Altered Intracortical Inhibition in Chronic Traumatic Diffuse Axonal Injury

Carregando...
Imagem de Miniatura
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
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
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
  1. Abbruzzese G, 2002, J CLIN NEUROPHYSIOL, V19, P307, DOI 10.1097/00004691-200208000-00005
  2. Vieira RDA, 2016, FRONT NEUROL, V7, DOI 10.3389/fneur.2016.00178
  3. Almeida-Suhett CP, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0102627
  4. Andrade AF, 2015, NEUROTRAUMATOLOGIA
  5. BECK AT, 1961, ARCH GEN PSYCHIAT, V4, P561
  6. Bernabeu M, 2009, J NEUROTRAUM, V26, P2185, DOI 10.1089/neu.2008.0859
  7. Campanholo Kenia Repiso, 2014, Dement. neuropsychol., V8, P26, DOI 10.1590/S1980-57642014DN81000005
  8. Cantu D, 2015, CEREB CORTEX, V25, P2306, DOI 10.1093/cercor/bhu041
  9. Castel-Lacanal E, 2014, ANN FR ANESTH, V33, P83, DOI 10.1016/j.annfar.2013.11.006
  10. Chen R, 2004, EXP BRAIN RES, V154, P1, DOI 10.1007/s00221-003-1684-1
  11. Croarkin PE, 2013, JAMA PSYCHIAT, V70, P291, DOI 10.1001/2013.jamapsychiatry.24
  12. Cueva AS, 2016, NEUROPHYSIOL CLIN, V46, P43, DOI 10.1016/j.neucli.2015.12.003
  13. Demirtas-Tatlidede A, 2012, J HEAD TRAUMA REHAB, V27, P274, DOI 10.1097/HTR.0b013e318217df55
  14. Dwason B, 2004, BASIC CLIN BIOSTATIS
  15. Gennarelli T. A., 1998, SEMIN CLIN NEUROPSYC, V3, P160
  16. Glantz SA, 2012, PRIMER BIOSTATISTICS
  17. Gorenstein C, 1996, BRAZ J MED BIOL RES, V29, P453
  18. Groppa S, 2012, CLIN NEUROPHYSIOL, V123, P858, DOI 10.1016/j.clinph.2012.01.010
  19. Hyder AA, 2007, NEUROREHABILITATION, V22, P341
  20. Johnson VE, 2013, EXP NEUROL, V246, P35, DOI 10.1016/j.expneurol.2012.01.013
  21. Lefaucheur Jean-Pascal, 2008, Expert Rev Neurother, V8, P799, DOI 10.1586/14737175.8.5.799
  22. Liuzzi G, 2014, NEUROLOGY, V82, P198, DOI 10.1212/WNL.0000000000000028
  23. Mhalla A, 2010, PAIN, V149, P495, DOI 10.1016/j.pain.2010.03.009
  24. Miller NR, 2014, BRAIN INJURY, V28, P1270, DOI 10.3109/02699052.2014.915987
  25. Miotto EC, 2012, ARQ NEURO-PSIQUIAT, V70, P962, DOI 10.1590/S0004-282X2012001200014
  26. Pascual-Leone A, 1998, J CLIN NEUROPHYSIOL, V15, P333, DOI 10.1097/00004691-199807000-00005
  27. Powers KC, 2014, BRAIN INJURY, V28, P465, DOI 10.3109/02699052.2014.888759
  28. Rabinowitz AR, 2014, PSYCHIAT CLIN N AM, V37, P1, DOI 10.1016/j.psc.2013.11.004
  29. Rossini PM, 2015, CLIN NEUROPHYSIOL, V126, P1071, DOI 10.1016/j.clinph.2015.02.001
  30. Rothwell J C, 1999, Electroencephalogr Clin Neurophysiol Suppl, V52, P97
  31. Spielberg CD, 1960, TEST MANUAL STATE TR
  32. Strauss E., 2006, COMPENDIUM NEUROPSYC
  33. Tiffin J., 1968, PURDUE PEGBOARD EXAM
  34. Wang JY, 2008, ARCH NEUROL-CHICAGO, V65, P619, DOI 10.1001/archneur.65.5.619
  35. Wassermann EM, 2002, CLIN NEUROPHYSIOL, V113, P1165, DOI 10.1016/S1388-2457(02)00144-X
  36. Wechsler D., 1997, WECHSLER ADULT INTEL
  37. World Health Organization (WHO), 2008, WORLD HLTH STAT 2008
  38. Wilson JTL, 1998, J NEUROTRAUM, V15, P573, DOI 10.1089/neu.1998.15.573
  39. Yasokawa YT, 2007, J NEUROTRAUM, V24, P163, DOI 10.1089/neu.2006.0073
  40. Zaninotto AL, 2017, ACTA NEUROPSYCHIATR, V29, P35, DOI 10.1017/neu.2016.29