Cognitive deterioration in adult epilepsy: clinical characteristics of "Accelerated Cognitive Ageing".

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.

Mental slowing in relation to epilepsy and antiepileptic medication.

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.