Grand Mal Seizure After Extradural Morphine Analgesia

Borgeat, Alain; Biollaz, J.; Depierraz, Blaise; Neff, Raymond K.

doi:10.1093/bja/60.6.733

Cited by 22 publications

(8 citation statements)

References 8 publications

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“…Our patient, and that described by Borgeat et al, 7 share a history of epilepsy and recent pregnancy. An epileptic pathology, even with the form of a dormant focus, might have interacted with the condition of pregnancy to produce a pro-convulsant environment for the seizure-inducing effect of small doses of morphine.…”

supporting

confidence: 77%

“…However, only one report in the literature describes the development of seizures after epidural morphine in a patient with a known history of epilepsy. 7 We report the case of a primiparous woman with a history of simple partial seizure with secondary generalization, who experienced recurrence of motor seizure activity after epidural administration of a small dose of morphine for postoperative pain control.…”

Section: Conclusion : Notre Article Indique Que Même Une Histoire Ancmentioning

confidence: 99%

“…4 Nonetheless, tonic-clonic activity has been reported in an epileptic woman who had elective Cesarean section, six hours after the epidural administration of 3 mg of morphine. 7 Human studies have shown that central effects of epidurally administered morphine, like delayed ventilatory depression 14 and nausea, 15 are mostly due to rostral spread of the drug through the cerebrospinal fluid and have an onset time between four and nine hours. In our case, myoclonic activity occurred three and eight hours after epidural administration of 1.5 and 1 mg of morphine, respectively.…”

mentioning

confidence: 99%

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Recurrent seizure activity after epidural morphine in a post-partum woman

Shih

Doufas

Chang

et al. 2005

Can J Anesth/J Can Anesth

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supporting

confidence: 77%

Section: Conclusion : Notre Article Indique Que Même Une Histoire Ancmentioning

confidence: 99%

mentioning

confidence: 99%

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Recurrent seizure activity after epidural morphine in a post-partum woman

Shih

Doufas

Chang

et al. 2005

Can J Anesth/J Can Anesth

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“…Landow (1985) described the occurrence of a focal seizure which was probably correlated with a high-pressure intrathecal injection in a patient with cancer. Borgeat et al (1988) reported the case of an epileptic woman who developed a generalised tonic-clonic seizure 6 hours after the administration of morphine 3mg into the extradural space.…”

Section: Morphinementioning

confidence: 99%

Clinical Features, Pathogenesis and Management of Drug-Induced Seizures

1990

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Many classes of pharmacological agents have been implicated in cases of drug-induced seizures. The list includes antidepressant drugs, lithium salts, neuroleptics, antihistamines (H1-receptor antagonists), anticonvulsants, central nervous system stimulants, general and local anaesthetics, antiarrhythmic drugs, narcotic and non-narcotic analgesics, non-steroidal anti-inflammatory drugs, antimicrobial agents, antifungal agents, antimalarial drugs, antineoplastic drugs, immunosuppressive drugs, radiological contrast agents and vaccines. For each of these classes of drugs, this article offers a revision of the literature and emphasises in particular the frequency of the adverse reaction, its clinical presentation, its presumed epileptogenic mechanism and the therapeutic strategy for the management of drug-induced seizures. An attempt is also made to distinguish seizures induced by standard dosages from those provoked by accidental or self-induced intoxication. For some classes of drugs such as antidepressants, neuroleptics, central nervous system stimulants (e.g. theophylline, cocaine, amphetamines) and beta-lactam antibiotics, seizures are a well recognised adverse reaction, and a large body of literature has been published discussing exhaustively the major aspects of the issue; sufficient data are available also for the other classes of pharmacological agents mentioned above. In contrast, several other drugs [e.g. allopurinol, digoxin, cimetidine, protirelin (thyrotrophin releasing hormone), bromocriptine, domperidone, insulin, fenformin, penicillamine, probenecid, verapamil, methyldopa] have not been studied thoroughly under this aspect, and the only source of information is the occasional case report. This review does not address the issue of seizures induced by drug withdrawal.

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“…Intracranial administration of morphine and opioid peptides elicit pathologic epileptiform activity in the electroencephalogram (Frenk et al., 1978; Tortella et al., 1978; Snead & Bearden, 1982; Urca et al., 1977). In humans, infusion of morphine into the cerebrospinal fluid (CSF) induces seizures in adults (Borgeat et al., 1988). A potential withdrawal condition caused by an abrupt discontinuation of opiate intake after an extended period of abuse may also induce seizure‐like activity (Pinsky et al., 1982; VanBaar & deGraaff, 1994).…”

mentioning

confidence: 99%

Morphine dependence increases the response to a brief pentylenetetrazol administration in rat hippocampal CA1 in vitro

et al. 2009

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SUMMARYPurpose: Herein we used electrophysiologic approaches in hippocampal area CA1 to estimate how morphine treatment alters the pentylenetetrazol (PTZ) effects. Methods: Hippocampal slices taken from either control animals or animals made dependent via chronic morphine administration were examined. Changes in the population spike and epileptiform amplitudes were used as indices to quantify the effects of PTZ exposure in the control and morphine-dependent slices. Hippocampal slices taken either from control animals or from animals made dependent upon morphine were exposed to PTZ, either with or without morphine, naloxone, or morphine + naloxone. Results: Morphine dependence increased a PTZinduced long-term potentiation (LTP) of the population spike in CA1 in vitro. This LTP was not found in rats that had spontaneously withdrawn morphine or withdrawn with naloxone in vivo after chronic morphine intake. Morphine or naloxone in vitro blocked the PTZ-induced LTP changes in control and morphine-dependent slices. However, PTZ-induced multiple population spikes (epileptiform activity) in CA1 was not blocked by naloxone. Discussion: It is concluded that dependence on morphine enhances PTZ-induced plastic and epileptic changes in CA1 excitability. We suggest that this model of neuronal activity in dependent slices could present an opportunity for studying the mechanisms underlying the increased likelihood of seizures in morphine users.

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Grand Mal Seizure After Extradural Morphine Analgesia

Abstract: Following an elective Caesarean section under extradural anaesthesia, a 30-yr-old known epileptic woman (gravida 4, para 3) developed a tonic-clonic seizure, 6 h after the administration of morphine 3 mg into the extradural space. Possible aetiological factors are discussed.

Cited by 22 publications

References 8 publications

Recurrent seizure activity after epidural morphine in a post-partum woman

Recurrent seizure activity after epidural morphine in a post-partum woman

Clinical Features, Pathogenesis and Management of Drug-Induced Seizures

Morphine dependence increases the response to a brief pentylenetetrazol administration in rat hippocampal CA1 in vitro

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