Here, we report of the use of an entropy module to measure the sedation in an adult sleepwalking patient with drug medication during intravenous anesthesia. The SE and RE values provided by the entropy module can provide reliable information about the level of sedation during surgery. Several studies suggest that SE and RE are useful parameters for determining the anesthetic effects of propofol, of the combination of propofol and remifentanil, and of sevoflurane.

Anesthetic requirement varies with a patient's age, clinical conditions, disease, and administration of other drugs. In this case, the patient was diagnosed with sleepwalking 2 years prior to the operation and has been administered benzodiazepines, valproic acid and selective serotonin reuptake inhibitors. Therefore, the patient's disease or possible drug interactions might have been responsible for an increase in anesthetic requirement and caused the unexpected increase in EEG entropy that occurred 10 min into surgery.

Psychiatric drugs usually given in combination with other, non-psychiatric drugs, or with each other, can often have an effect on peripheral or central neurotransmitter systems and ionic balances. Benzodiazepine-like clonazepam is known to increase blood concentrations of propofol by 25% through a decrease in the metabolic, rapid, and slow distribution clearance pathways of propofol; a decrease in mean arterial blood pressure would cause pharmacokinetic alterations of propofol and increase the blood propofol concentrations even further. Valproic acid may have significantly reduced the required dose of propofol due to its inhibitory action on the metabolic enzymes responsible for the metabolism of propofol [9]. Finally, propofol is known to inhibit norepinephrine and serotonin transporter protein functions in a drug-dependent manner. Therefore, selective serotonin reuptake inhibitors may be expected to alter the response of norepinephrine and serotonin transporter proteins to propofol. The psychiatric medications taken by our patient would be expected to decrease the anesthetic requirement.

Furthermore, our patient has been exposed to psychiatric medications for a period of 2 years. Propofol is metabolized primarily by glucuronidation through UDP-glucuronosyl-transferase 1A9. The cytochrome (CYP) enzymes CYP2B6, CYP3A4 and CYP1A2 play an important role in the liver metabolism of propofol, which is performed by oxidation of propofol via ring hydroxylation [10,11]. Under long-term use of psychiatric medications, the metabolism of the anesthetic drug can be changed such as transcriptional activation leading to increased synthesis of CYP 450 enzyme proteins. As a result, blood levels of the medication decrease, generally over the first 3 months of exposure to the medication [12]. This case also can be explained in the same way.

The measured EEG signal is primarily generated by cortical pyramidal cells and is the result of complex cortico-cortical and cortico-subcortical interactions. As such, diseases involving these structures or their connections may be expected to influence the EEG signal. For example, the EEG of patients with Alzheimer's disease or multi-infarct dementia has a lower bispectral index than the EEG of normal 'awake' adults, which correlates with the level of cognitive impairment in these patients [13]. Sleepwalking disorder may involve similar alterations within brain structures or connections. In support of this hypothesis, single photon emission computed tomography (CT scans) performed in patients during sleepwalking episodes reveal a persistent deactivation of thalamocortical arousal system and the thalamocingulate pathway as a dissociated state with concomitant motor arousal and sleep of mind. Furthermore, Oliviero and colleagues [14] suggested that functional abnormality of arousal circuits that widely project to the cortex could lead to changes in cortical excitability in adult sleepwalkers, even during wakefulness. The authors reported that adult sleepwalkers had reduced levels of short interval intracortical inhibition, reduced cortical silent period duration, and reduced short latency afferent inhibition during wakefulness. Their results suggested that sleepwalkers may have an impairment of inhibitory circuits that represents the immaturity of some neural circuits, synapses or receptors in the brain [14]. Therefore, the aforementioned changes may lead to drug resistance and EEG changes. This possibility is supported by the finding that patients who present with autism spectrum disorder as a result of deficient neural development have greater propofol requirements for anesthesia during ordinary dental treatment compared with intellectually impaired patients [15].

Finally, monitoring the sedation does not always coincide with a clinically-monitored level of consciousness. Cardiac pacing devices, electromagnetic systems, endoscopic shaver devices, forced-air warming devices and wire-reinforced EMG tubes can all have effects on the measured entropy value. However, in this case, the use of machinery or even the nociceptive stimuli that can affect the EEG or the entropy values may not be given during preparation of the surgical procedure.

In conclusion, sleepwalking patients with long-term use of psychiatric medications may need the increment of anesthetic requirement. It may be caused by the activation of the anesthetic drug metabolism leading to increased synthesis of CYP 450 enzyme proteins or an impairment or immaturity of inhibitory circuits due to somnambulism. Therefore, anesthesiologists may wish to consider a possible change in anesthetic requirement depending on the type of disease and prescribed medications. Furthermore, anesthesia depth monitoring through the use of devices such as an entropy module is recommended for the safety of patients.