Nonepileptiform EEG Abnormalities Research Articles

Concurrent EEG monitoring helps interpret neuropsychological testing results in patients with epilepsy

ObjectiveWe sought to determine if global cognitive function in patients with epilepsy (PWE) differs when electroencephalographic (EEG) abnormalities are present during concurrent neuropsychological (NP) evaluation. MethodsWe explored the association between subclinical epileptiform discharges (sEDs) and interictal epileptiform discharges (IEDs) and global aspects of cognition in 79 consecutive PWE who underwent continuous EEG monitoring during NP evaluation for diagnostic (15%) or presurgical (85%) purposes while on their standard antiseizure medication (ASM) regimens. As some researchers have suggested that the apparent link between IEDs and cognition represent epiphenomena of an underlying damaged neural substrate, we used functional status as a stratifying covariate to allow us to address this position. ResultsDespite being on their standard ASM regimen, EEG was abnormal in 68% of patients. Epileptiform abnormalities (IEDs, sEDs, or both) were seen in isolation or coupled with diffuse or focal slowing in 38% of patients. Individuals with IEDs occurring during their NP evaluation demonstrated poorer scores in attention/working memory (forward and backward digit span), processing speed (symbol searching and coding), and speeded components of language (semantic fluency) tests compared with those with normal EEG tracings matched by their real-world, functional status. In two high functioning patients, performance was significantly better when these individuals were tested in the absence of IEDs, with performances appearing invalid when tested during periods of IED activity. No significant association was found between NP performance and nonepileptiform EEG abnormalities. SignificanceA substantial proportion of PWE undergoing NP evaluation manifest concurrent EEG abnormalities, with epileptiform abnormalities associated with poorer global cognitive performance. As this pattern was observed regardless of functional status, this association appears to represent more than unrelated features coincidentally shared by the lowest functioning cohort. Coupled with our individual case data, our findings suggest that NP testing may be adversely affected by IEDs and sEDs going unrecognized in the absence of simultaneous EEG recordings, and set the stage for future studies to definitively establish this possible relationship.

O-20 Epileptiform and non-epileptiform EEG abnormalities in Autism Spectrum Disorder relate to opposite excitation-inhibition balance disturbances

Background Autism spectrum disorder (ASD) has been associated to balance alterations between neuronal excitation and inhibition (E/I). Part of this association is built upon the frequent concurrence of ASD with epilepsy and epileptiform abnormalities. Non-epileptiform EEG abnormalities are also frequent, yet their clinical relevance remains unclear. We hypothesize that subjects with EEG abnormalities – epileptiform and non-epileptiform – represent different physiological subgroups within the autism spectrum and have different effects on E/I balance. Using a novel algorithm involving critical-state dynamics we show that fluctuations in neuronal oscillations can be used to estimate E/I balance of neuronal networks. Here, we use this method to test the relationship between epileptiform and non-epileptiform abnormalities and E/I balance disturbance in ASD. Methods We investigated 64-channel EEG recordings of 100 unmedicated children with ASD and 29 typically developing children (age range 7–15 years). We assessed for EEG abnormalities according to Luders and Noachtar’s atlas and classification of electroencephalography and estimated the E/I ratio based on alpha oscillations. Results ASD subjects with EEG abnormalities (ASDabn, 46%) had lower E/I ratios than the group without abnormalities (p = 0.00035). From the ASDabn group, subjects with slowing of activity showed the lowest global E/I ratios (p = 0.0001), while epileptiform abnormalities were related to localized high E/I (p = 0.0063). Conclusions Epileptiform and non-epileptiform EEG abnormalities showed opposite excitation-inhibition balance disturbances identifying two subgroups within ASD – one with global increase of inhibition and one with locally increased excitation. This neurophysiological distinction may be determinant for targeting future treatment decisions.

Non-epileptiform EEG abnormalities: an overview

More than 80 years after its introduction by Hans Berger, the electroencephalogram (EEG) remains as an important supplementary examination in the investigation of neurological disorders and gives valuable and accurate information about cerebral function. Abnormal EEG findings may include ictal patterns, interictal epileptiform activity and non-epileptiform abnormalities. The aim of this study is to make an overview on the main non-epileptiform EEG abnormalities, emphasizing the pathologic findings and the importance of their recognition, excluding periodic patterns and EEG physiologic changes. Scientific articles were selected from MEDLINE and PubMed database. The presence of non-epileptiform EEG abnormalities provide evidence of brain dysfunction that are not specific to a particular etiology and may be related to a number of disorders affecting the brain. Although these abnormalities are not specific, they can direct attention to the diagnostic possibilities and guide the best treatment choice.

EEG does not predict response to valproate treatment of aggression in patients with borderline and antisocial personality disorders.

Previous investigations of the role of EEG in predicting response of aggressive patients to valproate therapy have yielded mixed results. In this study of borderline and antisocial personality disorder patients hospitalized with aggressive behavior, EEGs were obtained prior to treatment with valproate. Eight of 22 (36.4%) patients subsequently responsive to valproate had nonepileptiform EEG abnormalities, while 5 of 20 (25%) patients not responsive to valproate had nonepileptiform EEG abnormalities. Although more of the valproate responders than nonresponders had EEG abnormalities, the presence of nonepileptiform EEG abnormalities was not a statistically significant (X2 = 0.213, df = 1, p = 0.64) predictor of valproate response in personality disorder patients with aggression.

Does EEG predict response to valproate versus lithium in patients with mania?

A number of factors may suggest that a patient with mania may respond to valproate or to lithium. However, prediction of which patients will respond to either medication remains difficult. In this study nonepileptiform EEG abnormalities in responders to each medication were investigated. Six of 20 patients (30%) responsive to lithium but not to valproate had nonepileptiform EEG abnormalities while 14 of 20 patients (70%) responsive to valproate but not to lithium had nonepileptiform EEG abnormalities. Patients presenting with mania and EEG abnormalities, particularly sharp activity, are statistically more likely (chi2 = 4.9, df = 1, p = .027) to respond to valproate than to lithium. Whether such a finding will also hold true for other anticonvulsants used to treat mania remains to be seen.

Electroencephalogram alterations during treatment with olanzapine.

Olanzapine is similar in structure and pharmacology to clozapine. An increased incidence of electroencephalogram (EEG) abnormalities and seizures has been associated with clozapine but not with olanzapine, although isolated cases of seizures under olanzapine have been observed in high-risk patients. To evaluate the frequency of epileptic and non-epileptiform EEG abnormalities during treatment with olanzapine. Using a rating scale of demonstrated reliability, 43 EEGs of patients receiving 10-25 mg/day olanzapine in routine treatment were blindly rated and compared with EEG registrations from the same 43 patients with a different medication. There was no difference in epileptiform activity between the conditions with and without olanzapine. However, EEG slowing was significantly more frequent with olanzapine than under the other condition. This difference could not be attributed to concomitant medication. Although epileptiform activity did not increase under olanzapine, unspecific EEG abnormalities may be more frequent than with use of other neuroleptics. Careful surveillance of patients with risk factors for seizures is advisable. Further studies addressing the frequency and clinical relevance of EEG changes under olanzapine are necessary.

Avoiding the pitfalls of EEG interpretation in childhood epilepsy.

The accurate interpretation of the electroencephalogram (EEG) of infants and children being evaluated for suspected epilepsy is based on the appreciation of normal and expected age-dependent characteristics, an awareness of the significance of both epileptiform and non-epileptiform activity, and the correlation of epileptiform abnormalities with clinical findings. Avoiding the pitfalls of pediatric EEG interpretation include the recognition of such normal EEG features in wakefulness as posterior slow waves of youth, mu rhythm, and lambda waves. In addition, the understanding of age-dependent characteristics of EEG state-changes is essential, such as: monorhythmic and paroxysmal hypnagogic hypersynchrony, special features of vertex transients and sleep spindles, positive occipital sharp transients, initial arousal responses and post-arousal hypersynchrony. The EEG response to activation procedures such as hyperventilation and photic stimulation may also be a source of confusion. Patterns of uncertain diagnostic significance also may be present in children, including 14- and 6-Hz bursts and rhythmic temporal theta bursts of drowsiness (the so-called psychomotor variant). Some nonepileptiform EEG abnormalities may also be misinterpreted as epileptiform. The determination of the clinical significance of spike foci and generalized abortive spike-and-wave may pose more of a problem as a potential pitfall than the identification by visual analysis of these interictal discharges. Another problem posed to the electroencephalographer is the determination of the EEG response to antiepileptic drug therapy including effect on spike foci, generalized spike-and-wave and electrical seizure activity, and effect on background activity. The recognition of the differences between the EEG of children and adults will provide the basis for more accurate interpretation and assist the electroencephalographer in avoiding the identification of normal, age-dependent features as epileptiform.

Surgical treatment of epilepsy due to cortical dysplasia: clinical and EEG findings.

Seventeen patients with cortical dysplasia who had surgical resection for medically intractable partial epilepsy were studied. Compared with two groups of surgically treated patients with intractable epilepsy due to tumour (n = 20) and mesial temporal sclerosis (n = 40), patients with cortical dysplasia showed significantly more frequent extratemporal lesions, more frequent non-epileptiform EEG abnormalities and less favourable surgical outcome for seizure control. Patients with cortical dysplasia were younger at onset of seizures and had a lower detection rate of CT abnormalities compared with the tumour group, and lower IQ compared with the mesial temporal sclerosis group. MRI was abnormal in five of seven patients. Six patients became seizure-free or almost seizure-free but eight did not experience relief of seizures. Surgical outcome related to the extent of pathology but not to the histological abnormality. Lesions outside the temporal and frontal lobes were correlated with poor surgical outcome, as were generalised interictal EEG abnormalities, which may reflect extensive or multiple lesions. Ictal intracranial recordings were not useful for presurgical evaluation of cortical dysplasia.

Pathogenesis and Significance of Abnorma Nonepileptiform Rhythms in the EEG

In this article the present state of knowledge of physiological mechanisms underlying nonepileptiform EEG abnormalities is reviewed. Focal and widespread slow waves, background activity abnormalities, and bursts of rhythmic slow activity are discussed. Clinical and experimental data accumulated over the past four decades suggest that polymorphic slow activity is generated in cerebral cortex by layers of pyramidal cells and is probably due to partial deafferentation from subcortical areas. Unilateral background activity changes are probably due to thalamic dysfunction, and bilateral paroxysmal slow activity is due to abnormal thalamocortical circuits combined with cortical pathology. The fact that pathologic slow-wave phenomena are longer in duration than the average postsynaptic potential is also discussed.

Neuropsychological correlates of the electroencephalogram in epileptics: III. Generalized nonepileptiform abnormalities.

A broad battery of neuropsychological tests was given to 111 adult epileptics treated primarily with phenytoin. The patients were grouped according to degree of generalized nonepileptiform EEG abnormalities in waking EEGs. In patients classified as None/Mild, Moderate, or Marked in terms of these EEG abnormalities performances on 15 neuropsychological measures were contrasted. Statistically significant differences across the groups were found on 13 of the 15 neuropsychological variables. An orderly decrease in performance occurred as a correlate of an increase in EEG abnormalities. These results were compared to a similar analysis of the correlates of topographic distribution of epileptiform discharges (Absent, Focal, Generalized). It was discovered that degrees of generalized slow wave EEG abnormalities were more potent in differentiating levels of neuropsychological performance than epileptiform discharges. Nevertheless, when discharges and degree of nonepileptiform abnormalities were simultaneously considered, a maximal level of correlation was reached.