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Biomedical subjects

Andrew Parton

Publications and source records attributed to Andrew Parton.

7 recordsLinked to original sources
PubMed2006

Role of the human supplementary eye field in the control of saccadic eye movements.

The precise function of the supplementary eye field (SEF) is poorly understood. Although electrophysiological and functional imaging studies are important for demonstrating when SEF neurones are active, lesion studies are critical to establish the functions for which the SEF is essential. Here we report a series of investigations performed on an extremely rare individual with a highly focal lesion of the medial frontal cortex. High-resolution structural imaging demonstrated that his lesion was confined to the region of the left paracentral sulcus, the anatomical locus of the SEF. Behavioural testing revealed that the patient was significantly impaired when required to switch between anti- and pro-saccades, when there were conflicting rules governing stimulus-response mappings for saccades. Similarly, the results of an arbitrary stimulus-response associative learning task demonstrated that he was impaired when required to select the appropriate saccade from conflicting eye movement responses, but not for limb movements on an analogous manual task. When making memory-guided saccadic sequences, the patient demonstrated hypometria, like patients with Parkinson's disease, but had no significant difficulties in reproducing the order of saccades correctly on a task that emphasized accuracy with a wide temporal segregation between responses. These findings are consistent with the hypothesis that the SEF plays a key role in implementing control when there is conflict between several, ongoing competing saccadic responses, but not when eye movements need to be made accurately in sequence.

Association Learning↗
PubMed2006

Space re-exploration in hemispatial neglect.

Exploration of the space around us is a fundamental part of human behaviour. When it breaks down there is an important opportunity to understand its underlying mechanisms. Here we show that many right-hemisphere patients with left neglect re-explore rightward locations, failing to keep track of them during search. Importantly, such re-exploration occurred despite leftward stimuli being indistinguishable in peripheral vision, so it is unlikely to result from implicit processing of neglected targets. Revisits generally occurred after visits to other targets and are therefore not immediate perseverations. Finally, manipulating the visual salience of found targets altered the degree of neglect, but not revisit rates. Space exploration appears to be modulated both by the ability to keep track of spatial locations and by stimulus salience.

Aged↗
PubMed2005

Action control in visual neglect.

Patients with unilateral neglect show a variety of impairments when reaching towards objects in contralesional space. The basis of these deficits could be perceptual, motor or at one of the intermediate stages linking these processes. Here, we review studies of visually guided reaching in neglect and integrate these results with findings from normal human and monkey action control. We consider evidence which shows that neglect patients can be slow to initiate or execute reaches particularly to a contralesional target. We discuss the directional and spatial deficits that may interact to contribute to such reaching abnormalities and highlight the importance of effective target selection and on-line guidance, exploring the idea that deficits in these mechanisms underlie increased susceptibility to ipsilesional visual distraction in neglect. We also examine the relationship between optic ataxia and neglect by considering two illustrative cases, one with pure optic ataxia and the other with optic ataxia plus neglect, which reveal differences in the anatomical substrates of the two syndromes. We conclude that many patients with neglect make abnormal visually guided reaches, but the pattern of reaching deficits is highly variable, most likely reflecting heterogeneity of lesion location across subjects. Rather than being specific to the neglect syndrome, abnormalities of reaching in these patients may correspond to the extent of damage to the visuomotor control system which involves critical regions in both the parietal and frontal cortex, the white matter tracts connecting them and subcortical regions. Thus, the action control deficits in neglect may be conceptualised as a range of impairments affecting multiple stages in the visuomotor control process.

Attention↗
PubMed2005

Volition and conflict in human medial frontal cortex.

Controversy surrounds the role of human medial frontal cortex in controlling actions. Although damage to this area leads to severe difficulties in spontaneously initiating actions, the precise mechanisms underlying such "volitional" deficits remain to be established. Previous studies have implicated the medial frontal cortex in conflict monitoring and the control of voluntary action, suggesting that these key processes are functionally related or share neural substrates. Here, we combine a novel behavioral paradigm with functional imaging of the oculomotor system to reveal, for the first time, a functional subdivision of the pre-supplementary motor area (pre-SMA) into anatomically distinct areas that respond exclusively to either volition or conflict. We also demonstrate that activity in the supplementary eye field (SEF) distinguishes between success and failure in changing voluntary action plans during conflict, suggesting a role for the SEF in implementing the resolution of conflicting actions. We propose a functional architecture of human medial frontal cortex that incorporates the generation of action plans and the resolution of conflict.

Adult↗
PubMed2005

Spatial working memory capacity in unilateral neglect.

It has been proposed recently that a deficit in keeping track of spatial locations may contribute to the severity of unilateral neglect in some right hemisphere stroke patients. However, performance on traditional spatial working memory (SWM) tasks (e.g. Corsi blocks) might be confounded by failure to encode leftward locations, rather than a true deficit of maintaining locations in SWM. Here we introduced new procedures for circumventing this to measure SWM capacity in neglect. In a first experiment, 20 right hemisphere stroke patients (10 with and 10 without neglect) were tested on a computerized vertical variant of the Corsi task. Sequences of spatial locations in a vertical column were displayed and participants had to tap out the remembered sequence on a touchscreen. Patients with left neglect were impaired on this vertical SWM task compared with all control groups. However, poor performance on this task (as for Corsi blocks) might involve impaired memory for stimulus sequence, or poor visuomotor control of manual responding, rather than reduced SWM capacity per se. A second experiment therefore employed a purer measure of vertical SWM. After the displayed sequence, a single location was now probed visually, with observers judging verbally (yes/no) if it had been in the preceding sequence. Hence order no longer mattered, and no spatial motor response was required. Again, the neglect group was impaired relative to all others, now with very little overlap between the performances of individual neglect patients versus individuals in control groups. Poor performance on the second task, which provides a purer measure of SWM capacity, correlated with severity of left neglect on cancellation tasks (but not on line bisection), consistent with recent proposals that SWM deficits can exacerbate left neglect on visual search tasks when present conjointly. Lesion anatomy indicated that neglect patients with a SWM deficit were most likely to have damage to parietal white matter, plus, in the second experiment, to the insula also. These findings demonstrate that an impairment in SWM capacity can contribute to the neglect syndrome in patients with stroke involving regions within the right parietal lobe and insula.

Adult↗
PubMed2005

Neuropharmacological modulation of cognitive deficits after brain damage.

PURPOSE OF REVIEW: This review discusses recent studies that have implications for potential neuropharmacological interventions which target cognitive deficits resulting from traumatic brain injury or stroke. RECENT FINDINGS: An important new study concerning the activity of N-methyl-D-aspartate (NMDA) receptors after brain injury reveals that previous influential hypotheses about an increase in glutamate triggering neuronal death may need to be revised. Furthermore, the study suggests that cognitive function may be best preserved by stimulation of NMDA receptors with agonists rather than by the use of antagonists, as previously believed. Investigations of animal models of stroke and traumatic brain injury have further demonstrated the possibility of intervening in the acute and sub-acute stages to protect specific brain systems, such as preservation of the cholinergic system (via cholinesterase inhibitors) and hippocampal neurons (via a D2 agonist). Clinical trials in humans indicate it is also possible to target these neurotransmitter systems to enhance cognitive performance in patients with chronic deficits. In particular, recent studies demonstrated that it is possible to ameliorate the effects of two common cognitive syndromes, visual neglect and aphasia. SUMMARY: Cognitive deficits are an extremely common consequence of either traumatic brain injury or stroke. Recent studies demonstrate the potential for using neuropharmacological intervention after acquired brain injury to prevent or ameliorate the effects of cognitive impairments. These treatments, however, are still in their preliminary stages and further research is required to identify the most effective compounds.

Animals↗