Abstracts

Rationale: Neurofeedback (NF) - facilitated regulation of the arousal state has been used effectively in the treatment of closed head injury1, insomnia2, migraine, depression3, ADHD4, and posttraumatic stress disorder5. A recent meta-analysis review concluded epilepsy was positively impacted by neurofeedback (p = 0.001).6 We therefore hypothesized that NF could serve as a therapeutic modality for epilepsy patients with refractory comorbidities. In the present study we applied a NF protocol to two male patients with well controlled seizures but with medically refractory comorbidities: insomnia, intractable headaches and ADHD in Patient A; episodic dyscontrol (self-banging/ mutilating episodes) in Patient B. Methods: We obtained consent for NF therapy promoting central nervous system (CNS) self-regulation. Procedures were performed under physician direction and supervision (one of the authors). Patient A s implanted vagus nerve stimulator (VNS) device was temporarily inactivated for all his NF sessions. Initial NF trials sought an optimal reinforcement frequency (ORF) for each patient reflecting his optimal arousal state, based on subjective reporting by the patient as well as observer ratings of behavioral alertness. The ORF was established using bipolar training at T3-T4 (the ORF being within the clinical EEG band, particularly the infra-low region < = 0.1 - 1.5 Hz).7, 8 The T3-T4 bipolar recording was used to maximize the reward-based frequency feedback signal without promoting hemispheric coherence (of concern in individuals with seizures). Subsequently, each patient was scheduled to receive 21 separate 30-minute NF sessions (Othmer protocol9) over a period of four weeks. Baseline performance tests (symptom profiles, TOVA10, QEEGs, and observer evaluations) were to be repeated after 21 sessions to compare results to pre-treatment baseline. Results: (Table 1.) Patient A completed only 13 sessions (discontinuing for financial reasons). Nevertheless Patient A's medications for insomnia, headache, and ADHD were progressively discontinued and he remained seizure free on his original three antiepileptic drugs (oxcarbazepine, rufinamide, and zonisamide). Patient B s symptom profile was reduced 62.7% following 21 NF sessions; his seizures remained well-controlled on monotherapy (topiramate). Conclusions: Early results support the hypothesis that NF is a useful therapeutic modality for managing epilepsy comorbidities without compromising seizure control. Furthermore, NF treatment can allow medications other than AEDs to be discontinued thereby averting potential adverse effects arising from multiple drug interactions. The therapy is not widely covered by insurance, limiting its heuristic evaluation. Intrinsic cortical hyperexcitability underlying common epilepsy disorders reflects disturbed mechanisms of CNS control and regulation. Because many epilepsy comorbidites are syndromic expressions of the same CNS dysregulation that gives rise to seizures, physician-driven protocols investigating the mechanisms by which NF works to control comorbidities may shed light on mechanisms of epileptogenesis.