Sub-Saharan African Journal of Medicine

: 2017  |  Volume : 4  |  Issue : 3  |  Page : 57--61

Benign epileptiform variant electroencephalography

Frank A Imarhiagbe1, Oladunni V Ogundare1, Abiodun L Azeez2,  
1 Department of Medicine, Neurology Unit, Benin City, Nigeria
2 Department of Surgery, Division of Neurological Surgery, University of Benin Teaching Hospital, Benin City, Nigeria

Correspondence Address:
Frank A Imarhiagbe
P.O. Box 7184, GPO, Benin City


Background: Benign Epileptiform Variant EEG (BEV), are suspicious but innocuous EEG that are not predictive of epilepsy. The confident detection of BEV in routine EEG is vital so as not to misinterpret them as pathological, with its attendant clinical and sundry consequences. Objective: To profile BEV in routine EEG. Materials and Methods: Two hundred seventeen consecutive routine EEG done in 2013–2014 were reviewed for demographics of age and sex of the subjects, indications for EEG or clinical diagnosis, mental state of subjects during EEG procedure, EEG diagnosis and BEV. Operationally, EEG was done with an 18 channel machine without video recording and mental state of subjects was either awake and relaxed with eyes closed or asleep in uncooperative patients. Sleep was induced with parenteral or oral diazepam or chlorpheniramine. Procedure was done by EEG technologists and all records were interpreted by Consultant Neurologists. Results: The prevalence of BEV was 13.8%, mean age of subjects with BEV was significantly higher than that of subjects with essentially normal and abnormal EEG, sex distribution and handedness were however not significantly different. The distribution of BEV was wickets (5.5%), SREDA (4.1 %), FIRDA (1.4 %), RTTD (0.5%), Phantom spikes or 6-Hz spikes (1.0%) and POSTS (1.4%). Conclusion: BEV may be relatively infrequent in routine EEG, however their detection prevents the untoward consequences and the attendant clinical and other effects that a misinterpretation of EEG engenders. A second or third opinion is advised where there is equivocation in routine EEG or when BEV is suspected.

How to cite this article:
Imarhiagbe FA, Ogundare OV, Azeez AL. Benign epileptiform variant electroencephalography.Sub-Saharan Afr J Med 2017;4:57-61

How to cite this URL:
Imarhiagbe FA, Ogundare OV, Azeez AL. Benign epileptiform variant electroencephalography. Sub-Saharan Afr J Med [serial online] 2017 [cited 2022 Sep 27 ];4:57-61
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Benign epileptiform variants (BEVs) electroencephalography (EEG) are kinds of EEG patterns with morphology of waves or rhythms that appear abnormal and suspicious but are not pathological; rather they do not have any clinical significance different from normal EEG and they do not predict the occurrence of epilepsy.[1],[2],[3]

BEVs are not common but the significance of recognizing them is to prevent misinterpretation of EEG that are relatively innocuous as abnormal and thereby forcing a misdiagnosis with the attendant clinical corollary.[1],[2],[4],[5]

Recognition of BEV can be difficult, and it requires some level of expertise on the part of the interpreter to confidently decipher it. The skill to confidently interpret EEG is relatively scarce on a general note in the developing countries of sub-Saharan Africa and to recognize BEV appears to be far worse.[1],[2],[6]

There are several wave forms and rhythms that are labeled as BEV, and they include wickets or comb rhythm or “rhythm en arceau,” frontal intermittent rhythmic delta activity (FIRDA), subclinical rhythmic electrographic discharge of adults (SREDA), rhythmic temporal theta discharge of drowsiness (RTTD) or psychomotor variants, 6 Hz spikes or phantom spikes, 14 and 6 Hz positive spikes, mid temporal discharge of theta (ciganek rhythm), short sharp spikes of sleep which are also referred to as benign sporadic spike of sleep or benign epileptiform transients of sleep (BETS) and positive occipital sharp transients of sleep (POSTS) or lambdoids.[7],[8],[9] Some have for the ease of identification and nosology-differentiated BEV into those with alterations in rhythm and others with transients and those characteristically seen in sleep and age-dependent changes.[7],[10]

The clinical significance of recognizing BEV is particularly important where the semiology (clinical manifestation of a seizure) is not clear cut or doubtful as in psychogenic non-epileptic seizures, and the decision needs to be made as to whether antiepileptic drugs (AED) should be commenced or not.[6],[11]

Cases abound of misinterpretation of EEG and misdiagnosis of epilepsy with attendant avoidable clinical, social and financial consequences for the participants and family members.[5],[11]

This study looked at the profile of BEV EEG in the University of Benin Teaching Hospital, Benin City, Nigeria.


Two hundred and seventeen routine EEG taken between June 2013 and March 2014 were consecutively reviewed for demographics of age and sex of the participants, indications for EEG or clinical diagnosis, mental state of participants during EEG procedure, EEG diagnosis and BEV. Operationally, EEG was done with an 18-channel machine, Truscan Deymed®, manufactured in Czech republic in 2012 without video recording using the 10–20 electrode placement system, and the mental state of participants was either awake and relaxed with eyes closed or asleep in uncooperative patients. Sleep was induced with parenteral or oral diazepam or chlorpheniramine. Procedure was followed by EEG technologists for at least 30 min, and all records were interpreted by Consultant Neurologists, and a consensus opinion was agreed upon. Study was approved by the institutional review board or ethics committee of the study center.

Data were entered into a spreadsheet and exported to the Statistical Package for the Social Sciences software (SPSS® version 22; SPSS Inc., Chicago, IL, United States) for analysis. Mean age of study participants and other variables were described and data was compared between participants with BEV and others. Categorical and discrete data were compared with chi-square test and numerical data with Student’s t-test.

P-value of ≤0.05 was taken as significant for all tests.


Median age of total study participants was 17 years (interquartile range, IQR, 32.5–4.0), and sex distribution was 90 (41.5%) females and 127 (58.5%) males. Hand dominance was right in 196 (90.3%) and left in 13 (6%), and it could not be ascertained in 8 (3.7%). One hundred and sixty-five participants (76%) had the EEG recorded in the awake and relaxed state, and the other 52 (24%) had theirs during sleep [Table 1].{Table 1}

Indication for EEG was seizure disorders or epilepsy singly or in combination with other conditions in majority of the cases, that is, 205 (94.4%) participants.

EEG diagnosis was essentially normal in 99 (45.6%) cases, and BEV was the diagnosis in 30 (13.8%). The mean age of participants with BEV was 38.04 ± 23.09 years, and the sex distribution was female 15 (50%) and male 15 (50%). The distribution of BEV were wickets waves in 12 (5.5%), RTTD in 1 (0.5%), 6-Hz positive spike in 2 (1%), FIRDA in 3 (1.4%), SREDA in 9 (4.1%) and POSTS in 3 (1.4%) [Table 1] and [Figure 1],[Figure 2],[Figure 3],[Figure 4],[Figure 5],[Figure 6].{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}

Abnormal epileptiform EEG accounted for 88 (41.0%) of total EEG recorded. Abnormal findings were focal interictal epileptiform activity (FIEA) in 52 (23.9%) of cases and generalized interictal epileptiform activity (GIEA) in 34 (15.7%) of cases. There was one case each of burst suppression 1 (0.5%) and electrocerebral silence 1 (0.5%) [Figure 1].

Data were subsequently compared between participants with normal EEG and BEV. Mean age in years was significantly different (20.83 ± 22.47, n = 99, for normal versus 38.04 ± 23.09, n = 30, for BEV) (P < 0.01); however, sex (P = 0.06), hand dominance (P = 8.00), mental state (P = 0.15), and drugs used (P = 0.75) were not significantly different.

Also data were compared between participants with abnormal EEG and BEV. Mean age was also significantly higher in BEV (20.02 ± 18.51 years, n = 88 for abnormal EEG versus 38.04 ± 23.09 years, n = 30 for BEV) (P = 0.01). Sex, hand dominance, mental state, and drugs used were not significantly different.


The mean age of participants with BEV was significantly higher compared to those with essentially normal and abnormal EEG, and this may be due to the higher number of BEV with SREDA in this study. SREDA is predominantly seen with advancing age compared to other BEV[12] The sex distribution of BEV was remarkably the same for both male and female; however, it was different from that of the rest of the study participants where there was a male sex preponderance. Sex or gender, because it relates to BEV, is seen more in phantom or 6-Hz spikes where female occipitally predominant low-amplitude drowsiness and wake high-amplitude anterior male are variants.[3] Mental state of study participants (awake or sleep) and the AED that they were on did not differ significantly among BEV, those with essentially normal and abnormal EEG. Certain BEV-like lambdoids or POSTS and BETS are, however, known to be characteristically associated with sleep EEG compared to awake records.[9]

Remarkably, BEV accounted for nearly 14% of all the EEG, and the indication for EEG for over 94% of the participants was seizure-related. The corollary is that a further review of nearly 14% of the study participants would be warranted after the EEG report, particularly where the semiology (clinical manifestations of seizures) is not clear cut or doubtful. This may have huge clinical practice implications, and it therefore warrants a thorough and expert interpretation of EEG.[6] The prevalence of BEV in this work is close to two other similar but larger studies from India and Canada.[1],[2]

It is also noteworthy that wickets were the dominant BEV in this study.[13] Wickets are classified under BEV of rhythm disturbances and are characteristically found in the central regions with frequencies similar to alpha rhythm, and they are also variously referred to as comb or mu rhythm or “rhythm en arceau.” They only block with voluntary movements or thoughts of movement of the contralateral limbs.[3] Curiously, SREDA accounted for about a third of BEV in this study in sharp contrast to some earlier reports from western climes.[7],[8] SREDA is also a rhythm disturbance form of BEV seen more often in the those of middle age and in the elderly.[14] SREDA could be unilateral or bilateral and vary in morphology; it may appear during hyperventilation or other activation such as photic stimulation or stroboscopy.[15] FIRDA is also a rhythm disturbance, but RTTD or psychomotor variant, phantom spike or 6-Hz spike and POSTS or lambdoids are classified as BEV with epileptiform transients, and they occurred far less, and together they accounted for less than a third of BEV in this study.[9],[16],[17],[18],[19] 14- and 6-Hz spikes as well as mid temporal discharge of theta or ciganek rhythm, which are also forms of BEV, were not found among BEV in this study, probably due to the relatively small number of the total EEG studied.

A little less than half of the EEG were essentially normal, which corroborates the findings that a larger percentage of routine EEG in seizure disorders and epilepsy appear essentially normal.[13] Abnormal EEG accounted for over 40% of the EEG, and the large majority was FIEA far more than GIEA. This is in consonance with related studies where focal abnormality may account for as high as 60% of all epileptiform patterns on routine interictal EEG.[20]

In conclusion, BEV may be relatively infrequent, but the implication of recognizing them on routine EEG cannot be overemphasized because any misinterpretation of them could have more far-reaching clinical and non-clinical multiplier effects. This implies that EEG interpretation should be tempered with utmost caution, and second and possibly third opinions should be advisedly sought whenever there is a doubt.[21]


We acknowledge the contributions of EEG technologists and staff of the Neurology Unit of the University of Benin Teaching Hospital, Benin City, Nigeria.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Radhakrishnan K, Santoshkumar B, Venugopal A. Prevalence of benign epileptiform variants observed in an EEG laboratory from South India. Clin Neurophysiol 1999;110:280-5.
2Santoshkumar B, Chong JJ, Blume WT, McLachlan RS, Young GB, Diosy DC et al. Prevalence of benign epileptiform variants. Clin Neurophysiol 2009;120:856-61.
3Seyed MM. Benign epileptiform variants. EEG Course, CNSF, Quebec City, QE presented Friday June 11, 2010. Available from: [Last accessed on 2016 Dec 20].
4Berenguer-Sanchez MJ, Gutierrez-Manjarrez F, Senties-Madrid H, Estanol-Vidal B. Electroencephalographic normal variants or with uncertain significance. Rev Neurol 2012;54:435-44.
5Tatum WO 4th, Husain AM, Benbadis SR, Kaplan PW. Normal adult EEG and patterns of uncertain significance. J Clin Neurophysiol 2006;23:194-207.
6Tatum WO. Normal “suspicious” EEG. Neurology 2013;80 (1 Suppl 1):S4-11.
7Dash GK, Radhakrishnan A. What does “subclinical rhythmic electrographic discharge of adults” in EEG signify? J Clin Neurophysiol 2013;30:255-60.
8Poothrikovil RP, Al Asmi A, Gujjar A. Atypical presentation of subclinical rhythmic electrographic discharge of adults (SREDA) in a patient with idiopathic generalized epilepsy. Neurodiagn J 2012;52:42-53.
9Rey V, Aybek S, Maeder-Ingvar M, Rossetti AO. Positive occipital sharp transients of sleep (POSTS): A reappraisal. Clin Neurophysiol 2009;120:472-5.
10Batista MS, Coelho CF, de Lima MM, Silva DF. A case-control study of a benign electroencephalographic variant pattern. Arq Neuropsiquiatr 1999;57:561-5.
11Benbadis SR, Lin K. Errors in EEG interpretation and misdiagnosis of epilepsy. Which EEG patterns are overread? Eur Neurol 2008;59:267-71.
12Zumsteg D, Andrade DM, Del Campo JM, Wennberg R. Parietal lobe source localization and sensitivity to hyperventilation in subclinical rhythmic electrographic discharge of adults. Clin Neurophysiol 2006;117:2257-63.
13Krauss GL, Abdallah A, Lesser R, Thompson RE, Niedermeyer E. Clinical and EEG features of patients with EEG wicket rhythms misdiagnosed with epilepsy. Neurology 2005;64:1879-83.
14Nguyen Michel VH, Ourabah Z, Boudali Y, Gouronnec A, Elwan S, Motamed G et al. The yield of routine EEG in geriatric patients: A prospective hospital-based study. Neurophysiol Clin 2010;40:249-54.
15Westmoreland BF, Klass DW. Unusual variants of subclinical rhythmic electrographic discharge of adults (SREDA). Electroencephalogr Clin Neurophysiol 1997;102:1-4.
16Accolla EA, Kaplan PW, Maeder-Ingvar M, Jukopila S, Rossetti AO. Clinical correlates of frontal intermittent rhythmic delta activity (FIRDA). Clin Neurophysiol 2011;122:27-31.
17Watemberg N, Alehan F, Dabby R, Lerman-Sagie T, Pavot P, Towne A. Clinical and radiologic correlates of frontal intermittent rhythmic delta activity. J Clin Neurophysiol 2002;19:535-9.
18Brigo F. Intermittent rhythmic delta activity patterns. Epilepsy Behav 2011;20:254-6.
19Gelisse P, Crespel A. Phantom spike-and-wave bursts during REM-sleep. Neurophysiol Clin 2008;38:249-53.
20Lombroso CT. Consistent EEG focalities detected in subjects with primary generalized epilepsies monitored for two decades. Epilepsia 1997;38:797-812.
21Benbadis SR. “Just like EKGs!” Should EEGs undergo a confirmatory interpretation by a clinical neurophysiologist? Neurology 2013;80 (1 Suppl 1):S47-51.