J. Thomas Hutton
Texas Tech University Health Sciences Center
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by J. Thomas Hutton.
Journal of the American Geriatrics Society | 1986
Jean Pearson Scott; Karen A. Roberto; J. Thomas Hutton
This study examined the instrumental and social‐emotional support provided by families to the primary caregivers of Alzheimers patients. It was anticipated that the more adequate the support provided by the family, the less sense of burden and the better the coping effectiveness of the caregiver. Ratings of instrumental assistance, social‐emotional support, adequacy of support, and coping effectiveness were made by trained raters from transcribed interviews with 23 primary caregivers. Also, a second family member who was usually next closest of kin to the caregiver was interviewed in order to provide another perspective of the support the family provided.
Movement Disorders | 2001
J. Thomas Hutton; Leo Verhagen Metman; Thomas N. Chase; Jorge L. Juncos; William C. Koller; Rajesh Pahwa; Peter A. LeWitt; Ali Samii; Joseph K.C. Tsui; Donald B. Calne; Cheryl Waters; Vincent Calabrese; James P. Bennett; Richard Barrett; Jerry L. Morris
N‐0923 is a non‐ergot, dopaminergic D2 agonist designed to be transdermally available. It has anti‐parkinsonian effects when infused intravenously. An adhesive matrix patch was developed to deliver N‐0923 transdermally (N‐0923 TDS).
Neuropsychologia | 1986
J. Thomas Hutton; James Palet
Lateral saccadic latencies were determined in 18 right-handers and 18 left-handers. Within the right-handed group the mean latency was significantly shorter when looking from the left to the right (242.7 msec) than from right to left (265.0 msec), whereas no significant directional difference was found in the left-handed group. An age effect was also found with longer latencies being associated with increased age. These findings agree with those of Pirozzolo and Rayner (Neuropsychologia 18, 225-229, 1980) and provide further evidence of the pervasiveness of functional asymmetry in the human brain. The present findings suggest that motoric or central integrative mechanisms may contribute more to saccadic directional asymmetries than do perceptual differences.
Electroencephalography and Clinical Neurophysiology | 1983
J. Thomas Hutton; J.A Nagel; Ruth B. Loewenson
The effect of age and gender on eye tracking performance was studied in normal healthy subjects. Two measures of tracking performance, phase corrected cross-correlation coefficients and number of catch-up saccades were determined. The cross-correlation measures revealed a differential effect with the elderly men demonstrating significantly better tracking performance than elderly women. An aging effect was found in women and an aging trend in men using the catch-up saccade measure. Other variables influencing tracking performance, in addition to age and sex, were target speed and type of measure. Recognition of this differential effect largely explains the existing controversy as to whether age or sex variables influence tracking performance.
Experimental Aging Research | 1989
Sandra D. Netherton; Jeffrey W. Elias; Nettie N. Albrecht; Christine Acosta; J. Thomas Hutton; J. William Albrecht
Performance on the Benton Visual Retention Test was compared between those with Parkinsons disease (PD) and age-equivalent controls. The major difference between groups was that those with PD showed an increase in figural reproduction errors between test periods spaced six months apart, while controls showed little increase in errors over this time and made fewer errors at each time of testing. Age and IQ accounted for major proportions of variance in performance for both groups (about 50%), far more than that attributable to group membership. Within the PD group, however, age and disease onset were confounded (r = .92), indicating that age as a variable is quite when disease onset is considered. The results support the notion that PD is associated with change in visual-spatial memory, beyond that predicted by age per se.
Experimental Aging Research | 1987
Henrik K. Kulmala; Jw Boja; J. William Albrecht; J. Thomas Hutton
This study was initiated to confirm the existence of brain-reactive autoantibodies and to determine if such antibodies have higher affinity for brain regions especially affected in Alzheimers disease. Serum collected from 90, 300, and 600 day old mice was incubated against brain tissues from these same mice, followed by incubation with fluorescently tagged rabbit antimouse IgG. No antibodies were present in the youngest serum, but considerable antibodies were present at 300 and, especially, at 600 days. Such antibodies were present in the blood vessels, but not in the brains of older animals. These antibodies, applied exogenously, labeled cells equally in all three ages of brains including most cortical and many other neurons, indicating that they are not neurotransmitter specific. In a further study, kainic acid or saline was administered peripherally to 15-month old rats. Kainic acid damaged the blood brain barrier and allowed the CNS entry of brain-reactive antibodies, especially into the subregions of hippocampus most damaged in Alzheimers.
Neuro-Ophthalmology | 1987
J. Thomas Hutton; Raye Lynne Dippel; J. H. Sung
The authors report normal smooth pursuit eye tracking from a patient with pathologically confirmed Pick disease. This is contrasted to the abnormal pursuit tracking found in a group of nine Alzheimer patients, each of the same severity of dementia as the Pick patient, and to a group of 15 normal elderly controls. The Alzheimer patients demonstrated saccadic pursuit whereas the Pick patient showed smooth ocular pursuit. The parieto-occipital cortex, the area from which ocular smooth pursuit is believed to originate, is spared in Pick disease, but not in Alzheimer disease. Monitoring of ocular pursuit may differentiate Pick disease from Alzheimer disease.
Progress in Neuro-psychopharmacology & Biological Psychiatry | 1985
Henrik K. Kulmala; J. Thomas Hutton
Senile plaques participate in a cropping of the dendritic tree of enkephalinergic dentate granule cells and hl and subicular pyramidal cells. Somatostatin-containing pyramidal neurons are lost in Alzheimers disease, whereas nonpyramidal somatostatin neurons are less affected. Fibers containing somatostatin penetrate immature, but not end-stage senile plaques. The senile plaque may precipitate much of the hippocampal denervation seen in Alzheimers disease.
JAMA Neurology | 2001
Richard B. Dewey; J. Thomas Hutton; Peter A. LeWitt; Stewart A. Factor
JAMA Neurology | 1981
J. Thomas Hutton