For >75 years, electroencephalographers have appreciated that focal slowing is an ominous feature in adults. Indeed, electroencephalography (EEG) began its clinical application by localizing cerebral tumors (Walter, 1937). This occurred only 8 years after the first report of the human EEG and 1 year after Lord Adrian predicted the potential of its clinical application (Adrian, 1936). Walter coined the term, “delta” to refer to the slowing that accompanied various pathologic states of brain. In 1937, Walter reported the concordance of EEG and surgical findings in 12 patients, mostly adults. Numerous studies followed his seminal findings, and Goldensohn (2005) showed that EEG can localize lesions in 68% of patients with brain tumors (Niedermeyer & Silva, 2005).
By the end of the 1980s, researchers reported correlations between focal slowing and lesions on computerized tomography (CT) mostly in adults (Gilmore & Brenner, 1981; Schaul et al., 1986; Marshall et al., 1988). Over time, less interest was paid to focal slowing as attention shifted to advanced technologies such as positron emission tomography (PET), magnetoencephalography, and computerized analysis. This may have led to a reduced emphasis on slowing in EEG reports.
Today, imaging has largely replaced EEG for localizing tumors, and conventional EEG is used primarily to diagnose and manage patients with epilepsy. In children with epilepsy, magnetic resonance (MR) studies show a higher percentage of cortical malformations than brain tumors (King et al., 1998; Berg et al., 2009). This tendency is especially high in younger children (Hsieh et al., 2010). These observations led us to investigate the significance of EEG focal slowing in children with epilepsy and specifically to determine the correlation between focal slowing and focal lesions on brain magnetic resonance imaging (MRI). This information could inform the clinical neurophysiologist about the modern clinical significance of this important EEG finding.
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The main finding of this study was that 70% of children with nonsyndromic epilepsy and focal slowing and 56% of children with focal IEDs on their EEG had a brain MRI abnormality. About one third of these structural abnormalities were diffuse; however, the other two thirds were associated with a clear focal structural abnormality. There was a very high concordance with the laterality of the slowing and the presence of lesion on MR imaging, but not location.
Overall, 20% of children in this tertiary referral center sample with epilepsy and no focal slowing had a focal structural lesion on brain MR. This percentage is undoubtedly higher than would be seen in the general population due to the referral biases of children with more complicated epilepsy to our center. However, the difference between the groups with or without focal slowing is still significant.
Consistent with current guidelines on pediatric neuroimaging in patients with epilepsy, we excluded those who had syndromes in which imaging is unlikely to be of benefit including CAE, BECTS, JAE, and JME (Hirtz et al., 2000; Gaillard et al., 2009). Had we included these patients, the proportions of normal scans would have been higher.
MRI findings in different pathologic settings may change over time, including the number of foci or the size of the lesions. In 68% of patients, the interval was <6 months. In the patients who had a longer interval, 59% had MRI findings, which would not expected to change over time. Therefore, only 13% of all patients may have had MRI findings altered by this delay—not a number to change the overall trends.
Higher-strength magnets provide better resolution and sensitivity for detecting focal structural lesions, although it is difficult to quantify this benefit precisely as studies show variable results (Knake et al., 2005; Phal et al., 2008; Strandberg et al., 2008). Because our study combined the use of 1.5 and 3 T imaging, it is plausible that the proportion of subjects with abnormal results would have been greater had all scans been performed at the higher signal strength.
Cortical malformations were seven times more common than tumors in children with MRI lesions. These findings are similar to other modern imaging studies showing a higher percentage of cortical malformations in younger children and a higher proportion of atrophy and tumors in older individuals (King et al., 1998; Berg et al., 2009; Gaillard et al., 2009).
In contrast to the classic teaching that focal delta is seen with lesions of the cortical white matter (Schaul et al., 1986), we found that focal slowing in children with epilepsy was often associated with lesions that covered multiple layers including the cortical gray mantle. In other words, we did not find slowing was restricted to lesions involving the cortical white matter only.
Our findings are completely consistent with the latest recommendations set forth in guidelines for imaging children with epilepsy (Hirtz et al., 2000; Gaillard et al., 2009): “Imaging is recommended when localization-related epilepsy is known or suspected, when the epilepsy classification is in doubt, or when an epilepsy syndrome with remote symptomatic cause is suspected.” Furthermore, the results of this study show that focal slowing, as well as focal interictal epileptiform activity, are important and useful EEG indicators of a brain structural abnormality in children with nonsyndromic epilepsy.
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Dr. Noh reports no disclosures. Dr. Berg receives support from grant NINDS-R37-NS31146. She has received travel funding and honoraria from Eisai, the British Pediatric Neurological Association, and the Epilepsy Research Center (Melbourne); travel funding from UCB the American Epilepsy Society and the International League Against Epilepsy; BIAL, awards from the American Epilepsy Society and British Pediatric Neurological Association; and consulting fees from Dow Agro Science. She serves on the Editorial Boards of Epileptic Disorders, Epilepsy & Behavior, and Neurology. She is past Chair of the International League Against Epilepsy's (ILAE's) Commission on Classification and Terminology, Current Chair of the ILAE's Task Force on Classification-Diagnostic Manual, member of the American Epilepsy Society Psychiatric Task Force, Steward for the National Institute of Neurological Disorders and Stroke (NINDS) Benchmarks in Epilepsy Research. Dr. Nordli, Jr, has received funding as a co-investigator in NIH/NINDS 1-RO1-NS43209 and he is an associate editor for UpToDate. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.