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J A Wada

Publications and source records attributed to J A Wada.

At least 37 records · Page 2Linked to original sources
PubMed1977

Lateralisation of speech dominance by spectral analysis of evoked potentials.

A computerised evoked potential test for the lateralisation of speech dominance was compared with the intracarotid sodium amylobarbitone test in 22 epileptic patients. Based on spectral analysis, the computer test correctly predicted the speech dominance of 15 of 16 left speech dominant and five of six right speech dominant patients. This non-invasive test is simple, quick, and innocuous and can be easily implemented on a small laboratory computer.

Adolescent↗
PubMed1977

Transfer and interference in amygdaloid kindling in cats.

Examination of the effects of primary site kindling upon the development of secondary site amygdaloid kindling in cats showed that the former exerts powerful positive as well as negative after effects upon the latter. The positive after effect appears to be directed towards establishing a linkage between the secondary site and the Stage 6 generalized convulsive mechanism. The negative after effects were strikingly similar to those observed in animals with forebrain bisection subjected to amygdaloid kindling, suggesting that it is primarily directed towards functional accessibility of the cerebral structures interconnected by the forebrain commissure. The similarity of the findings in animals with anterior neocortical lesions supports such an assumption. The transient nature of the negative after effects was indicated by the development of a 'normal' clinical ictal pattern from the secondary site when it occurred spontaneously. Secondary site kindling exerted similar but less prominent negative after effects when the primary site was re-tested. Stage 6 seizure was elicited upon the first trial, however.

Amygdala↗
PubMed1977

Dorsal frontal, orbital and mesial frontal cortical lesion and amygdaloid kindling in cats.

Bilateral anteromesial or orbital cortical lesions do not affect sequential pattern of amygdaloid seizure development. However, orbital cortex lesions appear to significantly participate in the elaboration of a Stage 6 seizure pattern. Amygdaloid kindling ipsilateral to the side of anterodorsal cortical lesion or in animals with the same bilateral lesion appears to predispose them for the development of spontaneous, nonconvulsive (partial complex) seizures. It also significantly modifies clinical ictal patterns with practical ommission of Stages 2, 3 and 5, and largely lateralizes AD propagation to the stimulated hemisphere. The latter two features are strikingly reminiscent of the electroclinical manifestations of secondary site AM kindling in intact animals or AM kindling in animals with forebrain commissure bisection. Nonconvulsive (partial complex) status epilepticus was readily arrested by placement of electrolytic lesions ipsilateral to the AM stimulation, suggesting that MRF is essential for the perpetuation of the recurrent spontaneous seizure. Finally, the presence and absence of positive and negative aftereffects respectively, in animals with anterodorsal cortical lesion is consistent with the view that transfer and interference effects are mediated through the brain stem and forebrain commissures respectively.

Amygdala↗
PubMed1976

Prophylactic effects of phenytoin, phenobarbital, and carbamazepine examined in kindling cat preparations.

Prophylactic effects of phenobarbital, phenytoin (diphenylhydantoin), and carbamazepine were examined in amygdaloid kindling preparations in cats. Daily electrical stimulation was delivered at the time of peak plasma levels. Comparative examination of the chronological pattern of the clinical seizure development, after discharge growth, and formation of distant independent spike foci was made between periods of kindling with chronic drug administration and of rekindling without drugs. Both phenobarbital and carbamazepine were effective, but phenytoin was totally ineffective. Prophylactic action of phenobarbital and carbamazepine was mainly through the suppression of the development of motor seizures manifestations in the former and the same with the development of sustained after discharge in the latter. The kindling preparation appears to possess many desirable features as an ideal model of human epilepsy for the purpose of assessment and recruitment of potential antiepileptic drugs and development of a rational pharmacotherapeutic approach for the management and prevention of seizure disorder.

Animals↗
PubMed1976

Acute anticonvulsant effects of diphenylhydantoin, phenobarbital, and carbamazepine: a combined electroclinical and serum level study in amygdaloid kindled cats and baboons.

This preliminary study utilizing the kindling model of established epilepsy has provided information about the most effective routes of administration for diphenylhydantoin, phenobarbital, and carbamazepine in baboons and cats. The time of peak plasma levels for these drugs has been demonstrated in these animals so that experimental protocols can be designed to deliver the agents at appropriate times prior to the kindling stimulation. In addition, dose-effectiveness data is presented for these species. In 1 baboon, phenobarbital was also seen to suppress photosensitive seizures. The potential usefulness of the kindling model in anticonvulsant research is suggested.

Amygdala↗
PubMed1976

Spontaneous recurrent seizure state induced by daily electric amygdaloid stimulation in Senegalese baboons (Papio papio).

Daily electrical stimulation of the amygdala in Senegalese baboons (Papio papio) resulted in the development of generalized convulsive seizures focal onset through five distinct clinical stages in an average of 72 days. The chronologic pattern of electroclinical features suggested that vertical intrahemispheric ictal dissemination was of primary importance in the progressive seizure development. Some animals developed spontaneous recurrence of both partial complex and primary generalized seizures. The kindling preparation in P. papio represents a unique model of human epilepsy with its secondary generalized convulsive seizure development, spontaneously recurrent partial and primary generalized seizures in the background of predisposed epileptogenic susceptibility.

Amygdala↗
PubMed1975

Cerebral hemispheric asymmetry in humans. Cortical speech zones in 100 adults and 100 infant brains.

Morphological asymmetry of the frontal operculum and temporal planum becomes measurable at the 29th week of gestation. There is evidence of subsequent differential development of the planum in favor of the left, with the left planum larger than the right. While both the frontal operculum and left planum were always present, the right planum ranged in size from absent (10%)to larger than the left (about 10%). Females predominated (P less than .05) in the latter group. The findings suggest that (1) a higher percentage of persons may have right-sided cerebral representation for speech than has been assumed previously; (2) a predetermined morphological asymmetry contributes to establishing the ultimate pattern of cerebral speech representation following an early insult to a predisposed hemisphere; and (3) it is necessary to scrutinize clinical material for the differential organization of hemispheric development between sexes.

Adolescent↗
PubMed1975

Amino acids in human epileptogenic foci.

Free amino compounds were measured in 16 rapidly frozen epileptogenic foci excised from temporal or frontal cortex of nine patients with focal epilepsy, and in single cortical biopsy specimens obtained from 16 nonepileptic patients. Unlike the findings of a previous study, glutamic and aspartic acids were not diminished in the foci, nor was there a decrease in gamma-aminobutyric acid (GABA) or taurine levels. Glycine content was markedly elevated in two of 16 epileptogenic foci. These results do not suggest that deficiencies of GABA or of taurine, amino acids that may act physiologically as inhibitory neurotransmitters or modulators of inhibition, are causes of focal epilepsy, nor do they provide a logical basis for clinical trials of taurine in treatment of human epilepsy.

Adolescent↗
PubMed1975

Recurrent spontaneous seizure state induced by prefrontal kindling in senegalese baboons, Papio papio.

In our earlier study of amygdaloid kindling in Papio papio (Pp), the development of partial complex seizure and of focal motor seizure was correlated with bifrontal theta discharge and increasing Rolandic spike discharge respectively and the final stage was characterized by primary generalized convulsive seizure. Since the latter seizure pattern is known to originate from the frontal focus in man, the frontal cortex became suspect in the development of the final stage seizure pattern. Daily prefrontal stimulation showed that Pp can be kindled from this site, culminating in a recurrent spontaneous seizure state identical to that induced by amygdaloid kindling in this species. However, our observation did not support our original assumption regarding the genesis of primary generalized convulsive seizure. Prefrontal and amygdaloid kindling are significantly different with respect to morphology, distribution and propagation of after discharge and interictal spike discharge, and speed and pattern of clinical seizure development. Most intriguingly, inter-ictal behavioral aberration associated with depth EEG changes was observed only in the prefrontal animals and not in the amygdaloid animals.

Action Potentials↗
PubMed1975

Frontal cortical kindling in cats.

Our observaiton of amygdoloid seizure development in cats indicated early afterdischarge propagation into basal cortical areas prior to the development of bifrontal sharp theta discharge. In view of the implied participation of the frontal lobe in amygdaloid kindling, both fractional lesioning and kindling of selective areas were performed. This paper summarizes out stimulation study involving premotor, prefrontal, mesial frontal and orbital cortices. Except for the orbital series which showed a rather strikingly similar pattern of seizure development to that of amygdaloid kindling, all areas showed significantly different features in terms of the speed of seizure development, afterdischarge propagation, fragility of developing seizure, final stage 5 seizure and post-ictal behavior pattern, interictal discharge morphology and propagation, and generalized seizure triggering threshold intensity. All these findings suggest that the frontal lobe participates in, but is not essential for, the amygdaloid seizure development. The results of ongoing fractional lesion series support such a conclusion.

Action Potentials↗
PubMed1975

Frontal lobe and kindling in the rat.

To test the hypothesis that the cortex participates in amygdaloid kindling in rats, bilateral aspiration lesions were made in various cortical areas in rats prior to kindling. Lesions in orbital cortex (on the dorsal lip of the rhinal sulcus) or prefrontal cortex (area 10) significantly retarded the rate of amygdaloid kindling; lesions in motor cortex, anterior cingulate cortex, or visual cortex were without effect. Detailed analysis indicated that the orbital lesioned and frontal-lesioned rats kindled relatively normally up to the second-last stage of amygdaloid kindling, in which stage they perseverated significantly longer than the controls and the other lesioned rats. These results suggest that areas of the frontal lobe participate in the elaboration and generalization of amygdaloid seizures in rats. Although retarded in rate, kindling nonetheless occurred in the lesioned rats, indicating that these cortical areas are not essential for the development of amygdaloid seizures.

Action Potentials↗
PubMed1975

Cortical electrographic correlates of convulsive seizure development induced by daily electrical stimulation of the amygdala in rats and cats.

Increasing complexity of neocortical AD morphology was associated with clinical seizure development of amygdaloid origin in both rats and cats. Chronological examination of cortical AD and IID patterns in cats suggests very early involvement of basal cortical areas. Delayed but progressive ictal participation of anterior neocortical areas with eventual development of IID was coincident with eventual development of IID was coincident with recruitment of ictal motor manifestations while neocortical asymmetry with contralateral "desynchronization" pattern persisted throughout seizure development. It is suggested that anterior neocortex participates in the clinical expression of seizure development while verticle ictal propagation into the brain stem is responsible for seizure generalization.

Amygdala↗
PubMed1975

Effects of unilateral lesion in the midbrain reticular formation on kindled amygdaloid convulsion in cats.

Daily stimulation of the amygdala in cats resulted in progressive development of electroclinical seizures culminating in a generalized convulsion (kindling). An electrolytic lesion in the midbrain reticular formation, ipsilateral to the stimulated amygdala, markedly elevated the generalized seizure-triggering threshold and reduced susceptibility to pentylentetrazol challenge. In contrast, globus pallidus lesions had no appreciable effect upon the generalized seizure-triggering threshold and appeared to enhance susceptibility to pentylentetrazol. The results support the hypotheses that (1) the midbrain reticular formation participates significantly in the kindled amygdaloid seizures and (2) the effects of lesions in the midbrain reticular formation do not depend upon the presence of forebrain bisection.

Amygdala↗
PubMed1975

Effects of taurine on kindled amygdaloid seizures in rats, cats, and photosensitive baboons.

Acute administration of taurine produced a transient loss of susceptibility to photically induced seizures in photosensitive baboons, but failed to affect kindled amygdaloid convulsions in baboons, rats, and cats. In addition, it was totally ineffective in changing the course of spontaneous status epilepticus in kindled cats. These results suggest that a taurine-deficiency model of epilepsy applies only to certain types of seizure-generating conditions, apparently excluding kindled amygdaloid convulsions.

Amygdala↗
PubMed1975

The generalized convulsive seizure state induced by daily electrical stimulation of the amygdala in split brain cats.

Daily unilateral electrical stimulation of amygdala in forebrain bisected cats provoked the development of the final stage of the kindled convulsion with remarkable rapidity regardless of presence or absence of anterior commissure. The chronological and spatial pattern of propagation of afterdischarge, interictal spike discharge, and clinical manifestations strongly suggest the significant role played by the midbrain reticular formation and possibly other brainstem structures in the progressive electroclinical seizure development. This assumption was supported by the results of a lesion study in which placement of a destructive lesion in the ipsilateral midbrain reticular formation markedly increased the generalized seizure triggering threshold, lateralized the afterdischarge to the stimulated hemisphere when induced with increased intensity stimulation, fragmented clinical seizure manifestations, and failed to produce progression of clinical and electrographic events with prolonged daily stimulation. This is in contrast to the insignificant effect produced by a peduncular lesion. Our findings suggest that vertical (limbic-brainstem), but not horizontal (transhemispheric interlimbic) connection is critically involved in the amygdaloid seizure development while the forebrain commissures may play a role in the development of bisynchronous and bisymmetrical ictal and interictal electrographic and clinical manifestations. Finally, possible differential effect of forebrain bisection depending on developing in contrast with a established (cerebral) hemispheric epileptogenic process is postulated to explain the "facilitatory" effect observed in our series in contrast to the beneficial effects reported on some intractable seizure patients.

Amygdala↗
PubMed1975

Effects of tetrahydrocannabinols on kindled amygdaloid seizures and photogenic seizures in Senegalese baboons, Papio papio.

Intraperitoneal injections of delta 8-tetrahydrocannabinol (THC) and delta 9-THC failed to affect myoclonic response to photic stimulation in Senegalese baboons (Papio papio). However, both isomers of THC exerted dose-related antiepileptic effects upon established kindled convulsions provoked by electrical stimulation of amygdala in the same species. Delta 9-THC was more potent than delta 8-THC, in terms of both antiepileptic effects and general toxicity. The antiepileptic effects of the THC isomers appear to be due mainly to the suppression of propagation of the induced afterdischarge to distant cerebral structures, although high doses also seem to suppress afterdischarge at the site of stimulation.

Amygdala↗