Diagnostic pitfalls in patients with hypoxic brain damage: three case reports.
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.


CONCLUSIONS
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.
Zingler
Vera Carina
VC
Department of Neurology, Ludwig-Maximilians University, Klinikum Grosshadern, Marchioninistrasse 15, D-81366 Munich, Germany. vera-carina.zingler@nro.med.uni-muenchen.de
Pohlmann-Eden
Bernd
B
D016887:Cardiopulmonary Resuscitation; D005260:Female; D006323:Heart Arrest / Q000150:complications; D006801:Humans; D002534:Hypoxia, Brain / Q000175:diagnosis* / Q000209:etiology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D018458:Persistent Vegetative State / Q000209:etiology*; D011379:Prognosis; D016896:Treatment Outcome