We analyzed the dose-dependent effects of Sevoflurane anesthesia on high-frequency oscillations (HFOs) and spike discharges at non-epileptic sites and evaluated their effectiveness in identifying the epileptogenic zone.
We studied 21 children with drug-resistant focal epilepsy who achieved seizure control after focal resective surgery. Open-source detectors quantified HFO and spike rates during extraoperative and intraoperative intracranial EEG recordings performed before resection. We determined under which anesthetic conditions HFO and spike rates differentiated the seizure onset zone (SOZ) within the resected area from non-epileptic sites.
We analyzed 925 artifact-free electrodes, including 867 at non-epileptic sites and 58 at SOZ sites. Higher Sevoflurane doses significantly increased HFO and spike rates at non-epileptic sites, exhibiting spatial variability among different detectors. These biomarkers were elevated in the SOZ more than in non-epileptic sites under 2–4 vol% Sevoflurane anesthesia, with Cohen’s d effect sizes above 3.0 and Mann-Whitney U-Test r effect sizes above 0.5.
We provided normative atlases of HFO and spike rates under different Sevoflurane anesthesia conditions. Sevoflurane elevates HFO and spike rates preferentially in the epileptogenic zone.
Assessing the relative severity of biomarker levels across sites may be relevant for localizing the epileptogenic zone under Sevoflurane anesthesia.
Transcranial focused ultrasound (TUS) can suppress human motor cortical excitability. However, it is unclear whether the TUS may interact with transcranial magnetic stimulation (TMS) when they co-delivered in multiple trials.
Nineteen subjects received three different TUS-TMS co-stimulation protocols to the motor cortex including concurrent stimulation (TUS-TMS-C), separated stimulation (TUS-TMS-S), and TMS only. In each condition, two runs of 30 stimulation trials were conducted with a five-minute rest between runs. Motor-evoked potentials (MEP) were recorded during stimulation and at 0, 10, 20, and 30 min after stimulation. The MEP amplitudes after intervention were normalized to the mean pre-intervention MEP amplitude and expressed as MEP ratios. An additional test with TUS alone was applied to all participants to assess whether TUS itself can elicit after-effects.
There were no significant after-effects of all three interventions on MEP ratios. However, 11 subjects who showed online inhibition (OI + ) during the TUS-TMS-C protocol, defined as having MEP ratio less than 1 during TUS-TMS-C, showed significant MEP suppression at 10, 20 and 30 min after TUS-TMS-C. In 8 subjects did not show online inhibition (OI-), defined as having MEP ratios greater than 1 during TUS-TMS-C, showed no significant inhibitory after-effects. OI + and OI- status did not change in a follow-up repeat TUS-TMS-C test. TUS alone did not generate inhibitory after-effects in either OI + or OI- participants.
Our results showed that co-delivery of TUS and TMS can elicit inhibitory after-effect in subjects who showed online inhibition, suggesting that TUS and TMS may interact with each other to produce plasticity effects.
TUS and TMS may interact with each other to modulate cortical excitability.
To investigate sensorimotor integration by quantifying short-latency afferent inhibition (SAI) in people with MS who experience manual dexterity problems compared to controls.
22 people with MS with self-reported manual dexterity problems and 10 sex and age-matched controls were assessed using various upper extremity clinical tests. SAI was assessed by a transcranial magnetic stimulation pulse over the primary motor cortex preceded by peripheral nerve stimulation to the median nerve at 6 interstimulus intervals 2 – 8 ms longer than individualized N20 latencies.
Although within normal limits, persons with MS exhibited significantly slower Nine Hole Peg Test performance and pinch strength in the dominant hand. They also exhibited greater sensory impairment (monofilament test) in the dominant hand. Persons with MS showed significantly greater disinhibition of SAI in the dominant hand compared to controls, which was significantly correlated with weaker pinch strength.
Reduced SAI in people with MS, particularly in the dominant hand, signifies disruptions in cortical cholinergic inhibitory activity and is associated with lower pinch strength.
Evaluating changes in SAI may offer insight into the disrupted cortical cholinergic inhibitory activity that contributes to sensorimotor disintegration, potentially advancing disease management in persons with MS.
Early identification of infants at risk of cerebral palsy (CP) enables interventions to optimize outcomes. Central sleep spindles reflect thalamocortical sensorimotor circuit function. We hypothesized that abnormal infant central spindle activity would predict later contralateral CP.
We trained and validated an automated detector to measure spindle rate, duration, and percentage from central electroencephalogram (EEG) channels in high-risk infants (n = 35) and age-matched controls (n = 42). Neonatal magnetic resonance imaging (MRI) findings, infant motor exam, and CP outcomes were obtained from chart review. Using univariable and multivariable logistic regression models, we examined whether spindle activity, MRI abnormalities, and/or motor exam predicted future contralateral CP.
The detector had excellent performance (F1 = 0.50). Spindle rate (p = 0.005, p = 0.0004), duration (p < 0.001, p < 0.001), and percentage (p < 0.001, p < 0.001) were decreased in hemispheres corresponding to future CP compared to those without. In this cohort, PLIC abnormality (p = 0.004) and any MRI abnormality (p = 0.004) also predicted subsequent CP. After controlling for MRI findings, spindle features remained significant predictors and improved model fit (p < 0.001, all tests). Using both spindle duration and MRI findings had highest accuracy to classify hemispheres corresponding to future CP (F1 = 0.98, AUC 0.999).
Decreased central spindle activity improves the prediction of future CP in high-risk infants beyond early MRI or clinical exam alone.
Decreased central spindle activity provides an early biomarker for CP.