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.

Auditory evoked response during propofol anaesthesia after pre-induction with midazolam.

BACKGROUND: In clinical use, midazolam reduces the dose requirement for propofol. We studied the effect of midazolam given before anaesthesia on the amount of propofol needed and the time taken, to achieve loss of consciousness (LOC) in 20 patients. METHODS: We compared the auditory evoked responses (AER) in these patients with those in a group of 20 patients who were not given midazolam. RESULTS: LOC, as defined by a loss of response to verbal command and eyelash reflex, occurred after 113 (95% CI, 99-131) s in the control group and 75 (56-101) s in the midazolam group (P < 0.05). In the control group 2.3 (2.0-2.6) mg kg-1 propofol caused LOC compared with 1.3 (1.1-1.5) mg kg-1 in the group pretreated with midazolam (P < 0.001). Pa amplitude decreased by 60% in the control group and by 54% in the midazolam group while Nb latency increased by 24% in the control group and by 32% in the midazolam group following LOC. These differences were not significant. CONCLUSIONS: We confirmed that coinduction of anaesthesia with midazolam and propofol reduces the requirement of propofol. We also demonstrated that the AER reflects anaesthetic depth rather than plasma concentrations of anaesthetic drugs.