Abstracts

Rationale: Patients with focal cortical dysplasia (FCD) often suffer from intractable epilepsy. FCDs are grouped depending on pathology according to Palmini type 1a, 1b, 2a and 2b. There is conflicting evidence on whether the type of pathology is relevant for the prognosis of epilepsy. High frequency oscillations (HFOs, 80-500Hz) are linked to epileptic areas and their occurrence is more closely linked to the seizure onset zone than to lesional areas. Small studies on patients with FCD showed differing results for the occurrence of HFOs, with some patients having very high and others rather low rates of HFOs within the lesion. This study investigates the correlation between different types of FCDs and the generation of HFOs. Methods: Consecutive patients with FCD that were recorded with intracranial grid electrodes at the Freiburg Epilepsy centre with a 450Hz low pass filter and a sampling rate of 1024Hz were included. Postsurgical pathology was classified after Palmini. Ripples (80-200Hz) and fast ripples (200-450Hz) were visually identified by two independent reviewers during 5 minutes of slow wave sleep. Rates of HFOs were calculated for each channel and compared in areas inside and outside the seizure onset zone (SOZ) and patients with FCD type 1a&b with type 2a&b using ANOVA (p<0.05). Results: Twenty-one patients were included, with four having FCD type 1a, five type 1b, nine type 2a and five type 2b. HFO rates were significantly higher inside than outside the SOZ for all lesion types (p<0.001) and less common in patients with FCD types 1a&b than in FCD types 2a&b (ripple p<0.001, fast ripple p= 0.02) (Figure 1). Other clinical features (# of channels implanted, seizure frequency, postsurgical outcome) did not differ with the pathology. HFOs were not limited to the SOZ areas but also visible in areas adjacent to the SOZ within the FCD (Figure 2). Two types of HFO patterns were observed: pattern 1 was defined as channels with a continuously oscillating baseline with intermittently occurring higher voltage HFOs, with pattern 2 channels had a flat baseline without HF activity and intermittent very high voltage HFOs. The probability of pattern 2 being associated with the SOZ was significantly higher than in pattern 1 (p<0.05). Conclusions: HFOs are significantly correlated with the SOZ in patients with different types of FCD. Other areas of the lesion may also generate lower rates of HFOs. HFO patterns of occurrence may be important for the interpretation of their meaning; those occurring in channels with non-oscillating baselines were more closely linked to the SOZ than those occurring in continuously oscillating baselines. In FCD of Palmini type 1a&b, HFOs were rare compared to FCD type 2a&b, even if other clinical features did not vary between the different pathologies. Our study may indicate that generation of HFOs is more facilitated in patients with FCD type 2a&b and this may be related to the specific pathology. The generation mechanisms of pathological HFOs still remains unclear and thus reasons for the difference in HFO generation remain speculative.