A Study of Thalamic and Cortical Rhythms in Petit Mal

Williams, Denis

doi:10.1093/brain/76.1.50

Cited by 288 publications

(105 citation statements)

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“…This pattern is similar to the cortical recruiting due to stimulation of midline and intralaminary nuclei (26), in agreement with the currently accepted hypothesis of a thalamic origin for SWD (30). It thus seems that the slow wave originates and progresses in the thalamus as a recruiting response and ascends to the cortex, where it also recruits the spike (29). Probably, the thalamically originated delta wave triggers the cortical spike, which in turn is projected back to thalamic nuclei; a resonant loop might thus arise and be responsible for the epileptic fit, which fails to occur when the spike is not recruited (29).…”

Section: Discussionsupporting

confidence: 89%

“…The SWD we found in pilocarpine-treated rats evolved just as the human SWD in petit mal. Recent microelectrode studies have shown that the spikes of spike-wave complexes are associated with impulses leaving the cortex, thus supporting the hypothesis of the cortical origin of these potentials (29).…”

Section: Discussionmentioning

confidence: 61%

“…In humans, absence seizures are electroencephalographically characterized by spike-wave complexes oscillating at nearly 3 Hz in both hemispheres, mainly in the frontal lobe. Recordings of potentials from both cortex and thalamic nuclei of six children with frequent absence fits (29) showed that the spike-wave complexes start in thalamic nuclei as delta waves that are transmitted to the cortex with increasing voltage as a function of time. Williams (29) advanced the hypothesis that the spike originates in deep cortical layers and propagates to the thalamic nuclei, with the consequent occurrence of a wave-spike pattern.…”

Section: Discussionmentioning

confidence: 99%

“…It thus seems that the slow wave originates and progresses in the thalamus as a recruiting response and ascends to the cortex, where it also recruits the spike (29). Probably, the thalamically originated delta wave triggers the cortical spike, which in turn is projected back to thalamic nuclei; a resonant loop might thus arise and be responsible for the epileptic fit, which fails to occur when the spike is not recruited (29). The SWD we found in pilocarpine-treated rats evolved just as the human SWD in petit mal.…”

Section: Discussionmentioning

confidence: 99%

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Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life

Ferreira

Valle

Cavalheiro

et al. 2003

Braz J Med Biol Res

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Administration of pilocarpine causes epilepsy in rats if status epilepticus (SE) is induced at an early age. To determine in detail the electrophysiological patterns of the epileptogenic activity in these animals, 46 Wistar rats, 7-17 days old, were subjected to SE induced by pilocarpine and electro-oscillograms from the cortex, hippocampus, amygdala, thalamus and hypothalamus, as well as head, rostrum and vibrissa, eye, ear and forelimb movements, were recorded 120 days later. Six control animals of the same age range did not show any signs of epilepsy. In all the rats subjected to SE, iterative spike-wave complexes (8.1 ± 0.5 Hz in frequency, 18.9 ± 9.1 s in duration) were recorded from the frontal cortex during absence fits. However, similar spike-wave discharges were always found also in the hippocampus and, less frequently, in the amygdala and in thalamic nuclei. Repetitive or single spikes were also detected in these same central structures. Clonic movements and single jerks were recorded from all the rats, either concomitantly with or independently of the spike-wave complexes and spikes. We conclude that rats made epileptic with pilocarpine develop absence seizures also occurring during paradoxical sleep, showing the characteristic spike-wave bursts in neocortical areas and also in the hippocampus. This is in contrast to the wellaccepted statement that one of the main characteristics of absence-like fits in the rat is that spike-wave discharges are never recorded from the hippocampal fields. Correspondence

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life

Ferreira

Valle

Cavalheiro

et al. 2003

Braz J Med Biol Res

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“…Initially suggested by Jasper and Kershman (1941), the possible involvement of the thalamus in SW seizures was shown by recordings of thalamic nuclei in humans during absence attacks (Williams, 1953;Prevett et al, 1995). An important role for the thalamus also is supported by electrophysiological recordings in experimental models of SW seizures, which show that cortical and thalamic cells fire prolonged discharges in phase with the "spike" component, whereas the "wave" is characterized by a silence in all cell types (Pollen, 1964;Steriade, 1974;Avoli et al, 1983;McLachlan et al, 1984;Buzsáki et al, 1990;Inoue et al, 1993).…”

Section: Abstract: Computational Models; Thalamus; Cerebral Cortex; mentioning

confidence: 95%

Spike-and-Wave Oscillations Based on the Properties of GABA_BReceptors

1998

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Neocortical and thalamic neurons are involved in the genesis of generalized spike-and-wave (SW) epileptic seizures. The cellular mechanism of SW involves complex interactions between intrinsic neuronal firing properties and multiple types of synaptic receptors, but because of the complexity of these interactions the exact details of this mechanism are unclear. In this paper these types of interactions were investigated by using biophysical models of thalamic and cortical neurons. It is shown first that, because of the particular activation properties of GABA B receptor-mediated responses, simulated field potentials can display SW waveforms if cortical pyramidal cells and interneurons generate prolonged discharges in synchrony, without any other assumptions. Here the "spike" component coincided with the synchronous firing, whereas the "wave" component was generated mostly by slow GABA B -mediated K ϩ currents. Second, the model suggests that intact thalamic circuits can be forced into a ϳ3 Hz oscillatory mode by corticothalamic feedback. Here again, this property was attributable to the characteristics of GABA B -mediated inhibition. Third, in the thalamocortical system this property can lead to generalized ϳ3 Hz oscillations with SW field potentials. The oscillation consisted of a synchronous prolonged firing in all cell types, interleaved with a ϳ300 msec period of neuronal silence, similar to experimental observations during SW seizures. This model suggests that SW oscillations can arise from thalamocortical loops in which the corticothalamic feedback indirectly evokes GABA B -mediated inhibition in the thalamus. This mechanism is shown to be consistent with a number of different experimental models, and experiments are suggested to test its consistency.

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Experimental "Petit Mal" in Kittens

Guerrero-Figueroa¹,

Barros²,

Verster³

et al. 1963

Archives of Neurology

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in 1942. The technique does not readily lend itself, however, to the creation of focal deep lesions, since the fluid irritative agent backs up through the needle tract and often spreads through the ventricles or subarachnoid spaces. In our laboratories a method was introduced to produce epileptogenic foci in deep structures of the brain.2 Crystalline aluminum oxide was stereotaxically introduced into specific subcortical structures of the brain. A primary epileptogenic focus developed at the site of the alumina, and, subsequently, secondary discharge developed in the homotopic structure of the contralateral hemisphere. This report is concerned with the induction of petit mal-like patterns after the introduction of crystalline aluminum oxide into deep structures of the brains of kittens. Reports in the literature point to the importance of specific subcortical structures in the development of three per second spike and wave patterns.3"" This, however, is not a universal opinion. For example, Shimizu, Ref sum, and Gibbs 7 in 1952 contended that petit mal spike and wave discharges have a localized cortical origin and transmit over the entire cortex by means of corticocortical association pathways.In the study described here, introduction of aluminum oxide into the intralaminar nuclei of the thalamus and the mesencephalic reticular formation led to the development of spike and wave patterns in the electro¬ encephalographic recordings. The spike and wave patterns, typical of petit mal, did not develop, however, when aluminum oxide was introduced into several other deep structures or on the cortex. MethodThe experiments were carried out on 38 kittens between 21 and 30 days of age (200 to 300 gm body weight). Electrodes were introduced under pentobarbital (Nembutal) anesthesia by the tech¬ nique of Heath et al8 into deep structures, includ¬ ing the ventral mesencephalic reticular formation, the intralaminar nuclei of the thalamus, amygdala, hippocampus, septal region, and the following corti¬ cal areas : coronal gyrus, medial ectosylvian gyrus, posterior suprasylvian gyrus, and sigmoid gyrus. The epileptogenic foci were induced by a previously described technique employing aluminum oxide ( Fig 1 ). Recordings were obtained with a cathode ray oscilloscope and by an ink-writing electroen¬ cephalographic machine with eight or 16 channels. Hyperventilation of the animals was accomplished by manual manipulation of the thorax. Photostimu¬ lation of the animals was performed with a Grass Model PS-2 photostimulator at frequencies of 3, 6, 9, 12 and 18 cps. At the conclusion of the study the animals were sacrificed, and the brains were perfused and stained for location of the electrode tracts and site of the implanted aluminum oxide (Fig 2).Sites of alumina implantation were the reticular formation, intralaminar thalamic nuclei, hippo¬ campus, and over selected cortical areas. Alumina was introduced into only one site in each animal. Results Recordings in Animals WithFoci in the Thalamus and Reticular Formation.-The electroenc...

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A Study of Thalamic and Cortical Rhythms in Petit Mal

Cited by 288 publications

References 0 publications

Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life

Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life

Spike-and-Wave Oscillations Based on the Properties of GABA_BReceptors

Experimental "Petit Mal" in Kittens

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A Study of Thalamic and Cortical Rhythms in Petit Mal

Cited by 288 publications

References 0 publications

Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life

Absence-like seizures in adult rats following pilocarpine-induced status epilepticus early in life

Spike-and-Wave Oscillations Based on the Properties of GABABReceptors

Experimental "Petit Mal" in Kittens

Contact Info

Product

Resources

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Spike-and-Wave Oscillations Based on the Properties of GABA_BReceptors