The Nature of Bilateral and Synchronous Cerebral Spiking

Ogden, Thomas E.; Aird, Robert B.; Garoutte, Bill

doi:10.1111/j.1600-0447.1956.tb09693.x

Cited by 25 publications

(6 citation statements)

References 14 publications

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“…According to this view, the result of epileptiform activity of the centrencephalic system, whether primary or secondary, is the same\p=m-\i.e.,bilaterally synchronous waveand-spike complexes appearing simultane-ously in both cerebral hemispheres. The EEG pattern in these cases of secondary bilateral synchrony is often not precisely symmetrical or not exactly at a frequency of 3 per second, but similar irregularities are often seen in patients with classical petit mal (Ogden, Aird, and Garoutte, 1956). Some aspect of the patient's attack pat¬ tern often suggests that his seizure problem is a focal one, despite the bilaterally syn¬ chronous EEG abnormality, but the not infrequent focal ictal manifestations seen in patients with classical petit mal often makes this clinical differentiation between these 2 types of seizure problems difficult (Howell, 1955).…”

Section: Introductionmentioning

confidence: 79%

“…The results of carotid amobarbital injec¬ tion in the patients with idiopathic or primary centrencephalic epilepsy are of par¬ ticular interest in furnishing support for the concept that true petit mal epilepsy is due to an epileptic discharge in a hypothetical subcortical integrating mechanism, the cen¬ trencephalic system, as postulated by Penfield and Jasper (1946) and Penfield (1950). The failure of carotid amobarbital injection of either hemisphere to inhibit the spikeand-wave bursts of idiopathic or centren¬ cephalic epilepsy could be explained on the basis of one of several assumptions: (1) the centrencephalic wave-and-spike bursts represent a diffuse abnormality of both cerebral hemispheres that is more resistant to the effect of amobarbital than is a focal cortical epileptic lesion; (2) the primary discharges responsible for evoking these synchronized bursts in the 2 cerebral hemi¬ spheres arise in a region that lies mainly outside the carotid area of supply; (3) the primary discharging area, although mainly in the carotid area of supply, is less affected than the cortex by the same concentration of the drug in the carotid blood stream; (4) the primary discharging area involves both sides of the brain stem, rostrally and caudally, but the area inactivated by a unilateral carotid amytal injection is too small a por¬ tion of the total system to interfere with the epileptic process.…”

Section: Commentmentioning

confidence: 87%

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Intracarotid Amobarbital in Epileptic Patients

Rovit¹

1961

Arch Neurol

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Section: Introductionmentioning

confidence: 79%

Section: Commentmentioning

confidence: 87%

Intracarotid Amobarbital in Epileptic Patients

Rovit¹

1961

Arch Neurol

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“…The mechanisms for BSDs have not been well known [22][23][24] . Forebrain commissures [25][26][27] and subcortical structures [28][29][30] have been reported as possible origins for BSDs.…”

Section: Discussionmentioning

confidence: 99%

Magnetoencephalographic analysis of bilaterally synchronous discharges in benign rolandic epilepsy of childhood

Lin

Chang

Hsieh

et al. 2003

Seizure

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The purpose of this study was to examine the spatial and temporal relationship between bilateral foci of bilaterally synchronous discharges in benign rolandic epilepsy of childhood (BREC) using a whole-scalp neuromagnetometer. We simultaneously recorded interictal magnetoencephalographic (MEG) and electroencephalographic (EEG) signals in six children with BREC. Interictal spikes were classified into three groups: bilaterally synchronous discharges (BSDs), unilateral discharges on right side (UD-R), and unilateral discharges on left side (UD-L). We used equivalent current dipole (ECD) modelling to analyse the cortical sources of interictal spikes. Both BSDs and UDs were found in Patients 1-4, whereas only UDs were identified in Patients 5 and 6. The ECDs of interictal spikes were located in rolandic regions, 10-20mm anterior and lateral to hand somatosensory cortices. Multi-dipole analysis of BSDs showed two ECDs in homotopic motor areas of the hemispheres. During BSDs, the right-sided activation preceded the left-sided activation by 15-21 milliseconds in Patients 1 and 2. In Patients 3 and 4, the activation occurred 17-20 milliseconds earlier in the left than the right hemisphere. Within the same hemisphere, the sources of BSDs and UDs were located in similar areas. In conclusion, our results imply the cortical epileptogenicity in bilateral perirolandic areas in BREC. The sequential activation during BSDs in both hemispheres suggest the existence of synaptic connections, possibly via the corpus callosum, between bilateral irritative foci.

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“…That this "pacemaker" mechanism can be activated by the discharge of an epileptogenic focus has been documented in several cases (4, 21,22). Inter-hemispheric activation originating in an epileptogenic focus on one side and spreading to the opposite homologous areas may be detected at once by the technic described, since a close comparison of homologous areas is maintained throughout the study.…”

Section: Materials a N D Methodsmentioning

confidence: 97%

Propagation of Epileptic Discharge, as Revealed by Activated Electroencephalography

Aird

Garoutte

1959

Epilepsia

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SUMMARY 1. A detailed examination of 1300 consecutive EEGs revealed 151 (11%) in which gross foci were observed that were associated with exacerbations of activity sufficient to permit a study of the modes of propagation of focal discharge when recorded by means of homologous runs obtained simultaneously and when activated by hyper‐ventilation and other methods. 2. In addition to local cortical spread, two types of propagation of activated focal discharge were observed. 3. Gross generalized exacerbations were found in 51 % of the focal records, while focal exacerbation of the contralateral homologous region was definite in 47%. Both types were observed in the records of some patients. 4. The characteristics of the generalized and bilaterally synchronous exacerbations were such that they could only be explained in terms of a subcortical “pacemaker”. The characteristics of the more focal, contralateral homologous spread seemed to justify attributing it to commissural transmission. 5. Generalized activation occurred predominantly in the convulsive group, and activation of this type that was sufficient to obscure the primary focus occurred only in the convulsive cases. 6. Focal activation of contralateral homologous regions occurred predominantly in the nonconvulsive group. 7. The significance of these findings, in terms of the propagation of epileptic discharge and of EEG differential diagnosis was discussed. RÉSUMÉ 1. L'examen détaillé de 1300 EEG consécutifs révèle que dans 151 (11%) des cas on a observé de grands foyers associés à des exacerbations d'activité suffisantes pour permettre une étude des modes de propagation de la décharge focale enregistrée à l'aide de dérivations homologues obtenues simultanément et activée par hyperventilation ou autres méthodes. 2. Deux types de propagation d'une décharge focale activée ont été observés conjointement avec une extension corticale locale. 3. De fortes exacerbations généralisées ont été constatées en 51% des enregistrements focaux, tandis qu'une exacerbation focale de la région contralatérale homologue a été observée en 47% des cas. Les deux types ont été observés dans les enregistrements de quelques malades. 4. Les caractéristiques des exacerbations synchrones généralisées et bilatérales étaient telles qu'on ne peut les expliquer que par l'emploi du terme “pacemaker” subcortical. Il semble juste d'attribuer les caractéristiques d'une extension focale contralatérale et homologue à une transmission commissurale. 5. L'activation généralisée se produit principalement dans le groupe convulsif; l'activation de ce type suffisante pour masquer le foyer primaire ne se produit que dans des cas convulsifs. 6. Une activité focale de régions homologues contralatérales se présente surtout dans le groupe non‐convulsif. 7. Discussion de la signification de ces découvertes quant à la propagation d'une décharge épileptique et quant au diagnostic différentiel de l'EEG.

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The Nature of Bilateral and Synchronous Cerebral Spiking

Cited by 25 publications

References 14 publications

Intracarotid Amobarbital in Epileptic Patients

Intracarotid Amobarbital in Epileptic Patients

Magnetoencephalographic analysis of bilaterally synchronous discharges in benign rolandic epilepsy of childhood

Propagation of Epileptic Discharge, as Revealed by Activated Electroencephalography

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