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Updated: Aug 13, 2026
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 18, 2008
Diagnostic pitfalls in patients with hypoxic brain damage: three case reports
Vera Carina Zingler1, Bernd Pohlmann-Eden
1Department of Neurology, Ludwig-Maximilians University, Klinikum Grosshadern, Marchioninistrasse 15, D-81366 Munich, Germany. vera-carina.zingler@nro.med.uni-muenchen.de
Objective:
Our aim was to assess the possible diagnostic pitfalls in three patients with hypoxic brain damage who had partly conflicting clinical, biochemical, and electrophysiological data and were in a persistent vegetative state (PVS) following cardiac arrest (CA).
Methods:
Serum concentrations of the destruction proteins, neuron-specific enolase (NSE) and protein S-100B (S-100B), were measured on days 1-3, and 7; somatosensory evoked potentials (SEPs) were recorded within 48 h and on day 7 after CA.
Results:
Two patients had significantly increased concentrations of NSE and S-100B during the first 3 days after CA, a finding that indicates ongoing neuronal destruction. In contrast, the SEPs of these patients were normal or showed only a diminished amplitude configuration. In the third patient the SEPs demonstrated a bilateral loss of cortical responses repeatedly, but both destruction proteins were only slightly above the upper normal values on all study days.
Conclusion:
Our findings demonstrate that a poor prognosis can only be established if either SEPs, NSE, or S-100B are very abnormal. The conflicting results in our patients indicate that variable values may reflect different patterns of neuropathological damage caused by diffuse hypoxia. We, therefore, favour a multi-modal approach with a combination of clinical, biochemical, and electrophysiological investigations in order to predict neurological outcome after CA reliably.
