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Electroencephalogram desynchronization in brain trauma patients

Introduction

This study aimed at investigating the advantages of brain function monitoring in patients with subdural haematoma or spontaneous haemorrhage. We hypothesized that the reactivity of the EEG signal to stimuli could aid in the assessment of the condition of the brain and prediction of the outcome. We were also interested in the EEG patterns and features induced by midazolam in these critically ill patients as there are only a few studies on this subject in the literature.

Methods

Twenty-three patients with subdural haematoma and four patients with spontaneous haemorrhage were incorporated in the study. Midazolam and fentanyl were used as sedative agents. The EEG signal from four channels (C3, C4, Fp1, Fp2) was recorded for at least 24 hours following the surgery. Every 4–6 hours, on average, a well standardized sequence of stimuli (voice, noise, TOF, tetanic) was applied. Reactions to the stimuli were carefully annotated by the study nurse. Segments of the EEG signal from 20 seconds before up to 40 seconds after each stimulus were extracted. The segments were further divided into 10-second subsegments overlapping by 5 seconds. The modulation of alpha activity (8–13 Hz) by the phase of the delta rhythm (0.5–4 Hz) was estimated for each subsegment.

Results

The averaged results are shown grouped by the response of the patient to the stimuli (Figure 1). Deviation of the curves from a straight line indicates modulation. The lowermost curves correspond to the first subsegment (-20 to -10 s relative to the stimulus) and the uppermost curve to the last subsegment (30–40 s).

figure 1

Figure 1

Conclusion

Slight modulation of alpha activity by the delta rhythm can be seen. In cases where clinical response was noted, the modulation is stronger but tends to disappear at about 5–15 seconds post stimulus, indicating desynchronization. Further analysis is needed to draw final conclusions.

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Rätsep, I., Lipping, T. Electroencephalogram desynchronization in brain trauma patients. Crit Care 12 (Suppl 2), P119 (2008). https://doi.org/10.1186/cc6340

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  • DOI: https://doi.org/10.1186/cc6340

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