Skip to main content Accessibility help
×
Home

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

  • Dominik Zumsteg (a1), Richard Wennberg (a1), Eva Gütling (a2) and Klaus Hess (a2)

Abstract

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: 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.

    • Send article to Kindle

      To send this article to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle. Find out more about sending to your Kindle.

      Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

      Find out more about the Kindle Personal Document Service.

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

      Send article to Dropbox

      To send this article to your Dropbox account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Dropbox.

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

      Send article to Google Drive

      To send this article to your Google Drive account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Google Drive.

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

Copyright

Corresponding author

Krembil Neuroscience Centre, University of Toronto, Toronto Western Hospital, 5W-425, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada

References

Hide All
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;55:9438.
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;33:4428.
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;74:28197.
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;347:120711.
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;53:2936.
6. Kelly, JP, Rosenberg, JH. Diagnosis and management of concussion in sports. Neurology. 1997;48:57580.
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:S84105.
8. Practice parameter: The management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology. 1997;48:5815.
9. Riley, L, Long, D, Riley, LH. The science of whiplash. Medicine. 1995;74:2989.
10. Shaw, NA. The neurophysiology of concussion. Prog Neurobiol. 2002;67:281344.
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;11:408792.
12. Gaetz, M, Goodman, D, Weinberg, H. Electrophysiological evidence for the cumulative effects of concussion. Brain Inj. 2000;14:107788.
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;62:71122.
14. Goldring, S, Aras, E, Weber, PC. Comparative study of sensory input to motor cortex in animals and man. Electroencephalogr Clin Neurophysiol. 1970;29:53750.
15. Stöhr, PE, Goldring, S. Origin of somatosensory evoked scalp responses in man. J Neurosurg. 1969;31:11727.
16. Denny-Brown, D, Russell, WR. Experimental cerebral concussion. Brain 1941;64:93164.
17. Jane, JA, Steward, O, Gennarelli, T. Axonal degeneration induced by experimental noninvasive minor head injury. J Neurosurg. 1985;62:96100.
18. Ommaya, AK, Faas, F, Yarnell, P. Whiplash injury and brain damage: an experimental study. JAMA. 1968;204:2859.
19. Ommaya, AK, Gennarelli, TA. Cerebral concussion and traumatic unconsciousness. Correlation of experimental and clinical observations of blunt head injuries. Brain. 1974;97:63354.
20. Shaw, NA. Somatosensory evoked potentials after experimental head injury in the awake rat. J Neurol Sci. 1986;74:25770.
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;47:15062.
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;47:16377.
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;55:22736.
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;44:796802.
25. Moulton, RJ, Shedden, PM, Tucker, WS, Muller, PJ. Somatosensory evoked potential monitoring following severe closed head injury. Clin Invest Med. 1994;17:18795.
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;62:8898.
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;60:21326.
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;341:8558.
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;28:7216.
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;31:304.
31. Kullmann, F, Hollerbach, S, Holstege, A, Scholmerich, J. Subclinical hepatic encephalopathy: the diagnostic value of evoked potentials. J Hepatol. 1995;22:10110.
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;20:148794.
33. Yang, SS, Chu, NS, Liaw, YF. Somatosensory evoked potentials in hepatic encephalopathy. Gastroenterology. 1985;89:62530.
34. Yang, SS, Wu, CH, Chiang, TR, Chen, DS. Somatosensory evoked potentials in subclinical portosystemic encephalopathy: a comparison with psychometric tests. Hepatology. 1998;27: 35761.
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;23:5879.
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;17:947.
37. Hirsch, SA, Hirsch, PJ, Hiramoto, H, Weiss, A. Whiplash syndrome. Fact or fiction? Orthop Clin North Am. 1988;19:7915.
38. Jacome, DE. EEG in whiplash: a reappraisal. Clin Electro-encephalogr. 1987;18:415.
39. Torres, F, Shapiro, SK. Electroencephalograms in whiplash injury. Arch Neurol. 1961;5:2847.
40. Yarnell, PR, Rossie, GV. Minor whiplash head injury with major debilitation. Brain Inj. 1988;2:2558.
41. Zumsteg, D, Wieser, HG. Effects of aging and sex on middle-latency somatosensory evoked potentials: normative data. Clin Neurophysiol. 2002;13:6815.
42. Greenberg, RP, Ducker, TB. Evoked potentials in the clinical neurosciences. J Neurosurg. 1982;56:118.
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:S6875.
44. Holbourn, AHS. Mechanics of head injury. Lancet. 1943;2:43841.
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;12:56474.
46. Oppenheimer, DR. Microscopic lesions in the brain following head injury. J Neurol Neurosurg Psychiatry. 1968;31:299306.
47. Faden, AI, Demediuk, P, Panter, SS, Vink, R. The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science. 1989;244:798800.
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;73:889900.
49. Goff, WR, Allison, T, Shapiro, A, Rosner, BS. Cerebral somatosensory responses evoked during sleep in man. Electroencephalogr Clin Neurophysiol. 1966;21:19.
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;4:2759.
51. Grundy, BL, Brown, RH, Greenberg, BA. Diazepam alters cortical evoked potentials. Anesthesiology. 1979;51:538.
52. Lindenberg, R, Freytag, E. Brainstem lesion characteristics of traumatic hyperextension of the head. Arch Pathol. 1970;90: 50915.
53. Olsnes, BT. Neurobehavioral findings in whiplash patients with long-lasting symptoms. Acta Neurol Scand. 1989;80:5848.

Metrics

Full text views

Total number of HTML views: 0
Total number of PDF views: 0 *
Loading metrics...

Abstract views

Total abstract views: 0 *
Loading metrics...

* Views captured on Cambridge Core between <date>. This data will be updated every 24 hours.

Usage data cannot currently be displayed