Clinical EEG and Neuroscience

Sporadic Creutzfeldt-Jakob Disease (sCJD) is a rapidly progressive prion disease that can be challenging to distinguish from other dementias, especially in early stages or when classical EEG findings, such as periodic sharp wave complexes (PSWCs), are absent. This study aimed to assess the utility of quantitative EEG (QEEG) features—derived from Food and Drug Administration-approved software—in differentiating sCJD from non-sCJD dementias.

EEG data from 78 participants were retrospectively analyzed: 19 sCJD patients, 49 non-sCJD dementia patients, and 10 healthy controls. sCJD cases were sourced from three centers, while matched non-sCJD cases and controls were selected from a single-center EEG database. Sixty seconds of artifact-free EEG during wakefulness or drowsiness were selected per participant. QEEG parameters—amplitude-integrated EEG (aEEG) and rhythmicity spectrogram (RS)—were extracted using Persyst^® software. Intergroup comparisons were conducted using the Kruskal-Wallis test with Holm-Sidák correction. Group-level rhythmicity patterns were also evaluated visually.

sCJD patients had significantly higher aEEG and RS values than non-sCJD patients across both hemispheres (aEEG: left p = .001, right p = .010; RS: left p = .001, right p = .003). A distinct “tri-band rhythmicity” pattern involving delta, theta, and low beta frequencies was uniquely observed in sCJD patients, including those without PSWCs on conventional EEG.

QEEG using clinically available software can reveal disease-specific electrophysiological features in sCJD. Tri-band rhythmicity may serve as a non-invasive adjunctive marker for early or atypical sCJD diagnosis, warranting further validation in prospective studies.

Psychosocial stress—particularly bullying—has been recognized as a critical determinant of mental and neurophysiological health in children. Chronic stress exposure may disrupt cortical regulatory mechanisms detectable through quantitative electroencephalography (q-EEG).

This study examined the correlation between perceived psychological stress, involvement in bullying, and q-EEG spectral anomalies among Indonesian school-aged children, seeking to determine if bullying-related stress generates unique neurophysiological patterns or indicates a general dysregulation of stress responses.

A two-phase design was implemented. Phase I included 2781 8-13-year-olds who completed the PSS-10 and a validated bullying questionnaire. Using a Mitsar-EEG 201 equipment, Phase II selected 24 students with increased stress levels (PSS ≥ 27) for q-EEG examination. Electroencephalogram signals from 19 scalp sites were converted into z-scores using age-adjusted NeuroGuide database standards. Stress level and brain activity were correlated using Spearman's rho.

The majority of subjects (23 out of 25; 95.8%) had EEG activity above ±2 standard deviations, especially in the temporal and prefrontal areas. There was a negative correlation between stress and temporal alpha power (r = -0.43, p = 0.028) and a positive correlation between stress with enhanced prefrontal high-beta power (r = 0.47, p = 0.021). Neurophysiological alterations among bullied children closely paralleled those under non-bullying stressors such as academic overload or family conflict.

Elevated stress intensity, regardless of its psychosocial origin, was associated with convergent cortical dysregulation patterns. These results suggest that q-EEG may be a viable non-invasive method for early stress-related neurophysiological dysfunction diagnosis and that pediatric populations require integrated emotional regulation therapies.

Isolated paroxysmal eye deviation in children is often considered a benign nonepileptic phenomenon. When epileptic in origin, gaze deviation is usually accompanied by visual symptoms, autonomic features, impaired awareness, or additional motor manifestations.

We report a 6-year-old boy with frequent daily episodes of brief right upward eye deviation without impaired awareness, visual symptoms, head version, or other ictal features. Neurological and ophthalmological examinations, routine laboratory investigations, and brain magnetic resonance imaging were unremarkable. Video-electroencephalography demonstrated repetitive spike-wave discharges over the left occipital region, supporting an epileptic origin.

Carbamazepine treatment markedly reduced episode frequency, and the spells resolved completely after dose adjustment during follow-up. Next-generation sequencing analysis of calcium channelopathy-related genes revealed no pathogenic variants.

This case highlights that isolated paroxysmal right upward eye deviation, even in the absence of other ictal features, may represent a focal preserved consciousness seizure rather than a benign ocular phenomenon. Early electroencephalographic evaluation is essential in children with frequent or atypical paroxysmal eye movements to avoid misdiagnosis and delayed treatment.

There is a great need in distinguishing Dementia with Lewy Body (DLB) from Alzheimer's disease (AD) and elucidating its pathophysiology. Transcranial magnetic stimulation (TMS) evoked potentials (TEPs) offer a non-invasive measure of neurophysiological alterations associated with underlying disease pathology.

A total of 39 participants were included: 12 DLB, 10 AD, and 17 age-matched healthy controls (HC). TEPs were measured in the dorsolateral prefrontal cortex (DLPFC), primary motor cortex (M1), and primary visual cortex (V1).

Global mean field potential (GMFP) TEP (130-250 ms) showed a significant interaction of group and stimulation site (p = .0101, ηp² = 0.175) with a significant group effect (p = .0071, ηp² = 0.234), attributed to higher GMFP in DLB compared to AD and HC in response to V1 stimulation (p = .001, p = .001, respectively). TEP amplitude corresponding to P60 displayed a significant group*stimulation site interaction (p = .0037, ηp² = 0.202) arising from differences in DLPFC stimulation, between DLB compared to AD (p = .0013) and HC (p = .0032). DLPFC N45 presented a significant stimulation site effect not associated to a specific group in addition to DLPFC N45 amplitude being correlated to the UPDRS-III score (r = 0.9, p = .0002). A relative higher left over right DLPFC P30 amplitude was correlated with poorer MoCA scores in AD (r = −0.84, p = .002), as indicated by others before.

DLPFC may be a target for both diagnosis and assessment of severity of motor symptoms in DLB and cognitive impairment in AD. These results propose a promising method to non-invasively distinguish DLB from AD and monitor disease, based on DLPFC and V1 network characteristics.

Persistent depressed consciousness in severe coronavirus disease 2019 (COVID-19) is commonly attributed to hypoxemia, systemic inflammation, sedative exposure, or metabolic disturbance. Non-convulsive status epilepticus (NCSE), however, may be overlooked without electroencephalography (EEG). This diagnostic principle also applies to persistent unexplained encephalopathy more broadly, particularly when impaired consciousness remains disproportionate to systemic illness.

An 85-year-old woman with Parkinsonism, diabetes mellitus, and prior cerebrovascular disease developed severe COVID-19 pneumonia followed by persistent coma during intensive care. Brain computed tomography showed chronic atrophic change without acute structural lesions, and laboratory and cerebrospinal fluid findings did not identify a major alternative explanation for coma. On the day of EEG, arterial blood gas analysis showed adequate oxygenation without hypercapnia. EEG on hospital day 10 demonstrated abundant right-hemispheric rhythmic/periodic discharges at approximately 2 Hz and focal electrographic seizures arising from the right temporal region with spatiotemporal evolution, consistent with NCSE. Levetiracetam, lacosamide, and midazolam infusion were administered.

Midazolam infusion was followed by electrographic seizure resolution but did not produce immediate clinical awakening during sedation; spontaneous eye opening emerged approximately 4 days later. Follow-up EEG on hospital day 13 showed seizure resolution with residual diffuse slowing and a sporadic right-hemispheric spike.

This case highlights early EEG as a practical diagnostic and treatment-monitoring tool in severe COVID-19-associated encephalopathy when depressed consciousness is persistent or disproportionate to systemic illness. More generally, EEG should be considered in persistent unexplained coma or encephalopathy after stabilization of cardiopulmonary factors.

Posterior theta/alpha ratio (TAR) is among the best-validated qEEG biomarkers for dementia, yet remains largely unused in routine neurology practice — primarily because it is sensitive to the patient's arousal state, an uncontrolled variable in real-world clinical EEG. We evaluated whether aperiodic spectral correction can bridge this gap between research promise and clinical reality.

Routine EEGs from 73 participants (18 controls, 55 dementia patients) were analyzed across three arousal segments. Five correction strategies were evaluated for TAR, with the optimal method validated in an external dementia dataset (ds004504, n = 88) and a normative cohort (ds005385, n = 587, age 20-79).

Raw TAR was diagnostically significant at Alert (AUC=0.772) and HVT (AUC=0.812) segments but failed in the Drowsy segment (AUC=0.631, p = 0.110) — the state most representative of uncontrolled clinical EEG. FOOOF-based aperiodic correction restored significance (AUC=0.701, p = 0.014), improved intraclass correlation to 0.945, and generalised to the external dataset (AUC=0.830). In the normative cohort, FOOOF-corrected TAR was completely age-independent (r = 0.000), supporting a universal threshold of ≥0.45 (specificity 92.3%).

A single step of aperiodic correction transforms TAR from an arousal-sensitive research metric into a robust, age-independent clinical tool. Combined with cognitive assessment, FOOOF-corrected TAR offers practical, objective dementia screening within routine EEG practice.

This study evaluated whether quantitative electroencephalography (QEEG) guided neurofeedback (NF) improves intellectual functioning and attention in children with mild to severe intellectual disability (ID).

Sixty-five children (38 males, 27 females; mean age ≈11 years) with DSM-5 diagnoses of mild-to-severe ID (IQ 28-68) and histories of unsuccessful standard treatments were enrolled. Baseline assessments included 19-channel QEEG referenced to FDA-approved Nx-Link™, BrainDx™, and NeuroGuide™ databases, Wechsler Intelligence Scale for Children (WISC-R or WISC-IV),and the Test of Variables of Attention (TOVA). Participants underwent 80-120 QEEG-guided NF sessions. Training protocols targeted deviant z-scores, with hypercoherence addressed prior to amplitude abnormalities. IQ and attention were reassessed 6–12 months post-treatment. Outcomes were analyzed using paired t-tests, correlation analyses, and generalized linear models.

Mean full-scale IQ increased by approximately 10 points (≈53 to ≈63; +18.6%, p < 0.001). Significant gains were observed in both WISC-IV (+≈11 points) and WISC-R (+≈10 points), with improvements across verbal, perceptual, working memory, processing speed, and performance domains (all p < 0.001). Two thirds of participants' IQ increased by ≥6 points. TOVA scores improved but were not correlated with IQ changes. QEEG analyses showed normalization of resting-state networks, including increased alpha power in default mode network hubs and reduced coherence and phase lag; reductions in slow-wave coherence predicted IQ improvement.

QEEG-guided NF was associated with clinically meaningful improvements in intellectual functioning and attention in children with ID, exceeding gains expected from environmental enrichment. Findings support NF as a promising nonpharmacologic intervention warranting randomized controlled trials.

Subacute sclerosing panencephalitis (SSPE) is a rare progressive encephalitis due to persistent measles infection. While classically a childhood disorder, atypical, adult-onset, and subclinical variants are increasingly reported. Ocular findings may precede neurological involvement by years. We aimed to underline EEG's role in tracking disease evolution from isolated ocular signs to neurological progression.

A 31-year-old woman presented with isolated ocular complaints and bilateral optic atrophy. Cerebrospinal fluid revealed measles IgG and IgG index positivity, confirming SSPE. For four years, she remained neurologically asymptomatic. EEG initially showed bilateral central theta paroxysms, later progressing to generalized periodic discharges. Serial EEGs demonstrated progressively shortened inter-discharge intervals. Additional features emerged, including frontally predominant generalized rhythmic delta activity and hyperventilation-provoked discharges. Importantly, when EEG abnormalities first appeared, neuropsychometric testing detected deficits in attention and executive function, despite the absence of subjective complaints. With time, cognitive decline became clinically evident, and negative myoclonus appeared.

This case illustrates the importance of long-term surveillance in subclinical SSPE. EEG abnormalities preceded overt neurological decline, providing the earliest clues to disease progression. Careful interpretation of evolving EEG patterns may anticipate cognitive impairment and guide timely interventions. Our patient's trajectory underscores that even clinically silent SSPE carries a hidden risk of deterioration, and that vigilant EEG monitoring can act as a window into the disease course.

This study aimed to systematically assess ictal scalp electroencephalography (EEG) evolution by examining both ictal onset characteristics and late significant patterns (LSPs) in adults with focal epilepsy. We aimed to investigate their individual and collective descriptive roles in seizure lateralization and localization, as well as their correlation with seizure semiology, interictal EEG findings, and structural magnetic resonance imaging (MRI) within a multimodal presurgical assessment framework.

We retrospectively analyzed 67 adults with drug-resistant focal epilepsy who underwent extended video-EEG monitoring, during which 242 seizures were documented. The ictal EEG findings were categorized based on the morphology of the onset and subsequent rhythmic patterns. The yields of lateralization and localization were evaluated independently for ictal onset patterns, LSPs, and combined ictal interpretations. Cohen's κ statistics were used to look at multimodal concordance between ictal EEG, seizure semiology, interictal EEG, and MRI findings.

The most common types of ictal onset were non-rhythmic or unclassifiable activity (29.3%) and low-voltage fast activity (28.5%). Late significant patterns were detected in 36.8% of seizures, predominantly manifesting as rhythmic theta–alpha activity, followed by repetitive spikes or sharp waves. The integration of LSPs resulted in enhanced lateralization and localization yields, in contrast to the analysis of onset patterns in isolation. At the individual patient level, combined ictal interpretation lateralized seizures in 68.6% of cases and localized seizure-onset regions in 70.1% of cases. There was a high degree of agreement between ictal and interictal EEG (κ = 0.775, strict right-left), a high degree of agreement between ictal EEG and MRI (κ = 0.710), and moderate-to-high agreement between ictal EEG and seizure semiology (κ = 0.647).

A systematic evaluation of ictal EEG evolution, including the identification of LSPs, provides additional descriptive data that augments conventional ictal-onset analysis in focal epilepsy. The integration of ictal evolution findings with semiology, interictal EEG, and MRI validates a multimodal interpretative framework for presurgical evaluation. These results highlight the possible clinical importance of incorporating seizure evolution analysis into conventional scalp EEG interpretation, although further validation with surgical outcome data is required.

This study investigated whether P300, a component of event-related potentials (ERPs), and cognitive performance related to frontal lobe function can predict responsiveness to a brief cognitive behavioral intervention in individuals who consume alcohol on ≥3 days per week.

Participants were 35 habitual drinkers (drinking alcohol on ≥3 days per week). At baseline, they completed self-report questionnaires assessing alcohol consumption, neuropsychological tests reflecting frontal lobe function (eg, the Trail Making Test, Stroop Test, Digit Symbol Substitution Test, verbal fluency tests), and P300 assessment during a visual oddball task with alcohol-related images. All participants then received ∼30 min of structured counseling on drinking behavior, followed by a second brief intervention at 3 months. Alcohol intake was reported at both time points, and total daily alcohol consumption (in standard drinks) was calculated. Participants were categorized as successful reducers if their daily alcohol intake at three months was lower than at baseline (n = 27), and as unsuccessful if intake was unchanged or increased (n = 8). Baseline ERP and neuropsychological measures were compared between groups.

Participants who reduced their drinking had significantly lower P300 amplitudes at P3 and Fz at baseline compared with those who did not. No significant between-group differences were found in neuropsychological performance.

Lower P300 amplitudes may serve as a neurophysiological marker for predicting responsiveness to brief psychosocial interventions for alcohol reduction in individuals with high-risk drinking, potentially providing greater sensitivity than traditional neuropsychological tests.

Brain–computer interface-driven functional electrical stimulation (BCI-FES) is a promising approach for post-stroke upper limb rehabilitation. However, considerable variability exists in stimulation parameters and task designs across studies, and evidence remains insufficient to support definitive protocol recommendations.

We searched PubMed, Embase, Web of Science, and the Cochrane Library for randomized controlled trials (RCTs) up to September 2025. Eligible studies applied BCI-FES and reported the Fugl-Meyer Assessment for the upper extremity (FMA-UE). Risk of bias was assessed with the PEDro scale, and evidence certainty graded with GRADE. Random-effects meta-analyses were performed.

Twelve RCTs (n = 619) showed BCI-FES improved FMA-UE scores versus controls (MD = 5.82, 95% CI 3.04-8.59, p < 0.00001; I² = 39%), with larger benefits in subacute stroke (MD = 8.45). Dynamic-threshold paradigms and motor imagery were associated with higher effect sizes. Higher stimulation frequency (>50 Hz), narrow-pulse width (150 µs) more frequent sessions (≥5/week), shorter session duration (≤30 min), greater total sessions (>20), and longer intervention (>4 weeks) tended to be associated with larger effect sizes, though evidence is limited and based on few studies. Secondary outcomes (ARAT, WMFT, MBI) improved, and no serious adverse events were reported. Evidence certainty was moderate.

BCI-FES was associated with improvements in upper limb motor recovery after stroke, especially in subacute patients. Some stimulation and training features may relate to greater effects, but current evidence remains insufficient for definitive clinical guidance. Larger multicenter RCTs are needed to clarify dose-response relationships and support biomarker-guided, personalized interventions.

Interictal epileptiform discharges (IED) frequency is the most commonly studied interictal measure of ASM efficacy in patients with epilepsy, and IED suppression in a repeat pediatric EEG is usually interpreted as a reduced tendency towards seizures.

To assess whether the amplitude and morphology of IED can serve as surrogate measures of levetiracetam (LEV) efficacy in children with drug-resistant epilepsy.

Patients with refractory epilepsy, who were treated with oral LEV during a 5-year period, and who had at least 24 h long-term video-EEG recording (LTVEEG) before LEV was initiated and after attaining maximal dosage, were retrospectively selected from the database of the pediatric epilepsy clinic and LTVEEG monitoring unit. IED kurtosis (degree of peakedness), skewness (degree of asymmetry), and below-curve-area (area of the IED) were estimated by a signal processing analysis program.

IED analysis in 20 patients aged 3.6 months to 15 years at maximal LEV dosage revealed increased kurtosis, increased skewness positivity and decreased below-curve-area compared to pre-treatment values. Visual analysis revealed a mean IED amplitude decrease in 30% of the patients, mainly in patients with generalized seizures. Neither the changes in IED measures nor the decrease of the visually determined IED amplitude correlated with decreased seizure frequency.

IED amplitude, kurtosis, skewness and below-curve-area were not correlated with seizure outcome after LEV initiation. Further studies with larger samples and additional seizure outcome measures are warranted.

To describe demographics, semiology, etiology, and clinical features in individuals with insulo-opercular and pure insular onset presenting with hyperkinetic seizures (HKS).

Under PRISMA guidelines, Embase, PubMed, Medline, and Cochrane were searched for articles between 1969 and January 10, 2025, using terms for hyperkinetic/hypermotor seizures, insular epilepsy, sleep-related hypermotor epilepsy, nocturnal paroxysmal dyskinesia/dystonia, nocturnal frontal lobe epilepsy, and complex motor behavior. Eligible studies were reports or retrospective series of patients with pure insular or insulo-opercular epilepsy and HKS, documented with SEEG or subdural recordings, with at least 6 months of postsurgical follow-up and Engels class I. Of 271 studies, 14 met inclusion criteria.

Fourteen studies including 34 patients were analyzed; 61.8% had pure insular onset. Focal cortical dysplasia was the most common etiology, present in two-thirds of cases. Most HKS began with non-motor semiology (76.5%). Hyperkinetic automatisms type 3, defined by integrated/natural hyperkinetic behaviors, manipulation/utilization behaviors, and distal stereotypies, were reported in 49.9% of patients with pure insular onset. Compared with insulo-opercular onset, pure insular onset was associated with a higher frequency of these behaviors, along with agitation, vocalization, and breathing difficulties (p < 0.05). These findings are based on small, heterogeneous samples and should be interpreted cautiously.

HKS were more frequently associated with pure insular onset. Focal cortical dysplasia was the most common etiology, and integrated/natural hyperkinetic behavior was more frequent with pure insular onset. Given limited sample size, heterogeneity, and study design constraints, these findings should be considered exploratory rather than definitive.

Preschool children born preterm are at risk of developmental delay and cognitive deficits. However, the neurocognitive underpinnings of the cognitive deficits in preterm children remain unclear.

This study aimed to compare quantitative EEG (qEEG) profiles and cognitive function between preterm and full-term children aged 4 to 6 years.

Children's cognitive ability was assessed using the Griffiths Development Scales-Chinese (GDS-C). Resting-state EEG was recorded, and spectrum analysis was conducted. In addition to conventional band power analysis, aperiodic components (exponent and offset) and center frequency of the dominant oscillatory peak were calculated by fitting oscillations and one-over-f (FOOOF).

The study recruited 28 preterm-born children (15 girls, mean age = 62.14 months, SD = 7.31) and17 age-matched full-term children (7 girls, mean age = 59.8 months, SD = 8.49) Preterm children showed significantly elevated aperiodic offset and exponent. They also exhibited significantly slower center frequency of the dominant oscillatory peak and higher delta and theta band power compared to full-term children.

Preterm children demonstrated elevated aperiodic offset and exponent and slower center frequency of the dominant oscillatory peak compared to full-term children, at preschool age. These findings suggest that preschool children born preterm may exhibit less efficient functional neural connections and delayed brain maturation.

Vertex sharp waves(VSW) are sharply contoured waves with a duration of less than 500 mille-seconds and maximal over the central regions of the brain, that have been identified to appear during N1. Here we postulate that VSW are sleep stage-specific and can also identify a sleep stage shift to NREM sleep from REM sleep.

We retrospectively analyzed PSG data of 20 out of 74 consecutive patients who were studied with 18-channel EEG within the last year. Vertex sharp waves were visually and manually scored and analyzed by sleep stage.

Twenty patients(12 men, 60.0%) were analyzed. The median age was 37 years(95% CI 31.3—46.2 years) with a mean of 38.7 ± 14.4 years. Seventeen patients(85%) had VSW in both N1 and N2 sleep stage, only 6 patients(30%) had VSW in N3 sleep, and 10 patients(50%) in REM sleep. Regression analysis showed that the occurrence of VSW in N2 sleep(r² = 0.747,F = 44.366;p < 0.001) and REM sleep(r² = 0.473,F = 7.174; p = 0.028) was positively correlated with the presence of VSW in N1 sleep stage. The positive correlation during REM sleep was only spared for the VSW appearing following an arousal reaction(r² = 0.432, F = 5.329;p = 0.05).

Our results suggest that vertex sharp waves are state-dependent activities of NREM sleep, predominantly seen in N1 sleep stage, and also in N2 sleep. As they emerge in REM sleep, following an arousal reaction or not, it may be regarded as a sleep stage shift from REM to NREM sleep stage. These findings may help clarify scoring rules for REM sleep and arousal.