Brain Morphology in Children with Epilepsy and ADHD

Saute, Ricardo Lutzky; Dabbs, Kevin; Jones, Jana E.; Jackson, Daren C.; Seidenberg, Michael; Hermann, Bruce P.

doi:10.1371/journal.pone.0095269

Cited by 36 publications

(34 citation statements)

References 57 publications

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“…Although our current results for ADHD in children with BCECTS identified different abnormalities from a previous study of children with epilepsy and ADHD [34], the inclusion of heterogeneous types of epilepsy in that previous study may account for these differences. These structural alterations in ADHD patients disappear during adolescence [38] likewise supporting the paradigm of a delayed neurodevelopmental process leading to ADHD.…”

Section: Discussioncontrasting

confidence: 95%

“…A previous MRI study in children with epilepsy and ADHD [34] reported bilateral thinning in the frontal, parietal, and temporal lobes with diminution of subcortical structures similar to the findings of several previous MRI studies in children with ADHD alone [35][36][37]. Although our current results for ADHD in children with BCECTS identified different abnormalities from a previous study of children with epilepsy and ADHD [34], the inclusion of heterogeneous types of epilepsy in that previous study may account for these differences.…”

Section: Discussionsupporting

confidence: 83%

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Structural abnormalities in benign childhood epilepsy with centrotemporal spikes (BCECTS)

Kim

Yum

Shim

et al. 2015

Seizure

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Section: Discussioncontrasting

confidence: 95%

Section: Discussionsupporting

confidence: 83%

Structural abnormalities in benign childhood epilepsy with centrotemporal spikes (BCECTS)

Kim

Yum

Shim

et al. 2015

Seizure

View full text Add to dashboard Cite

show abstract

“…In children with epilepsy and an anxiety disorder, the volume of the amygdala was increased and the thickness of orbitofrontal cortices was reduced . Widespread changes in gray matter are also observed in children with epilepsy and ADHD . Although studies of connectivity and white matter integrity are lacking in these groups, fMRI may afford an additional marker of comorbid disease.…”

Section: Imaging Biomarkers Of Comorbiditiesmentioning

confidence: 99%

WONOEP appraisal: Biomarkers of epilepsy‐associated comorbidities

et al. 2016

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Neurologic and psychiatric comorbidities are common in patients with epilepsy. Diagnostic, predictive, and pharmacodynamic biomarkers of such comorbidities do not exist. They may share pathogenetic mechanisms with epileptogenesis/ictogenesis, and as such are an unmet clinical need. The objectives of the subgroup on biomarkers of comorbidities at the XIII Workshop on the Neurobiology of Epilepsy (WONOEP) were to present the state-of-the-art recent research findings in the field that highlighting potential biomarkers for comorbidities in epilepsy. We review recent progress in the field, including molecular, imaging, and genetic biomarkers of comorbidities as discussed during the WONOEP meeting on August 31-September 4, 2015, in Heybeliada Island (Istanbul, Turkey). We further highlight new directions and concepts from studies on comorbidities and potential new biomarkers for the prediction, diagnosis, and treatment of epilepsy-associated comorbidities. The activation of various molecular signaling pathways such as the "Janus Kinase/Signal Transducer and Activator of Transcription," "mammalian Target of Rapamycin," and oxidative stress have been shown to correlate with the presence and severity of subsequent cognitive abnormalities. Furthermore, dysfunction in serotonergic transmission, hyperactivity of the hypothalamic-pituitary-adrenocortical axis, the role of the inflammatory cytokines, and the contributions of genetic factors have all recently been regarded as relevant for understanding epilepsy-associated depression and cognitive deficits. Recent evidence supports the utility of imaging studies as potential biomarkers. The role of such biomarker may be far beyond the diagnosis of comorbidities, as accumulating clinical data indicate that comorbidities can predict epilepsy outcomes. Future research is required to reveal whether molecular changes in specific signaling pathways or advanced imaging techniques could be detected in the clinical settings and correlate with epilepsy-associated comorbidities. A reliable biomarker will allow a more accurate diagnosis and improved treatment of epilepsy-associated comorbidities.

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“…It was previously suggested that the utilisation of Se may be increased in epilepsy since a decreased level in Se in the serum and erythrocytes from epileptic patients was noted [163,164]. It is also believed that Se depletion in the brain during epilepsy constitutes a vital factor for the origin of seizures [163,165,166].…”

Section: Epilepsymentioning

confidence: 99%

Selenium in the therapy of neurological diseases. Where is it going?

Dominiak¹,

Wilkaniec²,

Wroczyński³

et al. 2015

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Selenium ( 34 Se), an antioxidant trace element, is an important regulator of brain function. These beneficial properties that Se possesses are attributed to its ability to be incorporated into selenoproteins as an amino acid. Several selenoproteins are expressed in the brain, in which some of them, e.g. glutathione peroxidases (GPxs), thioredoxin reductases (TrxRs) or selenoprotein P (SelP), are strongly involved in antioxidant defence and in maintaining intercellular reducing conditions. Since increased oxidative stress has been implicated in neurological disorders, including Parkinson's disease, Alzheimer's disease, stroke, epilepsy and others, a growing body of evidence suggests that Se depletion followed by decreased activity of Se-dependent enzymes may be important factors connected with those pathologies. Undoubtedly, the remarkable progress that has been made in understanding the biological function of Se in the brain has opened up new potential possibilities for the treatment of neurological diseases by using Se as a potential drug. However, further research in the search for optimal Se donors is necessary in order to achieve an effective and safe therapeutic income.

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Brain Morphology in Children with Epilepsy and ADHD

Cited by 36 publications

References 57 publications

Structural abnormalities in benign childhood epilepsy with centrotemporal spikes (BCECTS)

Structural abnormalities in benign childhood epilepsy with centrotemporal spikes (BCECTS)

WONOEP appraisal: Biomarkers of epilepsy‐associated comorbidities

Selenium in the therapy of neurological diseases. Where is it going?

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