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A A Ward

Publications and source records attributed to A A Ward.

At least 19 recordsLinked to original sources
PubMed1986

Multidisciplinary prediction of seizure relief from cortical resection surgery.

Preoperative variables from a full range of medical specialties were used to predict degree of seizure relief from cortical resection surgery as treatment for epilepsy in 100 patients. General, seizure history, electroencephalographic (EEG), radiological, surgical, and psychological/neuropsychological data were considered. The patients were divided into one large predictive group (n = 75) and a smaller independent cross-validation sample (n = 25). Eight predictive variables emerged: single EEG focus; anterior-midtemporal lobe discharges; discharges only from the side of surgery; rate of occurrence of discharges in surgical area; Wechsler Adult Intelligence Scale Digit Symbol subtest; Marching Test, preferred hand, time; Minnesota Multiphasic Personality Inventory (MMPI) Hysteria scale score; and MMPI Paranoia scale score. By use of multivariate procedures, increased predictability of surgical outcome was obtained not only with the predictive group but with the independent cross-validation sample. The results demonstrate that predictions of seizure relief from epilepsy surgery can be made with 80% accuracy using multiple, rather than single, predictors.

Adolescent↗
PubMed1986

New wave of research in the epilepsies.

The epilepsies affect at least 1 to 2 million people in the United States and 20 to 40 million people worldwide. Because the causes and basic mechanisms of the epilepsies have only started to unravel, there is still no cure for the disease. The purpose of this chapter is to present the new routes of navigation in epilepsy research, the salient theories on mechanisms of epilepsies, and their cogency to cause (generation of seizures) and effects (epileptic cell damage). In particular, it advances a comprehensible picture of the major cellular events involved in the generation, arrest, or spread of partial epileptic seizures; it also questions the major molecular events involved in the transmission and use of genetic information in the generalized epilepsies. In reviewing the many theories on mechanisms of epilepsies, this chapter establishes the connections between neurosciences, molecular genetics, and the epilepsies. The knowledge gained from such connections will certainly bear on the diagnosis of the subvarieties of epilepsies and is already promoting new methods of treatment of the disease. Indeed, it is this fusion between molecular genetics, neurosciences, and the clinical epilepsies that provides the excitement and new ferment in research of the epilepsies. This chapter also advances a conceptual blueprint for priority challenges in epilepsy research. It calls attention to the primary goal, namely, understanding the mechanisms of human epilepsies. In the most common of human epilepsies, namely, temporal lobe epilepsy, a priority challenge is to analyze paroxysmal depolarization shifts in hippocampal slices in vitro, slices excised from known sites of epileptogenicity. Parallel experiments exploring biochemical membrane abnormalities in neuronal and glial membranes isolated from the hippocampal seizure focus would be especially valuable. The role of kindling and the mirror focus in human temporal lobe epilepsy must be resolved. A second important goal is the search for polymorphisms of restriction endonuclease patterns in monogenic epilepsies in order to localize the abnormal gene to a specific chromosome. Because of the recent successful applications of positron emission tomography (PET), single-photon-emission computed tomography, and nuclear magnetic resonance computed tomography (NMR-CT), ion transport pathways, neurotransmitter systems, and metabolic processes may be constructed within the functioning brains of epileptic patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Neuronal firing patterns from epileptogenic foci of monkey and human.

The chronic, recurrent seizures induced in the monkey by cortical scarring occur spontaneously for years and share much of the phenomenology of spontaneous seizures of focal cortical onset in the human. Chronic extracellular recording in the focus of the chronic epileptic monkey reveals: A spectrum of abnormalities of unit firing ranging from grossly abnormal firing patterns to normal activity. Group I (highly epileptic) neurons fire exclusively in bursts, which are invariant during different behavioral states and during operant conditioning. Although firing within the bursts is not easily modified, the interburst interval can be modified indicating that these apparently denervated cells still have some synaptic input. All group I cells are pyramidal neurons. Group II (weakly epileptic) neurons exhibit variable burst firing, which may be intermixed with normal unit firing. The firing patterns of these cells can be modified by synaptic inputs. During operant conditioning, burst firing can decrease; during drowsiness or when inattentive, burst firing can approach that characteristic of group I cells. There is a direct relationship between the number of group I epileptic (pacemaker) neurons in the focus and the epileptogenicity of that focus as measured by frequency of spontaneous seizures in that monkey. The distribution of neurons encountered in the focus varies. On average, approximately 10% are group I (pacemaker) neurons; group II constitute 40%; and 50% of cells encountered exhibit normal firing patterns. In addition to firing in unstructured bursts, an unusual burst structure termed the long-first-interval (LFI) burst has been described that appears to be unique to the chronic focus. It is so named because the first interspike interval is longer than the remaining interspike intervals in the burst. The long first interval is extraordinarily invariant. There is little relationship between unit firing in bursts and the interictal EEG. During early parts of a spontaneous seizure, the two events become time-locked. During seizures, unit firing is synchronous with surrounding neurons and the spike portion of the EEG (as in penicillin foci). Firing of group I neurons does not change significantly preceding a spontaneous seizure. Thus, group I neurons appear to act as pacemakers to the focus and group II cells provide the critical mass that, when synchronized to the burst firing of the pacemakers, is capable of initiating the ictal event.

Animals↗
PubMed1985

Missing pieces in the epilepsy puzzle.

Research regarding the basic mechanisms of the epilepsies has been limited and has generated few clues that have led to dramatic improvements in the surgical therapy of epilepsy. It is now known that the epileptic focus is characterized by a population of pacemaker neurons that fire autonomously in bursts. When this high frequency discharge recruits bursting activity in neighboring neurons, a propagating seizure occurs. Such data as well as other recent data in neurobiology indicate that new forms of surgical therapy may be forthcoming including brain transplantation as well as local application of transmitter compounds which may significantly improve the therapy of epilepsy.

Animals↗
PubMed1984

Subdural strip electrodes for localizing epileptogenic foci.

Surgical removal of epileptogenic brain is indicated for treatment of many medically refractory focal seizure disorders. One of the important factors in providing good results from surgery is the accuracy of identifying the epileptogenic focus. However, accurate localization may be difficult when only standard scalp recordings are used. Many epilepsy centers have used intracranial recording techniques to better define regions of cortical epileptogenicity . Although subdural strip electrodes were first utilized many years ago, the more popular method of intracranial recording has been by intracortical depth electrodes. The authors present their method of placing subdural strip electrodes for extensive recordings from the cortex. To date, this method has been used to provide continuous monitoring of the electrocorticogram in 28 patients for periods up to 3 weeks, with only two minor complications. This procedure is relatively safe and a valuable alternative to placing intracortical depth electrodes.

Cerebral Cortex↗
PubMed1982

Neurons in human epileptic cortex: correlation between unit and EEG activity.

A total of 90 neurons were recorded extracellularly from 17 awake patients undergoing craniotomy for excision of epileptogenic cortex. Relationships between single-unit activity and gross epileptiform spikes recorded locally by the microelectrode or from the immediate overlying cortical surface by electrocorticography (ECoG) were examined. Similar relationships were also sought between interictal bursts from nearby cells when action potentials from several neurons had been recorded simultaneously by the tungsten electrodes. Although 40 single units fired action potentials in some relation to ECoG spikes, the relationships were variable between units and, often, for the same unit. For many units, action potentials were more consistently related to one phase of the local field potential recorded through tungsten microelectrodes than to the ECoG recorded from the overlying cortical surface. Synchronous firing between single units recorded simultaneously by the same microelectrode was rarely seen except at the onset of an ictal event. In addition, a high degree of synchrony between unit firing and local ECoG spikes was recorded in a few patients, but these patients had frequent focal spontaneous seizures. The data imply that in human epilepsy, unlike some animal models of the disorder, relationships between surface epileptiform events and single-unit burst firing are not easily found in interictal recordings. The data also suggest that synchrony between unit and surface events requires a high degree of synchrony among neurons within the epileptogenic focus.

Electroencephalography↗
PubMed1981

Intracellular records from chronic alumina epileptogenic foci in the monkey.

Neuronal records from the primate alumina focus revealed synaptic potentials with bursts of action potentials occurring on depolarizing potentials. These depolarizing potentials were not synchronous with electrocorticographic epileptic patterns. The configuration of the membrane potential changes was consistent with a dendritic generator for epileptic bursts. It is proposed that the genesis of these depolarizing potentials is postsynaptic.

Action Potentials↗
PubMed1981

Neurons in human epileptic cortex. Response to direct cortical stimulation.

During craniotomy for surgical treatment of medically intractable epilepsy, single neurons were recorded from the lateral temporal cortex of 11 awake patients. A total of 83 neurons were recorded, and their response to repetitive direct cortical stimulation with ascending and descending frequency ramps between 1 to 10 Hz was evaluated. More normal units from the suspected epileptogenic cortex responded to repetitive stimulation at frequencies between 5 to 20 Hz with augmented action potential bursts than did units from cortex thought not to be primarily epileptogenic. This burst response might persist for up to 30 seconds after the frequency ramp had descended from 10 to 1 Hz. Except in two cases, this augmentation of burst response was not accompanied by afterdischarge on electroencephalography. These data would indicate that neurons within the region of suspected epileptogenic cortex demonstrate a greater propensity for afterdischarge to repetitive stimuli than do neurons in more normal cortex.

Action Potentials↗
PubMed1979

Factors influencing future progress in neurosurgery.

The ever-widening horizons in the neurosciences are noted by the author. Maintenance of the bridges between research and clinical practice will result in improved therapy. Research interest is expanding, and involvement by neurosurgeons and neurosurgical training programs is vital for future progress. Techniques are required to evaluate and assess new surgical procedures that evolve from research endeavors.

Animals↗
PubMed1978

Chronic epileptic foci in monkeys: correlation between seizure frequency and proportion of pacemaker epileptic neurons.

A total of 1,802 neurons from 15 alert, undrugged Macaca mulatta monkeys were studied. Thirteen monkeys had chronic epilepsy induced by subpial alumina injections in precentral cortex. Precentral neurons were judged epileptic by the magnitude and variability of the percentage of interspike intervals less than 5 msec during periods when the monkeys were awake. This method of quantifying epileptic single neuron activity appears highly reliable in distinguishing epileptic neurons from precentral neurons in either normal cortex, cortex contralateral to, or within the focus. For the 13 epileptic monkeys, the relative proportion of strongly epileptic neurons found within foci was logarithmically correlated with the mean number of daily seizures. Because of the similarity between the physiology of the alumina focus in monkeys and epileptic foci in humans, these data imply that the severity of focal human epilepsy is a function of epileptic neuronal mass.

Action Potentials↗