• T Stelzl, M J von Bose, B Hogl, H H Fuchs, and K A Flugel.
• Städtisches Krankenhaus München-Bogenhausen, Department of Neurology, Munich, Germany.
• Eur J Emerg Med. 1995 Mar 1;2(1):24-7.

AbstractThirteen patients resuscitated after circulatory arrest due to cardiopulmonary aetiologies were studied with regard to survival and outcome. Exclusion criteria were known central nervous system disorders or death secondary to cerebrovascular accident. The serum level of neuron-specific enolase (NSE), presumably a reliable marker of neuronal death, was measured by enzyme immunoassay in peripheral blood samples over the course of 4 days at 12 h intervals. On the first and third day post-resuscitation, median nerve somatosensory evoked potentials (SSEPs) were recorded and evaluated for the absence of the cortical potential--presently the standard approach for assessing prognosis in terms of post-resuscitation hypoxaemic brain damage. Absent cortical potentials were found in six patients with NSE levels above 140 micrograms l-1. Five of these patients died; one patient survived with loss of cortical functioning. Five patients had normal SSEP findings, and their NSE maximum levels were below 25 micrograms l-1. All five patients survived without neurological deficits. One patient with a peak NSE level of 36 micrograms l-1 on the second day developed a prolonged delirium (according to DSM III-R criteria) and one patient with a peak level of 76 micrograms l-1 on the fourth day developed an acute respiratory distress syndrome; both patients had preserved cortical potentials. In conclusion, pathological SSEPs and increased NSE levels are of comparable prognostic value. They may well be complementary investigations. The neuron-bound enzyme NSE is a biochemical marker which varies with the extent of neuronal damage, while absence of the cortical potentials may indicate neurophysiological loss of function.

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