V. Rohde et al., Prediction of the post-comatose motor function by motor evoked potentials obtained in the acute phase of traumatic and non-traumatic coma, ACT NEUROCH, 141(8), 1999, pp. 841-848
Objective. To define the Value of electrically elicited motor evoked potent
ials (MEP), obtained during the initial phase of the coma, for correct pred
iction of the post-coma motor status. Methods: Fifty-two patients were inve
stigated by MEP within 72 hours after onset of the coma. It was the aim to
correlate the MEP findings to the motor function two months after coma onse
t. Results: Three patients with normal MEP showed no post-coma motor defici
t. In 21 patients, a bilateral, symmetric prolongation of the central motor
conduction time (CMCT) was registered. Eighteen of these 21 patients (86%)
showed a normal post-coma motor status. In 28 patients, unilaterally absen
t evoked potential, or unilaterally prolonged CMCT, or bilaterally prolonge
d CMCT with significant difference in each hemispere were observed. A post-
coma contralateral paresis was found in 25 of these 28 patients (89%). That
paresis was functionally important in 15 patients (54%) and functionally u
nimportant in 13 patients (46%). Conclusion. We identified certain MEP patt
erns (unilateral extinction of the evoked potential, unilateral, bilateral
prolongation of the CMCT with significant "side" difference), which indicat
ed a pyramidal tract lesion and a post-coma motor deficit with an accuracy
of 89%. This refers to the motor results, which may not be the final post-c
oma motor results which are usually assessed six months after the coma onse
t. The MEP changes did not allow one to predict the severity of the paresis
. The accuracy of prediction of a motor deficit increased from the MEP find
ing of unilaterally prolonged CMCT to the MEP finding of unilateral extinct
ion of the potential. The most common finding, bilateral central motor slow
ing without significant "side" difference, did not indicate a post-coma par
esis in 86%, leading to the assumption, that bilateral, symmetrical prolong
ation of the CMCT was not caused by lesions of the descending motor pathway
s, but by the drugs administered for treating the comatose patient. In conc
lusion, MEP allows one to predict the presence of a post-coma motor deficit
with a high degree of accuracy already in the initial phase of coma, but M
EP fails to predict the severity of that deficit.