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