Abstracts

Rationale: "Subclinical Spikes" (SCS) are electrographic spikes without known or observable clinical seizure manifestations, and may be associated with neuropsychological, behavioral and academic impairments. [Mintz et al. 2009]. Although related to ictal events, they are often considered less clinically significant. Many studies have shown SCS to be associated with momentary decrement in cognitive function. We examined our records to determine the frequency of SCS in our population, and the diagnoses and testing done on this population. Methods: Retrospective review and analysis of patients without known epilepsy with unexpected SCS found on digital dense array electroencephalography (dEEG). The records of 1592 patients who had an initial dEEG performed between Jan 2010 and Mar 2014 were examined. Baseline spike burden was determined from a 41-minute routine awake/drowsy dense array EEG recording. Patient records were analysed for diagnoses, neuropsychological (NP) testing results, and anti-epileptic drug (AED) treatments. Results: 133 of the subjects had a diagnosis of epilepsy, and were not analysed further. Of the remaining 1459 patients, 64 (4.5%) exhibited SCS. Thirty-three subjects had centrotemporal spikes, 19 frontal, and 12 parieto-occipital. The subjects (46 male, 18 female; 3-23 years, mean 7.8) had diagnoses of Autism Spectrum Disorder (ASD), Attention Deficit Hyperactivity Disorder (ADHD), learning disorders and/or behavioral issues. Of the 179 ASD subjects with dEEG performed, 11 (6.1%) exhibited SCS. Out of the 859 patients who presented with ADHD, Learning Disorders, or behavioral difficulties, 38 (4.5%) exhibited SCS. The remaining 340 patients were mainly diagnosed with anxiety, sleep disorders, obsessive-compulsive disorder (OCD), ataxia or headaches/migraine. Of these, 15 (4.4%) exhibited SCS. Of the overall 64 subjects identified with SCS, 52 (80%) had baseline NP assessments. These showed significant abnormalities, including cognitive deficits in working memory, attention and processing speed. 22 subjects (34%) were treated with antiepileptic drugs (AEDs), all associated with spike suppression. Seven (32%) of those subjects had repeat neuropsychological assessments post-treatment revealing improvements in cognitive functioning. Conclusions: Unexpected SCS can be found in patients presenting with cognitive and neurobehavioral disorders not obviously related to epilepsy. The noted impairments of neurological and NP functioning suggest that SCS may not be as "benign" as previously thought. SCS may be surrogate markers for unrecognized epilepsy, prodromal epilepsy, ion channelopathies causing neuronal disturbances, cerebral structural impairments or disconnectivity, or may be independently pathological. AEDs may result in improvements in clinical and NP surrogate markers in some patients, associated with concomitant spike suppression, suggesting the concept of "Epilepsy Spectrum Disorders".