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Biomedical subjects

D M Feeney

Publications and source records attributed to D M Feeney.

At least 37 records · Page 2Linked to original sources
PubMed1987

Recovery of tactile placing after visual cortex ablation in cat: a behavioral and metabolic study of diaschisis.

After bilateral visual cortex ablation, cats show a transient deficit in tactile placing and a permanent deficit in visual placing of both forelimbs. Amphetamine administration (four doses, 5 mg/kg, i.p., spaced at 4-day intervals beginning 10 days after surgery) accelerated the rate of recovery of tactile placing compared with saline controls whereas visual placing was not affected. The catecholamine antagonist, haloperidol (0.4 mg/kg, i.p.), blocked the amphetamine-enhanced recovery of tactile placing. Additionally, the visual cortex lesions produced a depression of oxidative metabolism, measured by cytochrome oxidase histochemistry, in subcortical regions remote from the injury. Animals treated with amphetamine exhibited an alleviation of this metabolic depression in the superior colliculus but not in other regions.

Amphetamine↗
PubMed1987

Pharmacotherapy for recovery of function after brain injury.

Considerable attention has recently been focused on the development of pharmacotherapies for promotion of recovery of function after brain injury. This article reviews both animal and human experimentation in two areas which appear to have considerable clinical applicability in the very near future for promoting recovery: drug manipulation of neurotransmitter systems and administration of gangliosides. Since the most important problem after brain injury is restoration of lost behavioral capabilities, this is the central theme of this review. The possible mechanisms of the effects of these pharmacological agents are only discussed for treatments with demonstrated beneficial or harmful effects on behavioral recovery. An attempt is also made to indicate possible common mechanisms and the clinical potential of the various treatments; future directions for research are suggested.

Animals↗
PubMed1985

Reinstatement of binocular depth perception by amphetamine and visual experience after visual cortex ablation.

In adult cats with bilateral visual cortex ablation the complete deficit in binocular depth perception, as measured on a visual cliff, was reversed by 4 doses of amphetamine. The amphetamine-induced recovery endured after the amphetamine treatment was discontinued. This enduring recovery of function was not obtained if the animals were housed in the dark during drug intoxication. Therefore, both amphetamine intoxication and visual experience are simultaneously required for recovery of binocular depth perception after visual cortex ablation.

Animals↗
PubMed1985

Striatal dopamine after cortical injury.

After right or left unilateral sensorimotor cortex ablation or a sham operation, dopamine concentrations were assayed in the right and left striatum of rats. In the sham-operated animals, a greater amount of dopamine was found in the left striatum compared with the right. Right or left sensorimotor cortex injury reduced dopamine in both striata. Right hemisphere lesions produced a greater loss of dopamine in the right striatum compared with the effect of a left lesion on dopamine in the left striatum. The results support the hypothesis of an asymmetric response to cortical injury.

Animals↗
PubMed1984

The electroencephalographic characteristics of the rhombencephalectomized cat.

The electroencephalographic responses in the rhombencephalectomized cat after the application of photic and epileptogenic agents resemble those phenomena in the normal animal. The spontaneous EEG of the motor region had fewer beta waves, a slower alpha but more delta components than the presection record. The response to photic stimulation in the occipital cortex was similar before and after the rhombencephalectomy, although the initial waves were slightly delayed. Epileptic activity upon topical application or intravenous administration of epileptogenic agents was demonstrated in the sensorimotor cortex.

Animals↗
PubMed1983

Amphetamine and apomorphine restore tactile placing after motor cortex injury in the cat.

Unilateral motor cortex injury in the cat results in a prolonged loss of tactile placing in the forelimb contralateral to the injury. Amphetamine (5 mg/kg) temporarily reverses this tactile placing deficit as early as 4 days following the injury. Racemic amphetamine was found to produce a significantly more prolonged restoration of placing than the d isomer, which was significantly more effective than the l isomer. Haloperidol (0.4 mg/kg) blocked the amphetamine-induced recovery of placing responses and also blocked placing in nondrugged cats showing partial spontaneous recovery. This dosage of haloperidol had no effect on tactile placing in normal cats. Apomorphine at moderate dosages (0.25 and 0.5 mg/kg) produced a weak restoration of tactile placing in motor cortex-injured animals. These pharmacological data suggest that the loss of tactile placing after motor cortex injury is due to a depression of catecholaminergic function, which is temporarily reversible by catecholaminergic stimulation.

Amphetamine↗
PubMed1982

Amphetamine, haloperidol, and experience interact to affect rate of recovery after motor cortex injury.

Rats subjected to unilateral ablation of the motor cortex and placed on a narrow beam displayed transient contralateral paresis. An immediate and enduring acceleration of recovery was produced by a single dose of d-amphetamine given 24 hours after injury. This effect was blocked by haloperidol or by restraining the animals for 8 hours beginning immediately after amphetamine administration. A single dose of haloperidol given 24 hours after injury markedly slowed recovery. This effect was also blocked by restraining the animals.

Animals↗
PubMed1981

Responses to cortical injury: I. Methodology and local effects of contusions in the rat.

In order to develop some understanding of the evolution of cortical contusions, interdisciplinary studies including behavior, morphology and histochemistry were conducted at varying intervals after standardized injuries. A method for producing graded and reproducible focal cortical contusions in the rat is described. When these impact injuries are made in the "hindpaw cortical area,' specific trauma dose dependent behavioral deficits can be readily observed in the contralateral hindlimb. While most functional recovery occurs in the first two weeks after trauma, with severe contusions, deficits persist beyond 90 days. Morphologically these injuries progress from hemorrhages in white matter directly under contused cortex during the first hours after injury to the development of a necrotic cavity by 24 hours. The cavitation appears to expand over the subsequent two weeks and by 15 days is lined with fibroblast-like elements and macrophages. Intense acid phosphatase activity is seen on the borders of the area of necrosis. This lysosomal enzyme may participate in autolysis and development of focal cavitation following cortical contusion.

Acid Phosphatase↗
PubMed1981

Responses to cortical injury: II. Widespread depression of the activity of an enzyme in cortex remote from a focal injury.

As a part of a broader study of the reaction of the brain to injury, we report here an interesting loss of the activity of an enzyme in areas quite remote from the site of direct injury. At 36 h following a laceration or contusion injury to the hindpaw area of the motor cortex, a peculiar loss of staining for the enzyme alpha glycerophosphate dehydrogenase (alpha-GPDH) was noted. alpha-GPDH activity was markedly depressed in cortical layers II and III throughout the hemisphere on the side of the injury. The depression of alpha-GPDH activity extended far laterally across the rhinal fissure into the pyriform cortex. The decrease in alpha-GPDH staining was prominent 4 days after the injury: however, the staining pattern had returned to normal at 9 days. Enzyme changes in animals lesioned in the occipital cortex paralleled that seen in animals with a lesion in the motor cortex. Animals which had received an undercut lesion in the motor cortex 56 days earlier were contused in the occipital cortex. The old injury site presented the same sequelae of changes as seen in other lesioned animals. Additionally, a suction ablation injury involving only a small part of motor cortex resulted in the same widespread reduction of staining for alpha-GPDH in layers II and III. The derangement in energy metabolism suggests that cells in layers II and III of the cerebral cortex may be particularly vulnerable to perturbations induced by cortical trauma. These findings may be related to the diffuse and transient functional losses observed after head injury in man.

Animals↗
PubMed1980

Chronic dorsal column stimulation: effects on H reflex and symptoms in a patient with multiple sclerosis.

In a case of severe multiple sclerosis primarily affecting the spinal cord, dorsal column stimulation over a 2-year period was followed by some functional improvement in locomotion. Additionally, the H reflex recovery cycle, which was quite abnormal before stimulation, showed a pronounced shift toward a more normal pattern with dorsal column stimulation. These data provide objective support for the apparent symptomatic relief by this procedure in such cases.

Adult↗
PubMed1979

Sensory neglect after lesions of substantia nigra or lateral hypothalamus: differential severity and recovery of function.

Sensory neglect was studied in cats after unilateral lesions of: lateral hypothalamus (LH); internal capsule (IC) adjacent to the LH; substantia nigra (SN) or the ventromedial hypothalamus (VMH). Special behavioral tests were employed to yield quantifiable data and also to exclude any confounding due to simple movement deficits. Lesions of SN or IC produced severe and enduring contralateral visual and somesthetic deficits and a facilitation of ipsilateral visual responsiveness. In contrast, LH lesions sparing the adjacent IC produced only weak and transient deficits and VMH lesions had no effects on sensory function. This suggests that lesions of the SN or its forebrain connections are important for producing sensory neglect and that sensory deficits after LH lesions are due to infringement on fibers of passage to or from the SN. Lesions which produced neglect often suppressed the amplitude of flash evoked responses in the ipsilateral caudate nucleus and visual and association cortex. However, these evoked potential effects were transient. There was no effect on the spontaneous EEG and this fails to support the hypothesis of a lack of hemispheric arousal in sensory neglect. The results are discussed in relation to nigrotectal projections and the process of attention. This lesion-behavior model is suggested for studies of recovery of function.

Animals↗
PubMed1979

The prediction of posttraumatic epilepsy. A mathematical approach.

Simple mathematical equations can be used to estimate the probability of posttraumatic seizures. Risk factors and time since the injury are taken into consideration in the calculations. The equations are based on a constant probability model derived from published data. When these formulae are applied to data from a variety of published studies, the predicted incidence of posttraumatic epilepsy based on the mathematical model agrees well with the incidence observed in the study groups.

Brain Injuries↗