Syster

spinothalamic tract

Figure 11-44. Schematic drawing of the "narcotic and the analgesic components" of potent ^-opioids when being administered in high dosages. (ARS = activation reticular system). Modified from [97]

Figure II-45. The nucleus limitans bordering the mesencephalon and the thalamic area, is an important relay station within the CNS, a necessary component for the mediation of identifying a stimulus as being painful and where the input receives its negative, throbbing component

vigilance is also reflected in the high density of opioid binding sites in the mesencephalon [99]. Physiologically this is mirrored by an arousal reaction following intense acoustic or a nociceptive stimulus, both of which induce a reversal from the low frequency delta- to high frequency beta-activity in the EEG (Figure II-47).

In summary, it is concluded that opioids primarily affect the limbic system, the specific site for inducing the negative component of nociception. Lastly such assumption is underlined by the result from Mc Kenzie and coworkers in the animal where the opioids morphine and pethidine were not able to sufficiently block any pain related nervous transmission from the mesencephalon to the higher cortical areas [100]. In contrast, both ligands were able to block nociceptive transmission from the mesencephalon to hippocampal areas of the limbic system, the part of the CNS, which is responsible for the identification of pain, causing the negative, grief, stinging and an intense emotional feeling associated with pain (Figure II-48).

Such differences in pain modulation were corroborated in patients undergoing stereotactic, painful stimulation within specific areas of the CNS [101]. Nociceptive afferents of the spinothalamic tract end in the nucleus ventrocaudalis parvo-cellularis

Figure 11-46. Selective perfusion of increasing doses of fentanyl through the fourth cerebral ventricle of the awake canine. Note, the direct sedative (delta-synchronisation in the EEG) effect via the underlying ARS. This effect is mediated through opioid receptors located on the floor of the ventricle, since it was reversible with naloxone (desynchronisation with beta activation in the EEG). Adapted from [98]

Figure 11-46. Selective perfusion of increasing doses of fentanyl through the fourth cerebral ventricle of the awake canine. Note, the direct sedative (delta-synchronisation in the EEG) effect via the underlying ARS. This effect is mediated through opioid receptors located on the floor of the ventricle, since it was reversible with naloxone (desynchronisation with beta activation in the EEG). Adapted from [98]

thalami, from where they further ascend to different cortical areas. Since these nuclei reflect a specific somatotopic differentiation, electrical stimulation within this area induced painful sensations in different parts of the body. Decoding of painful afferents was only possible when the stimulating electrode was placed within the nucleus limitans, where collaterals of the spinothalamic tract switch to the limbic system. There stimulation induced a less well-localized, however, intense unspecific displeasure [102].

Figure 11-47. Selective perfusion of the fourth cerebral ventricle with fentanyl in the canine results in the initiation of slow, high amplitude EEG-waves in the cortex. Auditory or nociceptive stimuli are able to reverse this pattern to a high frequency configuration pinpointing to the lesser sedative component of fentanyl. Adapted from [98]

Figure 11-47. Selective perfusion of the fourth cerebral ventricle with fentanyl in the canine results in the initiation of slow, high amplitude EEG-waves in the cortex. Auditory or nociceptive stimuli are able to reverse this pattern to a high frequency configuration pinpointing to the lesser sedative component of fentanyl. Adapted from [98]

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