Abstracts

Ictal focal beta activity (IFBA) is a rare electroencephalographic seizure pattern, predominantly reported in patients with intractable seizure disorders. One large prior study (n=16[apos]432) observed IFBA in only 0.024% of patients, most of them children with secondary epilepsies. More recently, ictal beta activity on scalp EEG and intracranial EEG was reported in patients with neocortical epilepsies undergoing presurgical evaluation. There is little data on this seizure pattern beyond such patients and studies describing it in human status epilepticus are lacking. Report of two patients, in whom IFBA became the only electroencephalographic seizure pattern in the late phase of refractory status epilepticus (RSE)(patient 1), and in non-convulsive status epilepticus (NCSE)(patient 2). Patient 1: 52 year old female patient with bitemporal non-lesional epilepsy since age 18. Non-adherence to AED treatment and methaqualone intoxication induced RSE lasting 54 days. Various treatments, pentobarbital anesthesia inclusively, failed. RSE eventually subsided under high-dose midazolam and carbamazepine. On day 42, serial episodes with complete loss of responsiveness and tonic upward-gaze were observed; EEG showed high-amplitude beta activity for 15-20 seconds, followed by attenuation. These seizures persisted until was RSE stopped.
Patient 2: 49 year old male schizophrenic patient without history of seizures admitted because of confusional state and hyperglycemia. Medications were quietiapine, biperiden, and risperidone. Repetitive episodes (up to 20/h) of slight tonic right-sided head version and starring started on day 2. Concomitant EEG showed high-amplitude beta-activity for 45-60 seconds followed by slowing and subsequent attenuation. NCSE responded well to lorazepam and valproic acid. Our patients both showed IFBA as the exclusive electroencephalographic seizure pattern in NCSE. IFBA must be differentiated from lateralized asymmetric non-epileptic beta activity occuring in patients with infarcts and tumors who do not experience seizures. Differential diagnosis of IFBA in our first patient additionally includes high-dose benzodiazepine treatment, but the clinical and electroencephalographic evolution render this cause very unlikely. In the second patient, seizure semiology during early NCSE allowed immediate recognition of the ictal nature of the beta activity. However, in the first patient, the ictal nature of beta activity was unequivocally recognized only after she showed a clear clinical seizure correlate (starring and upward-gaze deviation) in the late phase of RSE. With minimal or absent clinical seizure manifestations, antiepileptic treatment in NCSE is predominantly guided by EEG. Therefore, the recognition of rare or atypical electroencephalographic seizure patterns, such as IFBA, is essential in these patients.