PubMed Health⌕ Search

Biomedical subjects

A V Escueta

Publications and source records attributed to A V Escueta.

17 recordsLinked to original sources
PubMed1982

Complex partial seizures on closed-circuit television and EEG: a study of 691 attacks in 79 patients.

Automatisms of 691 complex partial seizures in 79 patients were studied on closed-circuit television (CCTV) and by electroencephalography. Simple stereotyped perseverative automatisms such as chewing, swallowing, and fumbling with clothes or sheets followed an initial motionless stare and lapse of consciousness in type I attacks. Ambulatory automatisms, bilateral arm and leg perseverative movements, and tonic adversive head or eye movements (or both) characterized type II attacks, in which a motionless stare was not observed. Type III started with a drop attack followed by confusion, amnesia, and gradual recomposure. Some type II and III attacks are suspected to begin in areas outside the temporal lobe, while type I attacks are thought to originate from the temporal lobe. Further studies using CCTV and depth electrode recordings are necessary to verify these suspicions.

Adult↗
PubMed1977

Lapse of consciousness and automatisms in temporal lobe epilepsy: a videotape analysis.

Videotape analysis of 76 attacks in 14 epileptics showed two electro-clinical types of psychomotor attacks. The first and most common type had three clinical phases, consisting of an initial motionless stare, stereotyped movements, and reactive automatisms during impaired consciousness. The second and less common type started with stereotyped and reactive automatisms. In the first type, focal temporal or lateralizing features were common. In the second type, there were only diffuse changes in the electroencephalogram. The value of recording attacks with nasopharyngeal electrodes was emphasized by a high yield for focal-lateralizing electroencephalographic features.

Adult↗
PubMed1975

The freezing lesion. III. The effects of diphenylhydantoin on potassium transport within nerve terminals from the primary foci.

Possible mechanisms by which dephenylhydantoin (DPH) controls seizures were examined. The effects of intraperitoneal DPH on seizure discharges within epileptogenic freeze lesions were correlated with DPH action on in vitro potassium uptake within synaptosomes isolated from the same freeze foci. When in vivo DPH suppressed seizure discharges, it stimulated in vitro potassium uptake within synaptosomes incubated in a high-Kplus (10 mM) media. With 2-5 mM Naplus and 10mM Kplus, DPH stimulation of synaptosome potassium uptake was reversed by ouabain. With 50 mM Naplus and 10 mM Kplus, DPH stimulation of potassium uptake was not reversed by ouabain. In low-Kplus (0.2-5 mM) media, DPH did not affect potassium uptake even when sodium concentrations were varied at 10-100 mM. In sham-operated controls and in non-epileptogenic lesions, the effects of DPH on synaptosome potassium uptake were identical to those previously reported in normal brains. These results strongly suggest that DPH controls the epileptogenic state by stimulating potassium uptake within synaptic terminals. DPH controls the epileptogenic state by stimulating potassium uptake within synaptic terminals. DPH enhances synaptic potassium uptake by stimulating the (Naplus-Kplus) pump and a second potassium uptake process which is insensitive to ouabain.

Animals↗
PubMed1975

Unconsciousness, automatisms, and myoclonic jerks with diffuse rhythmic 9-Hz discharges.

A 25-year-old man presented with seizures characterized by unconsciousness, automatic behavior, and myoclonic jerks lasting 0.5 to 8 sec. Videotape analysis of 300 simultaneously recorded electroencephalographic and clinical attacks revealed 8- to 9-Hz 150 to 200 muV sharp waves beginning in both medial temporal areas during eyelid flutters. When discharges spread diffusely on both sides and lasted 2 to 3 sec, 20 degrees forward flexion of the head, unconsciousness, pupil dilation, and staring became evident. Asymmetrical myoclonic jerks invariably appeared. When paroxysms were greater than 3 sec, automatisms and tonic posturing occurred. The electroencephalographic and clinical seizures appeared during the awake and relaxed states, i.e., with normal alpha rhythm. They were suppressed during physical and mental activities and during sleep, i.e., in the absence of alpha rhythm. Our studies suggest that these seizures associated with diffuse electroencephalographic alpha-like activities are subcortical in origin and should be tested in their responsivity to alpha suppressants and inducers.

Adult↗
PubMed1971

Diphenylhydantoin and potassium transport in isolated nerve terminals.

THE ANTIEPILEPTIC ACTION OF DIPHENYLHYDANTOIN (DPH) HAS BEEN EXPLAINED BY TWO DIFFERENT THEORIES: (a) that DPH stimulates the Na-K pump; (b) that DPH specifically blocks the passive translocation of sodium. Since electrophysiological experiments have recently suggested abnormal synaptic mechanisms as the basis for epileptogenic discharges, the action of DPH on K transport within synaptic terminals isolated from "normal" rat brain cortex was examined directly. A rapid filtration technique was used to assess in vitro potassium transport within synaptosomes. In vivo DPH did not significantly change endogenous K content within synaptosomes. With sodium (50 mM) and potassium (10 mM) concentrations optimal for Na-K pump activity, in vivo and in vitro DPH (10(-4) M) had minimal or no effects on total K uptake. DPH stimulated potassium uptake within synaptosomes under two situations: (a) at high sodium (50-100 mM) and low potassium (less than 2 mM) concentrations; (b) when synaptosomes were incubated with ouabain (10(-4) M) 50 mM Na and 10 mM K. In both situations, K was leaking out of synaptic terminals and the enhancement in net K uptake roughly corresponded to the ouabain inhibitable segment. In the absence of ouabain, the stimulatory effects of DPH were not observed when K was 2 mM or higher and when Na was 10 mM or lower. The stimulatory effects of in vitro DPH appeared over a range of concentrations from 10(-4) to 10(-10) M while single intraperitoneal injections of DPH had to be administered for 2 days before its effects were observed on synaptosomal K transport. The present data provided direct evidence for DPH stimulation of active potassium transport within synaptosomes under ionic conditions simulating the depolarized state. At other ionic conditions, DPH had inhibitory or no effects on K uptake. Although the results do not specify whether the effects of DPH on the Na-K pump are direct or indirect, they suggest that the action of DPH depends upon the state of the membrane and the specific ionic environment.

Adenosine Triphosphatases↗