IPSILATERAL MOTOR SEIZURES

R. PRATAP CHAND
Consultant Neurologist, Department of Medicine, University Hospital Kelantan, Malaysia

Abstract:
A patient presented with elementary partial motor seizures on the same side as the cerebral lesion.
A cerebral computerised tomographic scan showed a right medial frontal atrophic lesion and
an electroencephalogram showed seizure discharges from the same region. The clinical
significance and pathophysiology of ipsilateral seizures are discussed. (Aust NZ J Med 1986;
16: 234-235.)
Key words: lpsilateral seizures, epilepsy.

The motor and sensory phenomena of elementary partial
seizures occur on the side of the body contralateral to
the cerebral epileptogenic focus and are useful in
localising cerebral lesions. Partial seizures occurring on
the same side of the body as the cerebral hemispheric
lesion are termed ipsilateral seizures. These are exceedingly rare and have been reported in association with brain
tumours, tuberculosis, and cerebral infarct^.'.^ I describe
a patient with an atrophic lesion secondary to
craniocerebral trauma, who presented with ipsilateral
motor seizures with secondary generalisation.
CASE REPORT
A 21 year old, right handed Malay male presented with a history
of four episodes of seizures during the previous six months. The
attacks started with an aura of clonic twitching of the right upper
limb for a few seconds, followed by loss of consciousness, generalised tonic clonic convulsions lasting 5-10 minutes, and post-ictal
stupor and sleep. A partial seizure lasting a few minutes was
witnessed once and consisted of abduction of the right arm at
the shoulder and clonic jerking of the arm. Post-ictal paralysis
of the limb was not observed. He had suffered a head injury
at the age of 11 years owing to a fall from a tree, when he had
lost consciousness for about an hour and then recovered without
any residual deficits.
On examination, the patient had no neurological deficits. An
old healed scar was seen over the left frontal region. X-ray
examination of the skull was normal. A cerebral computerised
tomography (CT) scan showed a linear non-enhancing hypodense
lesion in the medial right fronto-polar region, suggestive of an
old cerebral contusion, and residual cortical atrophy (Figs 1 and
2). An electroencephalogram(EEG) showed infrequent spike and
slow wave discharges in the transverse runs, over the right medial
frontal and central regions (Fig. 3). The seizures were controlled
with oral carbamazepine (200 mg twice daily).

DISCUSSION
The exact mechanism of ipsilateral seizures is poorly
understood, although various hypotheses have been put

Figure I : Computerised tomographic (CT) scan shows the
linear non-enhancing lesion in the right medial frontal
lobe and right fronto-polar cortical atrophy.

Figure 2: Sagittal reconstruction of CT scan shows the
anatomical proximity of the lesion to the supplementary
motor cortex.

Reprinf requests to: Dr R. Pratap Chand, Consultant Neurologist, Dept of Medicine, University Hospital, Kubang Kerian, Kelantan, Malaysia.

234

Aust NZ J Med 1986; 16

CHAND

Fs - Fz

TI F7
Fs

F7

Fz- Fa
Fr- Fa
F8

- Tz
-

T3 C3
c3- cz

cz-c4
c4

- r4

T5- P5

PI -

P5 PZ

Pz PI
16

Figure 3: EEG shows infrequent spike and slow wave
discharges arising from the Fz-F4 and Cz-C4 linkages.

In the present case, the anatomic location of the lesion
on CT scan points to the supplementary motor cortex as
the epileptogenic area (Fig. 1). In four of the seven cases
reported by Ahuja and Tharakan, seizure discharges
could not be demonstrated in the EEG, although the
lesions had proximity to the above area. lpsilateral epileptiform discharges could be demonstrated in our patient,
and there was no evidence of a mirror focus. In view of
its anatomic location, epileptiform discharges arising
from the supplementary motor area may be difficult to
record using scalp electrodes. This may be the reason for
the absence of seizure discharges in the EEGs in the cases
previously reported. However, long term recording using
EEG telemetry may help to document the epileptogenic
focus adequately in similar cases where interictal seizure
discharges are scanty. In conclusion, ipsilateral seizure
constitutes a rare clinical phenomenon that can lead to
false clinical localisation of cerebral lesions. The EEG and
CT scan should help to give the correct localisation.
Accepted for publication: 7 January 1986.

forward. Experimental studies have shown that stimuReferences
lation of the supplementary motor cortex and secondary
I . Kofman 0 , Tasker R . Ipsilateral and focal inhibitory seizures.
somatosensory areas can give rise to motor and sensory
Neurology 1967; 17: 1082-6.
responses, respectively, in the ipsilateral e ~ t r e m i t i e s . ~ . ~ 2. Arseni C , Maretsis M. Focal epileptic seizures ipsilateral to the
tumour. Acta Neurochir (Wien) 1979; 49: 47-60.
Based on the anatomic proximity of the lesions to these
3. Ahuja GK, Tharakan J . lpsilateral seizures. Epilepsia 1982; 23:
areas, this mechanism has been invoked to explain
555-61.
ipsilateral seizures in most of the cases reported so f a ~ . I - ~
4. Penfield WG, Welch K. The supplementary area of cerebral cortex.
Chronic affection of t h e brain stem has been postulated
Arch Neurol Psychiatry (Chicago) 1951; 608: 289-317.
5 . Penfield WG, Jasper H A . Epilepsy and the functional anatomy of
to lead sometimes to ipsilateral epilepsy and was thought
human brain. Boston: Little, Brown and Co, 1954; 373-7.
to be the reason in one of the six cases reported by Arseni
6. Marsan CA, Gumnil JK. Neurophysiological aspects of epilepsy. In:
and Marehis.* The development of a mirror focus may
Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology.
explain ipsilateral seizures in some patients.6
Amsterdam: North Holland Publishing Co, 1974; IS: 30-5Y.

IPSILATEKAL MOTOR SEIZlJRES

Aust NZ J Med 1986; 16

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