Recurrent prolonged fugue states as the sole manifestation of epileptic seizures
A 15-year-old female, presented with 10 years history of recurrent episodes of acute onset, prolonged confusional states, accompanied by excessive somnolence, lasting for 15-24 h or more. The patient was a full-term normal delivery, with normal developmental milestones. The attacks first manifested at 5 years of age with a frequency of 1-2 per month, the current frequency being 2-3 per month. The attacks were stereotyped in nature and characterized by a prolonged fugue like state which would descend all of a sudden without any prior warning. During the attacks, the patient would appear dazed and become clumsy and ataxic. She displayed excessive sleepiness and remained confined to bed most of the day but remained partially responsive, answering in monosyllables, drinking and eating food when offered and would also attended to her toilet needs with assistance. The attacks were not accompanied by any jerks, tonic-clonic contractions, automatisms, or incontinence. The attacks would terminate as suddenly as they started and the patient would then resume her normal day to day activities as before. Interictally, her behavior was normal but her overall school performance was poor. There was no history of absence attacks, complex partial seizures (CPS), myoclonic jerks, or generalized tonic-clonic seizures. There was no history of head injury or family history of seizures. She had received valproate (600 mg/day) for 7 years following the onset of these attacks without any significant change in the frequency or duration of the attacks.\nOn examination, at the time of presentation, she was fully conscious and alert. Her minimum mean square error score was 27/30. On detailed higher mental function assessment, her fund of knowledge was poor and frontal lobe performance (literal fluency, mental flexibility, motor programming) was impaired. New learning ability, verbal memory tasks, and constructional ability was also impaired. There was no motor or sensory deficit.\nRoutine investigations including haemogram, blood biochemistry, and magnetic resonance imaging brain were normal. An interictal electroencephalogram (EEG) done at 8 years of age, showed normal background activity with frequent intermittent short lasting bursts of generalized 2.5-3 Hz spike wave discharges lasting for 4-s []. An ictal EEG done at 12 years of age revealed continuous generalized 2.5-3 Hz spike wave discharges throughout the trace without any discernable background activity []. A current EEG done 2 days following the last attack, revealed 3-4 Hz slow background activity with frequent intermittent bursts of generalized, bilateral symmetric and synchronous, high voltage slow wave activity intermixed with spike discharges and at places 3 Hz spike and wave discharges suggestive of a generalized seizure disorder []. Video EEG monitoring in the immediate postfugue state did not reveal any evidence of typical or subtle clinical absence attacks.\nOn the basis of the history and EEG findings, a diagnosis of prolonged fugue states or AS as the sole manifestation of epileptic seizures was made. In view of a history of lack of response to valproate, she was started on levetiracetam (1.5 g/day). Lacosamide (100 mg/day) was added subsequently because of persistence of epileptiform discharges in EEG after 1 week. There was, however, no decrease in frequency of attacks even after 1 month. However, on adding clobazam (30 mg/day) during one of the fugue states she became more responsive with improvement in her sensorium and the duration of attack was significantly reduced to 6 h. Subsequently, clobazam was continued and she remained seizure free over a 4 months follow-up period.