Abstracts

Rationale: Juvenile myoclonic epilepsy (JME) is a well defined type of idiopathic generalized epilepsy (IGE) that comprises 5-11% of patients with epilepsy. Literature data demonstrate frontal lobe dysfunctions possibly related to pathophysiologic mechanisms involved in the generation of epileptic activity in this epileptic syndrome. Personality traits characterized by emotional instability and immaturity, unsteadiness, lack of discipline, hedonism, frequent and rapid mood changes and indifference towards their disease have been associated to JME. These manifestations may possibly correspond to frontal lobe impairment, once there have been descriptions of similar behavioral abnormalities in patients with different types of frontal lobe injury. In addition, worse seizure control and more psychosocial dysfunctions among JME patients with those personality traits have also been reported. In this controlled study we aimed to verify the existence of a relation between thalamus and frontal lobe dysfunctions and the prevalence of personality disorders (PD) among patients with JME by using the technique of quantitative multivoxel magnetic resonance spectroscopy (MRS). Methods: Sixteen JME patients with cluster B PD, 41 JME patients without any psychiatric disorder and 30 healthy controls were submitted to a psychiatric evaluation and to a quantitative multivoxel MRS of thalamus, insula, cingulate gyrus, striatum, frontal, parietal and occipital lobes. Groups were paired according to age, gender and manual dominance. Psychiatric evaluation was performed through structured interviews based on DSM-IV (SCID I and SCID II). Results: The JME group with PD presented more patients with inadequate control of both myoclonic (p=0.007) and absence (p=0.04) seizures. A general tendency of lower values of NAA/Cr and higher values of GLX/Cr in the group of JME with PD was observed, mainly in frontal and thalamic regions. There was a significant reduction of NAA/Cr in right thalamus (p=0.03), left anterior thalamic (p=0.01) and in left medial primary motor regions (p=0.003) in the JME and PD group. In addition, an increase of the GLX/Cr in right medial primary motor (p=0.03) and in left lateral primary motor (p=0.02) regions in JME group with PD was also observed. Conclusions: These data from MRS might aid to support the hypothesis that PD in JME could represent a more severe form of thalamic and frontal lobe dysfunction as an underlying mechanism of epilepsy generation, consequently producing neuronal damage and PD. More studies involving neuroimaging and psychiatric evaluation in JME are therefore highly encouraged.