Interactions between relatively selective monoamine oxidase inhibitors and an inhibitor of 5-hydroxytryptamine re-uptake, clomipramine

Marley, E.; Wozniak, Krystyna M.

doi:10.1016/0022-3956(85)90079-2

Cited by 14 publications

(4 citation statements)

References 19 publications

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“…20 21 However, it may be noted that no expert animal pharmacologist has yet reviewed this subject in detail, and there remains much work to be done in relation to testing drugs in animal models of serotonin toxicity using more up-to-date techniques. The only systematic recent work since Marley's seminal papers [42][43][44][45][46] in the early 1980s has been done by Nisijima. In brief, from the very earliest experiments in 1958, 6 58 through to Nisijima's work, a wide variety of structurally different agents have been tested in animal models.…”

Section: Treatmentmentioning

confidence: 99%

Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity

Gillman

2005

British Journal of Anaesthesia

348

242

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Toxicity resulting from excessive intra-synaptic serotonin, historically referred to as serotonin syndrome, is now understood to be an intra-synaptic serotonin concentration-related phenomenon. Recent research more clearly delineates serotonin toxicity as a discreet toxidrome characterized by clonus, hyper-reflexia, hyperthermia and agitation. Serotonergic side-effects occur with serotonergic drugs, and overdoses of serotonin re-uptake inhibitors (SRIs) frequently produce marked serotonergic side-effects, and in 15% of cases, moderate serotonergic toxicity, but not to a severe degree, which produces hyperthermia and risk of death. It is only combinations of serotonergic drugs acting by different mechanisms that are capable of raising intra-synaptic serotonin to a level that is life threatening. The combination that most commonly does this is a monoamine oxidase inhibitor (MAOI) drug combined with any SRI. There are a number of lesser-known drugs that are MAOIs, such as linezolid and moclobemide; and some opioid analgesics have serotonergic activity. These properties when combined can precipitate life threatening serotonin toxicity. Possibly preventable deaths are still occurring. Knowledge of the properties of these drugs will therefore help to ensure that problems can be avoided in most clinical situations, and treated appropriately (with 5-HT(2A) antagonists for severe cases) if they occur. The phenylpiperidine series opioids, pethidine (meperidine), tramadol, methadone and dextromethorphan and propoxyphene, appear to be weak serotonin re-uptake inhibitors and have all been involved in serotonin toxicity reactions with MAOIs (including some fatalities). Morphine, codeine, oxycodone and buprenorphine are known not to be SRIs, and do not precipitate serotonin toxicity with MAOIs.

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Section: Treatmentmentioning

confidence: 99%

Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity

Gillman

2005

British Journal of Anaesthesia

348

242

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“…However, the hyperthermia of NMS is an idiosyncratic response to neuroleptics; the normal response is hypothermia. Indeed there is evidence that normal DA activity is needed for the expression of SS (Green and Grahame-Smith, 1974), thus lowering DA may help to ameliorate it (Marley and Wozniak, 1985). Chlorpromazine might cause problems by lowering the blood pressure and would be expected to worsen the clinical state if NMS is confused with SS; it should also be noted that bromocriptine, which has frequently been used to treat NMS, has been reported to increase brain 5-HT levels (Snider et al, 1975) with the attendant risk that this could worsen SS (Gillman, 1997a) when it is confused with NMS.…”

Section: Treatmentmentioning

confidence: 99%

“…There were reports of SS from animal research starting in 1958 (Bogdanski et al, 1958;Horita and Gogerty, 1958;Hess et al, 1959;Hess and Doepfner, 1961;Himwich and Petersen, 1961;Himwich, 1962;Curzon et al, 1963;Nymark and Moller Neilsen, 1963;Loveless and Maxwell, 1965;Rogers and Thornton, 1969;Penn and Rodgers, 1971;Fahim et al, 1972;Sinclair, 1973;Green and Grahame-Smith, 1976;Jounela et al, 1977;Felner and Waldmeier, 1979;Fjalland, 1979;Marsden and Curzon, 1979) and these continued to accrue until the seminal papers of Marley (Marley and Wozniak, 1983;Marley and Wozniak, 1984a,b;Marley and Wozniak, 1985), usually without percolating through to the corpus of psychiatric literature. These early studies indicated that some neuroleptics lessen symptoms of SS in animals (Bogdanski et al, 1958;Himwich and Petersen, 1961;Sinclair, 1973;Green and Grahame-Smith, 1974;Marley and Wozniak, 1984b) and that the hyperactivity syndrome which was seen when some analgesics were given in combination with MAOIs was related to excess intra-synaptic 5-HT.…”

Section: Introductionmentioning

confidence: 99%

The serotonin syndrome and its treatment

Gillman¹

1999

J Psychopharmacol

271

186

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Serotonin syndrome is caused by drug induced excess of intrasynaptic 5-hydroxytryptamine. The clinical manifestations are mediated by the action of 5-hydroxytryptamine on various subtypes of serotonin receptors. There is no effective drug treatment established. The history of the treatment of serotonin syndrome with 5-hydroxytryptamine blocking drugs is reviewed. A literature search was undertaken using both Medline and a manual search of the older literature. Reports of cases treated with the 5-HT2 blockers cyproheptadine and chlorpromazine were identified and analysed. There is some evidence suggesting the efficacy of chlorpromazine and cyproheptadine in the treatment of serotonin syndrome. The evidence for cyproheptadine is less substantial, perhaps because the dose of cyproheptadine necessary to ensure blockade of brain 5-HT2 receptors is 20-30 mg, which is higher than that used in the cases reported to date (4-16 mg).

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“…Pupils were mid size, equal and non-reacting. Arterial blood gas analysis (breathing air) revealed a marked metabolic acidosis (pH 7 Blood pressure was maintained at between 80 and 90 mmHg systolic with a central venous pressure of 9-15 cm H,O, and the heart rate decreased gradually to 110 beats/minute. He became normothermic but examination of his central nervous system revealed unreactive pupils.…”

Section: Case Historymentioning

confidence: 99%