Hippocampal high frequency oscillations in unilateral and bilateral mesial temporal lobe epilepsy

Řehulka, Pavel; Cimbálník, Jan; Pail, Martin; Chrastina, Jan; Hermanová, Markéta; Brázdil, Milan

doi:10.1016/j.clinph.2019.03.026

Cited by 9 publications

(11 citation statements)

References 44 publications

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“…It seems that fast ripples are more specific or pathological. Our MEG results are consistent with invasive recordings ( Zijlmans et al , 2012 ; Brázdil et al , 2017 ; Řehulka et al , 2019 ). Since HFBS are very weak, invasive recordings provide necessary and convincing data about the relationship between epilepsy and HFBS ( Engel and Lopes da Silva, 2012 ; Jacobs et al , 2012 ).…”

Section: Discussionsupporting

confidence: 90%

“…There is solid evidence that high-frequency brain signals (HFBSs > 80 Hz) play a key role in epilepsy ( Bragin et al , 2011 ; Engel and Lopes da Silva, 2012 ; Worrell et al , 2012 ). HFBS can be divided into high gamma oscillations (80–150 Hz), ripples (80–250 Hz), fast ripples (250–600 Hz) and very high-frequency oscillations (HFOs > 600 Hz) ( Zijlmans et al , 2012 ; Brázdil et al , 2017 ; Řehulka et al , 2019 ). Though the frequency ranges vary slightly among reports, the majority of studies of HFBS in epilepsy focus on oscillatory HFBS in 80–250 Hz (ripples) and 250–600 Hz (fast ripples), which are conventionally referred as HFOs ( Rampp, 2015 ; Lee et al , 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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Kurtosis and skewness of high-frequency brain signals are altered in paediatric epilepsy

Xiang

Maue

Fan

et al. 2020

Brain Communications

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Intracranial studies provide solid evidence that high-frequency brain signals are a new biomarker for epilepsy. Unfortunately, epileptic (pathological) high-frequency signals can be intermingled with physiological high-frequency signals making these signals difficult to differentiate. Recent success in non-invasive detection of high-frequency brain signals opens a new avenue for distinguishing pathological from physiological high-frequency signals. The objective of the present study is to characterize pathological and physiological high-frequency signals at source levels by using kurtosis and skewness analyses. Twenty-three children with medically intractable epilepsy and age-/gender-matched healthy controls were studied using magnetoencephalography. Magnetoencephalographic data in three frequency bands, which included 2–80 Hz (the conventional low-frequency signals), 80–250 Hz (ripples) and 250–600 Hz (fast ripples), were analysed. The kurtosis and skewness of virtual electrode signals in eight brain regions, which included left/right frontal, temporal, parietal and occipital cortices, were calculated and analysed. Differences between epilepsy and controls were quantitatively compared for each cerebral lobe in each frequency band in terms of kurtosis and skewness measurements. Virtual electrode signals from clinical epileptogenic zones and brain areas outside of the epileptogenic zones were also compared with kurtosis and skewness analyses. Compared to controls, patients with epilepsy showed significant elevation in kurtosis and skewness of virtual electrode signals. The spatial and frequency patterns of the kurtosis and skewness of virtual electrode signals among the eight cerebral lobes in three frequency bands were also significantly different from that of the controls (2–80 Hz, P < 0.001; 80–250 Hz, P < 0.00001; 250–600 Hz, P < 0.0001). Compared to signals from non-epileptogenic zones, virtual electrode signals from epileptogenic zones showed significantly altered kurtosis and skewness (P < 0.001). Compared to normative data from the control group, aberrant virtual electrode signals were, for each patient, more pronounced in the epileptogenic lobes than in other lobes(kurtosis analysis of virtual electrode signals in 250–600 Hz; odds ratio = 27.9; P < 0.0001). The kurtosis values of virtual electrode signals in 80–250 and 250–600 Hz showed the highest sensitivity (88.23%) and specificity (89.09%) for revealing epileptogenic lobe, respectively. The combination of virtual electrode and kurtosis/skewness measurements provides a new quantitative approach to distinguishing pathological from physiological high-frequency signals for paediatric epilepsy. Non-invasive identification of pathological high-frequency signals may provide novel important information to guide clinical invasive recordings and direct surgical treatment of epilepsy.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Kurtosis and skewness of high-frequency brain signals are altered in paediatric epilepsy

Xiang

Maue

Fan

et al. 2020

Brain Communications

View full text Add to dashboard Cite

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“…Fast ripples arose at a higher rate in the HS-vs. non-HS patients. This is in line with previous studies that found higher rates of fast ripples in patients with hippocampal sclerosis (15,23,24). Even though the mechanisms underlying the generation of HFOs are still unclear (6), it is suggested that this is due to excitotoxicity occurring in HS (25).…”

Section: Discussionsupporting

confidence: 91%

Are HFOs in the Intra-operative ECoG Related to Hippocampal Sclerosis, Volume and IQ?

et al. 2021

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Temporal lobe epilepsy (TLE) is the most common form of refractory focal epilepsy and is often associated with hippocampal sclerosis (HS) and cognitive disturbances. Over the last decade, high frequency oscillations (HFOs) in the intraoperative electrocorticography (ioECoG) have been proposed to be biomarkers for the delineation of epileptic tissue but hippocampal ripples have also been associated with memory consolidation. Healthy hippocampi can show prolonged ripple activity in stereo- EEG. We aimed to identify how the HFO rates [ripples (80–250 Hz, fast ripples (250–500 Hz); prolonged ripples (80–250 Hz, 200–500 ms)] in the pre-resection ioECoG over subtemporal area (hippocampus) and lateral temporal neocortex relate to presence of hippocampal sclerosis, the hippocampal volume quantified on MRI and the severity of cognitive impairment in TLE patients. Volumetric measurement of hippocampal subregions was performed in 47 patients with TLE, who underwent ioECoG. Ripples, prolonged ripples, and fast ripples were visually marked and rates of HFOs were calculated. The intellectual quotient (IQ) before resection was determined. There was a trend toward higher rates of ripples and fast ripples in subtemporal electrodes vs. the lateral neocortex (ripples: 2.1 vs. 1.3/min; fast ripples: 0.9 vs. 0.2/min). Patients with HS showed higher rates of subtemporal fast ripples than other patients (Z = −2.51, p = 0.012). Prolonged ripples were only found in the lateral temporal neocortex. The normalized ratio (smallest/largest) of hippocampal volume was correlated to pre-resection IQ (r = 0.45, p = 0.015). There was no correlation between HFO rates and hippocampal volumes or HFO rates and IQ. To conclude, intra-operative fast ripples were a marker for HS, but ripples and fast ripples were not linearly correlated with either the amount of hippocampal atrophy, nor for pre-surgical IQ.

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“…The automated detection of HFO was performed by an algorithm used in our previous studies (30,31). A statistical window of 10 s was used to compute z-scored amplitude envelopes using Hilbert transforms in a series of logarithmically spaced frequency bands (300 bands between 60 and 800 Hz).…”

Section: Hfo Detectionmentioning

confidence: 99%

Cognitive Processing Impacts High Frequency Intracranial EEG Activity of Human Hippocampus in Patients With Pharmacoresistant Focal Epilepsy

et al. 2020

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Hippocampal high frequency oscillations in unilateral and bilateral mesial temporal lobe epilepsy

Cited by 9 publications

References 44 publications

Kurtosis and skewness of high-frequency brain signals are altered in paediatric epilepsy

Kurtosis and skewness of high-frequency brain signals are altered in paediatric epilepsy

Are HFOs in the Intra-operative ECoG Related to Hippocampal Sclerosis, Volume and IQ?

Cognitive Processing Impacts High Frequency Intracranial EEG Activity of Human Hippocampus in Patients With Pharmacoresistant Focal Epilepsy

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