The effect of sleep on spike-wave discharges in absence seizures

Neurology ◽  
1973 ◽  
Vol 23 (12) ◽  
pp. 1335-1335 ◽  
Author(s):  
S. Sato ◽  
F. E. Dreifuss ◽  
J. K. Penry
2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Hudong Zhang ◽  
Xiaolong Tan ◽  
Yufeng Pan ◽  
Yuan Chai

Recent clinical practice has found that the spike-wave discharge (SWD) scopes of absence seizures change from small cortical region to large thalamocortical networks, which has also been proved by theoretical simulation. The best biophysics explanation is that there are interactions between coupled cortico-thalamic and thalamocortical circuits. To agree with experiment results and describe the phenomena better, we constructed a coupled thalamocortical model with bidirectional channel (CTMBC) to account for the causes of absence seizures which are connected by the principle of two-way communication of neural pathways. By adjusting the coupling strength of bidirectional pathways, the spike-wave discharges are reproduced. Regulatory mechanism for absence seizures is further applied to CTMBC via four different targeted therapy schemes, such as deep brain stimulation (DBS), charge-balanced biphasic pulse (CBBP), coordinated reset stimulation (CRS) 1 : 0, and (CRS) 3 : 2. The new CTMBC model shows that neurodiversity in bidirectional interactive channel could supply theory reference for the bidirectional communication mode of thalamocortical networks and the hypothesis validation of pathogenesis.


Neurosurgery ◽  
2020 ◽  
Vol 87 (5) ◽  
pp. E578-E583 ◽  
Author(s):  
Vasileios Kokkinos ◽  
Alexandra Urban ◽  
Nathaniel D Sisterson ◽  
Ningfei Li ◽  
Danielle Corson ◽  
...  

Abstract BACKGROUND AND IMPORTANCE At least 25% of patients with idiopathic generalized epilepsy do not obtain adequate seizure control with medication. This report describes the first use of responsive neurostimulation (RNS), bilaterally targeting the centromedian/ventrolateral (CM/VL) region in a patient with drug-refractory Jeavons syndrome (eyelid myoclonia with absences). CLINICAL PRESENTATION A patient, diagnosed with eyelid myoclonia with absences (EMA) and refractory to medication, was offered RNS treatment in the CM/VL region of the thalamus. Stimulation was triggered by thalamic neural activity having morphological, spectral, and synchronous features that corresponded to 3- to 5-Hz spike-wave discharges recorded on prior scalp electroencephalography. CONCLUSION RNS decreased daily absence seizures from a mean of 60 to ≤10 and maintained the patient's level of consciousness during the occurring episodes. This therapy should be evaluated further for its potential to treat patients with pharmaco-refractory generalized epilepsy.


1987 ◽  
Vol 41 (3) ◽  
pp. 448-449
Author(s):  
Hideo Nagao ◽  
Takehiko Morimoto ◽  
Mitsugi Takahashi ◽  
Shinji Habara ◽  
Hironao Nagai ◽  
...  

2019 ◽  
Vol 96 ◽  
pp. 200-209 ◽  
Author(s):  
Magdalena K. Smyk ◽  
Ilya V. Sysoev ◽  
Marina V. Sysoeva ◽  
Gilles van Luijtelaar ◽  
Wilhelmus H. Drinkenburg

2021 ◽  
Author(s):  
Cian McCafferty ◽  
Benjamin Gruenbaum ◽  
Renee Tung ◽  
Jing-Jing Li ◽  
Peter Salvino ◽  
...  

AbstractAbsence seizures are characterized by a brief behavioural impairment including apparent loss of consciousness. Neuronal mechanisms determining the behavioural impairment of absence seizures remain unknown, and their elucidation might highlight therapeutic options for reducing seizure severity. However, recent studies have questioned the similarity of animal spike-wave-discharges (SWD) to human absence seizures both behaviourally and neuronally. Here, we report that Genetic Absence Epilepsy Rats from Strasbourg recapitulate the decreased neuroimaging signals and loss of consciousness characteristic of human absence seizures. Overall neuronal firing is decreased but rhythmic in the somatosensory cortex and thalamus during these seizures. Interestingly, individual neurons in both regions tend to consistently express one of four distinct patterns of seizure-associated activity. These patterns differ in firing rate dynamics and in rhythmicity during seizure. One group of neurons showed a transient initial peak in firing at SWD onset, accounting for the brief initial increase in overall neuronal firing seen in cortex and thalamus. The largest group of neurons in both cortex and thalamus showed sustained decreases in firing during SWD. Other neurons showed either sustained increases or no change in firing. These findings suggest that certain classes of cortical and thalamic neurons may be particularly responsible for the paroxysmal oscillations and consequent loss of consciousness in absence epilepsy.


2013 ◽  
Vol 109 (10) ◽  
pp. 2505-2516 ◽  
Author(s):  
Fu-Zen Shaw ◽  
Yi-Fang Liao ◽  
Ruei-Feng Chen ◽  
Yu-Hsing Huang ◽  
Rick C. S. Lin

The contribution of the zona incerta (ZI) of the thalamus on spike-wave discharges (SWDs) was investigated. Chronic recordings of bilateral cortices, bilateral vibrissa muscle, and unilateral ZI were performed in Long-Evans rats to examine the functional role of SWDs. Rhythmic ZI activity appeared at the beginning of SWD and was accompanied by higher-oscillation frequencies and larger spike magnitudes. Bilateral lidocaine injections into the mystacial pads led to a decreased oscillation frequency of SWDs, but the phenomenon of ZI-related spike magnitude enhancement was preserved. Moreover, 800-Hz ZI microstimulation terminates most of the SWDs and whisker twitching (WT; >80%). In contrast, 200-Hz ZI microstimulation selectively stops WTs but not SWDs. Stimulation of the thalamic ventroposteriomedial nucleus showed no obvious effect on terminating SWDs. A unilateral ZI lesion resulted in a significant reduction of 7- to 12-Hz power of both the ipsilateral cortical and contralateral vibrissae muscle activities during SWDs. Intraincertal microinfusion of muscimol showed a significant inhibition on SWDs. Our present data suggest that the ZI actively modulates the SWD magnitude and WT behavior.


2011 ◽  
Vol 12 (3) ◽  
pp. 302-305
Author(s):  
Brendan P. Lucey ◽  
Cristina Toedebusch ◽  
Stephen P. Duntley

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