Brain development in children with new onset epilepsy: A prospective controlled cohort investigation

Abstract

Purpose To characterize prospective neurodevelopmental changes in brain structure in children with new and recent onset epilepsy compared to healthy controls. Methods 34 healthy controls (mean age = 12.9) and 38 children with new/recent onset idiopathic epilepsy (mean age = 12.9) underwent 1.5T MRI at baseline and two years later. Prospective changes in total cerebral and lobar gray and white matter volumes were compared within and between groups. Results Prospective changes in gray matter volume were comparable for the epilepsy and control groups with significant (p<.0001) reduction in total cerebral gray matter, due primarily to significant (p<.001) reductions in frontal and parietal gray matter. Prospective white matter volume changes differed between groups. Controls exhibited a significant (p=.0012) increase in total cerebral white matter volume due to significant (p<.001) volume increases in the frontal, parietal and temporal lobes. In contrast, the epilepsy group exhibited nonsignificant white matter volume change in the total cerebrum (p=.51) as well as across all lobes (all p’s > .06). The group by white matter volume change interactions were significant for total cerebrum (p=.04) and frontal lobe (p=.04). Discussion Children with new and recent onset epilepsy exhibit an altered pattern of brain development characterized by delayed age appropriate increase in white matter volume. These findings may affect cognitive development through reduced brain connectivity and may also be related to the impairments in executive function commonly reported in this population.

Temporal Lobe Epilepsy: Quantitative MR Volumetry in Detection of Hippocampal Atrophy

“…In addition, although HOC volumes have demonstrated superior ability to reveal conversion to AD when compared with ICV-adjusted volumes (11), neither the HOC volume nor its asymmetry was a strong classifier in patients with TLE. This may reflect the fact that the expansion of the ILV associated with AD reflects tissue loss that is predominantly secondary to neurodegeneration, whereas the HA associated with TLE is the product of both neurodevelopmental and neurodegenerative factors (23)(24)(25)(26). Therefore, adjusting for overall head size rather than ILV size better captures the hippocampal pathology associated with TLE.…”

Thalamofrontal neurodevelopment in new-onset pediatric idiopathic generalized epilepsy

“…Furthermore, the developmental trajectories for the thalamus and frontal lobes seen here are different from those observed for other nonfrontal cortical lobar regions in a mixed syndrome epilepsy group. 20 First, gray matter cortical lobe volumes were not significantly different from controls and only parietal lobe white matter development showed a similar trajectory to frontal white matter development in the mixed epilepsy syndrome group. Thus, the present findings appear to be fairly region specific.…”

Epilepsia Benigna da Infância com Paroxismos Centrotemporais - delineamento do perfil executivo

“…Em nosso grupo, 52,17% dos pacientes apresentaram TDAH. A prevalência deste transtorno nos pacientes com EBICT varia de 26 a 64% (Hermann et al, 2010;Kim, Yum, Kim, & Ko, 2014 Estudos anteriores demonstraram que os pacientes com EBICT possuem prejuízos em fluência verbal fonêmica (Croona et al, 1999;Neri, 2012;Baglietto et al, 2001;Lindgren et al, 2004;Riva et al, 2007 (Barkley, 1997;Barkley, 2010;Brown, Reichel, & Quinlan, 2009;Saylor, Buermeyer, Spencer, & Barkley, 2002).…”

“…Este resultado corrobora estudos anteriores, que postulam que o início precoce das crises epilépticas leva a maior interferência no desenvolvimento cerebral e, a médio e longo prazo, a maior efeito na cognição (Aldenkamp, 2006;Vingerhoets, 2006;Hoie et al, 2006). Além disso, o impacto das crises epilépticas em um córtex ainda em desenvolvimento poderia prejudicar o processo de maturação cortical, a mielinização e, consequentemente, a aquisição das habilidades cognitivas e, especificamente, das FE (Hermann et al, 2010;Hermann, Jones, Sheth, & Seidenberg, 2007;Hermann et al, 2017;Piccirilli, Alessandro, Tiacci, & Ferroni, 1988).…”

“…Neste contexto, quanto maior o tempo livre de crises epilépticas, melhor será o desenvolvimento do córtex (Baglietto et al, 2001;Jeong et al, 2011;Metz-Lutz et al, 2011;Northcott et al, 2005;Piccirilli et al, 1988) e o desempenho de suas funções sem interferências, assim como o aprendizado de estratégias para aprimorar seu desempenho (Aldenkamp, Baker, & Meador, 2004;Hermann et al, 2010Hermann & Seidenberg, 1995;Hermann et al, 2006 (Uijl et al, 2006;Lagae, 2006). Ao diminuírem a excitabilidade neuronal e, consequentemente, as crises epilépticas, afetam os mecanismos excitatórios do neurônio e podem prejudicar a cognição (Meador, 2006).…”