Network, clinical and sociodemographic features of cognitive phenotypes in temporal lobe epilepsy

Hermann, Bruce P.; Conant, Lisa L.; Cook, Cole John; Hwang, Gyujoon; Garcia‐Ramos, Camille; Dabbs, Kevin; Nair, Veena A.; Mathis, Jedidiah; Bonet, Charlene N. Rivera; Allen, Linda; Almane, Dace; Arkush, Karina; Birn, Rasmus M.; DeYoe, Edgar A.; Felton, Elizabeth A.; Maganti, Rama; Nencka, Andrew S.; Raghavan, Manoj; Shah, Umang; Sosa, Veronica N.; Struck, Aaron F.; Ustine, Candida; Reyes, Anny; Kaestner, Erik; McDonald, Carrie R.; Prabhakaran, Vivek; Binder, Jeffrey R.; Meyerand, M. Elizabeth

doi:10.1016/j.nicl.2020.102341

Cited by 44 publications

(65 citation statements)

References 105 publications

(137 reference statements)

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“…Concordantly, epileptogenic regions evince persistent hypometabolism during interictal periods 17 . The severity of both structural damage and hypometabolism is associated with cognitive decline in TLE patients [18][19][20] , suggesting that chronic neural dysfunction might be rooted in a reduced baseline metabolism underpinned by compromised structural integrity. Regional hypometabolism could hamper the attainment and maintenance of healthy activation levels, in turn decrementing the brain's dynamic repertoire and…”

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confidence: 99%

Pathological and metabolic underpinnings of energetic inefficiency in temporal lobe epilepsy

Caciagli

Parkes

et al. 2021

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The human brain consumes a disproportionate amount of energy to generate neural dynamics. Yet precisely how energetic processes are altered in neurological disorders remains far from understood. Here, we use network control theory to profile the brain's energy landscape, describing the rich dynamical repertoire supported by the structural connectome. This approach allows us to estimate the energy required to activate a circuit, and determine which regions most support that activation. Focusing on temporal lobe epilepsy (TLE), we show that patients require more control energy to activate the limbic network than healthy volunteers, especially ipsilateral to the seizure focus. Further, greater energetic costs are largely localized to the ipsilateral temporo-limbic regions. Importantly, the energetic imbalance between ipsilateral and contralateral temporo-limbic regions is tracked by asymmetric metabolic patterns, which in turn are explained by asymmetric gray matter volume loss. In TLE, failure to meet the extra energy demands may lead to suboptimal brain dynamics and inadequate activation. Broadly, our investigation provides a theoretical framework unifying gray matter integrity, local metabolism, and energetic generation of neural dynamics.

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confidence: 99%

Pathological and metabolic underpinnings of energetic inefficiency in temporal lobe epilepsy

Caciagli

Parkes

et al. 2021

Preprint

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“…Previous work on cognitive phenotypes has demonstrated that approximately 31% to 47% of young to middle-age adults do not demonstrate cognitive impairments despite having clinical features known to impact cognition. 7,[31][32][33] Furthermore, neuroimaging findings have shown that these patient demonstrate no or minimal brain abnormalities relative to healthy controls. This group of patients may represent a group with high cognitive or brain reserve or may have protective factors (eg, complex occupational histories, bilingualism, or genetics) that could protect against epilepsy-related pathology.…”

Section: The Tle-mci Phenotypementioning

confidence: 86%

“…Although a large proportion of the TLE patient cohort met criteria for MCI, 39% of the TLE patients did not meet criteria despite having similar clinical profiles. Previous work on cognitive phenotypes has demonstrated that approximately 31% to 47% of young to middle‐age adults do not demonstrate cognitive impairments despite having clinical features known to impact cognition 7,31–33 . Furthermore, neuroimaging findings have shown that these patient demonstrate no or minimal brain abnormalities relative to healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Diagnosing cognitive disorders in older adults with epilepsy

et al. 2020

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Objective To characterize the nature and prevalence of cognitive disorders in older adults with temporal lobe epilepsy (TLE) and compare their cognitive profiles to patients with amnestic mild cognitive impairment (ie, aMCI). Methods Seventy‐one older patients with TLE, 77 aMCI, and 69 normal aging controls (NACs), all 55‐80 years of age, completed neuropsychological measures of memory, language, executive function, and processing speed. An actuarial neuropsychological method designed to diagnose MCI was applied to individual patients to identify older adults with TLE who met diagnostic criteria for MCI (TLE‐MCI). A linear classifier was performed to evaluate how well the diagnostic criteria differentiated patients with TLE‐MCI from aMCI. In TLE, the contribution of epilepsy‐related and vascular risk factors to cognitive impairment was evaluated using multiple regression. Results Forty‐three TLE patients (60%) met criteria for TLE‐MCI, demonstrating marked deficits in both memory and language. When patients were analyzed according to age at seizure onset, 63% of those with an early onset (<50 years) versus 56% of those with late onset (≥ 50 years) met criteria for TLE‐MCI. A classification model between TLE‐MCI and aMCI correctly classified 81.1% (90.6% specificity, 61.3% sensitivity) of the cohort based on neuropsychological scores. Whereas TLE‐MCI showed greater deficits in language relative to aMCI, patients with aMCI showed greater rapid forgetting on memory measures. Both epilepsy‐related risk factors and the presence of leukoaraiosis on MRI contributed to impairment profiles in TLE‐MCI. Significance Cognitive impairment is a common comorbidity in epilepsy and it presents in a substantial number of older adults with TLE. Although the underlying etiologies are unknown in many patients, the TLE‐MCI phenotype may be secondary to an accumulation of epilepsy and vascular risk factors, signal the onset of a neurodegenerative disease, or represent a combination of factors.

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“…The life-history of the individual epilepsy patient and the variability of consequences of the seizure disorder may also influence the cognitive profile of the individual, in addition to localization and epilepsy diagnosis ( 63 ). For adults with temporal lobe epilepsy, three different cognitive phenotypes have been described, i.e., intact cognition, global impairment affecting all examined cognitive functions or focal impairment, most often affecting language, memory or executive function ( 64 , 65 ). In this recent important work the classical lesion-based profile was found only in 30.1% of the adults with temporal lobe epilepsy, while a higher proportion exhibited a cognitive profile comparable with healthy controls ( 64 ).…”

Section: Discussionmentioning

confidence: 99%

Similar Profile and Magnitude of Cognitive Impairments in Focal and Generalized Epilepsy: A Pilot Study

et al. 2022

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Introduction: Cognitive impairments in epilepsy are not well-understood. In addition, long-term emotional, interpersonal, and social consequences of the underlying disturbances are important to evaluate.Purpose: To compare cognitive function including language in young adults with focal or generalized epilepsy. In addition, quality of life and self-esteem were investigated.Patients and Methods: Young adults with no primary intellectual disability, 17 with focal epilepsy and 11 with generalized epilepsy participated and were compared to 28 healthy controls. Groups were matched on age (mean = 26 years), sex, and education. Participants were administered a battery of neuropsychological tasks and carried out self-ratings of quality of life, self-esteem, and psychological problems.Results: Similar impairments regarding cognitive function were noted in focal and generalized epilepsy. The cognitive domains tested were episodic long-term memory, executive functions, attention, working memory, visuospatial functions, and language. Both epilepsy groups had lower results compared to controls (effect sizes 0.24–1.07). The total number of convulsive seizures was predictive of episodic long-term memory function. Participants with focal epilepsy reported lower quality of life than participants with generalized epilepsy. Lowered self-esteem values were seen in both epilepsy groups and particularly in those with focal epilepsy. Along with measures of cognitive speed and depression, the total number of seizures explained more than 50% of variation in quality of life.Conclusion: Interestingly, similarities rather than differences characterized the widespread cognitive deficits that were seen in focal and generalized epilepsy, ranging from mild to moderate. These similarities were modified by quality of life and self-esteem. This study confirms the notion that epilepsy is a network disorder.

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Network, clinical and sociodemographic features of cognitive phenotypes in temporal lobe epilepsy

Cited by 44 publications

References 105 publications

Pathological and metabolic underpinnings of energetic inefficiency in temporal lobe epilepsy

Pathological and metabolic underpinnings of energetic inefficiency in temporal lobe epilepsy

Diagnosing cognitive disorders in older adults with epilepsy

Similar Profile and Magnitude of Cognitive Impairments in Focal and Generalized Epilepsy: A Pilot Study

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