Open Access Original Article

Assessing Brain Neurophysiology in COVID-19

Patients With Prolonged Cognitive Fatigue: A
Review began 06/18/2025
Comparison With Persistent Post-concussion
Review ended 07/09/2025
Published 07/17/2025 Symptoms
© Copyright 2025 David S. Oakley 1 , Mo Mortazavi 2, 3, Daniella K. Rivera 4 , Leila Samsam 2, Taylor P. Seitz 5, Leslie Streeter 2
Oakley et al. This is an open access article
distributed under the terms of the Creative
Commons Attribution License CC-BY 4.0., 1. Electrophysiology, WAVi Research, Boulder, USA 2. Trauma, Sports Medicine, Rehabilitation, and Concussion Center
which permits unrestricted use, distribution, (SPARCC), Tucson, USA 3. Trauma, Tucson Medical Center, Tucson, USA 4. Family Medicine, David Grant Medical
and reproduction in any medium, provided Center, Andrew Taylor (A. T. Still University School of Osteopathic Medicine, Fairfield, USA 5. Trauma, University of
the original author and source are credited.
Arizona, Tucson, USA

DOI: 10.7759/cureus.88160
Corresponding author: Daniella K. Rivera, [email protected]

Abstract
Introduction: Brain fog and cognitive dysfunction are frequently reported in post-viral fatigue syndromes
such as long COVID, yet these symptoms remain challenging to quantify objectively. Notably, many
individuals with long COVID describe clinical features that overlap with those observed in patients with
persistent post-concussion symptoms (PPCS), including cognitive fatigue, exertional intolerance, mood
disturbances, visual and balance problems, headaches, and neck pain. Emerging evidence suggests that
PPCS is associated with distinct electrophysiological abnormalities, including altered functional connectivity
(measured by electroencephalography (EEG) coherence), spatial changes in EEG amplitude distribution
(notably increased frontal alpha and left-right asymmetry), and reduced cognitive evoked potentials (e.g.,
the auditory P300 response). In this study, we investigated whether these electrophysiological markers of
PPCS are also present in individuals experiencing post-viral fatigue following COVID-19, aiming to provide
objective measures to better characterize and quantify cognitive impairment in this population.

Materials and methods: Thirty-one patients (mean age 45 ± 9 years) reporting persistent neurocognitive
symptoms following COVID-19 infection (10 ± 2 months post-infection) were evaluated at intake to a brain
injury clinic while seeking assessment/treatment for prolonged cognitive complaints. Over this time period,
64 PPCS patients (69% female; age: 42 ± 11 years) were evaluated at the same clinic for concussion-related
symptoms using identical protocols. These were compared to seventy age-matched controls (mean age 45 ±
5 years) without a history of COVID-19 or neurological conditions. Assessments comprised standard
concussion assessments with symptom profiles that included cognitive fatigue and EEG with event-related
potentials (ERP). We then compared the EEG and ERP metrics known to be sensitive to declines in mental
performance (i.e., PPCS) for both the long COVID group and age-matched controls.

Results: The long COVID cohort demonstrated neurophysiological alterations paralleling those observed in
PPCS, including significantly impaired processing speed and reduced physical reaction times compared to
controls (p < 0.001), as well as cognitive electrophysiological deficits, such as attenuated P300 amplitudes,
which reflect impaired attention allocation (p < 0.001). These biomarkers normalized concomitantly with
symptom resolution at long-term follow-up (mean 20 ± 8 months post-baseline assessment).

Conclusions: Our data demonstrate that ERP deficits, characteristic of cognitive decline in conditions like
concussion, PPCS, and aging, are replicable in long COVID patients. Notably, these electrophysiological
abnormalities (reduced P300 amplitude and altered coherence) correlate with quantifiable cognitive fatigue
and functional neurological impairments. Biomarker normalization tracked with symptom resolution at
follow-up (20 ± 8 months), confirming their clinical relevance. These accessible metrics provide objective
parameters to identify virally induced cognitive deficits, addressing a critical need for validated diagnostic
tools in post-viral syndromes.

Categories: Neurology, Internal Medicine, Infectious Disease

Keywords: cognitive fatigue, concussion, electroencephalogram, event related potentials, long covid

Introduction
A substantial proportion of individuals who have experienced COVID-19 develop persistent complications,
collectively referred to as long COVID or post-acute sequelae of SARS-CoV-2 infection. These complications
commonly include general fatigue and cognitive dysfunction, often described as brain fog [1-2]. Quantifying
brain fog and fatigue remains challenging; current assessments rely primarily on symptom inventories and
self-report questionnaires regarding memory impairment, reduced mental clarity, poor concentration,
subjective feelings of disorientation, headaches, and confusion.

How to cite this article

Oakley D S, Mortazavi M, Rivera D K, et al. (July 17, 2025) Assessing Brain Neurophysiology in COVID-19 Patients With Prolonged Cognitive
Fatigue: A Comparison With Persistent Post-concussion Symptoms. Cureus 17(7): e88160. DOI 10.7759/cureus.88160
 Numerous neuroimaging studies have identified structural and functional abnormalities in the brains of
individuals who have had COVID-19 [3-5]. Proposed mechanisms underlying these persistent symptoms
include ongoing neuroinflammation, vascular complications, and hypoxia, among others. A longitudinal
study of patients who underwent neuroimaging both before and after infection demonstrated alterations in
diffusion measures, which serve as proxies for tissue damage, as well as reductions in gray matter thickness.
In another relevant study of long COVID patients with persistent cognitive symptoms, including memory
problems, brain fog, increased fatigue, and reduced quality of life, cognitive test performance did not
significantly differ from that of controls at two years post-infection. However, MRI analysis revealed notable
differences, including decreased brain volumes and reduced cortical thickness in several brain regions,
among the COVID-19 group [6].

Despite the insights provided by neuroimaging studies, the absence of standardized neuroimaging protocols
in routine clinical practice for long COVID means that diagnosis and management often depend heavily on
patient self-report. This reliance can leave both patients and clinicians uncertain about the underlying
causes of symptoms and how best to address them. The resulting ambiguity is reflected in the literature,
where estimates of the prevalence of persistent brain fog among COVID-19 patients vary widely, ranging
from as low as 7% to as high as 70% [7].

This work aims to compare the clinical features of long COVID with those of persistent post-concussion
symptoms (PPCS), both of which manifest with overlapping symptom profiles. While most mild traumatic
brain injuries (mTBI) resolve within approximately one month, an estimated 10-30% of affected individuals
experience persistent symptoms beyond this period, resulting in PPCS. Similar to long COVID, PPCS is
characterized by brain fog, fatigue, memory impairment, reduced mental clarity, poor concentration,
subjective feelings of disorientation, headaches, and confusion [8]. As is the case with long COVID, the
absence of standardized neuroimaging protocols in routine clinical practice and the reliance on self-
reported symptoms have led to PPCS being frequently attributed to psychosocial factors. Notably, up to 40%
of patients with PPCS are referred for psychological evaluation [9].

Neuroimaging studies demonstrate that structural, functional, and/or metabolic alterations occurring
acutely after mTBI can persist in PPCS [9]. While neuroimaging elucidates physiological mechanisms in
PPCS and long COVID, its clinical implementation remains limited by practicality constraints. In contrast,
electroencephalography (EEG) with event-related potentials (ERPs), which are EEG responses time-locked to
sensory/cognitive stimuli, offers greater clinical accessibility for the longitudinal monitoring of cognitive
impairment [10-13]. Patients with mTBI exhibit electrophysiological deficits, such as reduced ERP
amplitudes, in both the acute and chronic phases of post-concussive syndrome (PCSS). Notably, PPCS
presents unique electrophysiological pathologies distinct from acute-phase abnormalities [12-13].

In this study, we retrospectively analyze patient data collected during routine clinical evaluations,
representing real-world, heterogeneous populations that self-report symptoms of PPCS or long COVID. Our
primary research question is whether EEG/ERP abnormalities observed in PPCS, including metrics
associated with reduced cognitive performance (CP), are also present in long COVID. Given the overlapping
symptom profiles and confounding psychosocial factors in both conditions, we designed this comparative
study to identify more objective neurophysiological markers that complement clinical findings. We
hypothesize that, to the extent these symptoms have a physiological basis, brain function analysis via
EEG/ERP will reveal similarities between PPCS and long COVID. Specifically, if subjective complaints such as
“brain fog” reflect underlying physiological dysfunction, we expect to observe reduced ERP amplitudes in
both patient groups, even if the specific pathophysiological mechanisms differ.

Materials And Methods

Study design
This is a retrospective analysis of data collected during clinical evaluations. These evaluations included EEG
with ERP, which is the primary focus of this study. Here, we rely on clinician assessments to determine the
diagnostic categories and historical data, collected with the same methods, for the control group. Solutions
Institutional Review Board issued approval 1MAY14-48

Study population
Thirty-one patients (50% female; age: 45 ± 9 years) with no history of concussion but presenting with
persistent long COVID symptoms were evaluated at a specialized PPCS clinic. Assessments occurred at 10 ± 2
months post-infection, with longitudinal follow-up at 20 ± 8 months post-initial evaluation. Over this
period, 64 PPCS patients (69% female; age: 42 ± 11 years) with no history of viral fatigue were evaluated at
the same clinic for concussion-related symptoms using identical protocols. Tests included the CP symptom
screening tool (scale of 0-3, none-to-severe) [14], a battery of visual testing that included vestibular-ocular
reflex, and the WAVi Scan (trail making test (TMT), reaction time, and EEG collected during an audio oddball
ERP protocol) [12-13]. Several studies have examined the patterns of relations between trail-making and
health, where TMT completion times have been seen to decline with concussion and cognitive impairment
[12,15]. Physical reaction time also represents a straightforward measurement that correlates with a host of

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 conditions, including concussion [16].

The non-long COVID, non-PPCS control group consisted of 70 WAVi assessments from healthy individuals
(mean age: 45 ± 5 years; 55% female), derived from three previous studies [17-19]. Participants were
measured during wellness exams across three independent clinics using identical EEG/ERP and TMT
protocols, software, and hardware as those used for the PPCS and long COVID evaluations described above.

Subjects who had a yield of less than 80% on evoked responses due to artifacts were excluded from the study
for all groups. In addition, those who had a history of head trauma, fatigue (including viral fatigue), or
psychiatric conditions, all related to PPCS and long COVID, were excluded from the control group.

EEG acquisition and extraction

The EEG was recorded using FDA-cleared WAVi Scan 1.1 (WAVi CO, Denver, CO, USA), sampled at 250 Hz
and bandpass filtered between 0.5 and 30 Hz. The electrodes were placed according to the International 10-
20 system (Figure 1), and linked reference electrodes were placed at the earlobes. Test administrators were
instructed to establish electrode impedances below 30 kW for EEG locations and below 20 kW for the ground-
to-ear locations where possible. These targets are well below the 1 GW input impedance of the WAVi
amplifiers, are practical in terms of preparation time, and produce a sufficient yield [20].

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 FIGURE 1: (Top) Alpha amplitude as a function of scalp location in
typical non-PPCS and PPCS patients. (Bottom) Occipital connectivity
from the O2 electrode as a function of scalp location in typical non-
PPCS and PPCS patients
PPCS: persistent post-concussion symptoms

Image Source: Mortazavi et al., 2023 [13]. Published with permission. Open access.

The testing details for the long COVID group were the same as those described elsewhere, with a continuous
four-minute, two-tone, eyes-closed protocol presenting 200 common tones (1000 Hz) and 40 rare tones
(2777 Hz) in random order, once per second [12-13,17]. This protocol was used to acquire both background
EEG and evoked ERP data, as discussed below.

WAVi Scan extracts EEG spectral information using standard Fourier transform methods. All trials included
automatic artifact rejection, which excluded sections of EEG data with higher than acceptable amplitudes
and excessive band frequency activities in the standard EEG bands (Delta, Theta, Alpha, and Beta) on an
individual channel basis. Files were also manually inspected to confirm the proper detection of
artifacts. Segments of data that contained synchronized eye blinks were also excluded from the study.
Finally, spectra were extracted from the background eyes-closed EEG acquired during the auditory oddball
ERP, consistent with the previous PPCS study against which we compare here [13].

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 Study measures
EEG Spectra

Spectral analysis characterizes the frequency composition of EEG, with the alpha band (8-12 Hz)
representing the dominant rhythm. We further examine alpha power topography, which in healthy
populations (eyes-closed condition) typically exhibits bilateral symmetry and posterior dominance. In PPCS,
however, deviations from this pattern occur, including anterior displacement of alpha power and
hemispheric asymmetries. These electrophysiological alterations have also been documented in other
conditions, such as emotional dysregulation [13,21-23].

In this work, we investigate whether these PPCS spectral physiologies are also present in long COVID. In
particular, we calculate the ratio of frontal to occipital alpha microvolt amplitudes using the sum of the
magnitudes at each of the alpha band frequencies (8-12 Hz) averaged across the five frontal locations FP1
and F3 (on the left), FP2 and F4 (on the right), and the central Fz and the two occipital locations O1 and O2.

In keeping with previous works, we calculate frontal left-right asymmetries between F3 and F4 as the
absolute value of the deviation from 1.0 (symmetry) [13].

EEG Coherence

EEG coherence quantifies frequency-dependent synchronization between electrode pairs, reflecting

functional connectivity. Post-mTBI studies demonstrate elevated coherence, particularly in long-range
interhemispheric pathways, where some of these abnormalities persist after symptom resolution or a return
to normal performance on neuropsychological evaluations [24-27]. It has been posited that concussed
participants may recruit additional brain resources to compensate for their inability to produce the
necessary level of amplitude, implying that functional recovery may occur faster than physiological recovery
[13,24].

Alpha band coherence was extracted using standard methods described elsewhere [12-13,17]. As with the
spectral analysis described above, eyes-closed coherence measures were extracted during the same eyes-
closed P300 protocol. There are many methods of presenting coherence, but with

pairs to choose from, care must be taken not to overfit the data. This study

employs an established connectivity quantification method [13,18-19], where strong functional connections
are defined as those exceeding two standard deviations above the mean of a reference control dataset. Our
control cohort exhibited a mean of three connections above this threshold (out of 171 possible), consistent
with expectations for a Gaussian distribution. This approach enables the standardized quantification of
network alterations in conditions such as post-viral fatigue (e.g., long COVID) and PPCS, where
hyperconnectivity patterns are anticipated. The method accounts for inter-individual variability in both
connection strength and spatial distribution of affected pathways.

It should be noted that coherence, like many other EEG metrics, is susceptible to artifacts, and the raw EEG
must be visually inspected to ensure that artifacts don't affect long- or short-distance coherences. We used
alpha band coherence because it is less susceptible to motion artifacts and/or muscle tension than the other
bands, and because alpha often accounts for the most significant amount of power in the EEG band, thus
yielding the most robust coherence estimates.

Evoked EEG

The final set of measures involves an auditory oddball ERP, a common protocol that measures the brain's
response to common rare tones. The brain typically identifies the rare as different by around 300 ms after the
delivery of the oddball stimulus, presenting as a positive EEG voltage, hence the name P300. The amplitude
of the P300 response is considered to be proportional to the number of attentional resources devoted to
detecting the rare tone, where larger amplitudes and smaller latencies (faster processing speeds) have been
associated with superior information processing. The P300 amplitude has been observed to decline after a
concussion and with PPCS, whereas the latency remains a more stable trait [12-13,19].

In this work, the depth (P300V) was extracted from the mean amplitude of the response to all stimuli. The
amplitudes of the P300 components reported here were measured by identifying the average positive
extremum in the latency range of 240-500 ms, relative to the average of the first 16 ms post-stimulus, with
baseline correction using the 100-ms pre-stimulus period. Here, we report the average P300 µV from the six
C-P scalp sites (C3, CZ, C4, P3, Pz, P4).

Statistical analysis
Following the procedure of the previous PPCS study [13], the mean of the metrics of interest for the long
COVID group was compared to that of the control group using unpaired two-sample t-tests, with a p-value

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 cutoff of 0.05 and a minimum meaningful effect size of Cohen's d > 0.50 [28].

Results
Initial evaluations
At their initial baseline evaluation, these long COVID patients exhibited similar symptom profiles to those
often seen in PPCS cases (Table 1), with cognitive fatigue being the most commonly reported symptom.

Profile category Mean symptom score

Cognitive fatigue 1.8

Mood 1.5

Sleep 1.4

Visual 0.9

Cervical 0.9

Vestibular 0.8

Migraine 0.8

TABLE 1: CP symptom screening in patients with post-viral fatigue, rated on a scale from 0 (none)
to 3 (severe)
CP: cognitive performance

While no reduction in TMT times was reported, physical reaction times were suppressed in both PPCS and
long COVID (Table 2). Electrophysical deficits were also seen in both the long COVID and PPCS populations
(Table 2), where cognitive resources, as measured by the P300 evoked response amplitude, were diminished
(Figure 2) with no reduction in latency. Here, 70% of the long COVID patients were one standard deviation
below that observed for the controls in amplitude (16% expected).

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 Metric Control (N=70) Long COVID (N=31) PPCS (N=64)

Performance

Reaction time (SD) 318 (87) ms 403 (122) ms 387 (118) ms

P-value (CohD) - <0.001 (0.8) <0.001 (0.7)

ERP

P300 voltage (SD) 9 (4) uV 5 (3) uV 6 (4) uV

P-value (CohD) - <0.001 (1.3) <0.001 (1.0)

P300 latency (SD) 290 (35) ms 286 (32) ms 294 (34) ms

P-value (CohD) - 0.6 (0.1) 0.6 (0.1)

Spectral

Frontal/OP a amplitude (SD) 0.8 (0.3) 1.1 (0.4) 1.0 (0.4)

P-value (CohD) - 0.001 (0.7) <0.001 (0.7)

Frontal asymmetry 0.05 (0.10) 0.15 (0.11) 0.38 (0.51)

P-value (CohD) - <0.001 (0.9) <0.001 (0.9)

Alpha-band connectivity

# coherence connections > 2 s 3.4 (1.8) 4.8 (5.0) 8.9 (7.4)

P-value (CohD) - 0.05 (0.4) <0.001 (1.0)

TABLE 2: EEG, ERP, and performance metrics in post-viral fatigue, PPCS, and control groups
COVID: coronavirus disease 2019, SD: standard deviation, CohD: Cohen's D, EEG: electroencephalography, ERP: event-related potential, PPCS:
persistent post-concussion symptom, OP: occipital-parietal

Bold: significant p-value difference from control

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 FIGURE 2: Evoked response amplitude (central-parietal) as a function of
time after the delivery of rare stimuli, averaged across control and long
COVID (viral fatigue) groups, showing a clear reduction in amplitude but
no change in latency of the P300 cognitive response
COVID: coronavirus disease

The alpha amplitude in the long COVID group, as in PPCS [13], trended toward reduction in occipital regions,
accompanied by a frontal increase, as illustrated in Figure 1 (top), and a marked trend of alpha asymmetry as
measured by the frontal alpha amplitude ratio. Concerning coherence differences, as in PPCS, the long
COVID group showed increased coherence in the alpha band compared to the control.

Follow-up evaluations
Patients with long COVID-related cognitive fatigue received multi-disciplinary management protocols
similar to those for PPCS patients within the same clinic. Multi-disciplinary treatments in these cohorts
included active rehabilitation protocols, physical therapy, occupational therapy, and cognitive behavioral
therapy, administered over 6-28 months (mean duration: 10.5 months). We compared ERP trajectories in 21
patients with long COVID versus 24 patients with PPCS (Figure 3) across serial assessments. Intermediate
testing was conducted during the ongoing symptoms, while final testing at 20 ± 8 months post-baseline
captured an improved clinical status.

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 FIGURE 3: Trajectories of P300 evoked response amplitudes measured
from intake through stages of symptom improvement. Both PPCS and
long COVID follow a similar path toward P300 normalization
PPCS: persistent post-concussion symptoms, COVID: coronavirus disease 2019

At the intermediate assessment, neither the long COVID nor the PPCS cohorts demonstrated symptomatic
improvement, as reflected by stable P300V values. By the final visit, however, both groups exhibited
significant symptom reduction, which was paralleled by a marked increase in P300V (p < 0.05, Cohen’s d >
0.5). These improvements were correlated with clinical improvements over time, as measured by the total
symptom score using the CP screen tool. Also of note, the number of excess coherence locations changed
from six on the initial and mid tests to the more expected three on the final tests.

Discussion
This study aims to characterize the electrophysiological abnormalities underlying cognitive symptoms in
patients with long COVID. By comparing these individuals against both healthy controls and PPCS cohorts,
who report similar cognitive complaints, we seek to identify objective electrophysiological signatures that
complement clinical symptom profiles.

In the long COVID group, as in the PPCS cohort, we observed a significantly reduced P300 amplitude,
indicative of diminished cognitive resources and consistent with patients’ subjective reports. This persistent
reduction in P300 amplitude in both groups aligns with the cognitive fatigue and “brain fog” frequently
described by affected individuals [11]. Despite the presence of psychosocial confounders and the
heterogeneity of the patient population, 70% of long COVID patients exhibited reduced P300 amplitude,
compared to only 16% of controls. Notably, this electrophysiological deficit resolved following several
months of multi-disciplinary neurorehabilitation in both PPCS and long COVID patients. These findings
may reflect underlying neuroinflammation, vascular complications, or metabolic disruptions previously
identified through neuroimaging [4,9]. However, it is essential to note that the resolution of symptoms and
functional (ERP) measures may not temporally coincide with the normalization of imaging findings.

We observed a frontal alpha power shift in long COVID patients with post-viral fatigue, mirroring patterns
previously documented in PPCS cohorts. While the neurophysiological basis of this shift requires further
investigation, preliminary evidence suggests it may represent a distinct electrophysiological phenotype [29].

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 Both long COVID and PPCS groups exhibited significantly greater alpha asymmetry than controls (p < 0.01),
a pattern potentially linked to emotional regulation deficits commonly reported in these populations [21-
23].

Both long COVID and PPCS cohorts exhibited increased alpha-band coherence, consistent with prior PPCS
literature. In PPCS, elevated long-range coherence emerges during subacute recovery phases (absent
acutely), suggesting neuroplastic reorganization. While the mechanistic basis of long COVID remains
unclear, similar increases may reflect compensatory processes following neural injury, as supported by
diffusion imaging evidence of microstructural damage. This interpretation is reinforced by our observation
of reduced excess coherence at final assessment (vs. baseline), which paralleled symptomatic improvement
in long COVID patients.

Finally, note that while the physical reaction time decreased, performance on the TMT was strong in long
COVID, consistent with some studies but not others [4,5]. This highlights the diagnostic challenge clinicians
face when patient-reported symptoms lack correlates in standard neuropsychological testing. Crucially, our
study demonstrates objective electrophysiological abnormalities that validate brain-related complaints in
both long COVID and PPCS cohorts.

Implications
Analysis of the long COVID cohort reveals electrophysiological abnormalities consistent with PPCS patients,
correlating with shared cognitive symptom profiles. These findings demonstrate measurable
neurophysiological dysfunction in long COVID. Moreover, similar intervention strategies may be employed.
With evidence of neurophysiological dysfunction such as frontal alpha, coherence, and P300 amplitude, the
results suggest that the combined use of EEG and ERP can help objectively assess long COVID diagnosis,
recovery, and prognosis to aid in the subjective assessment of patients with ongoing complaints of
persistent symptoms and help support decision-making in care.

Limitations
Potential limitations of the study include the fact that patient data were collected from clinical
examinations, which, by nature, creates a heterogeneous population and variable time course in disease
(i.e., wide ranges in chronicity and morbidity). While the neurophysiological findings matched
symptomology, the small sample size and the patient self-selection may limit the generalizability of this
clinic-based sample. Furthermore, the strong correlations between long COVID and PPCS versus the control
group support the notion that imaging studies do not directly address causation. Finally, while no gender
differences were observed, the sample size was insufficient to make any gender-related comparisons.

Conclusions
These findings suggest that the electrophysiological abnormalities observed in PPCS are also present in long
COVID. Such abnormalities may reflect cognitive fatigue, a symptom commonly reported in both
conditions. Notably, the amplitude of the P300 component of the ERP, an index of cognitive processing,
increased in both the PPCS and long COVID cohorts as symptoms resolved. These neurophysiological
markers may help clinicians identify affected individuals and facilitate earlier, evidence-based interventions,
which could be especially valuable in the context of confounding psychosocial factors.

Additional Information
Author Contributions
All authors have reviewed the final version to be published and agreed to be accountable for all aspects of the
work.

Concept and design: David S. Oakley, Mo Mortazavi, Daniella K. Rivera, Leila Samsam, Taylor P. Seitz,
Leslie Streeter

Acquisition, analysis, or interpretation of data: David S. Oakley, Mo Mortazavi, Daniella K. Rivera, Leila
Samsam, Taylor P. Seitz, Leslie Streeter

Drafting of the manuscript: David S. Oakley, Mo Mortazavi, Daniella K. Rivera, Leila Samsam, Taylor P.
Seitz, Leslie Streeter

Critical review of the manuscript for important intellectual content: David S. Oakley, Mo Mortazavi,
Daniella K. Rivera, Taylor P. Seitz, Leslie Streeter

Supervision: Daniella K. Rivera

Disclosures

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 Human subjects: Informed consent for treatment and open access publication was obtained or waived by all
participants in this study. Solutions Institutional Review Board issued approval 1MAY14-48. Retrospective
analysis of data collected during clinical evaluations using FDA-cleared devices is exempt under exemption
#4 of 45 CFR 46. Animal subjects: All authors have confirmed that this study did not involve animal
subjects or tissue. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors
declare the following: Payment/services info: All authors have declared that no financial support was
received from any organization for the submitted work. Financial relationships: David Oakley declare(s)
employment from WAVi Co. WAVi provided the EEG equipment whose data was used for the study. Other
relationships: All authors have declared that there are no other relationships or activities that could appear
to have influenced the submitted work.

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