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Gelastic seizures involving the left parietal lobe
Epilepsy & Behavior 23 (2012) 87–89
Contents lists available at SciVerse ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Case Report
Gelastic seizures involving the left parietal lobe René Andrade Machado ⁎, Adriana Goicoechea Astencio Epilepsy Section, National Neurology Institute, Havana, Cuba
a r t i c l e
i n f o
Article history: Received 2 November 2011 Accepted 4 November 2011 Available online 23 December 2011 Keywords: Gelastic seizure Parietal lobe Magnetic resonance imaging Ictal pattern
a b s t r a c t Gelastic seizures have been described in various epilepsies arising from the temporal or frontal lobes, although the most commonly encountered form is related to the presence of a hypothalamic hamartoma. We describe a patient with gelastic seizures involving the left parietal lobe. Our patient, an 8-year-old girl, underwent interictal video/EEG monitoring and MRI. The seizures consisted of brief staring followed by smiling and laughing. Electroencephalography during the gelastic seizures showed rhythmic spikes and waves in the left parietal lobe. MRI revealed the characteristic features of focal cortical dysplasia. Our findings suggest that the left parietal lobe may actively participate in the particular epileptogenic network generating gelastic seizures. © 2011 Elsevier Inc. All rights reserved.
1. Introduction Gelastic seizures (GSs) are characterized by bursts of laughter, often associated with other types of seizures, such as generalized tonic–clonic and atonic seizures, and are poorly responsive to antiepileptic drugs [1]. GSs, or laughter epilepsy, have been described in various epilepsies as arising most commonly from hypothalamic hamartomas and rarely from temporal [2] or frontal regions [3]. However, GSs have not been described in lesional parietal lobe epilepsy. We describe a girl with GSs arising from the left parietal lobe on the basis of video/EEG monitoring and MRI. 2. Case report An 8-year-old, right-handed girl has been attending our hospital for the evaluation of frequent motor partial seizures since the age of 7 years. Her seizures consisted of brief staring followed by smiling and then giggling. She could recall sensory symptoms prior to the seizures in her right hand. No postictal confusion has been observed. Family and personal past medical histories were unremarkable. Seizures occurred five to eight times per day despite treatment with clobazam 40 mg/day and carbamazepine 400 mg/day. Video/EEG monitoring captured seven seizures. During the ictal period, the patient stared for a few seconds and then suddenly started smiling and laughing for 23–45 seconds, senselessly, inappropriately, and involuntarily. She could not remember laughing afterward. Interictal EEGs showed frequent spike-and-wave discharges in the left parietal region (P4 electrode) and pre-ictal repetitive spike-and-wave
⁎ Corresponding author at: Epilepsy Section, National Neurology Institute, 20 y D street, Vedado, Plaza, Ciudad de la Habana, Cuba. E-mail addresses: [email protected], [email protected] (R.A. Machado). 1525-5050/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2011.11.009
discharges in the left parietal region and middle-line electrodes (Cz, Pz, Fz) (Fig. 1B) followed by ictal rhythmic spikes in the same region (Figs. 1A and 2A). MRI showed cortical thickness and blurred white and gray delineation in the left parietal lobe (Fig. 2B, see black arrow). Following epilepsy monitoring and adjustment of treatment, seizure frequency decreased to one per day on 700 mg of oxcarbazepine and 30 mg/day clobazam. The parents were appropriately counseled about the possibility of surgical treatment, but they remained reluctant to agree to surgery. 3. Discussion Daly and Mulder coined the term gelastic epilepsy from the Greek word gelos, “laughter,” to emphasize the main characteristic of these seizures [4]. The possibility of sudden emotions as a manifestation of an epileptic seizure has been recognized since the end of the 19th century. These emotions were usually characterized as unpleasant; emotions of fear were most often described. Laughing seizures were first described by Trousseau [5]. Gowers observed emotions "with a cheerful character" as part of a seizure [6]. Since then, ictal laughing, or gelastic seizures, has been described in different epileptic conditions associated with the temporal or frontal lobes. Gelastic seizures have been described most often in association with hypothalamic hamartomas. Gascon and Lombroso suggested the following criteria for the diagnosis of gelastic epilepsy: stereotyped recurrence; absence of external precipitants; concomitance of other manifestations generally accepted as epileptic; presence of ictal or interictal EEG epileptiform discharges; and absence of conditions in which pathological laughter might occur [7]. Our patient met all of the aforementioned criteria. We have described a patient with childhood-onset GSs with an ictal EEG-detected lesion localized to the left parietal lobe. Shin et al. previously reported GSs in an adult with right parietal lobe
88
R.A. Machado, A.G. Astencio / Epilepsy & Behavior 23 (2012) 87–89
Fig. 1. Electrographic pattern of a patient with gelastic seizures. (A) Ictal electographic pattern: black arrow indicates ictal electrographic onset. Spike-and-wave discharges followed by rhythmic low-amplitude spikes at 12.7-Hz frequency in the C3, P3 and P3, O1 channels. Four seconds later this electrographic activity appeared in the frontotemporal regions. (B) Interictal recording showing spike-and-wave discharges and rapid spikes at the Cz, Fz, Oz and C3, P3 electrodes.
epilepsy and without a lesion identified by MRI [8]. GSs are most commonly associated with hypothalamic hamartomas and earlier onset. The later onset of gelastic epilepsy in the presence of a hypothalamic hamartoma appears to be associated with a milder epilepsy syndrome—less severe learning difficulties and behavior problems [9]. Our patient did not manifest learning difficulties or behavior problems, but her seizures were not relatively well controlled by antiepileptic drugs. A previous case report including a SPECT study [8] showed ictal hyperperfusion in the right parietal lobe, suggesting that the parietal lobe could be either the origin or a part of the seizure pathway [10]. SISCOM revealed ictal hyperperfusion in the right parietal lobe, whereas ictal SPECT showed slightly increased perfusion in the right parietal region and in the medial portions of the right cerebellum including the vermis and fastigial and dentate nuclei, which suggests that the right cerebellum is activated during GSs. In the case described here, the EEG abnormalities were always focal interictally over the left parietal region. The ictal electrographic pattern arose in the left parietal lobe in all seizures. The rhythmic spikes and waves located at the P3 electrode and middle-line and
central electrodes (C3, Cz, Fz) preceded by seconds the spikes in the temporal lobe. Gelastic automatisms were always preceded by 2 seconds by spikes in the C3 and P3 electrodes. That is why we believe that cingulate structures played a pivotal role in the generation of gelastic automatisms in our patient. Electrical stimulation of the right cingulate gyrus has elicited smiling and laughter, but no mirth [1,11], suggesting that the motor act of laughing and the processing of its emotional content are represented separately in, respectively, the anterior cingulate area and the basal temporal area (fusiform gyrus, parahippocampal gyrus, or both). Fried et al. suggested not only that laughter and mirth are represented in the presupplementary motor area, but also that there is close linkage between the motor, affective, and cognitive components of laughter [12]. Our features are in concordance with a previous study reporting that an ictal smile arose from the parietal lobe during other complex partial seizures in two patients. They observed smiling during parietal (two patients) and temporal lobe (three patients) seizures, and the
Fig. 2. Ictal laughing and lesional left parietal epilepsy. (A) Ictal electrographic pattern associated with gelastic seizures. (B) MRI axial FLAIR image showing cortical and subcortical hyperintensities in the left parietal lobe (arrow). Coronal T1-weighted MR images show blurred delineation between gray and white matter (arrow), typical features of focal cortical dysplasia in the left parietal lobe.
R.A. Machado, A.G. Astencio / Epilepsy & Behavior 23 (2012) 87–89
right hemisphere appeared to be involved with greater frequency [13]. Neuroanatomic models of emotional processing, especially laughter, suggest the temporal lobe is the main site of initiation for emotional processing. The cerebellum is another important structure in emotional processing through the cerebropontocerebellar pathway [14]. In normal circumstances, a perceived external stimulus or a recalled one will trigger an emotional response, but only if the cognitive/social context is appropriate. Although the laughter components of the emotional responses are largely preprogrammed and stereotyped, their intensity and duration and certain aspects of the overall pattern depend on the cognitive/social context in which the triggering stimulus appeared [15]. It is suggested that the cerebellum plays an important role in the modulatory control described above [14]. Thus, the pathogenetic mechanisms underlying gelastic seizures are not fully understood. Interictal and ictal EEGs are nonspecific in gelastic seizures. Both focal spikes and generalized spike-and-wave discharges can be seen, thus indicating the involvement of both frontal and temporal lobes as well as subcortical structures [1]. Dipole source localization has been used in an attempt to investigate the relationship between hypothalamic hamartoma and gelastic seizures, but has demonstrated limited value, even though the findings suggest that gelastic seizures likely originate in the hypothalamic hamartoma [16]. Cascino et al. retrospectively studied 12 patients with gelastic seizures and hypothalamic hamartoma, in which ictal intracranial EEG recordings obtained in 8 patients indicated focal onset of seizures in the anterior temporal lobe in 7 and frontal lobe in 1 [17,18]. None of the 7 patients who underwent a focal cortical resection experienced a significant reduction in seizure activity. Stereo-EEG recordings from hypothalamic hamartoma, neighboring hypothalamic structures, and other bilateral cortical areas have shown that gelastic seizures are linked to ictal discharges localized in the hamartoma, whereas surface registrations have failed to define an epileptogenic cortical area [19]. Even though much effort has been put into understanding how gelastic seizures are generated, the relationship between a presumed epileptogenic focus and gelastic fits still remains a mystery. Although functional images and invasive recordings did not appropriately explain the structures involved in the generation of gelastic automatisms in our patient, ictal and interictal EEG abnormalities in our case were always focal, unlike in most diencephalic gelastic seizures in which ictal EEG abnormalities are diffuse and nonlocalizing [13]. The temporal synchrony demonstrated between the focal ictal pattern in the parietal lobe and gelastic automatism suggested that the parietal lobe was involved in the pathogenesis of ictal laughing behavior. Reciprocal connectivity among the hypothalamus, hippocampus, and parietal lobe could explain this complex behavior. Dottie et al. found that the inferior parietal lobe (IPL) is the target of disynaptic output from the hippocampus. In fact, each hippocampus innervates a different area of the IPL. IPL receives input from the CA1 region of the hippocampus [20]. The connection between hypothalamus and hippocampus has been largely studied
89
[20,21]. Because the electrical activation of hypothalamus and hippocampus is overlooked on scalp EEGs, activation of this circuitry could account for the lack of significant changes visible on scalp EEGs. Thus, despite the fact that rhythmic spikes were seen in the left parietal electrodes during ictal behavior, deeper subcortical activation could have taken place and may partially explain the GSs in our patient. In summary, we have described a patient with gelastic seizures whose EEG revealed ictal discharges in the left parietal region and whose MRI scan revealed a lesion in the left parietal lobe. Conflict of interest statement We have no conflicts of interest to declare. References [1] Arroyo S, Lesser RP, Gordon B. Mirth, laughter and gelastic seizures. Brain 1993;116:757–80. [2] Tassinari CA, Riguzzi P, Rizzi R, Passarelli D, Volpi L. Gelastic seizures. In: Tuxhorn I, Holthausen H, Boenigk H, editors. Paediatric epilepsy syndromes and their surgical treatment, vol. III. London: John Libbey; 1997. p. 429–46. [3] Sartori E, Biraben A, Taussig D. Gelastic seizures: video-EEG and scintigraphic analysis of a case with a frontal focus; review of the literature and pathophysiological hypotheses. Epileptic Disord 1999;1:221–8. [4] Daly DD, Mulder DW. Gelastic epilepsy. Neurology 1957;7:189–92. [5] Trousseau A. De L'Epilepsie. Clin Med 1877:89–155 Hotel-Dieu Paris. [6] Gowers WR. Epilepsy and other chronic convulsive diseases. New York: William Wood; 1881. p. 255. [7] Gascon GG, Lombroso CT. Epileptic (gelastic) laughter. Epilepsia 1971;12:63–76. [8] Shin HY, Hong SB, Joo EY, Tae WS, Han SJ. JW. Gelastic seizures involving the right parietal lobe. Epileptic Disord 2006;8:209–12. [9] Mullatti N. Hypothalamic hamartoma in adults. Epileptic Disord 2003;5:201–4. [10] Gordon BHJJ, Lesser RP, Arroyo S. Mapping cerebral sites for emotion and emotional expression with direct cortical electrical stimulation and seizure discharges. New York: Elsevier Science; 1996. [11] Sperli F, Spinelli L, Pollo C. Contralateral smile and laughter, but no mirth, induced by electrical stimulation of the cingulated cortex. Epilepsia 2006;47:440–3. [12] Fried I, Wilson CL, MacDonald KA. Electric current stimulates laughter. Nature 1998;391:650. [13] Berkovic SF, Andermann F, Melanson D. Hypothalamic hamartomas and ictal laughter: evolution of a characteristic epileptic syndrome and diagnostic value of magnetic resonance imaging. Ann Neurol 1988;23:429–39. [14] Parvizi J, Anderson SW, Martin CO. Pathological laughter and crying, a link to the cerebellum. Brain 2001;124:1708–19. [15] Provine RR. Contagious yawning and laughter: significance for sensory feature detection, motor pattern generation, imitation, and the evolution of social behavior. In: Heyes CM, Galef B, editors. Social learning in animals: the roots of culture. New York: Academic Press; 1996. p. 179–86. [16] Hiraiwa R, Pellouchoud E, Liow K. Source localization of epileptiform discharges in children with gelastic seizures associated with hypothalamic hamartoma. Epilepsia 2000;41(Suppl. 7):113. [17] Cascino GD, Hulihan JF, Sharbrough FW, Kelly PJ. Parietal lobe lesional epilepsy: electroclinical correlation and operative outcome. Epilepsia 1993;34:522–7. [18] Lehtinen L, Kivalo A. Laughter epilepsy. Acta Neurol Scand 1965;41:255–61. [19] Munari C, Kahane P, Francione S. Role of the hypothalamic hamartoma in the genesis of gelastic fits. EEG Clin Neurophysiol 1995;95:154–60. [20] Clower DM, Wes RA, Lynch JC, Strick PL. The inferior parietal lobule is the target of output from the superior colliculus, hippocampus, and cerebellum. J Neurosci 2001;21:6283–91. [21] Baizer JS, Desimone R, Ungerleider LG. Comparison of subcortical connections of inferior temporal and posterior parietal cortex in monkeys. Vis Neurosci 1993;10: 59–72.
Contents lists available at SciVerse ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Case Report
Gelastic seizures involving the left parietal lobe René Andrade Machado ⁎, Adriana Goicoechea Astencio Epilepsy Section, National Neurology Institute, Havana, Cuba
a r t i c l e
i n f o
Article history: Received 2 November 2011 Accepted 4 November 2011 Available online 23 December 2011 Keywords: Gelastic seizure Parietal lobe Magnetic resonance imaging Ictal pattern
a b s t r a c t Gelastic seizures have been described in various epilepsies arising from the temporal or frontal lobes, although the most commonly encountered form is related to the presence of a hypothalamic hamartoma. We describe a patient with gelastic seizures involving the left parietal lobe. Our patient, an 8-year-old girl, underwent interictal video/EEG monitoring and MRI. The seizures consisted of brief staring followed by smiling and laughing. Electroencephalography during the gelastic seizures showed rhythmic spikes and waves in the left parietal lobe. MRI revealed the characteristic features of focal cortical dysplasia. Our findings suggest that the left parietal lobe may actively participate in the particular epileptogenic network generating gelastic seizures. © 2011 Elsevier Inc. All rights reserved.
1. Introduction Gelastic seizures (GSs) are characterized by bursts of laughter, often associated with other types of seizures, such as generalized tonic–clonic and atonic seizures, and are poorly responsive to antiepileptic drugs [1]. GSs, or laughter epilepsy, have been described in various epilepsies as arising most commonly from hypothalamic hamartomas and rarely from temporal [2] or frontal regions [3]. However, GSs have not been described in lesional parietal lobe epilepsy. We describe a girl with GSs arising from the left parietal lobe on the basis of video/EEG monitoring and MRI. 2. Case report An 8-year-old, right-handed girl has been attending our hospital for the evaluation of frequent motor partial seizures since the age of 7 years. Her seizures consisted of brief staring followed by smiling and then giggling. She could recall sensory symptoms prior to the seizures in her right hand. No postictal confusion has been observed. Family and personal past medical histories were unremarkable. Seizures occurred five to eight times per day despite treatment with clobazam 40 mg/day and carbamazepine 400 mg/day. Video/EEG monitoring captured seven seizures. During the ictal period, the patient stared for a few seconds and then suddenly started smiling and laughing for 23–45 seconds, senselessly, inappropriately, and involuntarily. She could not remember laughing afterward. Interictal EEGs showed frequent spike-and-wave discharges in the left parietal region (P4 electrode) and pre-ictal repetitive spike-and-wave
⁎ Corresponding author at: Epilepsy Section, National Neurology Institute, 20 y D street, Vedado, Plaza, Ciudad de la Habana, Cuba. E-mail addresses: [email protected], [email protected] (R.A. Machado). 1525-5050/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2011.11.009
discharges in the left parietal region and middle-line electrodes (Cz, Pz, Fz) (Fig. 1B) followed by ictal rhythmic spikes in the same region (Figs. 1A and 2A). MRI showed cortical thickness and blurred white and gray delineation in the left parietal lobe (Fig. 2B, see black arrow). Following epilepsy monitoring and adjustment of treatment, seizure frequency decreased to one per day on 700 mg of oxcarbazepine and 30 mg/day clobazam. The parents were appropriately counseled about the possibility of surgical treatment, but they remained reluctant to agree to surgery. 3. Discussion Daly and Mulder coined the term gelastic epilepsy from the Greek word gelos, “laughter,” to emphasize the main characteristic of these seizures [4]. The possibility of sudden emotions as a manifestation of an epileptic seizure has been recognized since the end of the 19th century. These emotions were usually characterized as unpleasant; emotions of fear were most often described. Laughing seizures were first described by Trousseau [5]. Gowers observed emotions "with a cheerful character" as part of a seizure [6]. Since then, ictal laughing, or gelastic seizures, has been described in different epileptic conditions associated with the temporal or frontal lobes. Gelastic seizures have been described most often in association with hypothalamic hamartomas. Gascon and Lombroso suggested the following criteria for the diagnosis of gelastic epilepsy: stereotyped recurrence; absence of external precipitants; concomitance of other manifestations generally accepted as epileptic; presence of ictal or interictal EEG epileptiform discharges; and absence of conditions in which pathological laughter might occur [7]. Our patient met all of the aforementioned criteria. We have described a patient with childhood-onset GSs with an ictal EEG-detected lesion localized to the left parietal lobe. Shin et al. previously reported GSs in an adult with right parietal lobe
88
R.A. Machado, A.G. Astencio / Epilepsy & Behavior 23 (2012) 87–89
Fig. 1. Electrographic pattern of a patient with gelastic seizures. (A) Ictal electographic pattern: black arrow indicates ictal electrographic onset. Spike-and-wave discharges followed by rhythmic low-amplitude spikes at 12.7-Hz frequency in the C3, P3 and P3, O1 channels. Four seconds later this electrographic activity appeared in the frontotemporal regions. (B) Interictal recording showing spike-and-wave discharges and rapid spikes at the Cz, Fz, Oz and C3, P3 electrodes.
epilepsy and without a lesion identified by MRI [8]. GSs are most commonly associated with hypothalamic hamartomas and earlier onset. The later onset of gelastic epilepsy in the presence of a hypothalamic hamartoma appears to be associated with a milder epilepsy syndrome—less severe learning difficulties and behavior problems [9]. Our patient did not manifest learning difficulties or behavior problems, but her seizures were not relatively well controlled by antiepileptic drugs. A previous case report including a SPECT study [8] showed ictal hyperperfusion in the right parietal lobe, suggesting that the parietal lobe could be either the origin or a part of the seizure pathway [10]. SISCOM revealed ictal hyperperfusion in the right parietal lobe, whereas ictal SPECT showed slightly increased perfusion in the right parietal region and in the medial portions of the right cerebellum including the vermis and fastigial and dentate nuclei, which suggests that the right cerebellum is activated during GSs. In the case described here, the EEG abnormalities were always focal interictally over the left parietal region. The ictal electrographic pattern arose in the left parietal lobe in all seizures. The rhythmic spikes and waves located at the P3 electrode and middle-line and
central electrodes (C3, Cz, Fz) preceded by seconds the spikes in the temporal lobe. Gelastic automatisms were always preceded by 2 seconds by spikes in the C3 and P3 electrodes. That is why we believe that cingulate structures played a pivotal role in the generation of gelastic automatisms in our patient. Electrical stimulation of the right cingulate gyrus has elicited smiling and laughter, but no mirth [1,11], suggesting that the motor act of laughing and the processing of its emotional content are represented separately in, respectively, the anterior cingulate area and the basal temporal area (fusiform gyrus, parahippocampal gyrus, or both). Fried et al. suggested not only that laughter and mirth are represented in the presupplementary motor area, but also that there is close linkage between the motor, affective, and cognitive components of laughter [12]. Our features are in concordance with a previous study reporting that an ictal smile arose from the parietal lobe during other complex partial seizures in two patients. They observed smiling during parietal (two patients) and temporal lobe (three patients) seizures, and the
Fig. 2. Ictal laughing and lesional left parietal epilepsy. (A) Ictal electrographic pattern associated with gelastic seizures. (B) MRI axial FLAIR image showing cortical and subcortical hyperintensities in the left parietal lobe (arrow). Coronal T1-weighted MR images show blurred delineation between gray and white matter (arrow), typical features of focal cortical dysplasia in the left parietal lobe.
R.A. Machado, A.G. Astencio / Epilepsy & Behavior 23 (2012) 87–89
right hemisphere appeared to be involved with greater frequency [13]. Neuroanatomic models of emotional processing, especially laughter, suggest the temporal lobe is the main site of initiation for emotional processing. The cerebellum is another important structure in emotional processing through the cerebropontocerebellar pathway [14]. In normal circumstances, a perceived external stimulus or a recalled one will trigger an emotional response, but only if the cognitive/social context is appropriate. Although the laughter components of the emotional responses are largely preprogrammed and stereotyped, their intensity and duration and certain aspects of the overall pattern depend on the cognitive/social context in which the triggering stimulus appeared [15]. It is suggested that the cerebellum plays an important role in the modulatory control described above [14]. Thus, the pathogenetic mechanisms underlying gelastic seizures are not fully understood. Interictal and ictal EEGs are nonspecific in gelastic seizures. Both focal spikes and generalized spike-and-wave discharges can be seen, thus indicating the involvement of both frontal and temporal lobes as well as subcortical structures [1]. Dipole source localization has been used in an attempt to investigate the relationship between hypothalamic hamartoma and gelastic seizures, but has demonstrated limited value, even though the findings suggest that gelastic seizures likely originate in the hypothalamic hamartoma [16]. Cascino et al. retrospectively studied 12 patients with gelastic seizures and hypothalamic hamartoma, in which ictal intracranial EEG recordings obtained in 8 patients indicated focal onset of seizures in the anterior temporal lobe in 7 and frontal lobe in 1 [17,18]. None of the 7 patients who underwent a focal cortical resection experienced a significant reduction in seizure activity. Stereo-EEG recordings from hypothalamic hamartoma, neighboring hypothalamic structures, and other bilateral cortical areas have shown that gelastic seizures are linked to ictal discharges localized in the hamartoma, whereas surface registrations have failed to define an epileptogenic cortical area [19]. Even though much effort has been put into understanding how gelastic seizures are generated, the relationship between a presumed epileptogenic focus and gelastic fits still remains a mystery. Although functional images and invasive recordings did not appropriately explain the structures involved in the generation of gelastic automatisms in our patient, ictal and interictal EEG abnormalities in our case were always focal, unlike in most diencephalic gelastic seizures in which ictal EEG abnormalities are diffuse and nonlocalizing [13]. The temporal synchrony demonstrated between the focal ictal pattern in the parietal lobe and gelastic automatism suggested that the parietal lobe was involved in the pathogenesis of ictal laughing behavior. Reciprocal connectivity among the hypothalamus, hippocampus, and parietal lobe could explain this complex behavior. Dottie et al. found that the inferior parietal lobe (IPL) is the target of disynaptic output from the hippocampus. In fact, each hippocampus innervates a different area of the IPL. IPL receives input from the CA1 region of the hippocampus [20]. The connection between hypothalamus and hippocampus has been largely studied
89
[20,21]. Because the electrical activation of hypothalamus and hippocampus is overlooked on scalp EEGs, activation of this circuitry could account for the lack of significant changes visible on scalp EEGs. Thus, despite the fact that rhythmic spikes were seen in the left parietal electrodes during ictal behavior, deeper subcortical activation could have taken place and may partially explain the GSs in our patient. In summary, we have described a patient with gelastic seizures whose EEG revealed ictal discharges in the left parietal region and whose MRI scan revealed a lesion in the left parietal lobe. Conflict of interest statement We have no conflicts of interest to declare. References [1] Arroyo S, Lesser RP, Gordon B. Mirth, laughter and gelastic seizures. Brain 1993;116:757–80. [2] Tassinari CA, Riguzzi P, Rizzi R, Passarelli D, Volpi L. Gelastic seizures. In: Tuxhorn I, Holthausen H, Boenigk H, editors. Paediatric epilepsy syndromes and their surgical treatment, vol. III. London: John Libbey; 1997. p. 429–46. [3] Sartori E, Biraben A, Taussig D. Gelastic seizures: video-EEG and scintigraphic analysis of a case with a frontal focus; review of the literature and pathophysiological hypotheses. Epileptic Disord 1999;1:221–8. [4] Daly DD, Mulder DW. Gelastic epilepsy. Neurology 1957;7:189–92. [5] Trousseau A. De L'Epilepsie. Clin Med 1877:89–155 Hotel-Dieu Paris. [6] Gowers WR. Epilepsy and other chronic convulsive diseases. New York: William Wood; 1881. p. 255. [7] Gascon GG, Lombroso CT. Epileptic (gelastic) laughter. Epilepsia 1971;12:63–76. [8] Shin HY, Hong SB, Joo EY, Tae WS, Han SJ. JW. Gelastic seizures involving the right parietal lobe. Epileptic Disord 2006;8:209–12. [9] Mullatti N. Hypothalamic hamartoma in adults. Epileptic Disord 2003;5:201–4. [10] Gordon BHJJ, Lesser RP, Arroyo S. Mapping cerebral sites for emotion and emotional expression with direct cortical electrical stimulation and seizure discharges. New York: Elsevier Science; 1996. [11] Sperli F, Spinelli L, Pollo C. Contralateral smile and laughter, but no mirth, induced by electrical stimulation of the cingulated cortex. Epilepsia 2006;47:440–3. [12] Fried I, Wilson CL, MacDonald KA. Electric current stimulates laughter. Nature 1998;391:650. [13] Berkovic SF, Andermann F, Melanson D. Hypothalamic hamartomas and ictal laughter: evolution of a characteristic epileptic syndrome and diagnostic value of magnetic resonance imaging. Ann Neurol 1988;23:429–39. [14] Parvizi J, Anderson SW, Martin CO. Pathological laughter and crying, a link to the cerebellum. Brain 2001;124:1708–19. [15] Provine RR. Contagious yawning and laughter: significance for sensory feature detection, motor pattern generation, imitation, and the evolution of social behavior. In: Heyes CM, Galef B, editors. Social learning in animals: the roots of culture. New York: Academic Press; 1996. p. 179–86. [16] Hiraiwa R, Pellouchoud E, Liow K. Source localization of epileptiform discharges in children with gelastic seizures associated with hypothalamic hamartoma. Epilepsia 2000;41(Suppl. 7):113. [17] Cascino GD, Hulihan JF, Sharbrough FW, Kelly PJ. Parietal lobe lesional epilepsy: electroclinical correlation and operative outcome. Epilepsia 1993;34:522–7. [18] Lehtinen L, Kivalo A. Laughter epilepsy. Acta Neurol Scand 1965;41:255–61. [19] Munari C, Kahane P, Francione S. Role of the hypothalamic hamartoma in the genesis of gelastic fits. EEG Clin Neurophysiol 1995;95:154–60. [20] Clower DM, Wes RA, Lynch JC, Strick PL. The inferior parietal lobule is the target of output from the superior colliculus, hippocampus, and cerebellum. J Neurosci 2001;21:6283–91. [21] Baizer JS, Desimone R, Ungerleider LG. Comparison of subcortical connections of inferior temporal and posterior parietal cortex in monkeys. Vis Neurosci 1993;10: 59–72.