Abstract
Pharmacological treatment with antiepileptic medications (AEDs) in epilepsy is associated with a variety of neurocognitive side effects. However, the mechanisms underlying these side effects, and why certain brain anatomies are more affected still remain poorly understood. Advanced functional magnetic resonance imaging (fMRI) methods, such as pharmaco-fMRI, can investigate medication-related effects on brain activities using task and resting state fMRI and showing reproducible activation and deactivation patterns. This methodological approach has been used successfully to complement neuropsychological studies of AEDs. Here we review pharmaco-fMRI studies in people with epilepsy targeting the most-widely prescribed AEDs. Pharmco-fMRI has advanced our understanding of the impact of AEDs on specific brain networks and thus may provide potential biomarkers to move beyond the current “trial and error” approach when commencing anti-epileptic medication.
Highlights
Epilepsy is one of the most common neurological disorders, characterized by neurobiological, cognitive and psychosocial impairments
A growing number of recent pharmaco-functional magnetic resonance imaging (fMRI) studies have shed a light on mapping possible mechanisms behind cognitive side effects of anti-epileptic medications (AEDs) [18,19,20, 25], corroborating and extending the findings reported in previous neuropsychological studies
In comparison with healthy children, the untreated group showed increased functional connectivity and functional covariance connectivity (FCC) in rolandic regions and sensorimotor network, and decreased functional connectivity and FCC in dorsal frontal network while these abnormalities were not evident in the those children with AED treatment. These results are in consistence with our previous fMRI findings showing underlying functional network abnormalities in this “benign” type of epilepsy, which appear to be responsive to AED treatment [72]
Summary
Epilepsy is one of the most common neurological disorders, characterized by neurobiological, cognitive and psychosocial impairments. Given the importance that effective deactivation of the DMN has played an important role in executing task successfully in cognitive fMRI scans [40], these studies suggest an underlying mechanism by which TPM impairs cognitive processing during speech function They shared the following functional abnormalities: (i) Activation was reduced in brain areas relevant for language, including inferior frontal and middle frontal gyri (IFG and MFG), superior temporal gyrus in the language-dominant hemisphere [41,42,43]. One recent pharmaco-fMRI study in people with TLE using resting-state fMRI compared a subgroup of participants treated with CBZ or oxcarbazepine (OXC) with people with other AEDs. Using a graph-theoretical approach to characterize the organizational properties of functional networks, abnormal “hubness” was reported in people treated with CBZ/OXC [49]: FIGURE 2 | Group differences in the verbal fluency task fMRI activation maps between LEV, TPM, and ZNS.
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