Altered Intracortical Inhibition in Chronic Traumatic Diffuse Axonal Injury.

Cintya Yukie Hayashi,Priscila Aparecida Rodrigues,Ana Sofia Cueva,Wellingson Silva Paiva,Manoel Jacobsen Teixeira,Daniel Ciampi De Andrade,Iuri Santana Neville,Vinicius Monteiro De Paula Guirado,André Russowsky Brunoni,Ricardo Galhardoni,Ana Luiza Zaninotto

doi:10.3389/fneur.2018.00189

Abstract

Overactivation of NMDA-mediated excitatory processes and excess of GABA-mediated inhibition are attributed to the acute and subacute phases, respectively, after a traumatic brain injury (TBI). However, there are few studies regarding the circuitry during the chronic phase of brain injury. To evaluate the cortical excitability (CE) during the chronic phase of TBI in victims diagnosed with diffuse axonal injury (DAI). The 22 adult subjects were evaluated after a minimum of 1 year from the onset of moderate or severe TBI. Each of the subjects first had a comprehensive neuropsychological assessment to evaluate executive functions-attention, memory, verbal fluency, and information processing speed. Then, CE assessment was performed with a circular coil applying single-pulse and paired-pulse transcranial magnetic stimulation over the cortical representation of the abductor pollicis brevis muscle on M1 of both hemispheres. The CE parameters measured were resting motor threshold (RMT), motor-evoked potentials (MEPs), short-interval intracortical inhibition (SIICI), and intracortical facilitation (ICF). All data were compared with that of a control group that consisted of the healthy age-matched individuals. No significant differences between the left and right hemispheres were detected in the DAI subjects. Therefore, parameters were analyzed as pooled data. Values of RMT, MEPs, and ICF from DAI patients were within normal limits. However, SIICI values were higher in the DAI group-DAI SIICI = 1.28 (1.01; 1.87) versus the control value = 0.56 (0.33; 0.69)-suggesting that they had a disarranged inhibitory system (p < 0.001). By contrast, the neuropsychological findings had weak correlation with the CE data. As inhibition processes involve GABA-mediated circuitry, it is likely that the DAI pathophysiology itself (disruption of axons) may deplete GABA and contribute to ongoing disinhibition of these neural circuits of the cerebrum during the chronic phase of DAI.

Highlights

Traumatic brain injury (TBI) is one of the major health consequences of trauma from motor vehicle accidents having its highest incidence among young male adults [1, 2]
Three subjects had used medications in the past that could interfere with the neurophysiological tests, but by the time they were included in the study, they were no longer taking any medications and were not outliers on cortical excitability (CE) data
Diffuse axonal injury (DAI) Group Data Classified According to Normative Data On a group analysis, CE values for the DAI group were classified according to normative data (Table 2)

Summary

Introduction

Traumatic brain injury (TBI) is one of the major health consequences of trauma from motor vehicle accidents having its highest incidence among young male adults [1, 2]. Considering that this age group is at its prime economic productivity, should they suffer a TBI which can cause long-term motor and cognitive disabilities, the negative impact of TBI stretches beyond just the individual victim [3, 4]. Diffuse axonal injury (DAI) is a clinical condition often related to closed head traumas. There are few studies regarding the circuitry during the chronic phase of brain injury

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Results

Conclusion