Original Research ARTICLE
Altered intracortical inhibition in chronic traumatic diffuse axonal injury
- 1Department of Neurology, University of Sao Paulo, Brazil
- 2School of Medicine, Universidade da Cidade de Sao Paulo - UNICID, Brazil
- 3Institute of Psychiatry, Service of Interdisciplinary Neuromodulation, Brazil
Background: 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. However, there are few studies regarding the circuitry during the chronic phase of brain injury. Objective: To evaluate the cortical excitability (CE) during the chronic phase of traumatic brain injury (TBI) in victims diagnosed with diffuse axonal injury (DAI). Methods: 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 (MEP), 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. Results: 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 they had a disarranged inhibitory system (p < 0.001). In contrast, the neuropsychological findings had weak correlation with the CE data. Conclusion: 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.
Keywords: Transcranial magnetic stimulation (TMS), Craniocerebral Trauma, Diffuse Axonal Injury, Brain Injuries, Neurophysiology
Received: 28 Aug 2016;
Accepted: 12 Mar 2018.
Edited by:Kenneth Curley, Iatrikos Research and Development Solutions, LLC, United States
Reviewed by:Rao P. Gullapalli, School of Medicine, University of Maryland, United States
Ramon Diaz-Arrastia, University of Pennsylvania, United States
Copyright: © 2018 Hayashi, NEVILLE, Rodrigues, Galhardoni, Brunoni, ZANINOTTO, Guirado, Moscoso, De Andrade, Teixeira and Paiva. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Miss. Cintya Y. Hayashi, University of Sao Paulo, Department of Neurology, Sao Paulo, Sao Paulo, Brazil, firstname.lastname@example.org