Mu and delta, but not kappa, opioid agonists induce spastic paraparesis after a short period of spinal cord ischaemia in rats

Abstract

These results suggest that the effect of various opioids on motor function after a short period of spinal cord ischaemia depends upon individual opioid receptor subtypes.

Does high-dose opioid anesthesia exacerbate ischemic spinal cord injury in rabbits?

“…We gave pentazocine to the animals in the isofl urane and remifentanil groups after discontinuation of the drugs, but no analgesic was given to the fentanyl group, because an analgesic effect of fentanyl appeared to remain. Although the possibility cannot be completely excluded that the difference in the analgesic regimens for postsurgical care affected the results, we believe that this is unlikely, because pentazocine is known not to exacerbate ischemic spinal cord injury [2]. Third, there may have been a type-II error in the present study because of the limited number of animals in each group.…”

“…These authors then showed that, in rats, large intrathecal (IT) doses of morphine given during a post-ischemic period induced spastic paraparesis after a noninjurious interval (6 min) of spinal cord ischemia [1]. In addition, a series of experiments using the same ischemia model demonstrated that mu and delta, but not kappa, opioid agonists given intrathecally could induce spastic paraparesis [2]. It was suggested that opioids administered intrathecally during or shortly after transient aortic occlusion may be associated with a potential risk of paraparesis and the corresponding development of neurological dysfunction [3].…”

Central Sensory-Motor Deficit After Uneventful Single-Dose Spinal Morphine Administration in a Patient with Preexisting Migraine Headaches

“…12 Morphine-induced motor dysfunction has been reported after spinal ischemia in humans and laboratory animals. 13,14 Hemiparesis has resulted from spasm of the anterior and middle cerebral artery, which was exacerbated by IV morphine and reversed by naloxone. 13,14 In a rat model, neuraxial morphine administration was associated with transient motor dysfunction after a noninjurious interval of spinal ischemia.…”

“…13,14 Hemiparesis has resulted from spasm of the anterior and middle cerebral artery, which was exacerbated by IV morphine and reversed by naloxone. 13,14 In a rat model, neuraxial morphine administration was associated with transient motor dysfunction after a noninjurious interval of spinal ischemia. 14 Migraine is an independent risk factor for vascular dysfunction of the central nervous system including ischemic stroke in women younger than 45 yr. 12 Local changes in cerebral vessels during attacks including reduced oligemia, activation of the clotting system, vasoconstriction mediated by neural and endothelial alteration lead to vessel embolism, thrombosis, and ischemia.…”

“…12 For example, transient spastic motor dysfunction has been reported after a noninjurious interval of spinal cord ischemia in humans and laboratory animals. 13,14 We hypothesize that spinal morphine induced a permanent central motor deficit, facilitated by spinal cord vascular dysfunction associated with hemiplegic migraine.…”