Whereas Selleckchem URMC-099 morphological lesions or structural changes are associated with more or less irreversible deficits, epileptic activity, seizures, and the treatment of epilepsy can cause dynamic and principally reversible impairment. The relative contribution of these factors differs depending on the type of epilepsy, the age at lesion/epilepsy onset, the localization and lateralization of epilepsy and individual demographic patient characteristics.
Altered brain structure and function can result in epilepsy, but epilepsy can also alter the functional cerebral organization of the brain. Thus epilepsy-related cognitive impairment must be integrated within a developmental neuropsychological framework. The aetiology of epilepsy is strongly related to the age of onset. From a neuropsychological point of view, it makes a big difference for cognitive outcome as to whether epilepsy hits the maturing versus mature or aging brain. Dependent on this, epilepsy can result in retardation, loss of acquired functions, or accelerated mental decline. It will be demonstrated that cognitive impairments in epilepsy mostly exist from the beginning of epilepsy, that early onset lesions/epilepsy interfere with mental development, and that a progressive aetiology, severe seizures, and lesions secondary to epilepsy may accelerate
mental decline. It will furthermore be discussed that uncontrolled epilepsy and epileptic activity may reversibly and irreversibly contribute to cognitive impairment.
CBL0137 The same is demonstrated with regard to the pharmacological treatment of epilepsy. Finally, the cognitive risks and benefits of epilepsy surgery and the advantages of selective surgery will be addressed. The consequences for the neuropsychological assessment are discussed in part two of this review.”
“The extent AR-13324 nmr to which social cognitive changes reflect a discrete constellation of symptoms dissociable from general cognitive changes in Alzheimer’s disease (AD) is unclear. Moreover, whether social cognitive symptoms contribute to disease severity and progression is unknown. The current multicenter study investigated cross-sectional and longitudinal associations between social cognition measured with six items from the Blessed Dementia Rating Scale, general cognition, and dependence in 517 participants with probable AD. Participants were monitored every 6 months for 5.5 years. Results from multivariate latent growth curve models adjusted for sex, age, education, depression, and recruitment site revealed that social cognition and general cognition were unrelated cross-sectionally and throughout time. However, baseline levels of each were related independently to dependence, and change values of,each were related independently to change in dependence. These findings highlight the separability of social and general cognition in AD.