Biomedical subjects
Publications and source records attributed to C Kennard.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The exact role of the parietal lobe in spatial cognition is controversial. One influential hypothesis proposes that it subserves spatial perception, whereas other accounts suggest that its primary role is to direct spatial movement. For humans, it has been suggested that these functions may be divided between inferior and superior parietal lobes, respectively. In apparent support of a purely perceptual function for the inferior parietal lobe (IPL), patients with lesions to this structure, particularly in the right hemisphere, exhibit unilateral spatial neglect (deficient awareness for the side of space opposite to that of their lesion). Here we show that patients with right IPL lesions also have a specific difficulty in initiating leftward movements towards visual targets on the left side of space. This motor impairment was not found in neglect patients with frontal lesions, contrary to previous proposals that motor aspects of neglect are particularly associated with anterior damage. Our results suggest that the human IPL operates as a sensorimotor interface, rather than subserving only perceptual functions.
A patient with a lesion confined largely to the right inferior frontal gyrus was found to be impaired on tests of spatial working memory and executive functioning. By contrast, his pattern recognition was good. The patient's selective impairments are consistent with the view that prefrontal cortex contributes to processes involved in spatial working memory. The patient was also tested on a range of oculomotor paradigms, some of which required the temporary suppression of a saccadic response. He was unable to suppress making contra- or ipsilesional reflexive glances to peripheral stimuli on the "anti-saccade" paradigm, but his performance improved on delayed saccade, memory-guided saccade and fixation tasks. Although reflexive glances were observed under these conditions they occurred more frequently in response to contralesional stimuli than ipsilesional ones. Furthermore, the patient had no difficulty in performing anti-point movements with his ipsilesional hand. Thus, his inability to suppress reflexive glances on the anti-saccade task is not due to a generalised problem of "distractibility". The patient's deficits are discussed in terms of models of anti-saccade generation and are related to recent findings regarding the role of prefrontal cortex in working memory and visual attention.
BACKGROUND: Previous studies of oculomotor dysfunction in schizophrenia have tended to concentrate on abnormalities of smooth pursuit eye tracking in chronic medicated patients. We report the results of a study of smooth pursuit, reflexive and antisaccade performance in drug naive and antipsychotic treated first-episode schizophrenic patients. METHODS: Smooth pursuit and saccadic eye movements were recorded in 36 first-episode schizophrenic patients and 36 controls matched for age and estimated IQ. The schizophrenic patients were divided into drug-naive (N = 17) and antipsychotic treated groups (N = 19). RESULTS: Smooth pursuit velocity gain was significantly lower than controls only in the drug-naive patients. The treated patients did not differ significantly from either the controls or the untreated group. In an antisaccade paradigm both treated and drug-naive schizophrenic patients demonstrated an increased number of errors, but only drug-naive patients also demonstrated an increased latency in initiating correct antisaccades. CONCLUSIONS: These impairments are unlikely to be due to a generalized deficit in oculomotor function in the schizophrenic groups, as there were no differences between the groups in saccadic metrics on a reflexive saccade task. The results show that both smooth pursuit and saccadic abnormalities are present at the onset of schizophrenia and are integral to the disorder.
The project was an investigation into whether changes in the expression of G-proteins underlie altered cell signaling in migraine and cluster headache. The basis for this assumption is that altered physiological responses are seen in migraineurs and that differences in cell signaling are detected biochemically in various cell types isolated from peripheral blood. Levels of three G-protein mRNAs--Gs alpha, Gi alpha, and Gq alpha, were quantified in lymphocytes from clinically well-defined migraine and cluster headache patients and correlated with headache type and influence of drug treatment. Gi alpha mRNA was reduced by 50% in all migraine patients compared with control subjects; similarly in patients with or without aura, in patients with a migraine headache at the time of sampling, and patients in a quiescent state. No reduction in the levels of Gs alpha of Gq alpha mRNA were seen in migraine patients. A smaller reduction was seen in cluster headache patients, most marked in those without medication. Levels of Gs alpha mRNA were significantly reduced in cluster headache patients compared with migraine patients. The marked down-regulation of Gi alpha mRNA in migraine, whether quiescent or acute, indicates either an adaptive response to headache in this group of patients or that low levels of Gi alpha mRNA make individuals more susceptible to migraine.
Twelve patients with focal damage of the frontal cortex and 12 patients with mild, medicated, early stage Parkinson's disease switched between letter- and digit=naming tasks on every second trial of a task-switching paradigm. Compared with age- and IQ-matched control performance, patients with left-sided, but not right-sided, frontal damage exhibited markedly increased time costs associated with these predictable switches only when there was a general incidence of interference or 'crosstalk' between the tasks, and particularly so when the available task cues were relatively weak and arbitrary. The same patients also showed evidence of an increased sensitivity to the facilitatory and inhibitory effects of previous processing, when required to switch between tasks. Both groups of patients (with left- or right-sided frontal damage) exhibited slow, disorganized performance early in practice. In contrast to these frontal effects, the Parkinson's disease patients showed little indication of larger time costs of task switches but they did show progressive increases in the error costs, while age- and IQ-matched control subjects showed reductions. We propose that while both left and right frontal cortical areas are involved in the organization of cognitive and motor processes in situations involving novel task demands, only the left frontal cortex is involved in the dynamic reconfiguring between already-established task-sets, and specifically, that it is the site of an executive mechanism responsible for the modulation of exogenous task-set activity. Finally, dopaminergic transmission, along the nigrostriatal pathway, may be implicated in sustaining various cognitive and motor processes over prolonged periods, including the operation of those executive control mechanisms that accomplish reconfiguring between task-sets.
This review covers the recent developments in the diagnosis, natural history and treatment of several common neuro-opthalmological disorders, such as optic neuritis, pseudotumour cerebri and nonarteritic anterior ischaemic optic neuropathy. It also deals briefly with the effects on the eye of the ataxias and antiepileptic drugs.
Oculomotor abnormalities, particularly in smooth pursuit tracking, are one of the most widely investigated biological markers of schizophrenia. However, despite the wealth of published data, important questions concerning the exact nature of these abnormalities remain unanswered. Many of the studies use unreliable methodology, and few attempts have been made to interpret the observed oculomotor dysfunction in terms of current understanding of eye movement physiology. Also, the potential effects of antipsychotic medication have been poorly addressed. Recent research, using more reliable measurement techniques and novel saccadic paradigms are producing important results and may provide a more productive framework for future studies of oculomotor abnormalities in schizophrenia.
Saccades of patients with mild Parkinson's disease (PD) are said to be abnormal in the absence of a concurrently visible target or when they are part of a rapid sequence of eye movements. We tested this hypothesis using a predictive saccade paradigm in which target visibility is withdrawn for a period. Three rates of target alternation were used (0.25 Hz, 0.5 Hz and 1.0 Hz). Withdrawal of target visibility brought out the extremes of primary saccade gain for both the controls and the patients with PD, most undershoot being displayed at the lowest frequency, whereas the gain was greatest at the highest frequency, actually overshooting the target location. These results demonstrate that the spatial error of parkinsonian saccades does not invariably take the form of hypometria when part of a rapid sequence of eye movements.
When we identify a visual object such as a word or letter, our ability to detect a second object is impaired if it appears within 400ms of the first. This phenomenon has been termed the attentional blink or dwell time and is a measure of our ability to allocate attention over time (temporal attention). Patients with unilateral visual neglect are unaware of people or objects contralateral to their lesion. They are considered to have a disorder of attending to a particular location in space (spatial attention). Here we examined the non-spatial temporal dynamics of attention in patients, using a protocol for assessing the attentional blink. Neglect patients with right parietal, frontal or basal ganglia strokes had an abnormally severe and protracted attentional blink When they identified a letter, their awareness of a subsequent letter was significantly diminished for a length of time that was three times as long as for individuals without neglect. Our results demonstrate for the first time that visual neglect is a disorder of directing attention in time, as well as space.
The effect of distractor load on visual search was examined in a patient with visual neglect following infarction of the right frontal lobe. The spatial extent of his left-sided neglect was modified greatly by changing stimulus attributes. When targets were highly discriminable compared to distractors, or distractor density was low, or when the subject was asked to cancel distractors as well as targets, he was able to direct his search to the extreme left of search arrays and there was little or no evidence of neglect. By contrast, similar changes in distractor load had little or no effect on the neglect of a patient with a fronto-parietal lesion. These findings suggest that distractability towards ipsilesional stimuli may be an important component of neglect in individuals with only frontal lobe injury.
Explore the source record for details and available documents.
Five patients with left-sided visual neglect following focal infarction of the right frontal lobe are presented. Lesion location was assessed using computed tomography or magnetic resonance imaging. The common area of lesion overlap was small, being confined to the dorsal aspect of the inferior frontal gyrus (Brodmann's area 44) and the immediate underlying white matter. This cortical region is part of the homologue of Broca's area in the right hemisphere and is considered to be part of human premotor cortex. The association of neglect with injury to this area suggests it may play an important role in directing attention in visual space.
Recent research has shown that some patients with schizophrenia have a severe impairment in the suppression of reflexive saccadic eye movements in the ANTI-saccade task. This saccadic distractibility has previously been found in patients with lesions of dorsolateral prefrontal cortex, implicating an abnormality of prefrontal cortex. The objective of the present study was to determine the contribution of these and other areas to the ANTI-saccadic abnormality in schizophrenia by functional neuroimaging. Using 99mtechnetium-HMPAO high resolution multidetector single-photon emission tomography, regional cerebral blood flow (rCBF) during performance of the ANTI-saccade eye-movement task was compared, by statistical parametric mapping, in ten male schizophrenic patients on stable antipsychotic medication who had a high distractibility error rate on the task, and eight similar patients who had normal distractibility error rates. Compared with the normal error group, the patients with high error rates showed significantly decreased rCBF bilaterally, in the anterior cingulate, insula, and in left striatum. These same patients also had increased perseverative errors on the Wisconsin Card Sort Test.
Studies of patients with damage to the dorsolateral prefrontal cortex (DLPFC) and the basal ganglia have shown that these areas are involved in the control of remembered saccades. However, although positron emission tomography (PET) studies of remembered saccades have demonstrated extensive cortical and subcortical activation, they have failed to detect any significant increase in regional cerebral blood flow (rCBF) in these areas. This study was designed to see if these areas could be activated. Eight right-handed male volunteers were studied using H2(15)O PET. Comparison of the rCBF in the remembered saccade task to a rest control state revealed significant activation in both the DLPFC and the basal ganglia, and also the frontal eye fields, the supplementary motor area, the posterior parietal lobe, the cingulate cortex, the striate cortex, the extrastriate cortex and the superior temporal lobe. These findings confirm that remembered saccades are controlled by an extensive cortical and subcortical network, which includes the DLPFC and the basal ganglia.
We have examined visual functions, including colour vision, in a patient with bilateral cortical lesions involving mainly the fusiform and lingual gyri, areas known to be involved in the central processing of chromatic stimuli. The patient has near normal (6/9) acuity, and his responses to tests of binocular function and spatial vision are normal, as are his discrimination of changes in target speed and surface lightness. He does, however, exhibit minor losses in the upper visual field, mild prosopagnosia and topographical agnosia, all conditions commonly associated with cerebral achromatopsia. Colour matches and spectral response data establish that his cone photoreceptors have normal spectral characteristics and his spectral sensitivity measured against a white background reveals normal postreceptoral chromatic function. The patient's colour discrimination for differences in wavelength, hue or saturation is, however, impaired and his colour naming is significantly disturbed, particularly for blues and greens. We have determined the areas of the chromaticity chart that correspond to his naming categories for surface colours, and show that changes in illuminant cause him to alter the names of surface colours in a manner consistent with the changes in their chromaticities. Other subjects with normal or congenital red-green deficient colour vision make many fewer name changes under changes in illuminant. We conclude that the patient's colour constancy is impaired as a consequence of abnormal central processing of colour vision.