Authors:
Robert T. Knight
David L. Woods
Clay Clayworth
Date: 1987
PubMed: 3587487
Recovery From GABA-Mediated Hemiplegia in Young and Aged Rats: Effects of Catecholaminergic Manipulations
Abstract:
We investigated the participation of catecholaminergic mechanisms in the functional recovery from motor cortex lesions in young (9 months) and aged (26 months) rats. The animals were studied during the recovery period from an hemiplegic syndrome secondary to small motor cortex lesions potentiated by the localized, chronic (7 days) infusion of GABA into the lesion site. Acute administration of haloperidol (0.1 mg/kg IP) to these recovered animals induced a re-emergence of the contralateral motor syndrome in both groups. In the young group, the haloperidol-induced hemiplegia lasted one day whereas in the aged animals the deficit was significantly prolonged lasting three days. Apomorphine administration (0.5 mg/kg IP) prior to or immediately after haloperidol injection failed to prevent or reverse the reappearance of the motor deficit. Adult animals recovered from motor cortex aspirations performed 7 to 12 months prior were refractory to haloperidol effects. Amphetamine administration to young rats treated chronically with saline or GABA infusion into the somatomotor region also failed to alter the clinical evolution of the motor deficit. The evidence suggests that dopaminergic mechanisms are involved in the functional recovery from brain lesions and that these mechanisms are most susceptible to neuroleptic blockade during the early post-lesional period. The deleterious effects of dopaminergic blockade are heightened in aged populations. The use of dopaminergic antagonists in brain-lesioned subjects, and particularly in geriatric populations, is considered potentially harmful, particularly in the early stages of the recovery process.
Appraisal and diagnosis of neurogenic communicative disorders in remote settings
Authors:
Robert T. Wertz
Nina F. Dronkers
Ellen Bernstein-Ellis
Yvonne Shubitowski
Roberta Elman
Gregory K Shenaut
Robert T. Knight
Jon L. Deal
Date: 1987
Abstract:
Patients who suffer neurogenic communication disorders and reside in remote settings either do not receive services or they must travel long distances or become inpatients for extended periods. No services is unacceptable, because all patients merit appraisal and a diagnosis, and many respond to treatment with improvement in their communication. Traveling long distances for services is unacceptable, because it is expensive, inconvenient, may be contraindicated by the patient's medical condition, requires a means of transportation which often does not exist, and must be frequent and protracted. Hospitalization is also unacceptable, because the communication disorder does not necessitate hospitalization, it usurps a bed, carries a patient beyond DRG length-of-stay criteria, removes him or her from the home environment, and is expensive. There is a need to develop means for managing patients who live in remote settings.
Appraisal and diagnosis of neurogenic communicative disorders in remote settings
Authors:
Robert T. Wertz
Nina F. Dronkers
Ellen Bernstein-Ellis
Yvonne Shubitowski
Roberta Elman
Gregory K Shenaut
Robert T. Knight
Jon L. Deal
Date: 1987
Generators of middle- and long-latency auditory evoked potentials: implications from studies of patients with bitemporal lesions
Authors:
David L. Woods
Clay Clayworth
Robert T. Knight
Gregory V. Simpson
Margaret A. Naeser
Date: 1987
PubMed: 2435529
Abstract:
We recorded middle- and long-latency auditory evoked potentials (AEPs) in 5 patients (ages 39-72 years) with bilateral lesions of the superior temporal plane. Reconstructions of CT sections revealed that primary auditory cortex had been damaged bilaterally in four of the patients, while in the fifth an extensive left hemisphere lesion included primary auditory cortex while a right hemisphere lesion had damaged anterior auditory association areas but spared primary auditory cortex. Normal middle-latency AEPs (MAEPs) were recorded at the vertex electrode in all of the patients. In 3 of the 5 patients, MAEPs also showed normal coronal scalp distributions and were comparable in amplitude following stimulation of either ear. Two patients showed abnormalities. In one case, Na (latency 17 msec)-Pa (latency 30 msec) amplitudes were reduced over both hemispheres following stimulation of the ear contralateral to the more extensive lesion. In another, with both subcortical and cortical involvement, the Pa was abolished over the hemisphere with the more extensive lesion. Long-latency AEPs were normal in 2 patients whose lesions were largely confined to the superior temporal plane. In 2 patients with lesions extending into the inferior parietal lobe, N1s were abolished bilaterally. In the fifth patient, the N1 showed a slight reduction over the hemisphere with the more extensive lesion. Middle- and long-latency AEPs were differentially affected by some lesions. For example, patients with absent N1s could produce normal Pas. A review of these results and those of previous studies of bitemporal patients suggests that abnormalities in middle- and long-latency AEPs do not necessarily reflect damage to primary auditory cortex per se, but rather the degree of damage to adjacent areas. Abnormalities in MAEPs are associated with subcortical lesions, or cortical lesions extensive enough to denervate thalamic projection nuclei. Abnormalities in the long-latency N1 reflect lesion extension into the multi-modal areas of the inferior parietal lobule. This area appears to exert a critical modulatory influence over N1 generators outside of the superior temporal plane.
Aging decreases auditory event-related potentials to unexpected stimuli in humans
Abstract:
A P300 event-related potential (P3a) was recorded to unexpected, deviant auditory stimuli requiring no behavioral response. This brain potential underwent systematic latency prolongation and amplitude decrease with advancing age. The age-related changes paralleled those of the P300 (P3b) recorded in target detection tasks. These results provide physiological evidence of a decremented CNS response to unexpected stimuli with aging.