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Cursive epilepsy

and gelastic epilepsy

Rong-Chi Chen, M.D. and Francis M. Forster, M.D.
The occurrence of running or laughing
phenomena in the course of an epileptic attack
has been known for many years. Erastus in
1581 first described an epileptic patient who
ran for half an hour in a state of disturbed
consciousness. I n 1619, Bootius2 used the
term epilepsia cursiva for the first time to
characterize the phenomenon of running as a
symptom of a paroxysmal disorder. Trousseau3
and F&k4 are usually cited as giving the first
reports of epileptic laughter. However,
Erastus described a girl, if left to herself, she
laughed, talked to strange things, and after the
paroxysm had no memory of it. Daly and
Mulder5 coined the term gelastic epilepsy to
emphasize that laughter characterized the attacks. The occurrence of either gelastic or cursive phenomena is uncommon and the concurrence in the same patient is extremely rare.
T o establish the incidence of these forms of
epilepsy we have reviewed a series of 5000
consecutive cases of epilepsy, studied at this
epilepsy center over a 12 year period. We
found that 16 or 0.32 percent of the cases had
laughing or running epilepsy.

This incidence of 0.32 percent of the cases

is probably higher than the percentage that occurs in the total population of epileptics; the
cases studied in the center are predominantly
complex examples of epilepsy with a high incidence of temporal lobe seizures. The only
earlier report in the literature of a patient
having both running and laughing features is
by Sisler, Levy and Roseman,j but these components occurred in different seizure episodes.
Of the 16 cases in o u r series, eight haa
laughing epilepsy, six had running epilepsy
and two had both laughing and running
Table 1 presents the pertinent clinical and
laboratory features of our 16 cases. There is
From The Epilc sy Center, Department of Neurology.
University of &consin
Center for Health Sciences,
Mad ison.
This paper was read at the American Academy of Neurology,
Boston, April 27, 1973.
This work was supported by grant No. NB-03660.
Received for publication March 23, 1973.
Dr. Forsters address is Department of Neurology, University of Wisconsin, 1954 East Washington Avenue, Madison

Neurolo6y / Volume 23 /October 1973


Age a t
onset of
and types




0 th er


Age at onset
of running,


IQ 94-87-90,
short attention

PEG and angiogram, Head injury,

left hemiatrophy
hypoplasia, left

Psychomotor Spike-and-wave, Hyperactive, left

right sylvian
leg drifting (?)

Astrocytoma, right

Laugh 9
Run 9

IQ 89-18-83

Angiogram, right
frontal mass



Psychomotor, Spike, left
grand mal

IQ 106-98-103

PEG, negative

Head injury

Psychomotor, Delta, right

Lethargy, ataxia,
grand mal
anterior temporal diplopia

negative; PEG,

Run 21

Grand m 4
Spike-and-wave, Stutter,
left anterior
psychomotor, temporal
petit mal
IQ 98-86-89,

negative; PEG,
mild left


Run 12

Grand mal,
psychomotor bilateral

IQ 16-82-11,
left temporal
lobe dysfunction


Status epilepticus

Run 20

Psychomotor, Spike, left

grand mal

IQ 81-82-80,

Left lower facial

weakness (?)

Run 11

Psychomotor Spike-and-wave,
left anterior

(Marital problem) PEG, negative

Psychomotor, Sharp, right

grand mal








Laugh 8
Run 8

No. Age* Sex

*Age at admission for investigation.

PEG = pneumoencephalography.
IQ = verbal performance, full scale.
MMPI = Minnesota Multiphasic Personality Inventory.


N o . Age* Sex

Age a t onset

of running,
Laugh 8

and types

TABLE 1 (continued)


Behavior problem

Addition a1


PEG, negative

IQ 92-88-90,
PEG, negative
MMPI :depression,
anxiety, paranoid



Age a t
onset of


Psychomotor Spike-and-wave, Forcep delivery,

bilateral occipital congenital anomalies

Laugh 2


Spike, left

Petit mal,
grand mal



Birth trauma

Birth trauma,
cerebral anomaly ?


Laugh 2


Head injury

Psychomotor, Spike, left



Laugh 16

IQ 106-101-104, PEG, negative

MMPI: character
disorder, depression,
anxiety, compulsion



IQ 34





Laugh 9

Psychomotor Spike-and-wave, Meningitis (age

left temporal
two), right



Febrile con- Spike, left

vulsion, grand anterior
mal, petit mal, temporal


Head injury

Head injury,
left parieto-occipital,
arachnoid cyst, and
cortical atrophy


Grand mal,
psychomotor left temporal

Grand mal,
Spike, left
psychomotor temporal

IQ 61-60-56

Foamy cells,
liver, bone

Laugh 25

Laugh 42



Laugh 4





pyramidal signs,

IQ 90-103-96,
PEG and
MMP1:personality agiogram,
left hemisphere
mass (?)


Psychomotor Delta, right

tonic drop

*Age at admission for investigation.

PEG = pneumoencephalography.
IQ = verbal performance, full scale.
MMPI = Minnesota Multiphasic Personality Inventory.



no significant sex difference ( n i n e male, seven

female). Seizure onset ranged f r o m six months
t o 27 years. The gelastic or cursive c o m ponents o c c u r r e d usually early in the course of
the patient's epilepsy; however, a delay as long
as 27 years o c c u r r e d in o n e of o u r series (case
15). T h e patients who had b o t h laughing a n d
running epilepsy had a n almost c o n c u r r e n t o n set of b o t h types of seizures. M a n y of the
patients had multiple seizure types but all of
them had definite identifiable psychomotor
epilepsy. Electroencephalogram (EEG ) ab normalities were predominantly temporal lobe
in location. T h e psychometric levels in general
tend to be o n the low side of normal, even
when c o m p a r e d with o t h e r p s y c h o m o t o r
groups studied in o u r center,';' a n d there was
an above-average incidence of personality a n d
psychiatric problems in the g r o u p as a whole.
T h e presumed etiology a n d pathology varied
from posttraumatic (either acquired later in
life (ir a t birth) inflammatory diseases such as
meningitis a n d measles encephalapathy,
degenerative disease such as N i e n h n n - P i c k
disease, a n d brain t u m o r . Casss 1 a n d 2 a r e
presented in s o m e detail. These are. the two
patients with both cursive a n d gelastyc c o m ponents. Case 3 , with cursive epilepsy that o c curred with a brain t u m o r , is also presented in
s o m e detail.
Case reports
Case 1 . Patrice S . had the onset of major motor
seizures at the age of eight, with a frequency of approximately one per month. She was placed on
sodium pentobarbital therapy but it did not alter the
frequency of seizure. Some of her major motor
seizures were preceded by a d(ji vu sensation. At the
age of nine and one-half, the seizure pattern
changed; duration slowed to less than several
seconds (maximum of one minute) while frequency
increased to approximately one a day. Five weeks after initial onset she was admitted to the University of
Wisconsin medical center.
Her Family history states that her maternal uncle had seizures beginning at age seventeen. Physical
and neurologic examinations showed a moderately
hyperactive child with a suspicious drifting of left leg
when both legs were maintained in the air. Other
neurologic examinations were grossly negative.
Laboratory examinations revealed negative results
from blood chemistry, hemogram, x-rays, urinalysis
and u r i n a r y a m i n o - a c i d s c r e e n i n g , electrocardiogram (ECG) and brain scan. Neuropsychologic testing showed a verbal I Q of 94, performance IQ of 87 and a full scale IQ of 90 without
any gross lateralizing or focal sign. Resting EEG

showed continual slow wave activity with spikes in

the right hemisphere, and phase reversal at the right
sylvian region, with bilaterally synchronous spikeand-wave discharges. Hyperventilation induced a
rhythmic buildup of the delta in the right
hemisphere, with accompanying spikes lasting for 30
seconds followed by three seconds of bilaterally synchronous 4 to 5 cycles per second spike-and-slow
wave activity (figure I). During this period, the
patient's hyperventilation stopped and she stared at
the technician. The EEG then changed to a mixture
of movement artifact and high voltage sharp activity
at 6 cycles per second. A few seconds later, the activity changed to generalized 3 to 4 cycles per second
high voltage delta with spike activity most prominent
in the frontal regions, and the patient was noted to
be laughing, moving, pulling out the electrodes,
pushing the technician away, and trying to get out of
the chair to run away. Near the end of the seizure,
the patient was able to repeat numerals, counting after the technician, but did so with a southern accent.
(The patient could not recall the counting behavior
later on, and was unable to speak with a southern accent during interictal intervals.) This activity lasted
for 35 seconds and was followed by a short period of
diffuse slowing during which the patient seemed confused before she returned t<) preictal state both
clinically and electrically. Figure 1 done by the
audiovisual tape-recording of the split screen
technic, shows the EEG on the right side, the patient
on the left. The upper picture shows patient during
the period of gelastic component of the seizure. The
lower picture shows her abortive attempts at running
in the cursive phase of the seizure.
While in the hospital on the third day of her stay,
the patient had a spontaneous seizure during which
she suddenly started laughing and running across the
corridor into her room 20 m away without hitting
the walls or the door. She kept on laughing and tapping both hands on the edge of the bed. She
recovered about one minute later without falling and
with complete amnesia for the episode.
She was given phenobarbital, 60 mg, and diphenyldantoin sodium capsules (Dilantin @ Kapseals @), 200 mg a day, with regular follow-up, both
clinically and of her blood Icvels. Seizures came u n der quite good control.
Case 2. Gerald P.,a 1 6 year old youth began his
seizures at age eight, six months after a fall from a
haymow. The early episodes consisted of sudden
cessation of activity with eyes staring. He might
drop what he was holding and be unresponsive for
perhaps one minute or longer after which he would
resume what he had been doing previously, unaware
that anything had occurred. These seizures ranged i n
frequency from twice per week to twice per month.
Four months later an episode occurred at night when
the parents heard the child giggling and laughing
inappropriately and had difficulty in arousing him.
In other incidents, he would often stiffen, his eyes
rotate upward, and he would tend to turn to the
right. After turning one or more times, he would
begin running. If something was in his way, he would
frequently run into it and sometimes injure himself;



Figure 1. P.S. (case I)had both gelastic and cursive epilepsy. EEG showed focal spikes in the right
hemisphere at the beginning of seizure attack, followed by generalized spike-and-slow waves and then
obliteration of the tracing by muscle artifacts. Pictures show the patient laughing (upper right) and
trying to get out of chair to run (lower right) during one of her seizure attacks, with simultaneous EEG
tracing attached.
for example, once he he ran into a box of jars his
mother was using for canning and sustained several
lacerations on his hands. He had no recall of what
he did during the episodes. He was given
diphenylhydantoin sodium and had complete
freedom from seizures for the first two years. He was
admitted at age 16 because of frequent seizures.
Physical and neurologic examinations were
unremarkable. EEG showed frequent paroxysmal
spike discharges more prominent in the left
hemisphere, with phase reversal in the left temporal
area. Neuropsychology testing revealed a full scale
IQ of 83. Pneumoencephalogram showed hypoplasia
of the entire left cerebral hemisphere. Carotid
arteriogram revealed shifting of midline vessels to
the left side and hypoplasia of left carotid system.
Primidone (Mysoline @) was added to his regimen.
Case 3. A case of running epilepsy is reported in
some detail here because of the completeness of
studies (including autopsy) plus the patient's peculiar
awareness of an evoking factor for his cursive component. LeRoy J., a 35 year old man had the onset of
major motor and psychomotor seizures at the age of
27. The seizures started with an uncinate aura of an
odor of gasoline followed by uncontrollable running

for which he was amnesic. When asked about the

possible connection of gasoline and running, he
recalled that during childhood in the drought and
depression years, he took care of the gasoline
irrigation pump on his father's farm. The pump was
in poor repair and he was told not to let it stop. He
therefore had to refill it with gasoline and d o this
with the pump running. When he spilled gasoline o n
the exhaust pipe and smelled the aroma of gas he was
afraid and said that he "ran like heck to get away."
The uncinate aura o f an odor of gasoline reminded
h i m of these episodes.
I n other incidents, the patient's epileptic seizures
were characterized by sudden onset of an epigastric
sensation, brightening of environment, hyperacusis,
clenching of the fists, staring, drooling, chewing and
swallowing, lasting 30 seconds to several minutes.
Grand ma1 seizures occasionally would follow. He
continued to have poorly controlled seizures and
headaches in the following years in spite of various
treatments. Neuropsychologic studies revealed
moderate to severe impairment of abilities dependent upon organic brain function that appeared to he
bilateral. Full scale IQ was 103. At age 3 5 , he was
readmitted because of drug toxicity and poor seizure



Figure 2. L.J. (case 3) had F3-c3
cursive epilepsy. EEG shows
focal intermittent delta ac- C3-T3
tivity at right frontoternporal
F p 2-F4
control. Neurologic examination revealed lethargy,
ataxia and diplopia. EEG revealed intermittent delta
activity of the right anterior temporal and frontal regions (figure 2a). Carotid arteriogram revealed
evidence o f a mass lesion anterior to the sella near
the midline hut more on the right. A grand ma1
seizure developed 14 hours after the angiogram; the
patient went into coma and died. Autopsy revealed a
large deep-seated astrocytonia, grade I to 4, in the
right frontal lobe with extension into the right temporal lobe and basilary cisterns, and extending
through corpus callosum and septuni pellucidum
into left mesial hemispheric structures (figure 3).
The EEG of patients i n cases 9 and 14 with an

Figure 3.
tension to

L.J. (case 3):

in the right fronregion with exthe left mesial

isolated spike focus at the left anterior temporal

region is shown in figure 4.


Joy and fear a r e two components of human

emotions. Joy o r happiness may be expressed
by laughing or smiling while fear can be expressed by escape behavior manifested by running away. Disorders of laughter in the form
of forced laughter are widely recognized as occurring in organic brain syndromes such as
pseudobulbar palsy, generalized cerebral a r -



Figure 4. L.B. (case 14) and

P.P. (case 9) had gelastic
epilepsy. Both EEGs show
spike focus at the left anterior
temporal region.

1 second

,5o uv

teriosclerosis, amyotrophic lateral sclerosis,

multiple sclerosis, encephalitides (lethargic o r
syphilitic), hepatolenticular degeneration and
severe head trauma.7-8While these are diffuse
cerebral lesions, the occurrence of forced
laughter o r running as manifestations of
seizures suggests a more focal lesion in the
central nervous system. T h e study of laughing
epilepsy and running epilepsy could thus contribute to the understanding of the physiology
of human emotions.
The type and localization of lesions of
gelastic epilepsy are variable (table 2 ) . Diffuse
cerebral lesions manifested by infantile
massive spasm^,^ myoclonic seizures,'O and
mental retardation" with or without cerebral
palsy were reported in large series. Postencephalitic o r posttraumatic (birth injury) cases
also were reported."-I5 Metabolic o r
degenerative diseases such as Tay-Sachs
disease were noted.16 I n our series, we had o n e
Niemann-Pick disease (case 16), o n e as sequela
of measles encephalopathy (case 13), and one
meningitis (case 11). I n four cases ( 2 , 12, 14,
15) head injury was a possible etiology while
in two (9, 10) birth trauma may have been
responsible. Focal tumors of the temporal
lobe, frontal lobe o r basal frontal region were
n o t e d t o c a u s e g e l a s t i c seizure^.^,'^
Arachnoiditis of the frontal convexity,'8 a case
of frontal atrophyIg o r the report of temporal
atrophyZ0 argue for different kinds of focal
lesions. I n o u r series, case 2 had hemiatrophy
of the left hemisphere caused by trauma, and
case 14 had an arachnoid cyst and showed
cortical atrophy over the left parieto-occipital
Midline lesions with involvement at the

hypothalamic level are of special interest and

are repeatedly reported in the literature. They
include astrocytoma of the floor of the third
ventricle that originate from the region of the
mammillary bodies;" hypophyseal tumor;".':'
hamartoma o r other tumors of the hypothalamus that cause precocious puberty;'"."-"'
interpeduncular glioma that are invading
the superior portion of the pons;': radiosensit i ve in fu n d i b u I o t u b e r a I I e s io n s , I a n d
papilloma of the third ventricle with extension
to the temporal lobe.':' Foerster and Gage127.PH
reported that during an operation for a colloid
cyst of the third ventricle, whenever the floor
of the third ventricle was swabbed the patient
would burst into peals of laughter. Rupture of
a saccular basal aneurysm involving the corpora maminillaria was observed to produce
forced laughter and led Martin'):' t o postulate
the hypothalamus as the "laughing center."
From review of cases reported in the
literature and of our additional cases, it is obvious there is no single anatomic lesion that
can be held responsible for the occurrence of
gelastic epilepsy. Nor are the EEG studies indicative of a single electrophysiologic focus or
phenomenon. The EEG features of gelastic
epilepsy in reported cases are presented in
table 3. S o m e of the records were consistent
with subcortical discharges, some showed cortical features, and some were even normal.
The interictal EEGs might show: a normal
t r a c i n g;y.2fi-30gen e r a I ized d ys rhythm ia ;
paroxysmal abnormalities (delta waves and
spikes) diffusely;'!' hypsarrhythmia;!'."'.:" "some
spikes in the left hemisphere;"3' abnormalities
"mainly o n the right hemisphere;"lRR3temporal
o r frontotemporal foci;s~y~10~13~15~z~~34~35



waves independently in the central regions and

the vertex;': parieto-occipital or parietal
foci;".y and 14 and six per second positive
spikes."" In o u r 10 cases o f laughing seizures,
eight showed specific p a r o x y s m a l a b -

normalities in terms of spikes, spikes-andwaves. sharp-and-slow activity in the temporal,

anterior temporal or sylvian regions. One
showed bursts of slow waves in the anterior
temporal region. Only o n e patient, who was

A uthor(s)
Gelastic epilepsy


Druckman and Chaog

Diffuse cerebral lesion; massive infan tile spasm

Fukuyama and associates'


Diffuse cerebral lesion; myoclonic seizure; diffuse sclerosis;

influenza encephalitis; tuberculous meningitis
Diffuse cerebral lesion; feeble-minded


Giraud and associates'


Weil, Nosik and Demmy'



Encephalitis; papilloma of third ventricle; birth trauma


Inflammatory lesion of infundibulotuberal region; third

ventricle tumor

Lehtinen and Kivalo'


Head injury; inherited midline anomaly


Tay-Sachs disease

Daly and Mulder'

Oligodendroglioma, left temporo-occipital

Loiseau, Cohadon and Cohadon'

Martyrosyan and Sayomova'



Hypophyseal tumor
Hypophyseal tumor: basal aneurysm

List and associates2
Money and Hostal

Arachnoiditis of frontal convexity

Mass in third ventricle; hypothalamic glioma; right

hemisphere atrophy; right temporal lobe atrophy
Astrocytoma of mammillary bodies



Left subfrontal mass: corpus callosum cyst; left temporal


Cystic atrophy of frontal lobe

Gascon and Lombroso'






Hamartoma of hypothalamus
Tumors in hypothalamus
Interpeduncular glioma

Foerster and GageP z.

Colloid cyst of third ventricle (swabbing of floor of third


Chen and Forster

Niemann-Pick disease; measles encephalopathy; meningitis;

head injuryibirth trauma; left hemisphere atrophy

Cursive epilepsy


Pituitary adenoma

Chen and Forster

Astrocytoma, right frontotemporal; left hemisphere atrophy;

prematurity, head injury


examined at the age o f seven, had bioccipital
spikes-and-waves. S e v e n had interictal EEG
foci on the left side, tw o o n the right side a n d
o n e was bilateral. T h e following EEG patterns
d u r i n g the seizures have been r e p o r te d in the


literature: a discharge of temporal origin,

followed rapidly by generalization either of
bilaterally sy n ch r o n o u s slow waves, o r of
d e s y n c h r ~ n i z a t i o n ; : flattening
of the record;'Y
discrete d esy n ch r o n i zat i o n of the tracings,

A u tho@)
Gelastic epilepsy

EEG findings (interictal)

Druckman and Chaog

Money and Hosta'

Normal; generalized asynchronous spikes and sharp waves,

polyspikes; hypsarrhythmia; paroxysmal focus, right parietooccipital right central and temporal; 14 and six per second
positive spikes





Generalized dysrhythmia; right temporal focus

Gumpert, Hansotia and Upton*

Generalized slow waves with spikes

Fukuyama and associates'

Hypsarrhythmia; temporal spikes or sharps




Spikes in the left hemisphere

Martyrosyan and Sayomova'

Abnormality in right hemisphere

Stein and Dietze3'

Abnormality in right hemisphere

Daly and Mulder5

Fast spikes in posterior left hemisphere; slow waves in left

temporal region

Wed, Nosik and Demmy'


Focal temporal spike and slow: diffuse slow waves

Lehtinen and Kivalo'

Frontotemporal focus

Roger and associates3'

Temporal lobe focus (four left, one right)

Zecchini and Cecotto3

Temporal lobe focus

Loiseau, Cohadon and Cohadon'

Gibbs and Gibbs3

Chen and Forster
Cursive epilepsy


Sharp waves in central regions and vertex; left frontotemporal paroxysmal abnormalities; left Rolandic spikes:
diffuse spikes-and-waves; diffuse slow waves; left anterior
Fourteen and six cycles per second positive spikes
Specific paroxysmal abnormalities in temporal, anterior
temporal or sylvian regions (eight of 10 patients); anterior
temporal slow waves (one of 10 patients); bioccipital spikes
and waves (one of 10 patients)

Sisler, Levy and Rosemad

Diffuse dysrhythmia with temporal spikes (nine of nine



Spikes at frontal and anterior temporal regions

Chen and Forster

Specific paroxysmal abnormalities in temporal or sylvian

regions (seven of eight patients); delta focus in anterior
temporal region (one of eight patients)



sometimes followed by diffuse fast waves of

low amplitude with subsequent theta waves and
sometimes trains of spike-wave complexes,
chiefly at the vertex;; disappearance of
paroxysmal slow waves of high amplitude that
were replaced by a diffuse 10 to 1 1 cycles per
second activity;g absence of focal discharge at
the onset of the attacks, and a few seconds
later, a generalized rhythmic 5 cycles per
second discharge;5 and no apparent change.:
Our case 1 showed unilateral rhythmic buildup
of delta waves with spikes in the right
hemisphere followed by bilaterally synchronous spikes-and-waves.
According to H ay ni a ke r , e in o t i o n a I
movement has been thought to be dependent
on a neural mechanism in close association
with telencephalic and diencephalic centers
concerned in respiration, for in laughing o r in
crying, a series of respiratory arrests and accelerations occur. Two faciorespiratory pathways have been postulated: a respiratoryarresting pathway, originating in the inferior
surface of the frontal lobe, and a respiratoryaccelerating pathway arising in the parietal
cortex and extending to the striatum, then to
the globus pal lidus, and downward. Evidence
has suggested that they course rather closely
together in the region of the subthalamus, extend downward in the tegmentum medial to
the red nucleus and in the sagittal plane o f the
third nucleus to reach the medulla oblon-:I! Loiseau, Cohadon and Cohadon:
postulate that in the production of laughter,
three levels can be distinguished: a control
level in the cortex; the effector level in the
bulbar protuberance; and between these, a
level o f synkinesia in the posterior hypothalamus. Stearns argues that although epilepsy
is essentially considered a disorder of the
neurons o f the cerebral cortex, i t is generally
agreed upon that other sites of the brain also
may generate seizures; t.he hypothalamic area,
the reticular formation, the basal ganglia,
among others , may become epi leptogen ic
zones. The cerebral site from which the seizure
originates may, in rare instances, coincide with
circuit areas from which the efferent motor
pathways of reflex laughter arise.
The diversity of etiologies of the gelastic
seizures cited in the literature and in our cases
further prove that probably many lesions can
cause the same effect through a common center

or centers to cause laughing epilepsy. The

anatomic proximity of the temporal lobes
(especially the mesial temporal structures) to
midline hypothalamic structures, the complex
interrelationships in the limbic system, and the
presence of other psychomotor seizures and
temporal lobe epileptogenic foci i n most of
our patients lead us to postulate that the temporal lobe a n d its afferent and efferent pathways may be strongly implicated in the genesis
of gelastic epilepsy. I t seems likely that
variously localized lesions, either in the frontal or temporal cortex o r in hypothalamic
diencephalic structures, o r even possibly in the
parietal lobe, can exert their influence through
the limbic system and the temporal lobe to
cause seizure activity manifested by laughing.
Despite the numerous studies on experimental running fit^^^-^^ triggered by the
observation of canine hysteria, little is
known about the pathology of cursive epilepsy.
Few reported cases have pathologic study
available (table 2 ) . Lennox: documented a 54
year old patient, who for nine years had attacks of coma, convulsions, emotional outbursts and running fits, and had an adenoma
of the pituitary gland removed. Our case 3, a
35 year old man, who suffered from running
fits as well as psychomotor and grand ma1
seizures for eight years, had an astrocytoma in
the right frontotemporal regions extending
across the midline structures to the left side
(figure 2 ) .
Reported EEG findings in cursive epilepsy
a r e few (table 3). Sisler, Levy and Roseman6
described generalized dysrhythmia with temporal spikes, and
described single
and multiple spikes a t frontal and anterior
temporal regions as interictal EEGs. In our
eight patients who had cursive epilepsy, seven
had epileptogenic foci in the temporal o r
sylvian regions, and o n e had a delta focus in
the right anterior temporal region. Of these,
four were o n the left side, three o n the right
side and o n e was bilateral. Our case 1 is
probably the only reported ictal EEG recorded during the seizure. This record showed a
rhythmic buildup of delta waves in the right
he ni is p her e with a c c o m pan y i n g spikes,
followed by bilaterally synchronous spikesand-waves. The available E E G findings i n dicate that a temporal lobe focus is essential
for the genesis o f running epilepsy.


All three patients who had both cursive and
gelastic epilepsies, including the case (A.K.) of
Sisler, Levy and Rosemanfi and our cases 1
and 2, showed temporal lobe epileptogenic
foci caused their seizure manifestations.
Gelastic (laughing) and cursive (running)
epilepsy are considered relatively rare. In a
series of 5000 consecutive cases of epilepsy
studied at the University of Wisconsin epilepsy
center, 16 cases or 0.32 percent of the cases
had laughing or running epilepsy. Eight of the
patients had laughing epilepsy, six had running
epilepsy and two had both laughing and running epilepsy. The occurrence of laughing and
running epilepsy in the same patient is extremely rare. Our clinical material and the
reported cases in the literature were analy,zed
in regard to the clinical picture, seizure types,
EEG findings, neuropsychologic testing and
anatomic consideration of the lesions. It was
concluded that laughing and running epilepsy
are part of the manifestations of complex
psychomotor epilepsy with the origin of the
seizure discharge in the limbic system, and
especially of the temporal lobe or its afferent
and efferent pathways, or both.
I. Er;istus T. I S X I .

(Cited i n Temkin): The Falling

Sicknecs, Ed 2 . Baltimore. Johns Hopkins Press. 1971.
pp I Y O - I Y I
2. Bootius: Observationes medicae de affectis omissis.
London, 1619
3. Trousseau A. Clinique Midicale d e I'Hotel-Dieu d e
Paris, Ed 4, Paris, Bailliire, 1873, p 409
4. F<r<C: Aeces de rife chez u n enileDtique.
. . C R Soc Hi01
(Paris) 50:430, 1898
5. Daly DD, Mulder DW: Gelastic epilepsy. Neurology
(Minneaol 7:189. I957
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