EFFECTS OF MIDAZOLAM ON MEDIAN NERVE SOMATOSENSORY EVOKED POTENTIALS

• Published in: British journal of anaesthesia : BJA Vol. 64; no. 5; pp. 590 - 593
• Main Authors: SLOAN, T.B., FUGINA, M.L., TOLEIKIS, J.R.
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.05.1990; Oxford University Press
• Subjects: Adult; Anesthesia, Intravenous; benzodiazepines: midazolam; Biological and medical sciences; Cerebral Cortex - physiology; Evoked Potentials, Somatosensory - drug effects; Female; Hemodynamics - drug effects; Humans; Hypnotics; Hypnotics. Sedatives; Male; Median Nerve - drug effects; Median Nerve - physiology; Medical sciences; Midazolam - pharmacology; Middle Aged; Monitoring: somatosensory evoked potentials; Neuropharmacology; Pharmacology. Drug treatments; Psychology. Psychoanalysis. Psychiatry; Psychopharmacology; Spinal Cord - physiology; Time Factors; Monitoring: somatosensory evoked potentials; benzodiazepines: midazolam; Hypnotics; Human; Intravenous administration; Median nerve; Electrophysiology; Benzodiazepine derivatives; Hypnotic; Somatosensory evoked potential; Monitoring
• ISSN: 0007-0912; 1471-6771
• DOI: 10.1093/bja/64.5.590

We have studied the effect of i.v. midazolam on median nerve somatosensory evoked potentials (SSEP) in 10 unpremedicated adults. Anaesthesia was induced with midazolam by bolus administration (0.2 mg kg−1) followed by infusion (5 mg h−1). The latency and amplitudes of the SSEP responses over the second cervical vertebrae (SC2) and sensory cortex (P17, N20, P25) were recorded before and for 10 min after induction. Data were analysed over that period for time-related alterations. Small but statistically significant increases in latency of the cortical N20 (P < 0.005) and P25 (P < 0.001) waves and interwave conduction times of SC2 to P25 (P < 0.005) and N20 to P25 (P < 0.021) were observed. Cortical amplitude (N20–P25) decreased significantly (P < 0.012), to approximately 60% of baseline. These results demonstrated that midazolam produced a depression of cortical SSEP amplitude without clinically significant alterations in latency.