Auditory- and somatosensory-evoked potentials in cerebral malaria and anaesthesia: a comparison.

BACKGROUND AND OBJECTIVE

Parallels exist between the coma associated with cerebral malaria and general anaesthesia. They both produce reversible loss of consciousness. In the case of cerebral malaria and in the absence of other complications, patients recover without sequelae. General anaesthetics are so designed that patients recover from their anaesthetics very quickly and show no 'after effects'. This study compares brain function in these two clinical conditions by examining auditory- (AEPs) and median nerve somatosensory-evoked potentials (SEPs). The AEPs studied (waves Pa and Nb) are thought to arise from the primary auditory cortex and the median nerve SEPs (waves P15, N20, P25, N35, P45) from the pons, thalamus and primary somatosensory cortices.

METHODS

Six comatosed patients with malaria (three males, three females) aged between 19 and 38 yr were studied in Zimbabwe. Their Glasgow Coma Scores on admission were 4, 3, 6, 7, 7 and 11. Their AEPs and median nerve SEPs were recorded daily over 4 days. The data were compared with those previously collected in the UK on patients and volunteers anaesthetized with desflurane, isoflurane, sevoflurane and propofol.

RESULTS

In general, patients with cerebral malaria showed AEPs and SEPs similar to those of light to moderate anaesthesia i.e. 0.5-1.25 measure of anaesthetic potency (MAC), where 1 MAC is the minimum alveolar concentration necessary to prevent movement to surgical incision in 50% of patients. The appearance of the AEPs and SEPs bore no relationship to the degree of coma. The auditory brainstem-evoked response was retained in all degrees of coma, as would be expected. Otherwise, it would not be possible to interpret the waveform. In most instances, the early cortical complex Pa/Nb/Pb of the AER was present. When comatose patients emerged from malarial coma or were stimulated by talking loudly to them, they showed changes in the Pa/Nb/Pb complex similar to those seen on awakening from anaesthesia. The somatosensory-evoked response showed clear P15, N20 and P25 peaks at the expected latencies, and in some instances the waveforms of cerebral malaria and lightly anaesthetized volunteers were very similar.

CONCLUSIONS

The sensory-evoked responses of the cerebral malaria patients recorded in this study were not markedly different from those seen in light-to-moderately anaesthetized patients and volunteers. The profound depression of the AEPs and SEPs associated with deeper levels of anaesthesia were not seen, with the exception of one patient several hours before death.