 10 days after injury,77 another found cortical hypo-excitability persisting beyond the time of clinical recovery, up to 28 days after injury,78 and the third article showed increased inhibition in the motor system that persisted beyond 9 months post injury 79. The last article took a different approach and reported prolonged motor latencies that persisted through PID10 80…”

Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

“…[184][185][186] Several small TMS studies of young athletes in their early 20s with a history of concussion suggest imbalances in γ-aminobutyric acid and/or glutamate neurotransmission in the motor cortex that are associated with deficits in synaptic longterm potentiation and depression. 184,185,187,188 TMS has also revealed that concussion-related impairments in synaptic plasticity can impair aspects of motor learning, 188 and that these deficits are detectable decades after an individual's last concussion.…”

Theta burst stimulation to characterize changes in brain plasticity following mild traumatic brain injury: A proof-of-principle study

“…A common observation following mTBI is the presence of altered M1 intracortical excitability in the acute (Chistyakov et al, 2001; Pearce et al, 2014b; Miller et al, 2014; Powers et al, 2014) and chronic (De Beaumont et al, 2007,2009; Tremblay et al, 2011; Pearce et al, 2014b) phases of injury. More specifically, increased intracortical inhibition (Chistyakov et al, 2001; Pearce et al, 2014b; Miller et al, 2014) and decreased intracortical facilitation (Powers et al, 2014) have been reported in the acute and sub-acute phases of mTBI.…”

“…More specifically, increased intracortical inhibition (Chistyakov et al, 2001; Pearce et al, 2014b; Miller et al, 2014) and decreased intracortical facilitation (Powers et al, 2014) have been reported in the acute and sub-acute phases of mTBI. Despite strong evidence suggesting inhibitory/excitatory imbalance in the primary motor cortex of individuals with mTBI, the duration of such effects is unclear.…”

“…In humans, transcranial magnetic stimulation (TMS) has been used to non-invasively assess the neurophysiological impact of mTBI as it allows precise quantification of inhibitory and excitatory systems within primary motor cortex (M1; Hallet, 2007). Using this method, previous studies have shown sometimes long-lasting disruptions in M1 inhibitory/excitatory balance, usually taking the form of increased intracortical inhibition/reduced intracortical facilitation (Chistyakov et al, 2001; De Beaumont et al, 2007, 2009; Miller et al, 2014; Pearce et al, 2014a; Powers et al 2014; but see Tremblay et al, 2014; Pearce et al, 2014b) Moreover, chronic alterations in synaptic plasticity, possibly reflecting faulty long term potentiation (LTP) – and long term depression (LTD) - like mechanisms were found after multiple concussions, and were associated with intracortical inhibition abnormalities (De Beaumont et al, 2012). Taken together, these studies suggest the presence of impaired balance between primary motor cortex excitatory and inhibitory mechanisms following mTBI both in the acute and chronic phases, which may be related to abnormal M1 plasticity.…”