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Stimulus induced bursts in severe postanoxic encephalopathy.

Marleen C Tjepkema-Cloostermans1, Elisabeth T Wijers2, Michel J A M van Putten3

  • 1Department of Neurology and Clinical Neurophysiology, Medisch Spectrum Twente, The Netherlands.

Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology
|September 22, 2016
PubMed
Summary

External stimuli can trigger burst-suppression patterns on electroencephalograms (EEGs) in comatose patients with severe postanoxic encephalopathy. This stimulus-induced EEG activity is not a sign of favorable prognosis.

Keywords:
Burst-suppression EEGPostanoxic encephalopathyStimulus induced bursts

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Area of Science:

  • Neurology
  • Neurophysiology
  • Critical Care Medicine

Background:

  • Comatose patients with severe postanoxic encephalopathy often exhibit burst-suppression patterns on their electroencephalograms (EEGs).
  • The prognostic significance of EEG reactivity in such patients remains a critical area of investigation.

Observation:

  • This study examined two comatose patients with severe postanoxic encephalopathy and burst-suppression EEG patterns.
  • The effect of auditory and sensory stimuli on the induction of EEG bursts was investigated in an Intensive Care Unit (ICU) setting.

Findings:

  • Auditory or sensory stimuli induced EEG bursts in one patient.
  • Tactile stimuli applied to specific facial regions induced bursts in the second patient.
  • Stimulus-induced bursts were observed with longer stimulus intervals but not with intervals less than one second.
  • No myoclonic jerks accompanied the stimulus-induced bursts in either patient.
  • Both patients ultimately deceased.

Implications:

  • EEG bursts in severe postanoxic encephalopathy can be elicited by external stimuli, leading to stimulus-dependent burst-suppression.
  • Clinicians should exercise caution, as stimulus-induced EEG bursts do not indicate a favorable prognostic outcome.
  • This finding highlights the importance of carefully interpreting EEG reactivity in critically ill patients with severe brain injury.