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Acute repetitive pilomotor seizures
Letters to the Editor / Clinical Neurophysiology 116 (2005) 988–990
989
Fig. 1. Auditory cognitive ERPs of two comatose patients. The upper graph (a) shows ERPs of a patient from the MMN positive group. After an initial P1/N1 complex similar for rare (red) and frequent (green) tones, ERPs show a significant divergence the polarity (rare minus frequent is negative) and the latency (around 200 ms) of which correspond to the MMN. The lower graph (b) shows ERPs of a patient from the MMN negative group. The initial P1/N1 complex is still present, but delayed and small in amplitude. No significant difference could be observed between rare tones ERPs and frequent tones ERPs during the whole epoch of analysis. Fischer C, Luaute J, Adeleine P, Morlet D. Predictive value of sensory and cognitive evoked potentials for awakening from coma. Neurology 2004;63(4):669–73. Kane NM, Curry SH, Butler SR, Cummins BH. Electrophysiological indicator of awakening from coma. Lancet 1993;341(7905):688. Naccache L, Obadia M, Crozier S, Detante O, Guillerm C, Bonneville F, Dormont D, Willer JC, Samson Y. Preserved auditory cognitive ERPs in severe akinetic mutism: a case report. Brain Res Cogn Brain Res 2004;19(2):202–5. Tiitinen H, May P, Reinikainen K, Naatanen R. Attentive novelty detection in humans is governed by pre-attentive sensory memory. Nature 1994; 372(6501):90–2.
Lionel Naccachea,c, Louis Puybassetb, Raphae¨l Gaillardc, Emilie Serveb, Jean-Claude Willera a Clinical Neurophysiology Department, Hoˆpital de la Pitie´-Salpeˆtrie`re, Assistance Publique-Hoˆpitaux de Paris, 91 bd de l’Hopital, Paris 75013, France b Neuro-Intensive Care Unit, Hoˆpital de la Pitie´-Salpeˆtrie`re, Assistance Publique-Hoˆpitaux de Paris, Paris, France c INSERM U562, Cognitive Neuro-Imaging,
Service Hospitalier Fre´de´ric Joliot, CEA/DSV/DRM, Orsay 91, France E-mail address: [email protected]
1388-2457/$30.00 q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2004.10.009
Acute repetitive pilomotor seizures We read with interest the report of acute repetitive pilomotor seizures in a patient with right temporal epilepsy in this journal (Dove et al., 2004). The authors discuss the localizing and lateralizing value of pilomotor seizures. They state that this seizure symptom only occurs in temporal lobe epilepsy. Although the most frequent epileptogenic zone
990
Letters to the Editor / Clinical Neurophysiology 116 (2005) 988–990
associated with pilomotor seizures indeed is the temporal lobe, there are important exceptions (Brody et al., 1960; Seo et al., 2003). In our recent review we found that out of all 68 patients with pilomotor seizures published so far, seven patients (10%) clearly had seizure onset outside the temporal lobe (Loddenkemper et al., 2004). We also could demonstrate that there is no lateralizing value in this symptom if the goosebumps appear bilaterally. However, if they are (at least initially) limited to one body side, there is a 84% chance of ipsilateral seizure onset (Loddenkemper et al., 2004). Furthermore, the seizure onset zone (i.e. the area generating the seizure) should be distinguished carefully from the symptomatogenic zone (i.e. the area generating the seizure symptoms). Since most patients with ictal piloerection also have other autonomic symptoms during their seizures, the generator of ictal piloerection most likely is located in the immediate vicinity of the central autonomic network. However, the location within this network is not known. Ictal piloerection could be elicited by electrical stimulation of a variety of loci, including midbrain and prefrontal structures (Kitsikis and Steriade, 1981; Smith, 1945). Therefore it is uncertain whether the mesial temporal structures play a dominant role in generating this particular seizure symptom. We disagree with the authors statement ‘that there is only one previous case of acute repetitive pilomotor seizures’ and right temporal lobe seizure onset. Unless other information becomes available, we would like to credit Dr William M. Landau for the first report of repeated pilomotor seizures, most likely arising from the right temporal lobe. In his case report the seizures ‘continued to recur in intervals of a few minutes to a month’ (Landau, 1953) suggesting intermittent episodes of acute repetitive ictal piloerection which interestingly presented in a march-like pattern. Although no imaging except for a normal pneumencephalogram was available, EEG and clinical findings appeared ‘to place the disordered process in the (right) temporal lobe’ (Landau, 1953). Additionally, Andermann and Gloor (1984) reported that pilomotor seizures in their report of a 61-year-old man (also related to right temporal lobe pathology) ‘occurred every few minutes’. We appreciate the authors’ contribution to the literature of patients with repetitive pilomotor seizures.
References Andermann F, Gloor P. Pilomotor seizures. Neurology 1984;34:1623–5. Brody IA, Odom GL, Kunkle EC. Pilomotor seizures: report of a case associated with a central glioma. Neurology 1960;10:993–7. Dove GH, Buchhalter JR, Cascino GD. Acute repetitive pilomotor seizures (goose bumps) in a patient with right mesial temporal sclerosis. Clin Neurophysiol 2004;115:2511–3.
Kitsikis A, Steriade M. Immediate behavioral effects of kainic acid injections into the midbrain reticular core. Behav Brain Res 1981;3: 361–80. Landau WM. March of piloerection as a convulsive equivalent. Arch Neurol 1953;69:766–8. Loddenkemper T, Kellinghaus C, Gandjour J, Nair DR, Najm IM, Bingaman W, Lu¨ders HO. Localising and lateralising value of ictal piloerection. J Neurol Neurosurg Psychiatry 2004;75:879–83. Seo DW, Lee HS, Hong SB, Hong SC, Lee EK. Pilomotor seizures in frontal lobe epilepsy: case report. Seizure 2003;12:241–4. Smith WK. The functional significance of the rostral cingular cortex as revealed by its responses to electrical excitation. J Neurophysiol 1945; 8:241–55.
Christoph Kellinghausa, Tobias Loddenkemperb Department of Neurology, University of Mu¨nster, Albert-Schweitzer-Str. 33, Mu¨nster 48149, Germany b Department of Pediatrics, The Cleveland Clinic Foundation, Cleveland, OH, USA E-mail address: [email protected] a
1388-2457/$30.00 q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2004.11.021
Reply We wish to thank Drs Kellinghaus and Loddenkemper for their thoughtful comments on our manuscript and bringing to our attention their excellent review of the topic that was not available to us at the time of article submission. Dr Landau’s 1953 paper should be acknowledged as well as the possibility of extra-temporal onset for pilomotor seizures. We agree that the anatomic ictal onset zone cannot be determined with certainty unless intracranial electrodes are positioned in appropriate locations.
Jeffrey Buchhalter, Gerald Dove, Gregory Cascino Department of Child and Adolescent Neurology, Epilepsy Division, Mayo Clinic, 200 First Street SW, Rochester, MN 559805, USA E-mail address: [email protected]
1388-2457/$30.00 q 2004 Published by Elsevier Ireland Ltd. on behalf of International Federation of Clinical Neurophysiology. doi:10.1016/j.clinph.2004.11.022
989
Fig. 1. Auditory cognitive ERPs of two comatose patients. The upper graph (a) shows ERPs of a patient from the MMN positive group. After an initial P1/N1 complex similar for rare (red) and frequent (green) tones, ERPs show a significant divergence the polarity (rare minus frequent is negative) and the latency (around 200 ms) of which correspond to the MMN. The lower graph (b) shows ERPs of a patient from the MMN negative group. The initial P1/N1 complex is still present, but delayed and small in amplitude. No significant difference could be observed between rare tones ERPs and frequent tones ERPs during the whole epoch of analysis. Fischer C, Luaute J, Adeleine P, Morlet D. Predictive value of sensory and cognitive evoked potentials for awakening from coma. Neurology 2004;63(4):669–73. Kane NM, Curry SH, Butler SR, Cummins BH. Electrophysiological indicator of awakening from coma. Lancet 1993;341(7905):688. Naccache L, Obadia M, Crozier S, Detante O, Guillerm C, Bonneville F, Dormont D, Willer JC, Samson Y. Preserved auditory cognitive ERPs in severe akinetic mutism: a case report. Brain Res Cogn Brain Res 2004;19(2):202–5. Tiitinen H, May P, Reinikainen K, Naatanen R. Attentive novelty detection in humans is governed by pre-attentive sensory memory. Nature 1994; 372(6501):90–2.
Lionel Naccachea,c, Louis Puybassetb, Raphae¨l Gaillardc, Emilie Serveb, Jean-Claude Willera a Clinical Neurophysiology Department, Hoˆpital de la Pitie´-Salpeˆtrie`re, Assistance Publique-Hoˆpitaux de Paris, 91 bd de l’Hopital, Paris 75013, France b Neuro-Intensive Care Unit, Hoˆpital de la Pitie´-Salpeˆtrie`re, Assistance Publique-Hoˆpitaux de Paris, Paris, France c INSERM U562, Cognitive Neuro-Imaging,
Service Hospitalier Fre´de´ric Joliot, CEA/DSV/DRM, Orsay 91, France E-mail address: [email protected]
1388-2457/$30.00 q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2004.10.009
Acute repetitive pilomotor seizures We read with interest the report of acute repetitive pilomotor seizures in a patient with right temporal epilepsy in this journal (Dove et al., 2004). The authors discuss the localizing and lateralizing value of pilomotor seizures. They state that this seizure symptom only occurs in temporal lobe epilepsy. Although the most frequent epileptogenic zone
990
Letters to the Editor / Clinical Neurophysiology 116 (2005) 988–990
associated with pilomotor seizures indeed is the temporal lobe, there are important exceptions (Brody et al., 1960; Seo et al., 2003). In our recent review we found that out of all 68 patients with pilomotor seizures published so far, seven patients (10%) clearly had seizure onset outside the temporal lobe (Loddenkemper et al., 2004). We also could demonstrate that there is no lateralizing value in this symptom if the goosebumps appear bilaterally. However, if they are (at least initially) limited to one body side, there is a 84% chance of ipsilateral seizure onset (Loddenkemper et al., 2004). Furthermore, the seizure onset zone (i.e. the area generating the seizure) should be distinguished carefully from the symptomatogenic zone (i.e. the area generating the seizure symptoms). Since most patients with ictal piloerection also have other autonomic symptoms during their seizures, the generator of ictal piloerection most likely is located in the immediate vicinity of the central autonomic network. However, the location within this network is not known. Ictal piloerection could be elicited by electrical stimulation of a variety of loci, including midbrain and prefrontal structures (Kitsikis and Steriade, 1981; Smith, 1945). Therefore it is uncertain whether the mesial temporal structures play a dominant role in generating this particular seizure symptom. We disagree with the authors statement ‘that there is only one previous case of acute repetitive pilomotor seizures’ and right temporal lobe seizure onset. Unless other information becomes available, we would like to credit Dr William M. Landau for the first report of repeated pilomotor seizures, most likely arising from the right temporal lobe. In his case report the seizures ‘continued to recur in intervals of a few minutes to a month’ (Landau, 1953) suggesting intermittent episodes of acute repetitive ictal piloerection which interestingly presented in a march-like pattern. Although no imaging except for a normal pneumencephalogram was available, EEG and clinical findings appeared ‘to place the disordered process in the (right) temporal lobe’ (Landau, 1953). Additionally, Andermann and Gloor (1984) reported that pilomotor seizures in their report of a 61-year-old man (also related to right temporal lobe pathology) ‘occurred every few minutes’. We appreciate the authors’ contribution to the literature of patients with repetitive pilomotor seizures.
References Andermann F, Gloor P. Pilomotor seizures. Neurology 1984;34:1623–5. Brody IA, Odom GL, Kunkle EC. Pilomotor seizures: report of a case associated with a central glioma. Neurology 1960;10:993–7. Dove GH, Buchhalter JR, Cascino GD. Acute repetitive pilomotor seizures (goose bumps) in a patient with right mesial temporal sclerosis. Clin Neurophysiol 2004;115:2511–3.
Kitsikis A, Steriade M. Immediate behavioral effects of kainic acid injections into the midbrain reticular core. Behav Brain Res 1981;3: 361–80. Landau WM. March of piloerection as a convulsive equivalent. Arch Neurol 1953;69:766–8. Loddenkemper T, Kellinghaus C, Gandjour J, Nair DR, Najm IM, Bingaman W, Lu¨ders HO. Localising and lateralising value of ictal piloerection. J Neurol Neurosurg Psychiatry 2004;75:879–83. Seo DW, Lee HS, Hong SB, Hong SC, Lee EK. Pilomotor seizures in frontal lobe epilepsy: case report. Seizure 2003;12:241–4. Smith WK. The functional significance of the rostral cingular cortex as revealed by its responses to electrical excitation. J Neurophysiol 1945; 8:241–55.
Christoph Kellinghausa, Tobias Loddenkemperb Department of Neurology, University of Mu¨nster, Albert-Schweitzer-Str. 33, Mu¨nster 48149, Germany b Department of Pediatrics, The Cleveland Clinic Foundation, Cleveland, OH, USA E-mail address: [email protected] a
1388-2457/$30.00 q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.clinph.2004.11.021
Reply We wish to thank Drs Kellinghaus and Loddenkemper for their thoughtful comments on our manuscript and bringing to our attention their excellent review of the topic that was not available to us at the time of article submission. Dr Landau’s 1953 paper should be acknowledged as well as the possibility of extra-temporal onset for pilomotor seizures. We agree that the anatomic ictal onset zone cannot be determined with certainty unless intracranial electrodes are positioned in appropriate locations.
Jeffrey Buchhalter, Gerald Dove, Gregory Cascino Department of Child and Adolescent Neurology, Epilepsy Division, Mayo Clinic, 200 First Street SW, Rochester, MN 559805, USA E-mail address: [email protected]
1388-2457/$30.00 q 2004 Published by Elsevier Ireland Ltd. on behalf of International Federation of Clinical Neurophysiology. doi:10.1016/j.clinph.2004.11.022