Quantitative EEG Recordings Research Articles

EEG Abnormalities During Delirium as a Prodromal Feature of Dementia with Lewy Bodies: A Case Report

Background:A 79-year-old woman was admitted to the Neurology Clinic of the University of Chieti-Pescara for a syncope. At admission, the occurrence of an acute stroke was ruled out. Her cognitive status was unimpaired. After three days from the hospitalization, the patient experienced an episode of mixed delirium.Objective:The present case report shows a case of delirium-onset dementia with Lewy bodies (DLB) with a specific electroencephalographic (EEG) pattern from its prodromal stage.Methods:Delirium was assessed by 4AT test. During the hospitalization, the patient underwent a quantitative EEG (QEEG) with spectral analysis. At six months from the episode of delirium, she was tested by neuropsychological evaluation, QEEG, and 18F-fluorodeoxyglucose PET/CT to assess the onset of a possible cognitive decline.Results:At baseline, the QEEG exam showed a dominant frequency (DF) in the pre-alpha band (7.5 Hz) with a dominant frequency variability (DFV) of 2 Hz. This pattern is typical of DLB at early stage. After six months, she reported attention deficits in association with cognitive fluctuation and REM sleep behavior disorder. The neurological examination revealed signs of parkinsonism. Cognitive status resulted to be impaired (MoCA = 15/30). QEEG recording confirmed the presence of a DLB-typical pattern (DF = 7.5 Hz, DFV = 2.5 Hz). The 18F-FDG-PET/CT showed a moderate bilateral posterior hypometabolism (occipital and temporal cortex), with relative sparing of the posterior cingulate cortex compared to cuneus/precuneus (Cingulate Island sign), and mild bilateral hypometabolism in frontal regions (suggestive of a DLB diagnosis).Conclusion:EEGs may represent supportive and validated biomarkers for delirium-onset prodromal DLB.

Quantitative EEG recording of a migraine attack

Records of EEG during the post ictal period of migraine attack usually show electrical abnormalities of cortical activity mostly related to unspecific symptoms as drowsiness or hyperventilation. However, patients have abnormal EEG rhythms also during the visual aura with an overall slow activity and variation in power spectral values due to a decreased alpha activity in the posterior leads with an increased theta and delta power in the frontocentral regions mimicking some features of true epileptic patients.

Cortical Excitability and Activation of TrkB Signaling During Rebound Slow Oscillations Are Critical for Rapid Antidepressant Responses

Rapid antidepressant effects of ketamine become most evident when its psychotomimetic effects subside, but the neurobiological basis of this “lag” remains unclear. Laughing gas (N2O), another NMDA-R (N-methyl-d-aspartate receptor) blocker, has been reported to bring antidepressant effects rapidly upon drug discontinuation. We took advantage of the exceptional pharmacokinetic properties of N2O to investigate EEG (electroencephalogram) alterations and molecular determinants of antidepressant actions during and immediately after NMDA-R blockade. Effects of the drugs on brain activity were investigated in C57BL/6 mice using quantitative EEG recordings. Western blot and qPCR were used for molecular analyses. Learned helplessness (LH) was used to assess antidepressant-like behavior. Immediate-early genes (e.g., bdnf) and phosphorylation of mitogen-activated protein kinase—markers of neuronal excitability—were upregulated during N2O exposure. Notably, phosphorylation of BDNF receptor TrkB and GSK3β (glycogen synthase kinase 3β) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Subanesthetic ketamine and flurothyl-induced convulsions (reminiscent of electroconvulsive therapy) also evoked slow oscillations when their acute pharmacological effects subsided. The correlation between ongoing slow EEG oscillations and TrkB-GSK3β signaling was further strengthened utilizing medetomidine, a hypnotic-sedative agent that facilitates slow oscillations directly through the activation of α2-adrenergic autoreceptors. Medetomidine did not, however, facilitate markers of neuronal excitability or produce antidepressant-like behavioral changes in LH. Our results support a hypothesis that transient cortical excitability and the subsequent regulation of TrkB and GSK3β signaling during homeostatic emergence of slow oscillations are critical components for rapid antidepressant responses.

Electroencephalogram alpha-to-theta ratio over left fronto-temporal region correlates with negative symptoms in schizophrenia.

Negative symptoms impair outcomes on occupational functioning, social interaction and interpersonal relationships in patients with schizophrenia. Past researchers have reported reduced alpha and increased theta and delta spectral powers on quantitative EEG recordings in those with prominent negative symptoms. Present analysis aimed at exploring the relationships between lower-frequency EEG powers and negative symptoms, in schizophrenia, over a period of naturalistic antipsychotic treatment. Fifteen right-handed drug-free/drug-naïve schizophrenia patients (N=15;M=12,F=3) were recruited and assessed on PANSS. Spontaneous 192-channel resting-state EEG was recorded at baseline, and PANSS rating was repeated at 4 weeks. Baseline EEGs of patients were compared to 15 age-sex-handedness matched controls. Non-significant differences emerged between patient and controls in terms of socio-demographic characteristics. Over left frontal and left temporal regions, baseline ratio of alpha/theta power (bATR) was significantly lower (p<0.001) in patients, correlated negatively with baseline PANSS negative score (PNS) (p<0.05); and over 4-weeks of antipsychotic treatment, left temporal bATR correlated positively with relative improvements in PNS. Reduced alpha power over frontal regions might imply altered arousal and/or impaired attentional process, while abnormal theta range oscillations may relate to impairments in working memory via their influences on theta-gamma coupling. Our findings suggest left-predominant deficiencies in these processes might mediate negative symptoms. Further, since ATR might reflect integrity of certain cognitive processes, those with a higher bATR might possess better cognitive resource at baseline and therefore experience greater improvement in negative symptoms with antipsychotic treatments, at least during the first 4 weeks.

Attenuation of pathological spectral theta power by deep brain stimulation in a Parkinson patient

A patient (born in 1943) with generalized anxiety since 2008 developed Parkinsonian tremor in 2010. First quantitative EEG recording (neo-CATEEM software using 10/20 electrode positions) was obtained on 10.02.2011. Comparison of spectral power to a norm database of 500 healthy brains revealed enhanced theta power (5–7 Hz) at temporal electrode positions T5 and T6 with a statistical probability of 10000 to 1. This feature was seen under both recording conditions “eyes open” and “eyes closed”. In 11/2012 he got two deep brain electrodes implanted into the nucleus subthalamicus. EEG findings as seen before were reproduced on 22.02.2013 and 24.09.2013. In order to measure the effectiveness of the stimulation further recordings were taken without active stimulation and in the presence of active stimulation on 28.07.2014 and 24.09.2014. During stimulation spectral theta power was attenuated by 50% in comparison to the pre-stimulation recording only at electrode position T6 at both timings (videoclip). The results not only confirm the view that temporal spectral theta power seems to reflect movement problems like tremor but also signalizes that this pathological feature can be influenced successfully by deep brain stimulation. Quantitative EEG recordings might provide a reasonable control for deep brain stimulation in general.

Psychophysiological Effects of &amp;lt;i&amp;gt;Sideritis&amp;lt;/i&amp;gt; and &amp;lt;i&amp;gt;Bacopa&amp;lt;/i&amp;gt; Extract and Three Combinations Thereof—A Quantitative EEG Study in Subjects Suffering from Mild Cognitive Impairment (MCI)

Mild cognitive impairment (MCI) is regarded as a transitional stage during the development of Alzheimer’s disease. Diagnosis of MCI can be obtained by the questionnaire “DemTect” in German speaking countries. Quantitative assessment has been successfully performed using psychometric testing concomitantly with quantitative EEG recording. The present investigation aimed at the possible treatment of MCI with two botanicals, namely extracts from Sideritis scardica (500 mg) or Bacopa monnieri (320 mg) and three combinations thereof using this method in order to find a new treatment. The performance of the d2-test, an arithmetic calculation test (CPT) and a memory-test revealed better performance for the d2-test only in the presence of Sideritis extract or the combinations with Bacopa extract. Quantitative EEG assessment during the different experimental conditions showed massive differences between both extracts. Whereas Sideritis extract and its combination with a low amount of Bacopa extract (160 mg) induced increases of spectral power in fronto-temporal brain areas, Bacopa and the combination of Sideritis with high amounts of Bacopa extract produced attenuation of all waves except for delta in fronto-temporal brain areas. These differences were also documented by quantitative EEG maps in comparison to Placebo. A different action of both extracts was confirmed by discriminant analysis, where Sideritis extract and its combination with low Bacopa grouped together quite at distance to Bacopa and the combination of Sideritis with high Bacopa. A combination of Sideritis extract with a low amount of Bacopa should be tested with daily repetitive dosing for at least 4 weeks as a consequence.

Psychophysiological Effects of a Combination of Sideritis and Bacopa Extract (memoLoges&amp;lt;sup&amp;gt;&amp;#174;&amp;lt;/sup&amp;gt;) in 32 Subjects Suffering from Mild Cognitive Impairment. A Double-Blind, Randomized, Placebo-Controlled, 2-Armed Study with Parallel Design

Mild cognitive impairment (MCI) can be regarded as a non-demented transitional stage during the development of Alzheimer’s disease. Early recognition of this stage might increase the chance of prevention by early treatment. Within a pilot study, two plant-derived preparations and mixtures thereof were tested successfully in subjects suffering from MCI. A combination of Sideritis scardica and Bacopa monnieri extract (memoLoges®) was chosen now for a repetitive dosing during 4 weeks. Thirty-two subjects aged 50 to 80 years and suffering from MCI (having a DemTect questionnaire score between 8 and 13) were recruited for intake of 2 capsules of the preparation per day. Quantitative EEG recording during relaxation and concomitant performance of three 5 minutes lasting psychometric tests (d2-concentration test, arithmetic calculation test and memory test) was achieved at the first day and one day after the last repetitive intake. Seventeen channels of EEG and one channel EOG (for artefact rejection) were recorded. After frequency analysis (FFT) current source density was calculated as reported earlier. One, two and three hours after intake of the herbal extract or placebo the whole procedure was repeated. Brain imaging was achieved by conversion of numerical values of spectral EEG power into spectral colors and additive color mixture according to RGB as used in TV settings. Intake of memoLoges® induced a trend of improvement of performance in psychometric testing (all three tests). During relaxation quantitative assessment of EEG data revealed attenuation of delta and theta spectral power in frontal brain as likewise reported in the presence of the Alzheimer drug rivastigmine, bringing the spectrum back to “normality”. During mental work memoLoges® induced statistically significant increases of beta power. Since MCI subjects produce less beta power in comparison to healthy subjects, this increase must likewise be seen as a positive effect pointing to a healthier spectrum.

Comparing the effect of hypercapnia and hypoxia on the electroencephalogram during wakefulness

ObjectiveHypoxia has been postulated as a key mechanism for neurocognitive impairment in sleep-disordered breathing. However, the effect of hypoxia on the electroencephalogram (EEG) is not clear. MethodsWe examined quantitative EEG recordings from 20 normal volunteers under three 5-min ventilatory control protocols: progressive hypercapnia with iso-hyperoxia (pO2=150mmHg) (Protocol 1), progressive hypercapnia with iso-hypoxia (pO2=50mmHg) (Protocol 2), and progressive hypoxia with a CO2 scrubber in the circuit (Protocol 3). Each protocol started with a 5-min session of breathing room air as baseline. ResultsIn Protocol 1, compared to its baseline, iso-hyperoxia hypercapnia led to a lower Alpha% and higher Delta/Alpha (D/A) ratio. Similarly, in Protocol 2, the iso-hypoxia hypercapnia induced a higher Delta%, a lower Alpha% and higher D/A ratio. No difference was found in any EEG spectral band including the D/A ratio when Protocols 1 & 2 were compared. In Protocol 3, the Delta%, Alpha% and D/A ratio recorded during hypoxia were not significantly different from baseline. ConclusionsWe found that hypercapnia, but not hypoxia, may play a key role in slowing of the EEG in healthy humans. SignificanceHypercapnia may be a greater influence than hypoxia on brain neuroelectrical activities.

Electroencephalogram slowing in rapid eye movement sleep behavior disorder is associated with mild cognitive impairment

BackgroundIdiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) is a well-documented risk factor for synucleinopathies such as Parkinson disease (PD) and dementia with Lewy bodies (DLB). Moreover, approximately 50% of iRBD patients have mild cognitive impairment (MCI). The purpose of our study was to investigate waking electroencephalogram (EEG) abnormalities specific to iRBD patients with MCI. MethodsForty-two polysomnographically confirmed iRBD patients, including 23 iRBD [+]MCI patients 19 patients without MCI (iRBD [−]MCI), and 37 healthy subjects participated in the study. All participants underwent a complete neuropsychologic assessment for MCI diagnosis and a waking quantitative EEG recording. ResultsiRBD [+]MCI patients had a higher slow-to-fast frequency ratio than iRBD [−]MCI patients and controls in the parietal, temporal, and occipital regions. iRBD [+]MCI patients also had higher relative θ power in the parietal, temporal, and occipital regions and lower relative α power in the occipital region compared to iRBD [−]MCI patients and controls. Moreover, iRBD [+]MCI patients had higher relative θ power in the frontal and central areas and lower relative β power in the central, parietal, and temporal regions compared to controls. The dominant occipital frequency also was slower in iRBD [+]MCI patients compared to controls. No between-group differences were observed between iRBD [−]MCI patients and controls. ConclusionIn iRBD patients, only those with concomitant MCI showed waking EEG slowing in the posterior cortical regions, providing a potential marker for an increased risk for developing DLB or PD.

Different quantitative EEG alterations induced by TBI among patients with different APOE genotypes

Although several studies have revealed the EEG alterations in AD and TBI patients, the influence of APOE (apolipoprotein E) genotype in EEG at the early stage of TBI has not been reported yet. We have previously studied EEG alterations caused by TBI among different APOE genotype carriers. In this study, we firstly investigated the relationship between APOE polymorphisms and quantitative EEG (QEEG) changes after TBI. A total of 118 consecutive TBI patients with a Glasgow Coma Scale (GCS) of 9 or higher were recruited, and 40 normal adults were also included as a control group. APOE genotype was determined by PCR-RFLP for each subject, and QEEG recordings were performed in rest, relaxed, awake and with eyes closed in normal subjects and TBI patients during 1–3 days after TBI. In the normal control group, both APOEɛ4 carriers and non-carriers had normal EEG, and no significant difference of QEEG data was found between APOEɛ4 carriers and non-carriers. But in the TBI group, APOEɛ4 carriers had more focal or global irregular slow wave activities than APOEɛ4 non-carriers. APOE gene did not influence brain electrical activity under normal conditions, but TBI can induce different alterations among different APOE gene carriers, and APOEɛ4 allele enhances the EEG abnormalities at the early stage of TBI.

Pretreatment neurophysiologic function and ECT response in depression.

Recent brain imaging studies have provided evidence that brain function assessed prior to treatment of depression may be associated with eventual treatment response. The present study tested the hypothesis that brain activity in midline apical quantitative EEG (QEEG) electrodes would be associated with therapeutic response to electroconvulsive therapy (ECT). Ten treatment-refractory patients with unipolar or bipolar depression received a Hamilton Rating Scale for Depression (Ham-D) at baseline, during, and following ECT treatment. Resting, eyes-closed, 35-lead QEEG recordings were done 1 day before the initial ECT treatment. Data were analyzed using QEEG power and cordance. The mean of the theta-band pretreatment cordance from the central brain region was strongly associated with percentage decrease in Ham-D score over the course of treatment (r = 0.80, P = 0.005). QEEG cordance from other brain regions and power from all brain regions did not show an association with clinical improvement. Depressed subjects with higher pretreatment central cordance appear to be more likely to experience therapeutic benefits of ECT. The location of central electrodes over the cingulate cortex may indicate that pretreatment cingulate activity is associated with response to ECT.

Simultaneous central nervous system distribution and pharmacokinetic-pharmacodynamic modelling of the electroencephalogram effect of norfloxacin administered at a convulsant dose in rats.

The objective of this study was to investigate the contribution of norfloxacin blood-brain barrier (BBB) transport to its delayed electroencephalogram (EEG) effect in rats. Norfloxacin was injected as a bolus dose of 150 mg kg(-1). Blood samples were collected for total norfloxacin plasma concentration measurements. The corresponding unbound levels were determined in brain extracellular fluid (ECF) using microdialysis. Quantitative EEG recording was conducted during 9 h post-dose. Brain ECF norfloxacin concentrations were much lower than plasma levels (AUC ratio=9.7+/-2.8%) but peaked very early, and concentration versus time profiles were parallel in both biological fluids. The best pharmacokinetic (PK) modelling was obtained by considering that ECF concentrations were part of the central compartment, with a proportionality factor. The peak of EEG effect was delayed and the effect versus plasma concentration curves exhibited a dramatic hysteresis. A PK-pharmacodynamic (PD) effect compartment model with a spline function to describe the relationship between effect and concentration at the effect site successfully described the data. Comparisons of PK-PD parameters estimated from plasma and ECF concentrations show that most of the delayed norfloxacin EEG effect is not due to BBB transport, but also that PD parameters derived from plasma data must be carefully interpreted when drug distribution at the effect site is restricted, as may often be the case for centrally acting drugs.

QUANTITATIVE EEG PATTERNS FOLLOWING UNILATERAL STROKE: A STUDY IN CHRONIC STAGE

The aim of this study was to investigate the EEG power spectra obtained during rest and mental processing in chronic stroke patients. Seventeen patients with stabilized unilateral cerebral ischemia, grouped according to the side of lesion, underwent quantitative EEG recordings during rest and attentive/cognitive tasks. EEG spectral values were compared with those of 11 healthy subjects. Patients displayed different EEG patterns from controls, under rest condition: patients with left hemispheric lesion were characterized by a preserved alpha and beta band "reactivity," with a lack of significant changes in slow band components. In patients with right hemisphere lesion, no significant changes of the slow and fast band activities were evident during each task. These findings indicate that different EEG patterns of activation characterize stroke patients with left and right hemispheric damage.

EEG power changes are related to regional cerebral glucose metabolism in vascular dementia

Objective: In patients with vascular dementia (VD), the relationship between the EEG power within the 4 frequency bands and the regional metabolic disturbances was investigated.Methods: Twenty-eight patients (age 69.0±6.54 years) with VD according to NINDS-AIREN criteria underwent quantitative EEG recording, according to the 10–20 system, and fluodeoxyglucose F18 positron emission tomography (PET) at resting condition within 24 h. EEG power FFT-analysis was performed for delta (2–3.5 Hz), theta (4–7.5 Hz), alpha (8–13 Hz) and beta (13.5–20 Hz) frequency bands. Regional EEG power bands were related to regional glucose metabolism in anatomically defined regions corresponding to locations of the 10–20 system.Results: Correlation between slow frequency band power and glucose metabolism was found. A widespread inverse relationship of delta power to metabolism was found between various regions; additionally, delta power was negatively correlated to cerebral glucose metabolism in individual regions. Frontal theta power correlated especially with thalamic CMRglc. Alpha power correlated directly with metabolism in the occipital lobe. No significant relationships were found between beta power and metabolism.Conclusion: We conclude that EEG power in VD is linked to glucose metabolism, indicating specific regional dependencies.

Quantitative EEG and BPRS data following Haldol-Decanoate administration in schizophrenics.

Approximately one-third of schizophrenic patients receiving antipsychotic drugs obtain little or no benefit from them. In some reports, response has been linked with "prognostic" factors, including abnormal EEG and drug response (pharmaco-EEG). Measurements of topological EEG spectral power and Brief Psychiatric Rating Scale (BPRS) values were obtained in 15 schizophrenics over a period of 20 min immediately after the first application, and at weekly intervals after single intramuscular injection of 2 ml depot haloperidol (Haldol-Decanoate). A highly significant increase in the alpha-1 power density at almost all positions and an increase in theta power at parietotemporal regions can be described as electrophysiological parameters of the acute pharmaco-EEG. BPRS values decreased continuously within the first 2 weeks followed by an increase to the predrug level after the fourth week. Over the whole observation period there was a correlation between neurophysiological data (alpha-1 power) and clinical symptomatology (BPRS total score; r = -0.7). Therefore, it can be concluded that quantitative EEG recordings are able to serve as a tool for the optimization of the depot neuroleptic treatment in schizophrenics.