Potential Epileptogenic Potency Of Opioids

Following the administration of high dosages of opioids with different potency, epileptogenic activities in the EEG with tonic-clonic seizures can be induced in the animal. Pethidine (meperidine), morphine, alfentanil, fentanyl and sufentanil when administered in doses above 20, 180, 5, 4 and 4 mg/kg body weight respectively, induced epileptogenic discharges [103]. Because such massive dosages are never used in anesthesia or for analgesia in acute or chronic pain, epileptogenic effects, although being cited in the literature after fentanyl [104, 105] and sufentanil [106] are of insignificant nature. This is because the clinical picture resembles tonic-clonic seizures, however, in the EEG no such discharges could be derived [107]. Therefore, those high doses of opioids, which induced epileptogenic activity in the rat [108] or the canine [103] are far off from therapeutic range. Thus, in general, an epileptogenic activity of opioids can be canceled out. One exception is the use of high dosages of pethidine (meperidine), where the metabolic product norpethidine is a potent epileptogenic compound, which especially in the newborn is able to induce epileptogenic activity [109]. The cause for the few observations of a pseudo-epileptogenic activity of opioids when being administered within the therapeutic range very likely is due to a desinhibition of the cortical motor center within the CNS, as this phenomenon was observed during the induction of anesthesia or following a decline in plasma concentration. Such assumption is underlined by

Figure II-48. Two main components of painful afferents: localization of nociception (cortical area) and the initiation of the negative component (i.e. the limbic system within the mesencephalon). Opioids mainly modify the latter area

"epileptogenic activity" during the induction of anesthesia with the pure hypnotic etomidate, where desinhibition of the motor cortex activity was the cause of cortical discharges [110].

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