Focal cortical high-frequency oscillations trigger epileptic spasms: Confirmation by digital video subdural EEG

Akiyama, Tomoyuki; Otsubo, Hiroshi; Ochi, Ayako; Ishiguro, Taichi; Kadokura, Gemmu; RamachandranNair, Rajesh; Weiss, Shelly K.; Rutka, James T.; Snead, O. Carter

doi:10.1016/j.clinph.2005.08.029

Cited by 105 publications

(65 citation statements)

References 17 publications

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“…They have commonly been divided in two subtypes based on frequency: ripples and fast ripples (FRs, 250-500 Hz) (Ylinen et al, 1995;Bragin et al, 1999a,b, Staba et al, 2002. Ripples and FRs have been implicated in ictogenesis (Akiyama et al, 2005;Ochi et al, 2007;Ramachandrannair et al, 2008) and epileptogenesis (Bragin et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Contact size does not affect high frequency oscillation detection in intracerebral EEG recordings in a rat epilepsy model

Châtillon

Zelmann

Bortel

et al. 2011

Clinical Neurophysiology

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Objective-High frequency oscillations (HFOs) have been implicated in ictogenesis and epileptogenesis. The effect of contact size (in the clinical range: 1-10 mm 2 ) on HFO detection has not been determined. This study assesses the feasibility of HFO detection in a rat epilepsy model using macrocontacts and clinical amplifiers, and the effect of contact size on HFO detection within the macrocontact range.Methods-Eight epileptic rats were implanted with intracerebral electrodes containing three adjacent contacts of different sizes (0.02, 0.05 and 0.09 mm 2 ). HFOs were manually marked on 5 min interictal EEG segments. HFO rates and durations were compared between the different contacts.Results-10,966 ripples and 1475 fast ripples were identified in the recordings from 30 contacts. There were no significant differences in spike or HFO rates between the different contact sizes, nor was there a significant difference in HFO duration.Conclusions-HFOs can be detected in a rat epilepsy model using macrocontacts. Within the studied range, size did not significantly influence HFO detection.Significance-Using comparative anatomy of rat and human limbic structures, these findings suggest that reducing the size of macrocontacts (compared to those commercially available) would not improve HFO detection rates.

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Section: Introductionmentioning

confidence: 99%

Contact size does not affect high frequency oscillation detection in intracerebral EEG recordings in a rat epilepsy model

Châtillon

Zelmann

Bortel

et al. 2011

Clinical Neurophysiology

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“…The second, termed the "fast ripple" band (170-355 Hz), has been reported to occur overtly at seizure foci in patients with TLE (13,(15)(16)(17)(18). A number of studies using subdural grid electrodes (17,18,(28)(29)(30), depth macro- (14,31,32), and microelectrodes (33) have also reported a high correlation between VFO/pHFOs and regions of seizure onset. As far as a mechanism is concerned, in vivo recordings again show correlation between field VFO transients and interneuron unit activity (34), but in vitro studies suggest a primary causal role for gap-junctionally coupled principal cell axons (35).…”

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confidence: 99%

A nonsynaptic mechanism underlying interictal discharges in human epileptic neocortex

Roopun

Simonotto

Pierce

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

102

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Very fast oscillations (VFOs, >80 Hz) are important for physiological brain processes and, in excess, with certain epilepsies. Putative mechanisms for VFO include interneuron spiking and network activity in coupled pyramidal cell axons. It is not known whether either, or both, of these apply in pathophysiological conditions. Spontaneously occurring interictal discharges occur in human tissue in vitro, resected from neocortical epileptic foci. VFO associated with these discharges was manifest in both field potential and, with phase delay, in excitatory synaptic inputs to fast spiking interneurons. Recruitment of somatic pyramidal cell and interneuron spiking was low, with no correlation between VFO power and synaptic inputs to principal cells. Reducing synaptic inhibition failed to affect VFO occurrence, but they were abolished by reduced gap junction conductance. These data suggest a lack of a causal role for interneurons, and favor a nonsynaptic pyramidal cell network origin for VFO in epileptic human neocortex.epilepsy | fast ripple oscillation | ripple oscillation A dvances in electroencephalogram (EEG) techniques have revealed a much larger temporal window of oscillatory activity exists than has been previously thought (1-4). Of particular interest are very fast oscillations (VFOs), lying outside the traditional EEG frequency bands (5). These oscillations, at frequencies over c.80 Hz, are readily observable in animal models of epilepsy in vivo (6, 7), in vitro (8, 9), and clinically (10-14). In the epileptic human brain, VFOs are seen in structures involved in the pathology of temporal lobe epilepsy (TLE) (10,(15)(16)(17)(18).Although VFOs are seen in epileptic tissue, similar, transient expression of VFOs is also seen in normal cortex, albeit at lower power. As part of "physiological sharp waves," brief ripples of VFOs at c.200 Hz are seen and are suggested to be involved in the time-compressed replay of previous spike sequences in principal cells (19). A number of putative mechanisms of generation exist: Initial observations in vivo showed that principal cell unit activity was low during sharp waves, but that certain fast spiking (FS) interneurons were capable of spiking at VFO frequencies immediately before and sometimes during the event (20, 21). In vitro observations showed a predominantly inhibitory somatic input to principal cells during sharp waves (22). These observations suggest a role for rapid discharges from inhibitory interneurons as causal for the sharp wave and possibly the accompanying VFO. However, other studies have shown that brief VFO discharges in nonepileptic tissue survive synaptic blockade in low calcium ioncontaining media (23), with principal cell spikelets, rather than full spikes manifest as units, being generated at VFO frequency. Computational modeling predicted that VFO was generated as an emergent property of gap-junctionally coupled axons forming a plexus driven by ectopic action potential generation (24). This form of network is the only one to date shown to support frequen...

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“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14] They have been divided into ripples (80 -250 Hz) and fast ripples (FRs; 250 -500 Hz). 13 Ripples have been considered more physiologic in nature because they have also been recorded in healthy animal brains, whereas FRs are more frequent in affected hippocampi.…”

Section: Introductionmentioning

confidence: 99%

High-frequency oscillations mirror disease activity in patients with epilepsy

Zijlmans

Jacobs²,

Zelmann³

et al. 2009

Neurology

220

175

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Objective-High-frequency oscillations (HFOs) can be recorded in epileptic patients with clinical intracranial EEG. HFOs have been associated with seizure genesis because they occur in the seizure focus and during seizure onset. HFOs are also found interictally, partly co-occurring with epileptic spikes. We studied how HFOs are influenced by antiepileptic medication and seizure occurrence, to improve understanding of the pathophysiology and clinical meaning of HFOs.Methods-Intracerebral depth EEG was partly sampled at 2,000 Hz in 42 patients with intractable focal epilepsy. Patients with five or more usable nights of recording were selected. A sample of slow-wave sleep from each night was analyzed, and HFOs (ripples: 80-250 Hz, fast ripples: 250-500 Hz) and spikes were identified on all artifact-free channels. The HFOs and spikes were compared before and after seizures with stable medication dose and during medication reduction with no intervening seizures.Results-Twelve patients with five to eight nights were included. After seizures, there was an increase in spikes, whereas HFO rates remained the same. Medication reduction was followed by an increase in HFO rates and mean duration.Conclusions-Contrary to spikes, high-frequency oscillations (HFOs) do not increase after seizures, but do so after medication reduction, similarly to seizures. This implies that spikes and HFOs have different pathophysiologic mechanisms and that HFOs are more tightly linked to seizures than spikes. HFOs seem to play an important role in seizure genesis and can be a useful clinical marker for disease activity.High-frequency oscillations (HFOs) in intracranial EEG have been associated with epileptogenesis and seizure genesis and have been studied in humans and rats. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] They have been divided into ripples (80 -250 Hz) and fast ripples (FRs; 250 -500 Hz). 13 Ripples have been considered more physiologic in nature because they have also been recorded in healthy animal brains, whereas FRs are more frequent in affected hippocampi. 3,6,[15][16][17][18][19][20] Address correspondence and reprint requests to Dr. Jean Gotman, Montreal Neurological Institute and Hospital, 3801 University St., Montreal, Quebec, Canada H3A 2B4, jean.gotman@mcgill.ca. Disclosure: J.G. was a major shareholder of Stellate. The other authors report no disclosures. AUTHOR CONTRIBUTIONS CIHR Author Manuscript CIHR Author Manuscript CIHR Author ManuscriptHowever, both ripples and FRs have been correlated with the seizure onset zone (SOZ). 7,11,21 HFOs were first recorded with microelectrodes but can also be recorded with clinically used macroelectrodes. 11,13,[21][22][23] HFOs have been associated with seizure genesis because their localization is related to the seizure focus and they occur at seizure onset 1,6,11,24 and with epileptogenesis, as HFOs occurred before spontaneous seizures in kainic acid-injected rats. 7 They may result from a γ-aminobuteric acid-mediated feedback imbalance or pathologic neuronal connecti...

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Focal cortical high-frequency oscillations trigger epileptic spasms: Confirmation by digital video subdural EEG

Cited by 105 publications

References 17 publications

Contact size does not affect high frequency oscillation detection in intracerebral EEG recordings in a rat epilepsy model

Contact size does not affect high frequency oscillation detection in intracerebral EEG recordings in a rat epilepsy model

A nonsynaptic mechanism underlying interictal discharges in human epileptic neocortex

High-frequency oscillations mirror disease activity in patients with epilepsy

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