Blockade of Morphine-Induced Hindlimb Myoclonic Seizures in Mice by Ketamine

Kolesnikov, Yuri; Jain, Subash; Wilson, Roger S.; Pasternak, Gavril W.

doi:10.1016/s0091-3057(96)00221-3

Cited by 17 publications

(5 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 5 – 7 Ketamine is a noncompetitive N -methyl- d -aspartate receptor antagonist 23 that might play a role in treating seizure in status epilepticus by blocking N -methyl- d -aspartate receptor-mediated glutamatergic neurotransmission. 24 , 25 Besides, Kolesnikov et al 9 reported that ketamine could prevent morphine-induced myoclonus in mice, which is consistent with a clinical report introduced by Forero et al 10 that low-dose ketamine effectively relieved the painful myoclonus in a patient receiving long-term opioids treatment. In this study, we chose the low-dose ketamine because: low-dose ketamine has shown its capacity to prevent the painful myoclonus 10 ; low-dose ketamine administration over 30 seconds could get rid of the psychiatric symptoms induced by large doses (>2 mg/kg, IV) and rapid injection of ketamine (>40 mg/min) 26 ; low-dose ketamine premedication has been suggested to be beneficial in improving intubating condition and managing postoperative analgesia.…”

Section: Discussionmentioning

confidence: 54%

“… 5 – 7 Ketamine, a widely used anesthetic in clinical practice, has shown its therapeutic capacity for control of seizure. 8 In addition, it has also been demonstrated that ketamine could block the myoclonus induced by opioids administration both in animal 9 and human. 10 However, there is no investigation regarding the effectiveness of low-dose ketamine to prevent unwanted myoclonus caused by etomidate.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Low-Dose Ketamine Pretreatment Reduces the Incidence and Severity of Myoclonus Induced by Etomidate

Liu

et al. 2016

Medicine

View full text Add to dashboard Cite

Myoclonic movement induced by etomidate is a common but undesirable problem during general anesthesia induction. To investigate the influence of pretreatment with low-dose ketamine on the incidence and severity of myoclonus induced by etomidate, 104 patients were randomized allocated to 1 of 2 equally sized groups (n = 52) to receive either intravenous low-dose ketamine 0.5 mg/kg (group K) or an equal volume of normal saline (group S) 1 minute before induction of anesthesia with 0.3-mg/kg etomidate. The incidence and severity of myoclonus were assessed for 2 minutes after administration of etomidate. Here, we found that the incidence and intensity of myoclonus were both significantly reduced in low-dose ketamine-treated group compared with saline-treated group. The incidence of adverse effects was low and similar between groups. These results demonstrate that intravenous infusion of low-dose ketamine 0.5 mg/kg 1 minute prior to etomidate administration is effective in relieving etomidate-induced myoclonic movements during general anesthesia induction.

show abstract

Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Low-Dose Ketamine Pretreatment Reduces the Incidence and Severity of Myoclonus Induced by Etomidate

Liu

et al. 2016

Medicine

View full text Add to dashboard Cite

show abstract

“…The proconvulsant effect of higher doses of morphine has been previously linked to a putative inhibition of GABAergic tone (49) and increased activity of excitatory N-methyl-D-aspartate (NMDA) receptors (50,51). In the present study, this proconvulsant effect was potentiated by clonidine and inhibited by yohimbine.…”

Section: The Effects Of Clonidine and Yohimbinesupporting

confidence: 47%

The Role of α₂‐Adrenoceptors in the Modulatory Effects of Morphine on Seizure Susceptibility in Mice

2002

View full text Add to dashboard Cite

Summary: Purpose:To evaluate the effect of the ␣ 2 -adrenoceptor agonist clonidine and the antagonist yohimbine on the dual modulation of seizure susceptibility induced by morphine and the anticonvulsant effect of acute stress in mice.Methods: The thresholds for the clonic seizures induced after intravenous administration of pentylenetetrazole (PTZ) or bicuculline were assessed in mice weighing 23-30 g. Acute stress was induced by restraining mice for 2 h in a restrainer.Results: Morphine at lower doses (0.5, 1, and 3 mg/kg) increased and, at higher doses (15, 30, and 75 mg/kg), decreased the seizure threshold. Pretreatment with clonidine (0.001-0.1 mg/kg) inhibited the anticonvulsant effect of morphine, while potentiating its proconvulsant effect. Conversely, yohimbine (0.5-2 mg/kg) potentiated the anticonvulsant effect of morphine but inhibited its proconvulsant effects. Acute stress induced an anticonvulsant effect that was reversible by naloxone (1 mg/kg) or clonidine (0.05-0.1 mg/kg) or a combination of their lower doses (0.3 and 0.01 mg/kg, respectively), while being potentiated by yohimbine (1 mg/kg).Conclusions: ␣ 2 -Adrenoceptors play a dual role in the anticonvulsant effects of morphine. The activation of these receptors also can decrease the anticonvulsant effect of acute restraint stress in mice.

show abstract

“…Ketamine, an NMDA receptor antagonist, has also been reported to resolve hyperalgesia and myoclonus following chronic intrathecal opioid administration in a person when given as a low dose infusion (Forero and others 2011). Experimentally, a systemic bolus of ketamine resolved morphine induced hindlimb myoclonus in mice (Kolesnikov and others 1997). However, it was unsuccessful in resolving neuroexcitation in a dog following a perioperative dose of intrathecal morphine (Iff and others 2012).…”

Section: Discussionmentioning

confidence: 99%

Myoclonus and hyperalgesia following intended epidural morphine administration in a dog

Robson

Alderson

2014

Vet Record Case Reports

View full text Add to dashboard Cite

A West Highland White Terrier was presented after development of hindlimb myoclonus and hyperalgesia following intended epidural administration of morphine at a referring veterinary practice. MRI was unremarkable, except for the spinal cord extending to the caudal half of the L7 vertebrae. Treatment with systemic analgesia of methadone and sedation/analgesia with medetomidine resolved the clinical signs within 24 hours. The mechanism by which morphine causes adverse neurological side effects has yet to be fully determined; the morphine-3-glucuronide (M-3-G) metabolite is suspected to be responsible for the adverse effects seen. Hypotheses include action of morphine or the M-3-G metabolite on non-opioid inhibitory (glycine) or excitatory (N-methyl D-aspartate) receptors. However, more work is needed to determine the exact pathogenesis. Neuroexcitatory side effects are rarely reported following administration of morphine in dogs and this case demonstrates successful treatment with the use of an alternative opioid, methadone.

show abstract

Blockade of Morphine-Induced Hindlimb Myoclonic Seizures in Mice by Ketamine

Cited by 17 publications

References 11 publications

Low-Dose Ketamine Pretreatment Reduces the Incidence and Severity of Myoclonus Induced by Etomidate

Low-Dose Ketamine Pretreatment Reduces the Incidence and Severity of Myoclonus Induced by Etomidate

The Role of α₂‐Adrenoceptors in the Modulatory Effects of Morphine on Seizure Susceptibility in Mice

Myoclonus and hyperalgesia following intended epidural morphine administration in a dog

Contact Info

Product

Resources

About

Blockade of Morphine-Induced Hindlimb Myoclonic Seizures in Mice by Ketamine

Cited by 17 publications

References 11 publications

Low-Dose Ketamine Pretreatment Reduces the Incidence and Severity of Myoclonus Induced by Etomidate

Low-Dose Ketamine Pretreatment Reduces the Incidence and Severity of Myoclonus Induced by Etomidate

The Role of α2‐Adrenoceptors in the Modulatory Effects of Morphine on Seizure Susceptibility in Mice

Myoclonus and hyperalgesia following intended epidural morphine administration in a dog

Contact Info

Product

Resources

About

The Role of α₂‐Adrenoceptors in the Modulatory Effects of Morphine on Seizure Susceptibility in Mice