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N18 in median somatosensory evoked potentials: a new indicator of medullary function useful for the diagnosis of brain death
  1. Masahiro Sonooa,
  2. Yasunobu Tsai-Shozawaa,
  3. Makoto Aokib,
  4. Toshio Nakatanic,
  5. Yuuki Hatanakaa,
  6. Atsuko Mochizukia,
  7. Mikio Sawadaa,
  8. Kunio Kobayashic,
  9. Teruo Shimizua
  1. aDepartment of Neurology, bDepartment of Neurosurgery, cTrauma and Critical Care Center, Teikyo University School of Medicine, Tokyo, Japan
  1. Dr Masahiro Sonoo, Department of Neurology, Teikyo University School of Medicine, Kaga 2–11–1, Itabashi-ku, Tokyo 173, Japan. Telephone 0081 3 3964 1211 ext 1911; fax 0081 3 3964 6397; email sonoom{at}med.teikyo-u.ac.jp

Abstract

OBJECTIVES To record N18 in median somatosensory evoked potentials (SEPs) for deeply comatose or brain dead patients and to demonstrate the usefulness of N18 for the diagnosis of brain death in comparison with auditory brain stem responses (ABRs) and P13/14 in median SEPs, which have been conventionally used as complementary tests for the diagnosis of brain death.

METHODS Subjects were 19 deeply comatose or brain dead patients. Thirteen recordings were performed in deeply comatose but not brain dead conditions, and 12 recordings were performed in brain death. N18 was evaluated in the CPi-C2S lead (or other scalp-C2S leads) to obtain a flat baseline.

RESULTS N18 was preserved in 12 of 13 non-brain dead comatose recordings whereas it was completely lost for all of the 12 brain death recordings. P13/14 in median SEPs was preserved for all the comatose recordings, whereas apparent P13/14-like potentials, usually of low amplitude, were seen in nine of 12 brain death recordings—that is, frequent false positives. The ABRs already showed features which were characteristic for brain death (loss of components other than wave 1 or small wave 2) for four comatose recordings, in three of which N18 was preserved. The last result not only corresponds with the fact that ABRs can evaluate pontine and midbrain functions and not medullary function, but further supports the medullary origin of N18. In the four patients followed up for the course of progression from coma to brain death, N18s preserved in normal size during the comatose state were completely lost after brain death was established.

CONCLUSIONS The N18 potential is generated by the cuneate nucleus in the medulla oblongata in the preceding studies. N18 is suggested to be a promising tool for the diagnosis of brain death because there were no false positives and rare false negatives in the present series for detecting the remaining brain stem function.

  • somatosensory evoked potentials
  • N18
  • brain death
  • cuneate nucleus

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