Altered Intracortical Inhibition in Chronic Traumatic Diffuse Axonal Injury
Carregando...
Citações na Scopus
7
Tipo de produção
article
Data de publicação
2018
Título da Revista
ISSN da Revista
Título do Volume
Editora
FRONTIERS MEDIA SA
Citação
FRONTIERS IN NEUROLOGY, v.9, article ID 189, 8p, 2018
Resumo
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 (TBI). 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 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 (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. 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 that they had a disarranged inhibitory system (p < 0.001). By 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.
Palavras-chave
brain injuries, craniocerebral trauma, diffuse axonal injury, neurophysiology, transcranial magnetic stimulation
Referências
- Abbruzzese G, 2002, J CLIN NEUROPHYSIOL, V19, P307, DOI 10.1097/00004691-200208000-00005
- Vieira RDA, 2016, FRONT NEUROL, V7, DOI 10.3389/fneur.2016.00178
- Almeida-Suhett CP, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0102627
- Andrade AF, 2015, NEUROTRAUMATOLOGIA
- BECK AT, 1961, ARCH GEN PSYCHIAT, V4, P561
- Bernabeu M, 2009, J NEUROTRAUM, V26, P2185, DOI 10.1089/neu.2008.0859
- Campanholo Kenia Repiso, 2014, Dement. neuropsychol., V8, P26, DOI 10.1590/S1980-57642014DN81000005
- Cantu D, 2015, CEREB CORTEX, V25, P2306, DOI 10.1093/cercor/bhu041
- Castel-Lacanal E, 2014, ANN FR ANESTH, V33, P83, DOI 10.1016/j.annfar.2013.11.006
- Chen R, 2004, EXP BRAIN RES, V154, P1, DOI 10.1007/s00221-003-1684-1
- Croarkin PE, 2013, JAMA PSYCHIAT, V70, P291, DOI 10.1001/2013.jamapsychiatry.24
- Cueva AS, 2016, NEUROPHYSIOL CLIN, V46, P43, DOI 10.1016/j.neucli.2015.12.003
- Demirtas-Tatlidede A, 2012, J HEAD TRAUMA REHAB, V27, P274, DOI 10.1097/HTR.0b013e318217df55
- Dwason B, 2004, BASIC CLIN BIOSTATIS
- Gennarelli T. A., 1998, SEMIN CLIN NEUROPSYC, V3, P160
- Glantz SA, 2012, PRIMER BIOSTATISTICS
- Gorenstein C, 1996, BRAZ J MED BIOL RES, V29, P453
- Groppa S, 2012, CLIN NEUROPHYSIOL, V123, P858, DOI 10.1016/j.clinph.2012.01.010
- Hyder AA, 2007, NEUROREHABILITATION, V22, P341
- Johnson VE, 2013, EXP NEUROL, V246, P35, DOI 10.1016/j.expneurol.2012.01.013
- Lefaucheur Jean-Pascal, 2008, Expert Rev Neurother, V8, P799, DOI 10.1586/14737175.8.5.799
- Liuzzi G, 2014, NEUROLOGY, V82, P198, DOI 10.1212/WNL.0000000000000028
- Mhalla A, 2010, PAIN, V149, P495, DOI 10.1016/j.pain.2010.03.009
- Miller NR, 2014, BRAIN INJURY, V28, P1270, DOI 10.3109/02699052.2014.915987
- Miotto EC, 2012, ARQ NEURO-PSIQUIAT, V70, P962, DOI 10.1590/S0004-282X2012001200014
- Pascual-Leone A, 1998, J CLIN NEUROPHYSIOL, V15, P333, DOI 10.1097/00004691-199807000-00005
- Powers KC, 2014, BRAIN INJURY, V28, P465, DOI 10.3109/02699052.2014.888759
- Rabinowitz AR, 2014, PSYCHIAT CLIN N AM, V37, P1, DOI 10.1016/j.psc.2013.11.004
- Rossini PM, 2015, CLIN NEUROPHYSIOL, V126, P1071, DOI 10.1016/j.clinph.2015.02.001
- Rothwell J C, 1999, Electroencephalogr Clin Neurophysiol Suppl, V52, P97
- Spielberg CD, 1960, TEST MANUAL STATE TR
- Strauss E., 2006, COMPENDIUM NEUROPSYC
- Tiffin J., 1968, PURDUE PEGBOARD EXAM
- Wang JY, 2008, ARCH NEUROL-CHICAGO, V65, P619, DOI 10.1001/archneur.65.5.619
- Wassermann EM, 2002, CLIN NEUROPHYSIOL, V113, P1165, DOI 10.1016/S1388-2457(02)00144-X
- Wechsler D., 1997, WECHSLER ADULT INTEL
- World Health Organization (WHO), 2008, WORLD HLTH STAT 2008
- Wilson JTL, 1998, J NEUROTRAUM, V15, P573, DOI 10.1089/neu.1998.15.573
- Yasokawa YT, 2007, J NEUROTRAUM, V24, P163, DOI 10.1089/neu.2006.0073
- Zaninotto AL, 2017, ACTA NEUROPSYCHIATR, V29, P35, DOI 10.1017/neu.2016.29
Coleções
Artigos e Materiais de Revistas Científicas - FM/MNE
Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/IMREA
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - HC/IPq
Carregar mais Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/IMREA
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - HC/IPq