PubMed Health⌕ Search

Biomedical subjects

R M Dasheiff

Publications and source records attributed to R M Dasheiff.

At least 37 records · Page 2Linked to original sources
PubMed1992

Visual angle of the mind's eye before and after unilateral occipital lobectomy.

Do mental images occur in a spatially mapped (i.e., analog, or array-format) representational medium? Kosslyn's (1978) method was used to measure the visual angle of "the mind's eye" to estimate the extent of the imagery medium before and after unilateral occipital lobectomy. It was found that the overall size of the largest possible image was reduced following the surgery. In addition, only the horizontal extent, and not the vertical extent, of the imagery medium was reduced. Finally, it was determined that the S understood the tasks, was not aware of our predictions, and was unaffected by a strong demand characteristic in a different imagery task. These results are consistent with the hypothesis that imagery occurs in a spatially mapped representational medium dependent on occipital cortex.

Adult↗
PubMed1991

Sudden unexpected death in epilepsy: a series from an epilepsy surgery program and speculation on the relationship to sudden cardiac death.

Sudden unexpected death represents a significant cause of mortality in people with epilepsy. It derives this significance not because it is the most frequent cause of death but because it is apparently a direct consequence of a seizure. The implication is that epilepsy is an inherently lethal disorder. Seven patients who were studied in an epilepsy surgery program died a sudden unexpected death. This incidence of sudden unexpected death was five times higher than the 1-2/1,000 per year reported in the general epilepsy population. Sudden unexpected death shares some of the characteristics associated with sudden cardiac death, which kills 300,000 people in the United States each year. A cardiac arrhythmia, usually ventricular fibrillation, is the most common terminal event for sudden cardiac death and is the leading candidate as the mechanism for sudden unexpected death. Despite this knowledge, little is known on how to identify a high-risk group of patients for sudden death or how these deaths might be prevented.

Coronary Disease↗
PubMed1989

Regional voltage map of the hippocampus during seizures.

The hallmark of brain tissue is its electrical activity. However, few techniques are available to directly monitor voltage changes in neural tissue, especially in whole brain preparation. A technique has been developed using a fluorescent voltage-sensitive dye and digital image analysis to produce a high spatial resolution map of the voltage changes induced by seizures in the hippocampus. Eight different anatomical regions within the septal hippocampus of the rat were analyzed. Seizures were produced in vivo by methods which use entirely different mechanisms and produce electrographically and behaviorally different types of seizures. Kainic acid produced depolarization during the seizure, whereas bicuculline produced hyperpolarization. The results provide experimental evidence that all seizures do not induce a depolarized state in the brain.

Animals↗
PubMed1988

Fluorescent voltage-sensitive dyes: applications for neurophysiology.

Voltage-sensitive dyes are a means to optically monitor changes in membrane potential. Their application in research has grown steadily over the last two decades as better dyes have been developed. The techniques presently in use are providing unique information about biologic systems from bacteria to the functional organization of primate occipital cortex. This review provides a history of the dyes, the data supporting their voltage sensitivity, and the techniques required for their use. The limitations in using and interpreting the voltage-sensitive dyes, as well as their diverse applications in all areas of research, especially neurophysiology, are comprehensively presented.

Animals↗
PubMed1987

Epilepsy surgery improves regional glucose metabolism on PET scan. A case report.

A patient with medically intractable complex partial epilepsy was evaluated for epilepsy surgery by electro-encephalograph recording with depth electrodes and 18F-fluorodeoxyglucose positron emission tomography (PET). A small calcified arteriovenous malformation was excised from the left parietal lobe, and the patient became seizure free. Baseline and language stimulation PET scans were obtained preoperatively and 10 months postoperatively. There was a significant increase in glucose metabolism of the left temporal lobe postoperatively, which we interpret as evidence of improved neuronal function. We suggest that this case represents evidence for a functional, and reversible, inhibition of neuronal metabolism by epileptic activity.

Cerebral Cortex↗
PubMed1986

Sudden unexpected death of epileptic patient due to cardiac arrhythmia after seizure.

Sudden unexpected death (SUD) occurred in an epileptic patient after a seizure. The patient had a witnessed seizure with electrocardiographic evidence of a cardiac arrhythmia. Immediate cardiopulmonary resuscitation in the hospital was ineffective. Autopsy revealed no anatomic cause of death. This case supports a cardiac cause for SUD in this patient. The mechanism of death remains speculative despite its setting in an epilepsy center. The seven-year experience with SUD at the epilepsy center is reviewed.

Arrhythmias, Cardiac↗
PubMed1985

Abnormal somatosensory evoked potentials in amyotrophic lateral sclerosis.

A patient with typical clinical and electromyographic features of amyotrophic lateral sclerosis (ALS) was found to have abnormal somatosensory evoked potentials (SEPs). Evoked responses are generally considered to be normal in ALS despite occasional pathological and clinical evidence of sensory involvement. Thus, abnormal SEPs are considered to argue against a diagnosis of ALS. Based on the present case and a review of the literature, we suggest that abnormal SEPs need not exclude a diagnosis of ALS.

Adult↗
PubMed1985

d-Tubocurarine causes neuronal death when injected directly into rat brain.

d-Tubocurarine (d-TC) is a drug commonly used to produce muscle paralysis. Although it has been demonstrated to produce seizures when injected directly into the cerebral ventricles, no lasting neurotoxic effects have been reported. Data presented here suggest that amounts of d-TC as small as 1 microgram injected directly into rat hippocampus resulted in selective damage to dentate granule cells. Larger doses (5 to 10 micrograms) induced limbic and motor seizures with damage to hippocampal pyramidal cells. Other brain regions showed a differential sensitivity to direct injections. Pharmacologic studies suggest a nicotinic mechanism for both actions. The neurotoxic effects could not be elicited if d-TC was administered systemically, even when the blood-brain barrier was disrupted.

Animals↗
PubMed1985

The effects of colchicine in mammalian brain from rodents to rhesus monkeys.

The injection of colchicine into rats and monkeys produced two different types of brain damage. At selected doses, intradentate colchicine preferentially destroyed DGC in rats, whereas damage was less selective and more severe in monkeys. Experiments were performed with different tubulin-binding drugs to investigate the structure-function relationship of tubulin binding and DGC death. The tubulin-binding characteristics of these and other drugs reported in the literature did not correlate with their ability to damage DGC. The role of seizure-induced cell death was investigated by recording the EEG in monkeys and in rats treated with phenobarbital. The data suggest that seizures are an infrequent epiphenomenon of colchicine's action. We proposed that colchicine is not a selective neurotoxin and that it causes brain damage by inducing a non-specific inflammatory response. This response is both dose- and species-dependent. We concluded by discussing the medical implications of the present and proposed uses of colchicine.

Animals↗
PubMed1985

A new method of monitoring membrane potential in rat hippocampal slices using cyanine voltage-sensitive dyes.

A novel application of voltage-sensitive dyes is described. Hippocampal slices in vitro accumulated voltage-sensitive cyanine dyes under conditions presumed to cause depolarization and hyperpolarization. Increasing extracellular potassium caused a depression of dye uptake that correlated linearly with the membrane potential calculated from the Goldman equation. Veratrine depressed dye uptake, and this effect was blocked by addition of tetrodotoxin or removal of extracellular sodium. Ouabain also depressed dye uptake. Conversely, hyperpolarizing conditions using reduced extracellular sodium caused increased dye uptake. These results support a voltage-dependent mechanism for the uptake of cyanine dyes in hippocampal slices. Application of this phenomenon as an alternative to 2-deoxyglucose autoradiography for mapping neuronal activity will be presented.

Animals↗
PubMed1983

Kindled seizure-induced reduction of muscarinic cholinergic receptors in rat hippocampal formation: evidence for localization to dentate granule cells.

The binding of [3H] quinuclidinyl benzilate ( [3H] QNB) to muscarinic cholinergic receptors in dentate gyrus of rat hippocampal formation was analyzed by membrane binding assay and in vitro autoradiography. The destruction of dentate granule cells, either by neonatal irradiation or colchicine injection, resulted in nearly complete elimination of [3H] QNB binding sites in the molecular and granule cell layers. By contrast, neither perforant path transection nor destruction of the septal-hippocampal cholinergic afferents caused a decline of [3H] QNB binding sites. Amygdala kindled seizures resulted in a 30% reduction of [3H] QNB binding sites which was distributed uniformly across the entire molecular and granule cell layers. Thus, most, if not all, of the muscarinic cholinergic receptors present in dentate gyrus appear to reside on the somata and dendritic trees of the dentate granule cells. We propose that this kindled seizure-induced decline of muscarinic receptors represents an endogenous compensatory mechanism designed to stabilize granule cell excitability.

Afferent Pathways↗
PubMed1983

Benzodiazepine receptor declines in hippocampal formation following limbic seizures.

Electrolytic lesions of entorhinal cortex have previously been shown to consistently produce limbic seizures. We report a bilateral and symmetrical decline in benzodiazepine receptor number in dentate gyrus of the hippocampal formation in unilateral entorhinal cortex-lesioned animals. We think this decline is caused by seizures since phenobarbital pretreatment prevented the appearance of limbic seizures and blocked the receptor decline. We postulate that these receptor declines may contribute to decreased endogenous recurrent inhibition (a presumed GABAergic synapse) of dentate granule cells which could lead to their repetitive firing. Thus these benzodiazepine receptor declines may be a consequence of limbic seizures yet increase the likelihood of subsequent seizures.

Afferent Pathways↗
PubMed1982

Seizures down-regulate muscarinic cholinergic receptors in hippocampal formation.

Muscarinic cholinergic receptors (MCR) have been previously shown to decline in the hippocampal formation (HPF) of amygdala-kindled rats. Seizures have been proposed as the process responsible for this down-regulation. We now demonstrate similar down-regulation of MCR within HPF in 3 additional methods of inducing seizures: electroconvulsive shock, entorhinal kindling and entorhinal lesion. Two key parameters which causally link the MCR declines with seizures are their time course and reversal with anticonvulsants. The transient decline of MCR induced by entorhinal lesion-induced seizures parallels the time course established in amygdala kindling. Further, phenobarbital could block both these seizures and the MCR declines. Together, this supports the relationship of seizures causing the declines. We postulate that the MCR down-regulation represents an endogenous inhibitory response of neurons that are intensely and repeatedly depolarized during the seizures.

Amygdala↗
PubMed1982

Electrolytic entorhinal lesions cause seizures.

The entorhinal cortex is a key site of interneuronal communication between a variety of cortical and subcortical areas and hippocampal formation. Lesioning the entorhinal cortex is commonly used in studies of the hippocampal formation, animal behavior and neuronal plasticity. We have found that electrolytic destruction of the entorhinal cortex consistently produces limbic seizure activity in rats. The propensity of lesions in this area for producing seizure activity may facilitate insights into the normal function of this network of neural connections. This unexpected phenomenon represents a potential confounding variable for all researchers using this method for making brain lesions.

Animals↗
PubMed1982

Intradentate colchicine retards the development of amygdala kindling.

The mechanisms underlying the kindling model of epilepsy are unknown. Presumably, an altered network of neural circuits underlie amygdala kindling. Biochemical and radiohistochemical studies have pointed to the dentate granule cells (DGC) of the hippocampal formation as a member of this altered circuit. To test the role of these cells, colchicine, a neurotoxin of DGC, was directly injected into the dentate gyrus. Prior destruction of DGC retarded the development of amygdala kindling. Destruction of DGC after kindling was completed did not reverse the kindling effect. We conclude that DGC play a key role in the development, but not the permanence, of amygdala kindling. We propose a model whereby the greater the input to the hippocampal formation, the faster limbic kindling will proceed.

Amygdala↗