We present a patient with longstanding gelastic seizures due to a transmantle cortical dysplasia extending from the right lateral ventricle into the right superior frontal gyrus. Electrocorticography in this case demonstrated ictal involvement of the right anteromesial superior frontal gyrus in the generation of the ictal laughter, suggesting that this area serves as the symptomatogenic zone. Although other candidate areas, specifically the cingulate gyrus and the temporal lobe, were not evaluated with electrocorticography, the restriction of the ictal activity to three electrodes in the anteromesial superior frontal gyrus, the subsequent hypermotor activity, and, most importantly, postoperative seizure freedom all support frontal lobe origin. Absence of concomitant seizure characteristics such as autonomic symptoms and automatisms argue against anterior cingulate involvement (Devinsky et al., 1995). Although gelastic seizures are most often intracranially recorded from hypothalamic hamartomas (Kahane et al., 2003), ictal laughter can also be generated in the frontal lobe. Within the frontal lobe, the mesial and lateral aspects of the superior frontal gyrus, the cingulate gyrus, as well as the orbitofrontal gyrus, have been associated with gelastic seizures based on intracranial EEG recording and electrocortical stimulation in seven cases (Table 1). The most limited surgical approach resulting in seizure freedom was reported by Chassagnon et al. (2003). Following an invasive evaluation with stereo-EEG, their nonlesional patient became seizure free after radiofrequency stimulation, resulting in two distinct lesions in the left superior frontal and cingulate gyri. Ictal laughter occurred at a relatively late stage during the habitual seizures, suggesting propagation of the ictal activation. Although the typical seizure semiology was reproduced by low-intensity electrocortical stimulation of the contacts that were later used for the radiofrequency ablation, the only spontaneously recorded seizure during the stereo EEG evaluation had no gelastic features. A patient with a cavernous angioma in the left mesial superior frontal gyrus was evaluated using subdural grid and strip electrodes covering the lateral and mesial aspect of the left frontal lobe (Arroyo et al., 1993). At the time of the ictal laughter, four contacts overlying the mesial aspect of the frontal lobe were electrographically involved; however, at that time the seizure had already spread to involve more distant contacts in the anterior lateral frontal lobe and at the frontoparietotemporal junction. Electrocortical stimulation failed to elicit laughter in this patient. A low-grade glioma in the right anterior cingulum caused gelastic seizures in a patient described by Devinsky et al. (1995). Ictal onset was observed from contacts covering the right anterior cingulum, with spread to the right orbitofrontal cortex and the left cingulum within 500 msec. No details were provided with regard to correlation of ictal symptomatology and electrocorticography, or electrocortical stimulation. A patient with a right frontal cortical dysplasia resembling our case was recently reported (Cheung et al., 2007). Although resection of the cortical dysplasia resulted in seizure freedom following an invasive evaluation, no details are provided with regard to the correlation of ictal symptomatology and electrocorticography, or electrocortical stimulation. Lastly, a patient with a pleomorphic xanthoastrocytoma in the left cingulate gyrus, just anterior to the corpus callosum, was rendered free of gelastic seizures following resection of the tumor. Intracranial recordings were not utilized (Mohamed et al., 2007). In the preimaging era, one patient was cured from gelastic seizures after resection of a cystic mass in a similar location (Loiseau et al., 1971; “it looked as if the growth originated from the junction of the corpus callosum with the cingulate cortex, and had invaded both dorsally to the ventricle and rostrally to the mesial cortex.”). Laughter was induced by electrocortical stimulation of five subdural strip contacts covering the left superior frontal gyrus (Fried et al., 1998) and by depth electrode contacts in the right anterior cingulate gyrus (Sperli et al., 2006). It is noteworthy that in the latter case, no depth contacts were located in the superior frontal gyrus. Interestingly, in both these patients, laughter was not part of the patient’s habitual seizure semiology. Therefore, although freedom from gelastic seizures following lesionectomy in the cingulate gyrus suggests that the epileptogenic zone in these cases did indeed reside in this area, electrocorticography from our case in addition to the stimulation data by Fried et al., 1998 suggest that the symptomatogenic zone for the motor manifestations of laughter may reside inside the superior frontal gyrus. Given that epileptogenic lesions have been resected in the cingulate area of either hemisphere without resulting impairment of spontaneous laughter, the “generator” for the motor aspect of laughter is likely represented bilaterally. To our knowledge, no case to date has been reported in whom ictal laughter was reproduced during cortical stimulation. Many variables, such as stimulus duration, frequency, intensity, and anticonvulsant levels affect the results of electrocortical stimulation studies. In our case, stimulation had to be abandoned after definition of the posterior resection margin due to frequent spontaneous seizures. Lastly, one patient with gelastic seizures due to an orbitofrontal oligoastrocytoma has been described (Umeoka et al., 2008). Seizures lasted a few minutes and consisted of sudden motion arrest, unresponsiveness with or without staring, and followed by suspected mirthful laughter and postictal confusion. Intracranial EEG recording showed a leading epileptic discharge at orbitofrontal contacts before spreading to the temporal base where the laughter was observed. Laughter then recurred when the ictal discharge was seen exclusively at the temporal base electrodes. Therefore, the laughter in this case likely represents ictal propagation to the temporal lobe. This view is supported by the fact that stimulation of the parahippocampal gyrus and fusiform gyrus has been demonstrated to elicit laughter (Arroyo et al., 1993). To our knowledge, there is no report of laughter induced by stimulation of the orbitofrontal area.