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OBJECTIVE: This study aims at understanding the dynamic functional brain organization in Accelerated Cognitive Ageing (ACA) in epilepsy. We also assess to which extend the (abnormal) effective connectivity between brain networks correlates with the (estimated) decline in IQ scores observed in the ACA patients. MATERIAL AND METHODS: Two multi-echo resting-state fMRI scans of 10 ACA patients and 14 age- and education-matched healthy controls were acquired. A task-based fMRI was acquired in-between those two scans, for possible cognitive fatigue effects on reserve capacity. Granger causality (GC), a measure of effective connectivity between brain regions, was applied on 7 major cognitive networks, and group-wise compared, using permutation testing statistics. This was performed on each of the resting-state sessions independently. We assessed the correlation between the cognitive deterioration scores (representing cognitive decline), and the paired-networks granger causality values. RESULTS: The cingulate cortex appeared to be more engaged in ACA patients. Its dynamics towards the right fronto-parietal cortex, salience network, and the dorsal attention networks (DAN) was stronger than in controls, only in the first resting-state scan session. The Granger causality from the DAN to the default mode network (DMN) and from the ventral attention network (VAN) to the left fronto-parietal network (FPL) was also stronger in ACA patients and again only in the first scans. In the second resting-state scans, only the DMN was more strongly connected with the cingulate cortex in ACA patients. A weaker GC from DMN to FPL, and stronger GC from the salience network to cingulate cortex were associated with more decline in the Full-scale IQ and more GC from DMN to VAN would lead to more decline in the Perceptual Reasoning Index in ACA. CONCLUSION: The results are in line with the hypothesis of over-recruitment at low cognitive load, and exhaustion at higher cognitive load, as shown by the compensation-related utilization of neural circuits hypothesis (CRUNCH) model for ageing. Moreover, the DMN to VAN directed connectivity strongly correlates with the (estimated) decline in the Perceptual Reasoning Index, which is also in line with a recent study on ageing with mild cognitive impairment in elderly, and the posterior-anterior shift in aging (PASA) model. This study therefore supports the idea that the cognitive decline in our patients resembles the decline observed in healthy ageing, but in an accelerated mode. This study also sheds light on the directions of the impaired connectivity between the main networks involved in the deterioration process, which can be helpful for future development of treatment solutions.

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OBJECTIVES: "Epileptic dementia" is reported in adults with childhood-onset refractory epilepsy. Cognitive deterioration can also occur in a "second-hit model". MATERIALS AND METHODS: We studied the clinical and neuropsychological characteristics of patients with cognitive deterioration (≥1 SD discrepancy between current IQ and premorbid IQ). Memory function, reaction time and processing speed were also evaluated. Analyses were performed to investigate which clinical characteristics correlated with cognitive deterioration. RESULTS: Twenty-seven patients were included with a mean age of 55.7 years old, an average age at epilepsy onset of 33.9 years and a mean duration of 21.8 years. Over 40% had experienced at least one status epilepticus. About 77.8% had at least one comorbid disease (most of (cardio)vascular origin). Cognitive deterioration scores were significant for both Performance IQ and Full Scale IQ, but not for Verbal IQ. Impairments in fluid functions primarily affected the IQ-scores. Memory was not impaired. Epilepsy factors explained 7% of the variance in deterioration, whereas 38% was explained by relatively low premorbid IQ and educational level, high age at seizure onset and older age. CONCLUSIONS: A subgroup of patients with localization-related epilepsy exhibits cognitive decline characterized by deterioration in PIQ and FSIQ, but with preserved higher order functions (VIQ and memory). Patients typically have epilepsia tarda, comorbid pathology, relatively low educational level and older age. These are factors known to increase the vulnerability of the brain by diminishing cognitive reserve. Cognitive deterioration may develop according to a stepwise "second-hit model", affecting and accelerating the cognitive ageing process.

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Neuromodulation is a field of science, medicine, and bioengineering that encompasses implantable and non-implantable technologies for the purpose of improving quality of life and functioning of humans. Brain neuromodulation involves different neurostimulation techniques: transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), vagus nerve stimulation (VNS), and deep brain stimulation (DBS), which are being used both to study their effects on cognitive brain functions and to treat neuropsychiatric disorders. The mechanisms of action of neurostimulation remain incompletely understood. Insight into the technical basis of neurostimulation might be a first step towards a more profound understanding of these mechanisms, which might lead to improved clinical outcome and therapeutic potential. This review provides an overview of the technical basis of neurostimulation focusing on the equipment, the present understanding of induced electric fields, and the stimulation protocols. The review is written from a technical perspective aimed at supporting the use of neurostimulation in clinical practice.

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OBJECTIVES: Slowing of the central information-processing speed (CIPS) is frequently observed in epilepsy as a consequence of epileptic seizures and/or antiepileptic drugs (AEDs). A variety of neuropsychological tests are used to asses this 'mental slowing,' but it is highly questionable whether the different tasks measure the same cognitive process. Also, it remains unspecified to which degree the various tasks are sensitive to seizure- or treatment-related factors, or both. METHODS: We used an open clinical non-comparative study design. The sample consisted of adult patients with cryptogenic localization-related epilepsy who performed different cognitive measures of CIPS and psychomotor speed (PmS). Clinical data about their seizures and antiepileptic drug treatment were collected from an electronic patient database. RESULTS: Eighty patients were included. CIPS tasks mutually correlated significantly, but did not correlate with measures of PmS (finger tapping and reaction time). Also, the CIPS tasks were differently affected by treatment and seizure effects. Processing of complex information is affected by tonic-clonic seizures, while less complex tasks are more sensitive for AED effects. CONCLUSIONS: CIPS tasks are mainly measuring central processing, and the psychomotor component of these tasks is negligible. We propose a psychometric continuum on which PmS and CIPS tasks are ordered with ascending complexity. The model shows that the tasks are affected differently by seizures, treatment, age, and education level. In neuropsychological practice, this continuum can be helpful in the detection of treatment and seizure effects on the CIPS in epilepsy.

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A long-standing concern has been whether epilepsy contributes to cognitive decline or so-called 'epileptic dementia'. Although global cognitive decline is generally reported in the context of chronic refractory epilepsy, it is largely unknown what percentage of patients is at risk for decline. This review is focused on the identification of risk factors and characterization of aberrant cognitive trajectories in epilepsy. Evidence is found that the cognitive trajectory of patients with epilepsy over time differs from processes of cognitive ageing in healthy people, especially in adulthood-onset epilepsy. Cognitive deterioration in these patients seems to develop in a 'second hit model' and occurs when epilepsy hits on a brain that is already vulnerable or vice versa when comorbid problems develop in a person with epilepsy. Processes of ageing may be accelerated due to loss of brain plasticity and cognitive reserve capacity for which we coin the term 'accelerated cognitive ageing'. We believe that the concept of accelerated cognitive ageing can be helpful in providing a framework understanding global cognitive deterioration in epilepsy.

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