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Title: Cognitive impairment in epilepsy: the role of reduced network flexibility.
Austin Authors: Tailby, Chris ;Kowalczyk, Magdalena A;Jackson, Graeme D 
Affiliation: Florey Institute of Neuroscience and Mental Health, Heidelberg, Victoria, Australia
Institute for Social Neuroscience, Heidelberg, Victoria, Australia
Austin Health, Heidelberg, Victoria, Australia
The University of Melbourne, Parkville, Victoria, Australia
Issue Date: Jan-2018
Date: 2017-11-24
Publication information: Annals of clinical and translational neurology 2018; 5(1): 29-40
Abstract: The dominant model of cognitive impairment in focal epilepsy has emphasised structural bases for cognitive deficits. Current theories of cognition in the healthy brain emphasise the importance of the reweighting of brain network interactions in support of task performance. Here, we explore the hypothesis that cognitive deficits in epilepsy arise through abnormalities of dynamic functional network interactions. We studied 19 healthy controls and 37 temporal lobe epilepsy (TLE) patients, using a behavioural measure of verbal fluency (the Controlled Oral Word Association Test) and an fMRI verbal fluency paradigm (Orthographic Lexical Retrieval). Behaviourally, verbal fluency was significantly impaired in TLE. Psychophysiological interaction analyses of the fMRI data, which capture state-dependent changes in network connectivity, revealed reduced task-dependent modulations of connectivity from left superior medial frontal cortex to left middle frontal gyrus in TLE patients. Individual differences in verbal fluency among TLE cases was correlated with task-dependent changes in connectivity from left posterior cingulate to left superior medial frontal cortex, and from left superior medial frontal cortex to a range of right predominant brain areas. These data reveal that the typical pattern of task-driven shifts in network connectivity is not observed in TLE. Our observations go beyond simple structure-function associations and suggest that failure of network flexibility can be an important contributor to cognitive impairment in epilepsy.
DOI: 10.1002/acn3.503
ORCID: 0000-0002-1320-5924
Journal: Annals of clinical and translational neurology
PubMed URL: 29376090
ISSN: 2328-9503
Type: Journal Article
Appears in Collections:Journal articles

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