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Stimulus-Sensitive Burst- Spiking in Burst-Suppression in Children: Implications for Management of Refractory Status Epilepticus

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Stimulus-Sensitive Burst- Spiking in Burst-Suppression in Children: Implications for Management of Refractory Status Epilepticus Original article Epileptic Disord 2006; 8 (2): 143-50 Stimulus-sensitive burst- spiking in burst-suppression in children: implications for management of refractory status epilepticus Bernard Dan1, Stewart G. Boyd2 1 Department of Neurology, Hôpital Universitaire des Enfants Reine Fabiola, Free University of Brussels (ULB), Belgium 2 Department of Clinical Neurophysiology, Great Ormond Street Hospital for Children, London, United Kingdom Received June 29, 2005; Accepted February 13, 2006 ABSTRACT – Status epilepticus refractory to sequential trials of multiple medi- cation is a rare but significant problem in children. We describe stimulus sensitivity arising during the treatment of convulsive status epilepticus in children (stimulus-sensitive burst-spiking in burst-suppression). We reviewed retrospectively clinical and EEG features in six children (three months to ten years), with status epilepticus requiring intensive care, in whom tactile, auditory and visual stimulation induced myoclonic jerks and bursts of EEG spikes. Sensitivity was not present at onset, but appeared after 24 hours as myoclonic jerks of the eyes, face and limbs, irrespective of the modality and site of stimulation. These were associated with burst-suppression in the EEG, the induced spiking forming the burst component. Various antiepileptic drugs, including GABAergic and NMDA blockers had no effect, but halogenated agents (used in two patients) abolished the sensitivity. Two children died, but the remainder returned to their previous clinical state. We conclude that stimulus sensitivity may appear in the context of refractory status epilepticus treated with high-dose barbiturates. Outcome may be more favorable than previously reported in adults, mostly in the context of post-anoxic or toxic coma. Evalua- tion of ventilated children in status epilepticus should include electroclinical assessment using sensory stimulation. If present, the drug regime should be reviewed and halogenated agents considered. Key words: status epilepticus, stimulus sensitivity, child, barbiturate, isoflurane, Correspondence: halothane, post-anoxic myoclonus B. Dan Department of Neurology, Hôpital Universitaire des Enfants Reine Refractory status epilepticus has been anesthesia. Outcome is often poor, Fabiola, Free University of Brussels (ULB), defined as seizures continuing for particularly in children (Sahin et al. 15 avenue J.J. Crocq, more than 60-90 minutes after initia- 2001, Sahin et al. 2003, Baxter et al. 1020 Brussels, tion of therapy (Shorvon 1994). Pa- 2003). Some authors have reported Belgium tients who reach this stage are often (Jäntti et al. 1994), or illustrated (wi- Tel.: (+00 322) 477 3174; Fax: (+00 322) 477 2176. unresponsive to sequential trials of thout directly addressing) (Baxter et al. <[email protected]> multiple agents and usually require 2003), one uncommon phenomenon Epileptic Disord Vol. 8, No. 2, June 2006 143 B. Dan, S.G. Boyd in children with refractory status epilepticus. This consis- Ormond Street Hospital for Children (London, United ted of bursts of spikes in response to sensory stimulation in Kingdom) were included in the study. While they were in an otherwise “suppressed” EEG. A similar phenomenon status epilepticus, EEGs were taken using conventional has been well-described in adults with post-anoxic coma electrode placements according to the International 10-20 (Van Cott et al. 1996, Morris et al. 1998) or carbamazepine system. In addition, the examiner touched the patients overdose (De Rubeis et al. 2001), perhaps pointing to lightly on the arms and face (tactile stimulation), made common pathophysiological mechanisms. Recently, hand claps (auditory stimuli) and flashed lights on and off Hirsch characterized various patterns of EEG discharges in in front of the patients face (visual stimulation) during the intensive care patients in response to alerting stimuli such recordings. A retrospective review of the clinical notes and as auditory and tactile stimulation, suggesting that these investigations was then carried out. might be linked to arousal mechanisms in critically ill patients (Hirsch et al. 2004). We present six children with prominent evidence of sti- Results mulus sensitivity during status epilepticus and report on its phenomenology and response to pharmacological mani- Six children (clinical details in table 1) with prolonged pulation. convulsive status epilepticus refractory to medication showed clinical and EEG sensitivity to stimulation. This sensitivity appeared after more than 24 hours in response Materials and methods to tactile, auditory and/or visual stimuli. At this time, EEGs showed burst-suppression (not present initially) in all but Five consecutive children with refractory status epilepti- one patient (Case 4) who showed brief periods of low EEG cus admitted to the pediatric intensive care unit of the amplitude. Although none had myoclonic status epilepti- Hôpital Universitaire des Enfants Reine-Fabiola (Brussels, cus, motor responses to stimulation consisted mainly of Belgium) and one child with refractory status epilepticus myoclonic jerks of the eyelids and extremities. The same admitted to the pediatric intensive care unit of Great response was observed irrespective of the modality or site Table 1. Characteristics of patients and stimulus-sensitive status epilepticus. Case No. 123456 Age 9 years 4 months 10 years 21 months 6 years 3 months Gender MFFMFM Previous epilepsy No No Yes No Yes No Underlying None Tracheal Cortical Tracheomalacia Cortical None condition stenosis dysplasia dysplasia Status epilepticus Post-infectious Cardio- Poor epilepsy Respiratory Poor epilepsy Upper airway precipitant encephalitis? respiratory control arrest control infection arrest Duration of status 8 weeks 6 days 24 h 3 days 2-3 days 2-3 days epilepticus EEG features Generalized Generalized Brief focal Generalized Brief focal Brief focal runs of fast complexes complexes of bursts of fast complexes of complexes of activity and including spikes spikes spiking spikes spike-waves spike-waves and fast activity Other clinical SSEP increased none SSEP normal; SSEP normal; none none neurophysiology amplitude; fVEP fVEP absent, fVEP absent, initially normal, later normal; later normal; later absent; BAEP increased BAEP normal BAEP increased I-V latency I-V latency Medication DZP PHT PHB LZP PHB PHT VPA LMT LEV LZP PHT PHB VPA CLB CZP DZP PHB PHT VPA CZP TP CLM TP LZP PHB TP LC PHT PHB TP MDZ TP CLM MP LC ISO+ HAL+ CLM PPF VGB TPM KTM ISO+ Outcome Died Died No sequelae No sequelae No sequelae Hemiplegia SSEP: somatosensory-evoked potentials, fVEP: flash visual-evoked potentials, BAEP: brainstem auditory-evoked potentials, DZP: diazepam, PHT: phenytoin, VPA: valproic acid, CZP: clonazepam, TP: thiopental, CLM: chlormethiazole, MP: methylprednisolone, LC: lidocaine, VGB: vigabatrin, TPM: topiramate, KTM: ketamine, ISO: isoflurane, LZP: lorazepam, LMT: lamotrigine, LEV: levetiracetam, PHB: phenobarbital, HAL: halothane, CLB: clobazam, PPF: propofol, MDZ midazolam; + indicates a clear positive response. 144 Epileptic Disord Vol. 8, No. 2, June 2006 Stimulus-sensitive burst-spiking in refractory status epilepticus of stimulation. The clinical response was intermittent and spiking over a flat background (figure 2). Thiopental with- only appeared in association with EEG spikes. The epilep- drawal did not alter this electroclinical state, nor did tiform EEG bursts were markedly stereotyped, and more subsequent chlormethiazole (10 mg/kg/h), corticosteroids readily seen against a low amplitude EEG background, (30 mg/kg methylprednisolone), vigabatrin (up to constituting the bursts of activity during burst-suppression 120 mg/kg via nasogastric tube), topiramate (up to (figures 1-3). In three documented cases (Cases 1, 2 30 mg/kg via nasogastric tube), lidocaine (up to and 5), the phenomenon persisted when the burst- 0.6 mg/kg/h) or ketamine (up to 7 mg/kg/h). In particular, suppression pattern was clearly not related to medication EEG burst-suppression persisted. However, isoflurane in- but to the time course of the status epilpticus. There was duced a response with increased doses (from 2%), al- some slowing in the rate of spiking before the end of many though clinical seizures recurred whenever the infusion of the bursts (figure 1B), without any slow activity after the was reduced. With effective doses of isoflurane, the phe- run of spikes (figure 1C). The electroclinical phenomenon nomenon was abolished and the EEG activity changed, lasted from hours to days, though it persisted for eight consisting of low amplitude, bi-occipital spikes without weeks in Case 1. Drugs that enhance GABA (barbiturates, clinical correlates followed by total electrocerebral inac- bendzodiazepines, vigabatrin), or that reduce NMDA ac- tivity, however the patient developed tachyphylaxis. MRI tivity (ketamine) as their main mode of action did not alter (T1, T2, FLAIR sequences) performed after one week of it. However, halogenated agents abolished it. status epilepticus was normal. A subsequent scan ob- Three children survived without sequelae; Case 4 who is tained one month later showed diffuse cortical edema and normal, and Cases 3 and 5 with pre-existing seizures who increased signal in the basal ganglia on T2-weighted se- recovered their previous state, but subsequently required quences. A brain biopsy taken on the 42nd day of status surgical excision of focal dysplasia. One infant (Case 6) epilepticus showed focal subcortical necrosis with mac- was left with hemiplegia
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