There are common pathogenic mechanisms shared by depression, anxiety, and epilepsy. Serotonin (5HT), NE, dopamine, GABA, and glutamate are likely involved in the expression of all three disorders (Jobe et al., 1999 , Ressler and Nemeroff
2000). In depression and anxiety, changes in the noradrenergic and serotoner-gic systems are implicated as playing a significant role in the expression of these disorders. There appears to be increased noradrenergic activity, contrasting with decreased activity in the serotonergic systems. Pharmacological treatments attempt to modulate this activity. Depending on which medication is introduced, there is a combination of increased or decreased release of the serotonin or NE along with an increase or decrease in receptor activity (Stahl, 1997 ) Ressler and Nemeroff, 2000). It is suggested that selective serotonin reuptake inhibitors (SSRIs) reduce noradrenergic transmission and increase serotonergic transmission (Ressler and Nemeroff, 2000) . If there is a sudden reduction in serotonin there will be an increase in depressive symptoms (Stahl, 1997 ) Ressler and Nemeroff, 2000) . A related hypothesis explaining the effectiveness of SSRIs in treating anxiety indicates that if there is excess serotonin, the receptors downregulate to prevent excessive neuronal activity, reducing symptoms of anxiety; and in depression, an upregulation occurs to enhance neuronal activity (Stahl, 1997). This is a significant simplification of the process, but illustrates the relationship nonetheless.
In epilepsy, if there is a decrease in serotonergic or noradrenergic transmission, kindling of seizures occurs, seizure activity increases, and severity intensifies (Jobe et al.) 1999). Increasing serotonin and NE transmission helps to prevent seizures and a reduction will increase the likelihood that a seizure will occur (J obe et al.) 1999). There have been no randomized controlled trials examining the effects of SSRIs on seizure frequency; however, open trials of fluoxetine and citalopram indicated some improvement in seizure frequency (Favale et al.) 1995 ) Specchio et al.) 2004). Additionally, there was one controlled trial using imipramine, a tricy-clic antidepressant (TCA); it was reported to reduce absence and myoclonic seizures (Fromm et al.) 1978).
In a similar fashion, antiepileptic drugs (AEDs) play a dual role with antiepilep-tic effects and psychotropic properties. All AEDs can have psychiatric side effects (Ketter )t al., 1994) Schmitz, 1999 ) Ettinger, 2006) . Valproate, lamotrigine, car-bamazepine, and oxcarbazepine have been used as mood stabilizers (Stahl, 2004; Kanner, 2005 ) Ettinger, 2006). There are two broad categories that can be utilized to classify AEDs — sedating and activating (Ketter et al.) 1999). The sedating effects are linked to the GABA inhibitory neurotransmission. These medications result in side effect symptoms of fatigue, cognitive slowing, weight gain, and somnolence. There are possible anxiolytic effects of these drugs as well. The medications included in this category are barbiturates, benzodiazepines, valproate, tiagabine, and vigabatrin. The second category is the activating group, and the resulting symptoms include weight loss, activation, and anxiogenic effects and reduce excitatory glutamate neurotransmission. The medications in this group include felbamate and lamotrigine. Topiramate, zonisamide, and levetiracetam have mixed effects with both activating and sedating profiles (Ketter et al.) 1999).
In summary, the common pathogenic mechanisms shared by depression, anxiety, and epilepsy reveal a neurobiological connectedness among the disorders. Serotonin
(5HT), NE, dopamine, GABA, and glutamate are likely involved in the expression of each disorder (Jobe et al, 1999 ; Ressler and Nemeroff, 2000). It will be important to continue to conduct further investigations of these complex networks to provide a greater understanding of these complicated and interconnected processes.
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