Epilepsy & Behavior 8 (2006) 773–775
www.elsevier.com/locate/yebeh

Brief Communication

Laughter and the mesial and lateral premotor cortex
J.J. Schmitt *, J. Janszky, F. Woermann, I. Tuxhorn, A. Ebner
Department of Presurgical Evaluation, Epilepsy Center Bethel, Maraweg 21, 33617 Bielefeld, Germany
Received 28 September 2005; revised 28 February 2006; accepted 4 March 2006

Abstract
We report the induction of laughter and smiling by cortical electrical stimulation of the frontal lobe of two patients: an 18-month-old boy
with a left frontal cortical lesion extending to the vertex and the central gyrus, and a 35-year-old woman with a lesion in the right supplementary sensorimotor area (SSMA). The subjects underwent presurgical epilepsy evaluation with subdural grid electrodes to determine surgical candidacy. Stimulation of the prefrontal area reproducibly induced laughter. The adult patient reported absence of emotional content.
Slowing of speech occurred under stimulation of electrodes in the upper and posterior vicinity. In this patient laughter was elicited in the
anterior part of the SSMA. In the child, this response was induced by stimulation of the lateral prefrontal cortex near the midline. We conclude that the anterior portion of the SSMA/lateral premotor cortex is involved in generating the motor pattern of laughter.
Ó 2006 Elsevier Inc. All rights reserved.
Keywords: Electrical stimulation; Laughter; Gelastic epilepsy

1. Introduction
Laughter and smiling have been reported as ictal symptoms in patients with epilepsy and as inappropriate signs of
affect in neurological disease [1]. Cortical electric stimulation
has so far demonstrated a reproducible site responsible for
the generation of laughter in only a very limited number of
subjects, none of whom had been suffering from lesion-associated focal epilepsy, as will be pointed out in Section 4. We
report the induction of laughter and smiling by cortical electrical stimulation in the frontal lobe in two patients.
2. Subjects and methods
Subject 1 was an ambidextrous (as documented by self-declaration)
woman, aged 35, with a lesion in the right supplementary sensorimotor
area (SSMA). She experienced tonic seizures associated with preserved
consciousness and complex involuntary movements of the right hand
(alien hand), preceded by an ascending somatosensory aura in the left
hand. Surface EEG monitoring demonstrated interictal epileptiform
potentials and seizure patterns over the vertex.
*

Corresponding author. Present address: Evangelisches Krankenhaus
Unna, Holbeinstrasse 10, D-59423 Unna, Germany.
E-mail address: jsh@gmx.org (J.J. Schmitt).
1525-5050/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.yebeh.2006.03.003

Subject 2 was an 18-month-old boy with a left frontal cortical
lesion extending to the vertex and posterior to the motor area. He
experienced hypomotor and tonic seizures. Surface EEG monitoring
demonstrated intermittent slowing, interictal epileptiform potentials,
and seizure patterns over the left frontal lobe, the last with rapid
generalization.
Histology in both cases was classified as tuberal cortical dysplasia.
Lesions were solitary, and there were no other signs indicating the presence of clinical tuberous sclerosis (TS). Neither patient had skin manifestations or other features of TS. The adult patient later underwent genetic
testing for TSC1 and TSC2 and was reported to be negative for both. The
boy had been in our care several years earlier, and nothing is known about
his genetic status with respect to TS.
Both subjects remained seizure-free for at least 2 years after resection
without focal neurological deficits. Neither subject ever had gelastic seizures. When they underwent presurgical epilepsy evaluation with subdural
grid electrodes to determine surgical candidacy, we applied biphasic, predominantly bipolar electrical stimulation at 0.3 ms, 50 Hz, and 1- to 15mA levels in both patients while they were undergoing subdural EEG
diagnostics for identification of the epileptogenic zone and delineation
of the adjacent functionally eloquent cortex.

3. Results
In both patients, stimulation of the premotor area
induced reproducible laughter (Figs. 1 and 2, hatched electrodes). In the child, this response was induced by stimula-

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Brief Communication / Epilepsy & Behavior 8 (2006) 773–775

Fig. 1. Subject 1, adult. Image of SSMA lesion obtained by sagittal and axial FLAIR on stimulation of the right SSMA. Hatched circle: laughter. Grey
circle: slowing of speech.

Fig. 2. Subject 2, child. Stimulation of left lateral premotor cortex. Hatched circle: laughter. Circle with black sector: motor response of right arm/hand to
stimulation. Black circle: motor response of face. Black area: frontolateral cortical lesion.

tion of the lateral premotor cortex near the falx cerebri
(hatched electrodes). In the adult patient laughter was elicited under an electrode in the cranial anterior part of the

SSMA. She reported absence of emotional content: ‘‘That
is not me!’’ Slowing of speech occurred during stimulation
of electrodes in the upper and posterior vicinity (grey).

Brief Communication / Epilepsy & Behavior 8 (2006) 773–775

None of the stimulation tests that caused laughter were
associated with afterdischarges.
4. Discussion
Of 44 publications on ‘‘gelastic epilepsy’’ listed in Medline since 1985, 35 (including 5 reviews) concerned, predominantly or exclusively, patients with hypothalamic
hamartoma. This well-established cause of gelastic epilepsy
is, nevertheless, a largely unsuitable condition for studying
the generation of laughter, as gelastic seizures in these
patients are typically associated with heterogeneous spread
of surface EEG seizure patterns [2], which does not allow
demonstration of an unequivocal relationship between ictal
laughter and a specific brain region. This study [2] demonstrated that temporal and generalized EEG changes were
common, and the most common concomitant seizure type
(11 of 17 patients) was psychomotor seizures. Noncortical
brain structures are obviously involved in the generation of
laughter, although for methodological reasons, it is even
more difficult to define the role of certain subcortical structures in the generation of laughter. We know exactly the
part of the cortex to which the electric current was applied
in our cases. We cannot exclude that our paradigm activated other, possibly remote, subcortical brain structures via
cortical–subcortical circuits. Tassinari et al. [3], in their
review of 60 cases from the literature, concluded that the
laughter of patients with hypothalamic hamartoma and
frontal lobe seizures usually lacked emotional content,
whereas patients with temporal lobe epilepsy usually manifested a sense of mirth. Iwasa et al. [4] described two
patients with nonlesional gelastic epilepsy whose gelastic
seizures were accompanied by a subjective feeling of mirth;
interictal EEG dipoles were calculated in the right or left
mediobasal temporal regions in these two patients, whereas
in their third patient, with gelastic seizures without a sense
of mirth, the dipole sources were localized in the right frontal region corresponding to the anterior cingulate.
The anterior portion of the SSMA/lateral premotor
cortex is involved in generating the motor pattern of
laughter. Whether other cortical areas are also involved
in the generation of laughter is not certain, but there
are four other cases in three published studies in the biomedical literature in which laughter could be elicited by
cortical electric stimulation. Laughter response was
evoked in one patient [5] by stimulation of the left posterior superior frontal gyrus, representing the anterior border of the lateral premotor cortex. In the other three
patients [6,7], laughter could be elicited in the temporal

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lobe by electric stimulation of the left temporobasal
region, and all patients experienced some disruption of
speech with stimulation of adjacent electrodes. Krack
et al. [8] reported the very interesting finding of mirthful
laughter induced by stimulation of the subthalamic nucleus (in one patient, right-sided, and in the other, bilateral).
In conclusion, laughter can be elicited in at least three
areas of the brain: the frontal premotor cortex and the
basal cortex of the dominant temporal lobe and the subthalamic nucleus. Of the cortical areas, the temporal site
seems to be involved mostly in generating the associated
emotional content. Laughter resulting from deep brain
stimulation in both reported cases was associated with
emotional content, which may be due to activation of corticobasal connections to the adjacent temporal lobe,
whereas the motor component of laughter in our adult
patient could be generated in the premotor cortex without
emotional content and, therefore, probably without temporal involvement. We are aware that because only a very
limited number of the patients being stimulated in these
areas laugh while the remainder do not, and because the
brain lesion may well have altered localization of cerebral
functions, these findings must be interpreted with caution.
The striking coincidence that in both cases histology was
classified as tuberal cortical dysplasia is interesting,
although the significance of this finding cannot be
interpreted with the data available and remains subject to
further research.
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