It is important to state at the outset that there is only one controlled trial of the effects of an intervention for mood disorders in epilepsy, and the evidence for treatment strategies relies heavily on clinical experience.
Psychiatric symptoms temporally related to the occurrence of seizures (preceding or following a seizure or a cluster of seizures; occurring when the patient achieves a sudden and complete seizure control or when seizures worsened) do not need any specific psychotropic treatment and a better control of seizures is often the sole solution.
In the case of a mood disorder characterized by symptoms occurring independently of seizures, psychopharmacotherapy can be required but evidence in favor of a particular drug is lacking. The only published controlled trial involved nomifensine, an antidepressant no longer available (Robertson and Trimble, 1985).
Selective serotonin reuptake inhibitors (SSRIs) have become the first-line of pharmacotherapy for primary major depressive and dysthymic disorders in psychiatric but also in neurological practice. However, studies about efficacy and safety in epilepsy are lacking. During recent years, a number of authors have approached the clinical problem of treating mood disorders in epilepsy from different points of view (Mula et al., 2004; Kanner and Balabanov, 2005; Prueter and Norra, 2005). A few open studies have been published about sertraline (Kanner et al., 2000; Thome-Souza et al., 2007e , citalopram (Hovorka et al., 2000; Kuhn et al., 2003; Specchio et al., 2004e , reboxetine (Kuhn e t al., 2003e , mirtazapine (Kuhn et al. , 2003), and fluoxetine (Thome-Souza et al. , 2007) . The study by Thome-Souza et al. (2007) is of particular interest because it is the only published paper involving children and adolescents with epilepsy and depression.
In general, all presented studies showed antidepressant drug treatment to be well tolerated, but the reported response rates were highly variable, ranging, for example, with citalopram, between 38% (Khun et al., 2003} and 65% (Hovorka et al.e 2000) at eight weeks. It is evident that the reported variability is influenced by the selection of patients, the lack of a rigorous psychiatric assessment for a correct diagnosis (dysthymia, major depression, bipolar depression, IDD), the presence of other comorbid Axis I disorders, the presence of brain damage, cognitive impairment, a family history for mood disorders and so on. All these variables are taken into consideration very rarely in these studies, but they are essential for a correct interpretation of results.
If studies about psychoactive drugs in epilepsy are rare, studies about psychological therapies for mood disorders in epilepsy are really exceptional. We are aware of only two papers, one involving adult patients (Tan and Bruni, 1986) and the other with children (Martinovic et al, 2006) . Both showed some utility of cognitive behavioral therapies in the management of mood disorder symptoms in epilepsy.
The issue of psychotropic drug treatment of depression in epilepsy is interlinked with that of the "proconvulsant" or "anticonvulsant" effects of antide-pressants. Tricyclic antidepressants developed a clinical reputation for convulsant liability soon after their introduction into therapeutics (Dailey and Naritoku, 1996). The concept that antidepressant medications are more likely to produce convulsions in patients with epilepsy than in patients without this disorder is intuitively appealing, and is seemingly compatible with the concept that seizure predisposition is fundamental to the definition of epilepsy. However, it is clear that the biology of seizure predisposition is not a single entity; moreover, it is not clear whether the risk of seizure expression arises from the seizure liability itself or from a more complex predisposition inherent in the mechanisms of comorbidity between affective disorders and the epilepsies (Jobe and Browning, 2005).
A number of authors claimed possible anticonvulsant properties for SSRIs speculating about the antagonistic role of serotonin transmission in epileptogenesis (Favale et al, 1995 ) Albano et al, 2006). Although some neurobiological explanations have been suggested, further studies are needed to clarify whether SSRIs can exhibit direct anticonvulsant properties or are indirectly effective, for example by ameliorating sleep and circadian patterns.
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