Neuropsychology of late-onset epilepsies.

In an increasingly ageing society, patients ageing with epilepsy and those with late-onset epilepsies (LOE) represent a challenge for epilepsy care and treatment. Senescence itself bears risks of pathologies which in the form of acute focal damage (e.g. stroke) or slowly progressive degenerative damage can cause seizures and substantial cognitive impairment. There is converging evidence from studies in LOE that cognitive impairments are present from epilepsy onset before treatment is initiated and may even precede the emergence of seizures. This suggests that these impairments (like the seizures) are expressions of the underlying disease. Indeed, both seizures and cognitive impairments can be early indicators of disease conditions which lead to mental decline. Cognitive decline over time poses the challenge of disentangling the interrelation between seizures, treatment effects and underlying disease. This issue must be considered as some of the etiologies for causing neuropsychological decline can be addressed. Medication and active epilepsy can contribute to impairments and their impact may be reversible. Dementia is rare if seizures are what has brought the person to attention, and if this is not accompanied by other slowly developing features (such as cognitive of psychiatric changes). From a neuropsychological point of view choosing the right screening tools or assessments, obtaining the history and timeline of impairments in relation to epilepsy, and most importantly longitudinally following the patients regardless of whether epilepsy is ultimately controlled or not appear essential.

Temporal response properties of koniocellular (blue-on and blue-off) cells in marmoset lateral geniculate nucleus.

Visual perception requires integrating signals arriving at different times from parallel visual streams. For example, signals carried on the phasic-magnocellular (MC) pathway reach the cerebral cortex pathways some tens of milliseconds before signals traveling on the tonic-parvocellular (PC) pathway. Visual latencies of cells in the koniocellular (KC) pathway have not been specifically studied in simian primates. Here we compared MC and PC cells to "blue-on" (BON) and "blue-off" (BOF) KC cells; these cells carry visual signals originating in short-wavelength-sensitive (S) cones. We made extracellular recordings in the lateral geniculate nucleus (LGN) of anesthetized marmosets. We found that BON visual latencies are 10-20 ms longer than those of PC or MC cells. A small number of recorded BOF cells (n = 7) had latencies 10-20 ms longer than those of BON cells. Within all cell groups, latencies of foveal receptive fields (<10° eccentricity) were longer (by 3-8 ms) than latencies of peripheral receptive fields (>10°). Latencies of yellow-off inputs to BON cells lagged the blue-on inputs by up to 30 ms, but no differences in visual latency were seen on comparing marmosets expressing dichromatic ("red-green color-blind") or trichromatic color vision phenotype. We conclude that S-cone signals leaving the LGN on KC pathways are delayed with respect to signals traveling on PC and MC pathways. Cortical circuits serving color vision must therefore integrate across delays in (red-green) chromatic signals carried by PC cells and (blue-yellow) signals carried by KC cells.

Transmission of blue (S) cone signals through the primate lateral geniculate nucleus.

This study concerns the transmission of short-wavelength-sensitive (S) cone signals through the primate dorsal lateral geniculate nucleus. The principal cell classes, magnocellular (MC) and parvocellular (PC), are traditionally segregated into on- and off-subtypes on the basis of the sign of their response to luminance variation. Cells dominated by input from S-cones ('blue-on and blue-off') are less frequently encountered and their properties are less well understood. Here we characterize the spatial and chromatic properties of a large sample of blue-on and blue-off neurons and contrast them with those of PC and MC neurons. The results confirm that blue-on and blue-off cells have larger receptive fields than PC and MC neurons at equivalent eccentricities. Relative to blue-on cells, blue-off cells are less sensitive to S-cone contrast, have larger receptive fields, and show more low-pass spatial frequency tuning. Thus, blue-on and blue-off neurons lack the functional symmetry characteristic of on- and off-subtypes in the MC and PC pathways. The majority of MC and PC cells received no detectible input from S-cones. Where present, input from S-cones tended to provide weak inhibition to PC cells. All cell types showed evidence of a suppressive extra-classical receptive field driven largely or exclusively by ML-cones. These data indicate that S-cone signals are isolated to supply the classical receptive field mechanisms of blue-on and blue-off cells in the LGN, and that the low spatial precision of S-cone vision has origins in both classical and extraclassical receptive field properties of subcortical pathways.