Interactions Between Anticonvulsant and Psychoactive Drugs

Monaco, Francesco; Cicolin, Alessandro

doi:10.1111/j.1528-1157.1999.tb00888.x

Cited by 53 publications

(30 citation statements)

References 54 publications

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“…Fluoxetine was found to be effective against maximal electroshock-induced tonic extension in rats (44), audiogen seizures in mice and rats (21,25), and focally evoked limbic motor seizures in rats (22). Several clinical observations and animal studies showed that fluoxetine enhanced the anticonvulsant potency of various antiepileptic drugs (19,20,(45)(46)(47). Regarding the effective anticonvulsant dose of the drug, fluoxetine exerted 50% protective effect at 5 mg/kg in the limbic motor seizure model, whereas, in the genetically epilepsy-prone rats (GEPR-9) the ED 50 was ~16 mg/kg.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues

et al. 2003

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Abstract. Racemic fluoxetine is a widely used SSRI antidepressant compound having also anticonvulsant effect. In addition, it was shown that it blocked several types of voltage gated ion channels including neural and cardiac calcium channels. In the present study the effects of enantiomers of fluoxetine (R(-)-fluoxetine and S(+)-fluoxetine) were compared on neuronal and cardiac voltage-gated Ca 2+ channels using the whole cell configuration of patch clamp techniques, and the anticonvulsant action of these enantiomers was also evaluated in a mouse epilepsy model. In isolated pyramidal neurons of the dorsal cochlear nucleus of the rat the effect of fluoxetine (S(+), R(-) and racemic) was studied on the Ca 2+ channels by measuring peak Ba 2+ current during ramp depolarizations. All forms of fluoxetine reduced the Ba

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Section: Discussionmentioning

confidence: 99%

Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues

et al. 2003

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“…The drug interactions between these two classes of agents focus on the cytochrome P450 enzymes. For example, the enzyme-inducing AEDs PB, PHT, and CBZ stimulate the metabolism of tricyclic antidepressants (TCAs), and the TCAs have an inhibitory effect on the metabolism of some AEDs (120), resulting in a reduction in the plasma concentration of TCAs, with a concomitant increase in the plasma concentration of the coadministered AED. Examples of TCAs that interact in this complex manner include nortryptiline, imipramine, nomifensine, and trazodone (121,122).…”

Section: Psychotropic Drugsmentioning

confidence: 99%

The Importance of Drug Interactions in Epilepsy Therapy

et al. 2002

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Summary: Long-term antiepileptic drug (AED) therapy is the reality for the majority of patients diagnosed with epilepsy. One AED will usually be sufficient to control seizures effectively, but a significant proportion of patients will need to receive a multiple AED regimen. Furthermore, polytherapy may be necessary for the treatment of concomitant disease. The fact that over-the-counter drugs and nutritional supplements are increasingly being self-administered by patients also must be considered. Therefore the probability of patients with epilepsy experiencing drug interactions is high, particularly with the traditional AEDs, which are highly prone to drug interactions. Physicians prescribing AEDs to patients with epilepsy must, therefore, be aware of the potential for drug interactions and the effects (pharmacokinetic and pharmacodynamic) that can occur both during combination therapy and on drug discontinuation. Although pharmacokinetic interactions are numerous and well described, pharmacodynamic interactions are few and usually concluded by default. Perhaps the most clinically significant pharmacodynamic interaction is that of lamotrigine (LTG) and valproic acid (VPA); these drugs exhibit synergistic efficacy when coadministered in patients with refractory partial and generalised seizures. Hepatic metabolism is often the target for pharmacokinetic drug interactions, and enzyme-inducing drugs such as phenytoin (PHT), phenobarbitone (PB), and carbamazepine (CBZ) will readily enhance the metabolism of other AEDs [e.g., LTG, topiramate (TPM), and tiagabine (TGB)].The enzyme-inducing AEDs also enhance the metabolism of many other drugs (e.g., oral contraceptives, antidepressants, and warfarin) so that therapeutic efficacy of coadministered drugs is lost unless the dosage is increased. VPA inhibits the metabolism of PB and LTG, resulting in an elevation in the plasma concentrations of the inhibited drugs and consequently an increased risk of toxicity. The inhibition of the metabolism of CBZ by VPA results in an elevation of the metabolite CBZepoxide, which also increases the risk of toxicity. Other examples include the inhibition of PHT and CBZ metabolism by cimetidine and CBZ metabolism by erythromycin. In recent years, a more rational approach has been taken with regard to metabolic drug interactions because of our enhanced understanding of the cytochrome P450 system that is responsible for the metabolism of many drugs, including AEDs. The review briefly discusses the mechanisms of drug interactions and then proceeds to highlight some of the more clinically relevant drug interactions between AEDs and between AEDs and non-AEDs. Understanding the fundamental principles that contribute to a drug interaction may help the physician to better anticipate a drug interaction and allow a graded and planned therapeutic response and, therefore, help to enhance the management of patients with epilepsy who may require treatment with polytherapy regimens.

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“…However, some clinically relevant interactions may occur by inhibition of CYP isoenzymes, especially when in a regimen of multiple drugs, which is the case of our patients 12 . Serotonin reuptake inhibitors can also cause an increase in plasma levels of AEDs through inhibition of P450 2D6 isoenzyme 13 . As the concomitant administration of AEDs and serotonin reuptake inhibitors is common, therapeutic drug monitoring may be useful in designing correct and rational therapy, but further studies are necessary 13 .…”

Section: Discussionmentioning

confidence: 99%

“…Serotonin reuptake inhibitors can also cause an increase in plasma levels of AEDs through inhibition of P450 2D6 isoenzyme 13 . As the concomitant administration of AEDs and serotonin reuptake inhibitors is common, therapeutic drug monitoring may be useful in designing correct and rational therapy, but further studies are necessary 13 . We can conclude by these data that patients with chronic neurological diseases, such as epilepsy and headaches, have a high number of comorbidities.…”

Section: Discussionmentioning

confidence: 99%

Comorbidities associated with epilepsy and headaches

Ferreira

Coan

Guerreiro

2012

Arq. Neuro-Psiquiatr.

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Epilepsy and headache are the two most common neurologic disorders affecting individuals of all ages worldwide. They constitute an important health and socioeconomic problem 1,2 . Approximately 50 million people suffer from epilepsy 3 , while in the adult population the prevalence of active headache is around 46% 2 . Drug treatment of epilepsy, with antiepileptic drugs, and headache, with prophylactic drugs, is prolonged in most cases (years to decades). Moreover, although for both pathologies it is recommended the use of a single antiepileptic or prophylactic drug, the use of polytherapy is very common [4][5][6] . Therefore, there is high risk of interactions between the drugs used for the primary neurologic disorder and other ones necessary throughout life for different acute or chronic conditions.In the treatment of chronic diseases, such as epilepsy and migraines, it is important to know the side effects of the prescribed drugs, as well as their contraindications and interactions, since most patients will need at some point to use medications for other associated diseases [4][5][6][7] . Once they are diseases that affect individuals at any age, chronically, comorbidities are common in people with epilepsy and headache and they lead to the use of other medications, which are added to the primary neurological drugs. In subjects with migraine, the second most common type of chronic headache, a long list of comorbidities are reported, AbsTRACT Comorbidities are often associated with chronic neurological diseases, such as headache and epilepsy. Objectives: To identify comorbidities associated with epilepsy and headaches, and to determine possible drug interactions. Methods: A standardized questionnaire with information about type of epilepsy/headache, medical history, and medication was administered to 80 adult subjects (40 with epilepsy and 40 with chronic headache). Results: Patients with epilepsy had an average of two comorbidities and those with headache of three. For both groups, hypertension was the most prevalent. On average, patients with epilepsy were taking two antiepileptic medications and those with headache were taking only one prophylactic medication. Regarding concomitant medications, patients with epilepsy were in use, on average, of one drug and patients with headache of two. Conclusions: Patients with chronic neurological diseases, such as epilepsy and headaches, have a high number of comorbidities and they use many medications. This may contribute to poor adherence and interactions between different medications.Key words: epilepsy, headache, drugs interaction. REsumoAs comorbidades geralmente estão associadas a doenças neurológicas crônicas, tais como cefaleia e epilepsia. Objetivos: Identificar comorbidades associadas à epilepsia e cefaleia e determinar as possíveis interações de drogas. Métodos: Questionário padronizado com informações sobre o tipo de epilepsia/cefaleia, os antecedentes médicos e as medicações foi aplicado a 80 indivíduos adultos (40 com epilepsia e 40 com cefaleia crônica). ...

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Interactions Between Anticonvulsant and Psychoactive Drugs

Cited by 53 publications

References 54 publications

Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues

Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues

The Importance of Drug Interactions in Epilepsy Therapy

Comorbidities associated with epilepsy and headaches

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