scholarly journals P.029 Limbic system involvement in absence seizures

2017 ◽  
Vol 44 (S2) ◽  
pp. S21-S21
Author(s):  
R Ajaz ◽  
SM Mirsattari ◽  
R Mousavi ◽  
S Leung
Keyword(s):  
Limbic System ◽  
Neural Activity ◽  
High Frequency ◽  
Phase Modulation ◽  
Absence Epilepsy ◽  
Field Potentials ◽  
High Frequency Oscillations ◽  
Ventrolateral Thalamus ◽  
Long Evans ◽  
The Right

Background: Absence epilepsy (AE) is believed to be generated by a thalamocortical network. Our laboratory showed that hippocampal neuronal firings were synchronous with the SWDs in the gamma butyrolactone (GBL) model of AE in rats. Here, we hypothesize that high frequency oscillations (HFOs) in the hippocampus and other parts of the limbic system were phase modulated by SWDs Methods: GBL (200 mg/kg i.p) was injected to induce SWDs in 6 male Long-Evans rats. Spontaneous local field potentials (LFPs) were recorded from electrodes implanted in the hippocampus and ventrolateral thalamus bilaterally and the right frontal cortex. For each LFP, modulation index (MI) gives the cross-frequency amplitude modulation of the HFOs (;90-250 Hz) by the phase of the SWD frequency at 2-8 Hz Results: Phase modulation of the HFOs by 2-8 Hz frequency increased for >45 min after GBL injection. MI increase was higher for hippocampal than thalamic LFPs, and not significant for frontal cortical LFP. MI for the nucleus accumbens LFP (N= 1 rat) also increased after GBL Conclusions: The modulation of HFOs (presumed local neural activity) by SWD frequency provides further support that the hippocampus and connected limbic system may become synchronous with the SWDs in AE

scholarly journals Ictal onset patterns of local field potentials, high frequency oscillations, and unit activity in human mesial temporal lobe epilepsy

Epilepsia ◽  
2015 ◽  
Vol 57 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Shennan Aibel Weiss ◽  
Catalina Alvarado-Rojas ◽  
Anatol Bragin ◽  
Eric Behnke ◽  
Tony Fields ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Local Field ◽  
Unit Activity ◽  
High Frequency ◽  
Local Field Potentials ◽  
Mesial Temporal Lobe Epilepsy ◽  
Field Potentials ◽  
High Frequency Oscillations ◽  
Mesial Temporal Lobe

scholarly journals Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks: Correlations with thalamocortical activity and clinical features

Cephalalgia ◽  
2015 ◽  
Vol 36 (6) ◽  
pp. 568-578 ◽  
Author(s):  
Gianluca Coppola ◽  
Martina Bracaglia ◽  
Davide Di Lenola ◽  
Elisa Iacovelli ◽  
Cherubino Di Lorenzo ◽  
...  
Keyword(s):  
Somatosensory Cortex ◽  
Clinical Features ◽  
Lateral Inhibition ◽  
High Frequency ◽  
Migraine Without Aura ◽  
High Frequency Oscillations ◽  
Cortical Excitation ◽  
Cycle Dependent ◽  
The Right ◽  
Stimulation Of

Background We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features. Participants and methods Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20–P25 component by using the formula [(100)–MU/(M + U)*100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation. Results In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack ( r = −0.510, p = 0.01), monthly attack duration ( r = −0.469, p = 0.02) and severity ( r = −0.443, p = 0.03), but positively with thalamocortical activity ( r = −0.463, p = 0.02). Conclusions We hypothesize that abnormal migraine cycle-dependent dynamics of connectivity between subcortical and cortical excitation/inhibition networks may contribute to clinical features of MO and recurrence of attacks.

scholarly journals Neural signatures of loss of consciousness and its recovery by thalamic stimulation

2019 ◽  
Author(s):  
Jacob A. Donoghue ◽  
André M. Bastos ◽  
Jorge Yanar ◽  
Simon Kornblith ◽  
Meredith Mahnke ◽  
...  
Keyword(s):  
General Anesthesia ◽  
Local Field ◽  
Neural Activity ◽  
High Frequency ◽  
Loss Of Consciousness ◽  
Field Potentials ◽  
Thalamic Stimulation ◽  
Cortical Rhythms ◽  
Up States ◽  
Slow Frequency

AbstractWe know that general anesthesia produces unconsciousness but not quite how. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with propofol. Unconsciousness was marked by slow frequency (∼1 Hz) oscillations in local field potentials, entraining local spiking to Up states alternating with Down states of little spiking, and decreased higher frequency (>4 Hz) coherence. The thalamus contributed to cortical rhythms. Its stimulation “awakened” anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness thus resulted from slow frequency hypersynchrony and loss of high-frequency dynamics, partly mediated by the thalamus, that disrupts cortical communication/integration.

scholarly journals Intrinsic coupling modes reveal the functional architecture of cortico-tectal networks

2015 ◽  
Author(s):  
Iain Stitt ◽  
Edgar Galindo-Leon ◽  
Florian Pieper ◽  
Gerhard Engler ◽  
Eva Fiedler ◽  
...  
Keyword(s):  
Neural Activity ◽  
High Frequency ◽  
Large Scale ◽  
Sensory Stimulation ◽  
Correlation Structure ◽  
Spatial And Temporal Scales ◽  
Cortical Oscillations ◽  
High Frequency Oscillations ◽  
Rich Information ◽  
The Rich

In the absence of sensory stimulation or motor output, the brain exhibits complex spatiotemporal patterns of intrinsically generated neural activity. However, little is known about how such patterns of activity are correlated between cortical and subcortical brain areas. Here, we investigate the large-scale correlation structure of ongoing cortical and superior colliculus (SC) activity across multiple spatial and temporal scales. Cortico-tectal interaction was characterized by correlated fluctuations in the amplitude of delta, spindle, low gamma and high frequency oscillations (> 100 Hz). Of these identified coupling modes, topographical patterns of high frequency coupling were the most consistent with anatomical connectivity, and reflected synchronized spiking in cortico-tectal networks. Ongoing high frequency cortico-tectal coupling was temporally governed by the phase of slow cortical oscillations. Collectively, our findings show that cortico-tectal networks can be resolved through the correlation structure of ongoing neural activity, and demonstrate the rich information conveyed by high frequency electrocorticographic signals.

scholarly journals High-frequency oscillations in the internal globus pallidus: a pathophysiological biomarker in Parkinson's disease?

2020 ◽  
Author(s):  
Luke A Johnson ◽  
Joshua E Aman ◽  
Ying Yu ◽  
David Escobar Sanabria ◽  
Jing Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Globus Pallidus ◽  
High Frequency ◽  
Neural Oscillations ◽  
Field Potentials ◽  
Internal Globus Pallidus ◽  
High Frequency Oscillations ◽  
Deep Brain

AbstractAbnormal oscillatory neural activity in the basal ganglia is thought to play a pathophysiological role in Parkinson’s disease. Many patient studies have focused on beta frequency band (13-35 Hz) local field potential activity in the subthalamic nucleus, however increasing evidence points to alterations in neural oscillations in high frequency ranges (>100 Hz) having pathophysiological relevance. Prior studies have found that power in subthalamic high frequency oscillations (HFOs) is positively correlated with dopamine tone and increased during voluntary movements, implicating these brain rhythms in normal basal ganglia function. Contrary to this idea, in the current study we present a combination of clinical and preclinical data that support the hypothesis that HFOs in the internal globus pallidus (GPi) are a pathophysiological feature of Parkinson’s disease. Spontaneous and movement-related pallidal field potentials were recorded from deep brain stimulation (DBS) leads targeting the GPi in five externalized Parkinson’s disease patients, on and off dopaminergic medication. We identified a prominent oscillatory peak centered at 200-300 Hz in the off-medication rest recordings in all patients. High frequency power increased during movement, and the magnitude of modulation was negatively correlated with bradykinesia. Moreover, high frequency oscillations were significantly attenuated in the on-medication condition, suggesting they are a feature of the parkinsonian condition. To further confirm that GPi high frequency oscillations are characteristic of dopamine depletion, we also collected field potentials from DBS leads chronically implanted in three rhesus monkeys before and after the induction of parkinsonism with the neurotoxin 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP). High frequency oscillations and their modulation during movement were not prominent in the normal condition but emerged in the parkinsonian condition in the monkey model. These data provide the first evidence demonstrating that exaggerated, movement-modulated high frequency oscillations in the internal globus pallidus are a pathophysiological feature of Parkinson’s disease, and motivate additional investigations into the functional roles of high frequency neural oscillations across the basal ganglia-thalamocortical motor circuit and their relationship to motor control in normal and diseased states. These findings also provide rationale for further exploration of these signals for electrophysiological biomarker-based device programming and stimulation strategies in patients receiving deep brain stimulation therapy.

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