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Whiplash and Concussion: Similar Acute Changes in Middle-Latency SEPs

Published online by Cambridge University Press:  02 December 2014

Dominik Zumsteg ,
Richard Wennberg ,
Eva Gütling  and
Klaus Hess
Dominik Zumsteg*
Affiliation:
Krembil Neuroscience Centre, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada
Richard Wennberg
Affiliation:
Krembil Neuroscience Centre, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada
Eva Gütling
Affiliation:
Department of Neurology, University Hospital, Zurich, Switzerland
Klaus Hess
Affiliation:
Department of Neurology, University Hospital, Zurich, Switzerland
*
Krembil Neuroscience Centre, University of Toronto, Toronto Western Hospital, 5W-425, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada
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Abstract

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Objective:

Middle-latency somatosensory evoked potentials (SEPs) following median nerve stimulation can provide a sensitive measure of cortical function. We sought to determine whether the mechanical forces of whiplash injury or concussion alter normal processing of middle-latency SEPs.

Methods:

In a cross-sectional pilot study 20 subjects with whiplash were investigated (50% between 0.5-2 months and 50% between 6-41 months post injury) and compared to 83 healthy subjects using a standard middle-latency SEP procedure. In a subsequent prospective study subjects with either acute whiplash (n=13) or Grade 3 concussion (n=16) were investigated within 48 hours and again three months post injury.

Results:

In the pilot study the middle-latency SEP component N60 was significantly increased in the ten subjects investigated within two months after whiplash. In contrast, the ten subjects examined more than six months after injury showed normal latencies. In the prospective study N60 latencies were increased after whiplash and concussion when tested within 48 hours of injury. At three months, latencies were improved though still significantly different from controls post whiplash and concussion.

Conclusion:

Both whiplash injury and concussion alter processing of the middle-latency SEP component N60 in the acute post traumatic period. The acute changes appear to normalize between three-six months post injury. The SEP similarities suggest that the overlapping clinical symptomatology post whiplash and concussion may reflect a similar underlying mechanism of rotational mild traumatic brain injury.

Résumé:

RÉSUMÉ:Objectif:

Les potentiels évoqués somesthésiques (PÉSs) de latence moyenne obtenus par stimulation du nerf médian constituent une mesure sensible de la fonction corticale. Le but de cette étude était de déterminer si les forces mécaniques impliquées dans le coup de fouet cervical et dans la commotion cérébrale altèrent le traitement normal des PÉSs de latence moyenne.

Méthodes:

Il s’agit d’une étude pilote transversale au cours de laquelle nous avons évalué 20 sujets qui avaient subi un coup de fouet cervical. La moitié des sujets ont été évalués entre 0,5 à 2 mois après l’incident et l’autre moitié de 6 à 41 mois après. Nous les avons comparés à 83 sujets témoins en santé au moyen de la technique standard d’évaluation des PÉSs de latence moyenne. Au cours d’une étude prospective subséquente, nous avons évalué des sujets présentant soit un coup de fouet cervical aigu (n = 13) ou une commotion cérébrale de grade 3 (n = 16) dans les 48 heures de l’incident et 3 mois après.

Résultats:

Dans l’étude pilote, la composante de latence moyenne N60 était significativement augmentée chez les dix sujets évalués dans les deux premiers mois après l’incident. Par contre, les dix sujets examinés plus de six mois après l’incident avaient des latences normales. Dans l’étude prospective, les latences N60 étaient augmentées après le coup de fouet cervical et la commotion cérébrale lors de l’évaluation faite dans les 48 heures de l’incident. Après trois mois, les latences étaient améliorées chez les sujets ayant subi un coup de fouet cervical ou une commotion cérébrale, même si elles demeuraient significativement différentes de celles des témoins.

Conclusions:

Le coup de fouet cervical et la commotion cérébrale modifient le traitement de la composante N60 des PÉSs de latence moyenne au cours de la période post-traumatique aiguë. Les changements aigus semblent se normaliser entre trois et six mois après la blessure. La similitude des PÉSs suggère que le chevauchement de la symptomatologie clinique après le coup de fouet cervical et après la commotion cérébrale puisse refléter un mécanisme sous-jacent similaire soit une légère lésion cérébrale traumatique rotatoire.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 33 , Issue 4 , November 2006 , pp. 379 - 386
Copyright
Copyright © The Canadian Journal of Neurological 2006

References

1. Ettlin, TM, Kischka, U, Reichmann, S, Radii, EW, Heim, S, Wengen, D, et al. Cerebral symptoms after whiplash injury of the neck: a prospective clinical and neuropsychological study of whiplash injury. J Neurol Neurosurg Psychiatry. 1992;55:943–8.Google Scholar
2. Radanov, BP, Sturzenegger, M, Di Stefano, G, Schnidrig, A. Relationship between early somatic, radiological, cognitive and psychosocial findings and outcome during a one-year follow-up in 117 patients suffering from common whiplash. Br J Rheumatol. 1994;33:442–8.CrossRefGoogle ScholarPubMed
3. Radonov, BP, Sturzenegger, M, Di Stefano, G. Long-term outcome after whiplash injury. A 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychological findings. Medicine. 1995;74:281–97.Google Scholar
4. Schrader, H, Obelieniene, D, Bovim, G, Surkiene, D, Mickeviciene, D, Miseviciene, I, et al. Natural evolution of late whiplash syndrome outside the medicolegal context. Lancet. 1996;347:1207–11.Google Scholar
5. Leininger, BE, Gramling, SE, Farrell, HD, Kreutzer, JS, Peck, EA. Neuropsychological deficits in symptomatic minor head injury patients after concussion and mild concussion. J Neurol Neurosurg Psychiatry. 1990;53:293–6.Google Scholar
6. Kelly, JP, Rosenberg, JH. Diagnosis and management of concussion in sports. Neurology. 1997;48:575–80.Google Scholar
7. Carroll, LJ, Cassidy, JD, Peloso, PM, Borg, J, von Holst, H, Holm, L, et al. Prognosis for mild traumatic brain injury: results of the WHO collaborating centre task force on mild traumatic brain injury. J Rehabil Med. 2004; 43 Suppl:S84–105.Google Scholar
8. Practice parameter: The management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology. 1997;48:581–5.Google Scholar
9. Riley, L, Long, D, Riley, LH. The science of whiplash. Medicine. 1995;74:298–9.Google Scholar
10. Shaw, NA. The neurophysiology of concussion. Prog Neurobiol. 2002;67:281–344.CrossRefGoogle ScholarPubMed
11. Dupuis, F, Johnston, KM, Lavoie, M, Lepore, F, Lassonde, M. Concussions in athletes produce brain dysfunction as revealed by event-related potentials. Neuroreport. 2000;11:4087–92.Google Scholar
12. Gaetz, M, Goodman, D, Weinberg, H. Electrophysiological evidence for the cumulative effects of concussion. Brain Inj. 2000;14:1077–88.Google Scholar
13. Allison, T, McCarthy, G, Wood, CC, Williamson, PD, Spencer, DD. Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity. J Neurophysiol. 1989;62:711–22.Google Scholar
14. Goldring, S, Aras, E, Weber, PC. Comparative study of sensory input to motor cortex in animals and man. Electroencephalogr Clin Neurophysiol. 1970;29:537–50.Google Scholar
15. Stöhr, PE, Goldring, S. Origin of somatosensory evoked scalp responses in man. J Neurosurg. 1969;31:117–27.Google Scholar
16. Denny-Brown, D, Russell, WR. Experimental cerebral concussion. Brain 1941;64:93–164.Google Scholar
17. Jane, JA, Steward, O, Gennarelli, T. Axonal degeneration induced by experimental noninvasive minor head injury. J Neurosurg. 1985;62:96–100.Google Scholar
18. Ommaya, AK, Faas, F, Yarnell, P. Whiplash injury and brain damage: an experimental study. JAMA. 1968;204:285–9.Google Scholar
19. Ommaya, AK, Gennarelli, TA. Cerebral concussion and traumatic unconsciousness. Correlation of experimental and clinical observations of blunt head injuries. Brain. 1974;97:633–54.Google Scholar
20. Shaw, NA. Somatosensory evoked potentials after experimental head injury in the awake rat. J Neurol Sci. 1986;74:257–70.Google Scholar
21. Greenberg, RP, Mayer, DJ, Becker, DP, Miller, JD. Evaluation of brain function in severe human head trauma with multimodality evoked potentials. Part 1: evoked brain-injury potentials, methods, and analysis. J Neurosurg. 1977;47:150–62.Google Scholar
22. Greenberg, RP, Becker, DP, Miller, JD, Mayer, DJ. Evaluation of brain function in severe human head trauma with multimodality evoked potentials. Part 2: localization of brain dysfunction and correlation with posttraumatic neurological conditions. J Neurosurg. 1977;47:163–77.CrossRefGoogle ScholarPubMed
23. Greenberg, RP, Newlon, PG, Hyatt, MS, Narayan, RK, Becker, DP. Prognostic implications of early multimodality evoked potentials in severely head-injured patients. J Neurosurg. 1981;55:227–36.Google Scholar
24. Lindsay, KW, Carlin, J, Kennedy, I, Fry, J, McInnes, A, Teasdale, GM. Evoked potentials in severe head injury--analysis and relation to outcome. J Neurol Neurosurg Psychiatry. 1981;44:796–802.Google Scholar
25. Moulton, RJ, Shedden, PM, Tucker, WS, Muller, PJ. Somatosensory evoked potential monitoring following severe closed head injury. Clin Invest Med. 1994;17:187–95.Google ScholarPubMed
26. Pfurtscheller, G, Schwarz, G, Gravenstein, N. Clinical relevance of long-latency SEPs and VEPs during coma and emergency from coma. Electroencephalogr Clin Neurophysiol. 1985;62:88–98.Google Scholar
27. He, F, Liu, X, Yang, S, Zhang, S, Xu, G, Fang, G, et al. Evaluation of brain function in acute carbon monoxide poisoning with multimodality evoked potentials. Environ Res. 1993;60:213–26.Google Scholar
28. Madl, C, Grimm, G, Kramer, L, Yeganehfar, W, Sterz, F, Schneider, B, et al. Early prediction of individual outcome after cardiopulmonary resuscitation. Lancet. 1993;341:855–8.Google Scholar
29. Madl, C, Kramer, L, Domanovits, H, Woolard, RH, Gervais, H, Gendo, A, et al. Improved outcome prediction in unconscious cardiac arrest survivors with sensory evoked potentials compared with clinical assessment. Crit Care Medicine. 2000;28:721–6.Google Scholar
30. Kramer, L, Tribl, B, Gendo, A, Zauner, C, Schneider, B, Ferenci, P, et al. Partial pressure of ammonia versus ammonia in hepatic encephalopathy. Hepatology. 2000;31:30–4.Google Scholar
31. Kullmann, F, Hollerbach, S, Holstege, A, Scholmerich, J. Subclinical hepatic encephalopathy: the diagnostic value of evoked potentials. J Hepatol. 1995;22:101–10.Google Scholar
32. Madl, C, Grimm, G, Ferenci, P, Kramer, L, Yeganehfar, W, Oder, W, et al. Serial recording of sensory evoked potentials: a noninvasive prognostic indicator in fulminant liver failure. Hepatology. 1994;20:1487–94.Google Scholar
33. Yang, SS, Chu, NS, Liaw, YF. Somatosensory evoked potentials in hepatic encephalopathy. Gastroenterology. 1985;89:625–30.Google Scholar
34. Yang, SS, Wu, CH, Chiang, TR, Chen, DS. Somatosensory evoked potentials in subclinical portosystemic encephalopathy: a comparison with psychometric tests. Hepatology. 1998;27: 357–61.Google Scholar
35. Eisenhuber, E, Madl, C, Kramer, L, Ratheiser, K, Grimm, G. Detection of subclinical brain dysfunction by sensory evoked potentials in patients with severe diabetic ketoacidosis. Intensive Care Med. 1997;23:587–9.Google Scholar
36. Grimm, G, Madl, C, Oder, W, Druml, W, Schneeweiss, B, Laggner, AN, et al. Evoked potentials in severe herpes simplex encephalitis. Intensive Care Med. 1991;17:94–7.CrossRefGoogle ScholarPubMed
37. Hirsch, SA, Hirsch, PJ, Hiramoto, H, Weiss, A. Whiplash syndrome. Fact or fiction? Orthop Clin North Am. 1988;19:791–5.Google Scholar
38. Jacome, DE. EEG in whiplash: a reappraisal. Clin Electro-encephalogr. 1987;18:41–5.Google Scholar
39. Torres, F, Shapiro, SK. Electroencephalograms in whiplash injury. Arch Neurol. 1961;5:28–47.Google Scholar
40. Yarnell, PR, Rossie, GV. Minor whiplash head injury with major debilitation. Brain Inj. 1988;2:255–8.Google Scholar
41. Zumsteg, D, Wieser, HG. Effects of aging and sex on middle-latency somatosensory evoked potentials: normative data. Clin Neurophysiol. 2002;13:681–5.Google Scholar
42. Greenberg, RP, Ducker, TB. Evoked potentials in the clinical neurosciences. J Neurosurg. 1982;56:1–18.CrossRefGoogle ScholarPubMed
43. Allison, T, Goff, WR, Abrahamian, HA, Rosner, BS. The effects of barbiturate anesthesia upon human somatosensory evoked responses. Electroencephalogr Clin Neurophysiol. 1963; Suppl 24:S68–75.Google Scholar
44. Holbourn, AHS. Mechanics of head injury. Lancet. 1943;2:438–41.Google Scholar
45. Gennarelli, TA, Thibault, LE, Adams, JH, Graham, DI, Thompson, CJ, Marcincin, RP. Diffuse axonal injury and traumatic coma in the primate. Ann Neurol. 1982;12:564–74.Google Scholar
46. Oppenheimer, DR. Microscopic lesions in the brain following head injury. J Neurol Neurosurg Psychiatry. 1968;31:299–306.CrossRefGoogle ScholarPubMed
47. Faden, AI, Demediuk, P, Panter, SS, Vink, R. The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science. 1989;244:798–800.Google Scholar
48. Katayama, Y, Becker, DP, Tamura, T, Hovda, DA. Massive increases in extracellular potassium and the indiscriminant release of glutamate following concussive brain injury. J Neurosurg. 1990;73:889–900.Google Scholar
49. Goff, WR, Allison, T, Shapiro, A, Rosner, BS. Cerebral somatosensory responses evoked during sleep in man. Electroencephalogr Clin Neurophysiol. 1966;21:1–9.Google Scholar
50. Kitamura, Y, Kakigi, R, Hoshiyama, M, Koyama, S, Nakamura, A. Effects of sleep on somatosensory evoked responses in human: a magnetoencephalographic study. Brain Res Cogn Brain Res. 1996;4:275–9.Google Scholar
51. Grundy, BL, Brown, RH, Greenberg, BA. Diazepam alters cortical evoked potentials. Anesthesiology. 1979;51:538.CrossRefGoogle Scholar
52. Lindenberg, R, Freytag, E. Brainstem lesion characteristics of traumatic hyperextension of the head. Arch Pathol. 1970;90: 509–15.Google Scholar
53. Olsnes, BT. Neurobehavioral findings in whiplash patients with long-lasting symptoms. Acta Neurol Scand. 1989;80:584–8.Google Scholar