540647 research-article2014
EEGXXX10.1177/1550059414540647Clinical EEG and Neuroscience
Letter to the Editor Clinical EEG and Neuroscience 2015, Vol. 46(2) 169 © EEG and Clinical Neuroscience Society (ECNS) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1550059414540647 eeg.sagepub.com
Transcranial Direct Current Stimulation–Induced Seizure: Analysis of a Case
Dear Editor, Transcranial direct current stimulation (tDCS) is a form of neurostimulation that constantly delivers low current to the brain for facilitating or inhibiting spontaneous neuronal activity. tDCS causes polarity-dependent changes at the resting neuronal membrane potential, and modulates spontaneous neuronal network activity. Unlike transcranial magnetic stimulation, tDCS does not induce neuronal firing by suprathreshold stimuli.1 Induction of seizure by tDCS has not been reported previously. On the contrary, cathodal stimulation was reported to be well tolerated in children with epilepsy, and is associated with a decrease in seizure frequency.2 Here, we report a child who had a seizure after consecutive daily tDCS protocol. A 4-year-old boy with left dominant spastic tetraparesis was consulted for tDCS, at the pediatric neurology outpatient clinic, to reduce spasticity and improve upper limb function. The patient was born to nonconsanguineous parents after 28 weeks of gestation as one of twin sons. He was diagnosed with idiopathic infantile spasms, and ACTH (adrenocorticotropic hormone) was administered at 12 months of age. Our patient remained seizure free with valprote and topiramate, but developed left dominant spastic paresis. He had his last seizure during a viral infection at 3 years of age. Interictal EEG showed absence of active epileptiform discharges. Dosage of valproate was adjusted to 30 mg/kg and topiramate was tapered. Two weeks after completion of topiramate tapering, anodal stimulation with 25-cm2 electrodes was initiated to right motor cortex for 20 minutes at 1.2 mA. Stimulation protocol included 2.5 mg escitalopram administration 2 hours before each session, as serotonergic reinforcement enhances facilitatory aftereffects. The first 2 consecutive stimulations were uneventful, but the patient had a seizure 4 hours after the completion of third stimulation. Seizure started with confusion and speech arrest, followed by deviation of the eyes to the left and clonic jerks of the left arm. Rectal diazepam and intravenous midazolam were administered for secondary generalized seizure. Diagnostic workup for possible infection or electrolyte disturbances revealed no pathologies. The patient remained seizure free after the cessation of the stimulation protocol. The possible etiologies of the induction of seizure after tDCS in this patient might be related to recent adjustment in antiepileptic treatment regimen, premedication with escitalopram, or anodal stimulation. Our patient was seizure free for the past 12 months, and his last EEG revealed no epileptiform activity; subsequently, topiramate treatment was withdrawn. The glutaminergic antagonism and sodium channel blocking effects of topiramate might inhibit facilitatory aftereffects of
anodal stimulation.3 As the seizures did not recur after the cessation of the protocol, changes in the antiepileptic regimen might not be responsible for the seizure. In a previous study, it was reported that serotonin reuptake blockers may enhance facilitatory aftereffects, so we used escitalopram premedication in our protocol.4 A multicenter retrospective review of cases with escitalopram and citalopram demonstrated that escitalopram causes fewer seizures in human overdose than citalopram at comparable doses.5 Hence, escitalopram premedication is not considered as a main trigger for seizure. Animal studies showed that cathodal stimulation could increase the threshold for localized seizure activity. On the other hand, anodal stimulation has no significant effect on the threshold for localized seizure.6 Although no seizure induction after tDCS has been reported previously in the literature, the practice of the procedure is limited in pediatric groups. Unlike in adult patients with stroke, epilepsy is a particular comorbidity in children with cerebral palsy. In the near future, more pediatric patients suffering from cerebral palsy will be eligible for tDCS, and induction of the seizures by stimulation is expected to be reported more frequently. References 1. Brunoni AR, Nitsche MA, Bolognini N, et al. Clinical research with transcranial direct current stimulation (tDCS): challenges and future directions. Brain Stimul. 2012;5:175-195. 2. Auvichayapat N, Rotenberg A, Gersner R, et al. Transcranial direct current stimulation for treatment of refractory childhood focal epilepsy. Brain Stimul. 2013;6:696-700. 3. Nitsche MA, Fricke K, Henschke U, et al. Pharmacological modulation of cortical excitability shifts induced by transcranial direct current stimulation in humans. J Physiol. 2003;553(pt 1):293-301. 4. Nitsche MA, Kuo MF, Karrasch R, Wächter B, Liebetanz D, Paulus W. Serotonin affects transcranial direct current-induced neuroplasticity in humans. Biol Psychiatry. 2009;66:503-508. 5. Yilmaz Z, Ceschi A, Rauber-Lüthy C, et al. Escitalopram causes fewer seizures in human overdose than citalopram. Clin Toxicol (Phila). 2010;48:207-212. 6. Liebetanz D, Klinker F, Hering D, et al. Anticonvulsant effects of transcranial direct-current stimulation (tDCS) in the rat cortical ramp model of focal epilepsy. Epilepsia. 2006;47:1216-1224.
1
Derince Research Hospital, Kocaeli, Turkey
Corresponding Author: Baris¸ Ekici, Department of Pediatric Neurology, Derince Research Hospital, Kocaeli, Turkey. Email: [email protected]
Downloaded from eeg.sagepub.com at UNIV OF MICHIGAN on April 18, 2015
EEGXXX10.1177/1550059414540647Clinical EEG and Neuroscience
Letter to the Editor Clinical EEG and Neuroscience 2015, Vol. 46(2) 169 © EEG and Clinical Neuroscience Society (ECNS) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1550059414540647 eeg.sagepub.com
Transcranial Direct Current Stimulation–Induced Seizure: Analysis of a Case
Dear Editor, Transcranial direct current stimulation (tDCS) is a form of neurostimulation that constantly delivers low current to the brain for facilitating or inhibiting spontaneous neuronal activity. tDCS causes polarity-dependent changes at the resting neuronal membrane potential, and modulates spontaneous neuronal network activity. Unlike transcranial magnetic stimulation, tDCS does not induce neuronal firing by suprathreshold stimuli.1 Induction of seizure by tDCS has not been reported previously. On the contrary, cathodal stimulation was reported to be well tolerated in children with epilepsy, and is associated with a decrease in seizure frequency.2 Here, we report a child who had a seizure after consecutive daily tDCS protocol. A 4-year-old boy with left dominant spastic tetraparesis was consulted for tDCS, at the pediatric neurology outpatient clinic, to reduce spasticity and improve upper limb function. The patient was born to nonconsanguineous parents after 28 weeks of gestation as one of twin sons. He was diagnosed with idiopathic infantile spasms, and ACTH (adrenocorticotropic hormone) was administered at 12 months of age. Our patient remained seizure free with valprote and topiramate, but developed left dominant spastic paresis. He had his last seizure during a viral infection at 3 years of age. Interictal EEG showed absence of active epileptiform discharges. Dosage of valproate was adjusted to 30 mg/kg and topiramate was tapered. Two weeks after completion of topiramate tapering, anodal stimulation with 25-cm2 electrodes was initiated to right motor cortex for 20 minutes at 1.2 mA. Stimulation protocol included 2.5 mg escitalopram administration 2 hours before each session, as serotonergic reinforcement enhances facilitatory aftereffects. The first 2 consecutive stimulations were uneventful, but the patient had a seizure 4 hours after the completion of third stimulation. Seizure started with confusion and speech arrest, followed by deviation of the eyes to the left and clonic jerks of the left arm. Rectal diazepam and intravenous midazolam were administered for secondary generalized seizure. Diagnostic workup for possible infection or electrolyte disturbances revealed no pathologies. The patient remained seizure free after the cessation of the stimulation protocol. The possible etiologies of the induction of seizure after tDCS in this patient might be related to recent adjustment in antiepileptic treatment regimen, premedication with escitalopram, or anodal stimulation. Our patient was seizure free for the past 12 months, and his last EEG revealed no epileptiform activity; subsequently, topiramate treatment was withdrawn. The glutaminergic antagonism and sodium channel blocking effects of topiramate might inhibit facilitatory aftereffects of
anodal stimulation.3 As the seizures did not recur after the cessation of the protocol, changes in the antiepileptic regimen might not be responsible for the seizure. In a previous study, it was reported that serotonin reuptake blockers may enhance facilitatory aftereffects, so we used escitalopram premedication in our protocol.4 A multicenter retrospective review of cases with escitalopram and citalopram demonstrated that escitalopram causes fewer seizures in human overdose than citalopram at comparable doses.5 Hence, escitalopram premedication is not considered as a main trigger for seizure. Animal studies showed that cathodal stimulation could increase the threshold for localized seizure activity. On the other hand, anodal stimulation has no significant effect on the threshold for localized seizure.6 Although no seizure induction after tDCS has been reported previously in the literature, the practice of the procedure is limited in pediatric groups. Unlike in adult patients with stroke, epilepsy is a particular comorbidity in children with cerebral palsy. In the near future, more pediatric patients suffering from cerebral palsy will be eligible for tDCS, and induction of the seizures by stimulation is expected to be reported more frequently. References 1. Brunoni AR, Nitsche MA, Bolognini N, et al. Clinical research with transcranial direct current stimulation (tDCS): challenges and future directions. Brain Stimul. 2012;5:175-195. 2. Auvichayapat N, Rotenberg A, Gersner R, et al. Transcranial direct current stimulation for treatment of refractory childhood focal epilepsy. Brain Stimul. 2013;6:696-700. 3. Nitsche MA, Fricke K, Henschke U, et al. Pharmacological modulation of cortical excitability shifts induced by transcranial direct current stimulation in humans. J Physiol. 2003;553(pt 1):293-301. 4. Nitsche MA, Kuo MF, Karrasch R, Wächter B, Liebetanz D, Paulus W. Serotonin affects transcranial direct current-induced neuroplasticity in humans. Biol Psychiatry. 2009;66:503-508. 5. Yilmaz Z, Ceschi A, Rauber-Lüthy C, et al. Escitalopram causes fewer seizures in human overdose than citalopram. Clin Toxicol (Phila). 2010;48:207-212. 6. Liebetanz D, Klinker F, Hering D, et al. Anticonvulsant effects of transcranial direct-current stimulation (tDCS) in the rat cortical ramp model of focal epilepsy. Epilepsia. 2006;47:1216-1224.
1
Derince Research Hospital, Kocaeli, Turkey
Corresponding Author: Baris¸ Ekici, Department of Pediatric Neurology, Derince Research Hospital, Kocaeli, Turkey. Email: [email protected]
Downloaded from eeg.sagepub.com at UNIV OF MICHIGAN on April 18, 2015
