![]() ![]() Based on the hypothesis that deep hypothermia produces considerable effects on a patient’s analgesia and hypnosis levels, in one study, 39 patients who underwent elective on-pump coronary artery bypass graft surgery under hypothermia were monitored using the bispectral index (BIS) and Conox monitors. Thermoregulatory processes are essential for the activation of analgesic mechanisms, given the physiologically strong negative association between nerve conduction velocity and temperature, in addition to having significant repercussions on the pharmacological dynamics of analgesic drugs (decreased clearance rates with a subsequent increase in effect-site concentrations). Furthermore, the qNOX index increased faster at the end of surgery, leading to the hypothesis that the response to stimuli is recovered faster than the consciousness recovering. In a study of 140 patients scheduled for propofol-remifentanil GA, the qCON index was found to be better for predicting loss of consciousness, such as loss of verbal command and eyelash reflex, than the qNOX index, while the qNOX index had a better predictive value for response to noxious stimuli. The qCON and qNOX indices behave differently for detecting loss of consciousness and loss of response to nociceptive stimulation. If the qCON and qNOX values equal 0, this indicates an isoelectric EEG signal, and consequently, a burst suppression ratio of 100%. The recommended qNOX index values for GA are between 40 and 60, where a value > 60 corresponds to a high probability of response to external noxious stimuli and a value < 40 corresponds to a low likelihood of response. The likelihood of movement response to external stimuli is described on a scale ranging from 0 to 100. Similar to the qCON index, which links different EEG spectral components to distinct aspects of hypnosis (loss of consciousness event, hypnotic concentrations, level of alertness/sedation scales) using a quadratic model, the qNOX index integrates the spectral components into an equivalent model that best predicts whether a patient will respond to noxious stimuli. The qCON index is an indication of the patient’s level of consciousness, and the qNOX index can be used to gauge the probability that a patient will respond to noxious stimuli. Similar to the spectral entropy monitor, the Conox monitor (Fresenius Kabi AG, Germany) integrates two EEG-based indices. ![]() Once nociceptive signaling reaches the thalamus, it is projected to widespread areas of the forebrain through third-order neurons, from the somatosensory cortex and limbic system to the frontal cortex. In general, the intensity of the stimuli is proportional to the frequency of the nociception discharges along the ascending pathway. ![]() Despite this, there is a variable relationship between nociceptor input and perceived pain intensity. Primary afferent nociceptors release transmitter substances to the spinal terminals (substance P), stimulating second-order pain transmission cells. This neuron has its cell body in the dorsal root ganglion, with one axon branching out to the periphery and another into the spinal cord, ending near second-order nerve cells in the dorsal horn of the gray matter (substantia gelatinosa) that project over the anterolateral quadrant of the spinal cord to the brain stem and thalamus. Focusing on the ascending pain pathway, the nociceptive message is coded in the pattern and frequency of action potentials triggered by different chemicals released by injured cells (e.g., prostaglandins) and transmitted to the spinal cord through the axon of the primary afferent nociceptor (first-order cell). These differences in sensory modalities and locations at the transduction level influence nociceptive processing and perception. In addition, processing depends on the location of the stimuli, from the cutaneous nerves to the visceral or deep musculoskeletal tissues. 2), meaning whether stimuli are mechanical (pressure, pitch), thermal (heat), or chemical, and their specific pain receptors or nociceptors. The complexity of nociception begins with the nature of the stimuli, where differences in nociception processing depend on the type of sensory modality involved ( Fig. ![]()
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