Deep grey matter MRI abnormalities and cognitive function in relapsing-remitting multiple sclerosis.

Although deep grey matter (GM) involvement in multiple sclerosis (MS) is well documented, in-vivo multi-parameter magnetic resonance imaging (MRI) studies and association with detailed cognitive measures are limited. We investigated volumetric, diffusion and perfusion metrics in thalamus, hippocampus, putamen, caudate nucleus and globus pallidum, and neuropsychological measures, spanning 4 cognitive domains, in 60 relapsing-remitting MS patients (RRMS) (mean disease duration of 5.1 years, median EDSS of 1.

Reduced grey matter perfusion without volume loss in early relapsing-remitting multiple sclerosis.

Background: Grey matter (GM) pathology in multiple sclerosis (MS) is associated with progressive long-term disability. Detection of GM abnormalities in early MS may therefore be valuable in understanding and predicting the long-term course. However, structural MRI measures such as volume loss have shown only modest abnormalities in early relapsing-remitting MS (RRMS).

A perceptual discrimination task results in greater facilitation of voluntary saccades in Parkinson's disease patients.

Many studies have shown that Parkinson's disease (PD) affects not only the ability to generate voluntary saccades but also the ability to suppress reflexive saccades (hyper-reflexivity). To further investigate these apparently contradictory effects of PD on the saccade system we adapted a well-known dual-task paradigm (Deubel, 2008) to measure saccades with and without a peripheral discrimination task. Previously we reported that the concurrent performance of a perceptual discrimination task abnormally reduced the latencies of reflexive saccades in PD.

The influence of motor and cognitive impairment upon visually-guided saccades in Parkinson's disease.

Studies of saccades in Parkinson's disease (PD) have seldom examined the influence of cognitive status, ranging from normal cognition, through mild cognitive impairment, to dementia. In a large and heterogeneous sample, we examined how motor and cognitive impairment was reflected in the performance of reflexive, visually-guided saccades. We examined 163 people with PD and 47 similar-aged controls.

Impairment of voluntary saccades and facilitation of reflexive saccades do not co-occur in Parkinson's disease.

Reflexive saccades (fast eye movements) and voluntary saccades activate overlapping parts of the oculomotor system. It is assumed that striatal dopamine depletion in Parkinson's disease (PD) only affects the voluntary saccadic system and that the often-reported facilitation of the reflexive saccadic system in PD is secondary to impairment of the voluntary saccadic system. If this assumption is correct, facilitation of reflexive saccades should co-occur with impaired performance of voluntary saccades in patients with PD.

A perceptual discrimination task abnormally facilitates reflexive saccades in Parkinson's disease.

Numerous studies have shown that Parkinson's disease (PD) affects the ability to generate voluntary saccades and the ability to suppress reflexive saccades. The effects of PD on the generation of reflexive saccades, however, are not clear. Some studies report impairments, but there are also reports of abnormal facilitation or hyper-reflexivity of the saccade system in PD.

Bottom-up effects modulate saccadic latencies in well-known eye movement paradigm.

A well-known eye movement paradigm combines saccades (fast eye movements) with a perceptual discrimination task. At a variable time after the onset of a central arrow cue indicating the target direction [the stimulus onset asynchrony (SOA)], discrimination symbols appear briefly at saccade target and non-target locations. A previous study revealed an unexpected effect of SOA on saccadic latencies: latencies were longer in trials with longer SOAs.

Don't look now or look away: two sources of saccadic disinhibition in Parkinson's disease?

Recent studies found evidence of impaired inhibition of saccades (fast eye movements) in non-demented people with PD. It has been suggested that impaired eye movement control reflects a general deficit of automatic response inhibition associated with impaired cognitive function in Parkinson's disease (PD). This study investigated the nature and source of saccadic disinhibition in PD.