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Favourable outcome of a brain trauma patient despite bilateral loss of cortical somatosensory evoked potential during thiopental sedation
  1. P A Robe1,
  2. A Dubuisson1,
  3. S Bartsch2,
  4. P Damas2,
  5. S Laureys3
  1. 1Service of Neurosurgery, University Hospital of Liége, Liége, Belgium
  2. 2Service of Critical Care Medicine, University Hospital of Liége
  3. 3Service of Neurology, University Hospital of Liége
  1. Correspondence to:
 Dr P A Robe, Department of Neurosurgery, CHU de Liége, Domaine universitaire du Sart Tilman, B35, 4000 Liége, Belgium;
 pierre.robe{at}ulg.ac.be

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We would like to present an observation that somewhat questions the predictive value of somatosensory evoked potentials on the outcome of brain trauma patients treated with thiopental coma.1,2

A 30 year old woman suffered a high velocity car accident resulting in a diffuse brain injury. Her Glasgow coma scale score on admission was E2V2M5 (9/15), with preserved pupillary reflexes and gross motor function. Computed tomography of the head showed a traumatic disjunction of the lambdoid suture and multiple left frontobasal and temporal cerebral contusions. The patient was sedated with propofol, intubated, and monitored for intracerebral pressure (ICP) through an external ventricular drain. Her clinical condition rapidly worsened because of brain swelling around the contusions, and cerebrospinal fluid drainage, manitol boluses, and mild hyperventilation were started. Three days after admission, a further ICP increase was treated with thiopental coma (10 mg/kg/h × 24 h loading dose followed by 3 mg/kg/h maintenance dose to obtain a burst suppression EEG pattern). On day 7, the patient developed a left sided mydriasis and a left temporal partial lobectomy was performed to remove contused brain. The ICP returned to normal and thiopental administration was stopped on day 8. On day 10, the EEG was isoelectrical and on day 11, somatosensory evoked potentials (SSEP) of the median nerve showed no cortical response (N20) despite normal brachial plexus (Erb) and lemniscal (P14) potentials. Levels of thiopental and phenobarbital, its main metabolite, were then respectively 65 ng/l and 56 ng/l. The patient remained areactive (GCS 3/15T) and without brain stem reflexes, including the ocular-cardiac response, until day 20. The transcranial Doppler however showed normal flow patterns and the brain CT scan did not reveal any post-herniation ischaemic lesion. On day 21, the patient opened her eyes. The serum concentration of thiopental was then 12 ng/l whereas that of phenobarbital remained around 40 ng/l until day 23. A 1–2 Hz low amplitude EEG activity with right sided predominance was observed, and the SSEP cortical peak N20 recovered on day 22 when the thiopental concentration was 5.9 ng/l. A steady improvement followed. On discharge to a rehabilitation facility (day 57), the patient could follow simple commands but suffered mixed dysphasia and generalised weakness. At four months, she presented no residual motor deficit, an improved verbal expression and comprehension, and a moderate frontal behaviour. At two years, the patient only still suffered some episodes of labile mood, and although she had not resumed her previous job, she was active as a farm worker, read and wrote, drove her car, and could live an independent and social life, with a Glasgow outcome score (GOS) of 5/5.

SSEP are commonly used to monitor comatose patients even under barbiturate sedation.2,3 Indeed, although their morphology can become changed, short latency SSEPs in humans supposedly do not disappear in response to barbiturate doses sufficient to render the EEG isoelectrical and the neurological examination similar to brain stem death.3,4 The bilateral loss of SSEP N20 responses is regarded as a predictor of ominous outcome after a trauma. There are only a few reports on the recovery of initially absent or lost N20 potentials after severe brain injury with increased ICP, some of them with a good outcome as was the case in our patient.5,6 In our case, the disappearance of the cortical evoked responses correlated with both the ICP increase and the induction of thiopental coma. As their reappearance closely matched the elimination of thiopental from the bloodstream and was quite delayed relative to the normalisation of the ICP, our observation suggests that barbiturates may contribute to the suppression of N20 evoked potentials in brain trauma patients. Awaiting further observations, caution is thus warranted on the use of SSEP to monitor the clinical evolution and predict the outcome of such patients under barbiturate coma.

Funding: PAR and SL are post-doctoral researchers at the Fonds National de la Recherche Scientifique (FNRS).

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