Etiology and pathogenesis of anxiety and depression in epilepsy

D`ALESSIO L

Singapore

Congreso; 27th International Epilepsy Congress.; 2007

Liga Internaciona contra la epilepsia

Anxiety and depression are the most frequent psychiatric comorbidities in patients with epilepsy. More recent epidemiological studies indicate that 10-20 % of the patients with controlled epilepsy and 20-60% with recurrent seizures have a depressive disorder. Similarly, a history of depression is more common in patients who develop new onset epilepsy. In the last years, it has been proposed that anxiety and depression shared “partially” neurobiological mechanisms with epilepsy. The etiology of anxiety and depression in epileptic patients remains unclear. However both genetic/neurobiological and environmental factors are involved in its etiology and pathogenesis. Neuroimaging studies of patients with depression and anxiety disorders post-traumatic stress disorder (PTSD), reveal structural and functional alterations in prefrontal cortex, and other limbic regions (hippocamus-amygdala). Similar anatomical areas are affected in the temporal and frontal lobe epilepsies. Deficits in serotonin transmission and in 5-HT1A receptors have been described in anxiety, depression and epilepsy. Furthermore, selective serotonin reuptake inhibitors have demonstrated a better response in treating depression and anxiety associated to epilepsy, without seizure worsening. A new group of hypotheses for the development of anxiety and depression in humans has been postulated over the last years. These hypotheses involve stress mediators, changes in neurotrophic factors (brain-derived neurotrophic factor or BDNF), hippocampal volume loss and alterations in hippocampal function with a reduction of neurogenesis and changes in the information processing within neuronal networks. Antidepressants increase hippocampal neurogenesis and neural connectivity during the recovery process from the depressive state. Hippocampal atrophy with mesial sclerosis is the most frequently identified abnormality in patients with temporal lobe epilepsy and depression. Experimental models of temporal lobe epilepsy revealed changes in BDNF expression and in hippocampal neurogenesis with controversial functional implications.