Epilepsia, 23555-561, 1982.
Raven Press. New York

Ipsilateral Seizures
G. K. Ahuja and John Tharakan
Department of Neurology, AH India Institute of Medical Sciences,
New Delhi, India

Summary: Seven patients who had partial elementary seizures on the same
side as the cerebral lesion are described. In six patients the seizures were
partial motor, and one patient had seizures which were partial elementary with
sensory symptomatology. Four patients had frontal lesions, two parietal, and
one parietotemporal. Five patients out of seven had lesions in the right cerebral
hemisphere. There were three cases with astrocytoma, two with infarction, and
one each with rneningioma and tuberculoma. The clinical significance and
pathophysiological mechanisms of this rare ipsilateral sign are discussed.

Partial seizures have a localizing value
in neurological evaluation. The partial elementary seizures with motor and sensory
phenomena occur o n the side opposite
to the cerebral lesion. Ipsilateral seizure,
that is, seizure occurring on the same side
as the hemispheric lesion, is an exceedingly
rare clinical event, and may mislead to false
localization of cerebral lesion. Experimental studies have shed light on the anatomic
localization of cortical areas concerned
with ipsilateral motor and sensory responses (Penfield and Welch, 1951; Penfield
and Jasper, 1954). There are very few reports of ipsilateral epilepsy in the literature
(Kofman and Tasker, 1967; Arseni and
Maretsis, 1979). We are reporting seven
patients, six cases with partial motor and
one case with partial sensory seizures in
whom, on investigation, there was evidence
of ipsilateral cerebral lesion. Brief case
summaries are given below.

CASE REPORTS
Case 1

J.P., a 32-year-old male was admitted
complaining of partial motor seizures of 2
years' duration which would begin with
clonic movements in the right upper limb
and spread to the right side of the face and
right leg. There was no loss of consciousness. Each attack lasted for 3-4 min, and
he had two to three such attacks per month.
Examination showed minimal pyramidal
signs on the right side and bilateral papilledema. EEG revealed delta activity from
the right frontal region. There was no
epileptic activity. A contrast enhanced CT
scan (Fig. 1) showed a uniformly enhancing
basifrontal mass on the right side. A right
frontal craniotomy and total excision of
meningioma were done. The patient was
continued on antiepileptic drugs and his
seizures were controlled.

Received October 19, 1981; revision received June 30, 1982.
Address correspondence and reprint requests to Dr. Ahuja at Department of Neurology, All India Institute of
Medical Sciences, New Delhi-I 10029, India.
Key Words: lpsilaterul seizures-Epilepsy.

555

556

G . K . AHUJA A N D J . THARAKAN
showed papilledema and bilateral sixth
nerve palsy. EEG revealed delta activity in
the right temporal region (Fig. 2). CT scan
demonstrated a right parietotemporal mass
lesion. Surgical decompression of the
tumor was done, and the histopathological
diagnosis was malignant astrocytoma. The
patient was subjected to postoperative
radiotherapy and antiepileptic medicines
were continued. His seizures were partially
controlled.

Case 4
M.K., a 12-year-old girl, had a single attack of seizure starting with clonic movements of the right side of the face spreading
FIG. 1. CT scan showing basifrontal mass on the right to the right arm followed by loss of conside.
sciousness in a few seconds 1 month prior
t o admission. S h e also complained of
headaches and vomiting for the same peCase 2
On examination she had early papillriod.
T.K., a 42-year-old male, presented with
edema.
There was no focal neurological
an 8-month history of two attacks of partial
motor fits which started with clonic movements of the right leg with secondary
generalization and episodes of generalized
headaches of the same duration. The seizures occurred two t o three times per
month. Neurological examination was
negative except for bilateral papilledema.
EEG showed delta activity in the right
frontal region, and no epileptic discharges
were seen. Right carotid angiogram as well
as a CT scan visualized a right frontal mass
lesion, which was partially excised. Histopathology revealed this to be a pleomorphic astrocytoma. The patient received
postoperative radiotherapy and anticonvulsants. His epilepsy was partially controlled.
Case 3
S.K., a 20-year-old male, developed recurrent attacks of partial sensory epilepsy
involving the right side of the face and
upper limb for 20 days prior to admission.
Each attack lasted for 1-2 min with a
frequency of three to four times a day.
He also had symptoms of increased intracranial pressure. Neurological examination
Epilepsia, Vol. 23, October 1982

FIG. 2. EEG showing delta activity in the right temporal region.

IPSILATERAL SEIZURES
deficit. EEG demonstrated delta activity
over the right frontal region, occasionally
spreading to the left. N o epileptic discharges were seen. A CT scan revealed an
area of decreased attenuation in the right
frontal region. The patient was given
anticonvulsant medicatiofi. Her vomiting
and headaches subsided in 2 weeks, and
there was no recurrence of convulsions. A
repeat scan after 1 month showed complete
resolution of the area of decreased attenuation. In view of the resolution of the abnormality on CT scan it was interpreted as
an infarction.

557

showed a parietal mass lesion. Tumor excision was done and the histologic diagnosis was malignant astrocytoma. The patient received postoperative radiotherapy.
There was only partial control of her convulsions with antiepileptic drugs.

Case 7
M.M., a 22-year-old woman, was admitted with complaints of two attacks of left
focal motor seizure with secondary generalization, during the week prior to admission. Neurological examination was negative except for bilateral mild papilledema.
Her EEG record was within normal limits.
A contrast enhanced CT scan visualized a
left frontal lesion (Fig. 3 , left). Based on the
image morphology and experience of CT
scan findings on a large number of histologically proved cases of CNS tuberculoma
at this Institute (Bhargava and Tandon,
1980) the lesion was presumed to be a
tuberculoma. She was given anticonvulsants and antituberculous therapy. A repeat scan 2 months later showed regression
of the lesion (Fig. 3, right). Her convulsions were completely controlled and papilledema regressed.
Table 1 gives a summary of the clinical
findings in all seven patients.

Case 5
H.S. a 50-year-old man, was admitted
with a 2-month history of partial seizures,
which would start with clonic movements
of the fingers and spread to the right side of
the face and right leg without loss of consciousness. Each attack lasted for 2-3 min
with a frequency of two to three times per
day. Examination revealed a hypertensive
patient with no neurological deficit. EEG
showed theta activity over the right frontal
region. CT scan visualized an infarction in
the right parietal region. The patient was
treated with antihypertensive and antiepileptic agents, and seizures were controlled.
A follow-up examination 3 months later did
not show any neurological deficit.
DISCUSSION
Case 6
A.H., a 35-year-old woman, presented
with convulsions starting with clonic
movements of the left upper limb with secondary generalization of 18 months’ duration. She also developed headaches, vomiting, and progressive diminution of vision
for 6 months prior to admission. Examination revealed bilateral papilledema and left
sixth nerve palsy. There was no motor or
sensory deficit. EEG showed theta activity
over the left parietal region. No epileptic activity was seen. A right carotid angiogram done in view of left focal epilepsy
demonstrated an ipsilateral shift of anterior
cerebral artery. A left carotid angiogram

Partial elementary seizures are helpful in
lateralization of cerebral disease, somatic
seizure manifestations occurring on the side
contralateral to the hemispherical lesion.
The seizures may occur rarely on the ipsilateral side and thus serve as a false localizing sign.
Byrom Bramwell (quoted by Gasel, 1961)
in 1899 coined the term “pseudo-lateralizing symptoms” in practice of clinical
neurology. The first comprehensive article
on this subject review pointed out that
third, sixth, and seventh cranial nerve
palsy, pyramidal signs, cerebellar signs,
extrapyramidal signs, and neck stiffness
were the more commonly seen false loEpilepsia, Vol. 23, October 1982

558

G. K . AHUJA A N D J . THARAKAN

FIG. 3. CT scan before ([eft) and after (right) antituberculous treatment, showing regression of the lesion

calizing signs. These false localizing signs
are mentioned as being more frequently
seen in cases of intracranial tumors by Tandon and Singh (1970). Focal seizures are
not mentioned as a false localizing sign in
any of the above reports. Though the experimental evidence for cortical areas concerned with ipsilateral responses was put
forth by earlier workers (Penfield and
Welch, 1951; Penfield and Jasper, 1954) it
was in 1967 that Kofman and Tasker reported two cases of ipsilateral and focal inhibitory seizures in patients with brain
tumor. Arseni and Maretsis (1979) reported
six cases of focal epilepsy ipsilateral to the
tumor.
In six out of seven patients reported here,
EEG showed focal slowing in the ipsilateral
cerebral hemisphere with a normal contralateral tracing; it was normal in one patient. The pathologic lesion was in the cerebral hemisphere, ipsilateral to focal
epilepsy as demonstrated by CT scan and
carotid angiography. No abnormality was
visualized in the opposite cerebral hemisphere in any of the patients. Surgical excision and histopathological examination
confirmed the nature of lesion as astrocytoma in three patients and meninEpilepsia. V n l . 23, October 1982

gioma in one patient. In two patients infarction was thought to be the nature of
abnormality, and in a single patient the
diagnosis was presumed to be tuberculoma.
Four patients had frontal lesions, two had
parietal, and one had parietotemporal lesion. In five out of the seven cases, the cerebral abnormality was on the right hemisphere. In all these cases, focal epilepsy
was ipsilateral and hence can be labeled as
a false localizing sign.
Various mechanisms are put forth to explain the pathophysiology of false localizing
signs (Gassel, 1961; Tandon and Singh,
1970). These include vascular lesions, local
spreading edema of brain, hydrocephalus,
and raised intracranial pressure. It is generally agreed that gross brain displacement
and various intracranial herniations constitute the most important pathogenetic
mechanism of false localizing signs. Incidence of false localizing signs is higher in
those patients with raised intracranial pressure than those without (Gassel, 1961).
These factors may also play a role in the
pathogenesis of ipsilateral epilepsy. Several
other mechanisms are postulated to explain
the occurrence of ipsilateral epilepsy. A
secondary epileptogenic area may develop

28

M

56

I

F

12

F

F

M

20

35

Right focal motor, starting
in face with secondary
generalization

M

42

6

Focal motor, starting in the
right arm, spreading to
face and leg. No loss of
consciousness
Right focal motor, starting
in leg and becoming
generalized
Right focal sensory, starting
in face and spreading to
right upper limb

M

32

1

Right focal motor, starting
in fingers and spreading
to right half of the body.
No loss of consciousness
Left focal motor, starting in
upper limb and becoming
generalized
Focal motor, starting in left
upper limb and becoming
generalized

Type of convulsion

Sex

Age

Case no.

Normal record

Theta activity over left
parietal region

Low voltage, fast activity in
background. Delta rhythm
in the right temporal
region. No epileptic
discharges
Normal background. High
voltage delta activity in
the right frontal region.
No epileptic discharges
Normal background. Occasional
theta activity from right
frontal region

Normal background. Delta
activity over right
frontal region. No
epileptic discharges
-do-

EEG findings

Left frontal

Left parietal

Right parietal

Right frontal

Right parietotemporal

Right frontal

Right basifrontal

Site of lesion

TABLE 1. Summary of the clinical findings in seven cases of ipsilateral seizures

-

Tuberculoma

Astrocytoma

Infarction

Infarction

Astrocytoma

Astmcytoma

Meningioma

Nature of lesion

560

G . K . A H U J A A N D J . THARAKAN

as a mirror focus and this may explain the
ipsilateral epilepsy in some cases (Marsan
and Gumnit, 1974). We could not demonstrate such a focus in any of our patients.
Stimulation of the supplementary motor
area as well as the stimulation of the secondary somatosensory area can give rise to
responses in the ipsilateral extremities
(Penfield and Welch, 1951; Penfield and
Jasper, 1954). Stimulation of these areas
was thought to be responsible for ipsilateral
epilepsy in the cases of Kofman and Tasker
(1967). Subfalxian herniation and compression of the opposite hemisphere against the
inner vault of the skull can cause focal seizures, homolateral to the tumor. Evidence
of herniation will be present in the
angiogram in such cases. Chronic affection
of the brainstem may sometimes lead to ipsilateral epilepsy (Penfield and Jasper,
1954). A mainly theoretical proposition is
the absence of decusation of sensorimotor
fibers.
Stimulation of irritation of the supplementary motor area is thought to be the
probable mechanism of ipsilateral convulsions in cases 1, 2, 4, and 7, because of the
proximity of lesions to this area. Case 3 had
ipsilateral, focal sensory convulsions and
the pathology was in the parietotemporal
region, that is, near the secondary somatosensory area. The irritation of this area
was probably responsible for the ipsilateral sensory epilepsy in this patient. Case
5 was a hypertensive patient with cerebral infarction. It is presumed that the
ischemia was responsible for irritating the
nearby supplementary motor areas resulting in ipsilateral seizures. In case 6 cerebral
edema associated with tumor produced seizures by irritating the neighboring supplementary motor area. All patients except
one had papilledema and raised intracranial
pressure might have been contributing to
the pathogenesis of this phenomenon. We
believe that in all cases probably more than
one factor contributed to the occurrence of
ipsilateral seizures. Arseni and Maretsis

Epilepsin, Vol. 23, Ortoher 1982

(1979) in their series considered involvement of the supplementary motor area to be
the cause of ipsilateral convulsions in three
cases, secondary somatosensory area in
two cases, and chronic compression of
brainstem in one case. Besides ipsilateral
epilepsy, other false localizing signs observed in our cases were sixth nerve palsy
in two cases and ipsilateral pyramidal tract
signs in one patient. With the availability of
CT scan, the false localizing signs may not
have the same practical significance as in
the past; still these may confuse the planning of investigations. This is exemplified
by case 6 in our series in which a carotid
angiogram was done on the opposite side
first.
We should emphasize that though there
are numerous cases of voluminous infiltrating cerebral t u m o r s with cerebral
edema, ipsilateral epilepsy is seen only
rarely and the actual mechanism still remains hypothetical.
REFERENCES
Arseni C, Maretsis M. Focal epileptic seizures ipsilateral to the tumor. A c t n Neurochir ( W i e n )
1979;49:47 -60.
Bhargava S , Tandon PN. CNS tuberculosis: Lessons
learned from CT studies. Neurology ( I n d i a )
1980;28:207 - 12.
Gassel MM. False localising signs-A review of the
concepts and analysis of occurrence in 250 cases of
intracranial meningioma. A r c h Neurol 1961;
4:526-54.
Kofman 0, Tasker R. Ipsilateral and focal inhibitory
seizures. Neurology 1967;17:1082-6.
Marsan CA, Gumnit JR. Neurophysiological aspects
of epilepsy. In: Vinken PJ, Bruyn GW, eds. Hundbook of clinical neurology (vol 15). Amsterdam:
North-Holland Publishing Co., 1974:30 -59.
Penfield WG, Jasper HA. Epilepsy and the functional
anatomy of human brain. Boston: Little, Brown &
CO., 1954:373-7.
Penfield WG, Welch K. The supplementary area of
cerebral cortex. Arch Neurol Psychiatr (Chicago)
1951;606:289- 3 17.
Tandon PN, Singh B. False localising sign in intracranial tumors. Ann Ind Acad Med Sci 1970;6:24-33.

RESUME
7 Patients qui avaient des crises partielles elementaires du m&me cBte que la lesion cerebrale sont decrits. Chez 6 patients les crises etaient des crises mot-

56 1

IPSILA TERAL SEIZURES
rices partielles et le septieme avait des crises partielles
elementaires a semiologie sensitive. Quatre patients
avaient des lesions frontales, deux d e s lesions
parietales, e t dans un cas la lesion etait parietotemporale. Cinq des sept patients avaient une lesion de
I’hemisphere cerebral droit. Dans trois cas il s’agissait
d’un astrocytome. Dans deux cas d’un infarctus, dans
un cas d‘un meningiome et dans un cas d’un tuberculome. La signification clinique et les mecanismes
physiopathologiques de cette symptomatologie ip,
silaterale rare sont discutes.
(Ch. Dravet, Marseille)

RESUMEN
Se describen siete pacientes que presentaban ataques parciales elementales en el mismo lado de la
lesi6n cerebral. En seis pacientes 10s ataques eran
motores parciales y un enfermo tenia ataques que eran
parciales elementales con sintomatologia sensorial.
Cuatro pacientes tenfan lesiones frontales, dos parietales y, en un caso, la lesi6n era parieto-temporal.
Cinco de 10s siete enfermos tenfan lesiones en el hem-

isferio cerebral derecho. Se encontraron tres casos
con astrocitomas, dos con infartos, uno con meningioma y uno con tuberculoma. Se discuten 10s mecanismos fisiopatol6gicos de esta rara manifestaci6n
ipsilateral y su significado clinico.
(A. Portera Sanchez, Madrid)

ZUSAMMENFASSUNG
Beschreibung von 7 Patienten, die partielle elementare Anfalle auf der Seite der cerebralen Lasion hatten.
6 Patienten hatten partielle motorische Anfalle, 1 Patient partielle elementare Anfalle mit sensorischer
Symptomatologie. 4 Patienten hatten frontale
Lasionen, 2 parietale und einer eine parieto-temporale.
5 der 7 Patienten hatten Lasionen in der rechten
Hemisphare. Es handelte sich dabei dreimal um Astrozytome, zweimal um Infarkte und je 1 Patient hatte
ein Meningiom bzw. ein Tuberculom. Die klinische
Bedeutung und die pathophysiologischen Mechanismen, die sehr seltenen ipsilateralen Symptome
werden diskutiert.
(D. Scheffner, Heidelberg)

Epilepsia, V d . 23, October 1982