Acta Neurologica Belgica
https://doi.org/10.1007/s13760-020-01466-4

LETTER TO THE EDITOR

Abdominal epilepsia partialis continua due to cortical ischemia:
a video‑documented case report and review
Morgane Soler‑Rico1 · Roger Denays1 · Eléonore Sinzobahamvya1
Received: 20 July 2020 / Accepted: 3 August 2020
© Belgian Neurological Society 2020

Keywords Epilepsia partialis continua · Abdominal muscles · Cerebrovascular disease

Introduction
Epilepsia partialis continua (EPC) is an uncommon form
of status epilepticus, characterized by repetitive myoclonic
jerks of a defined part of the body, that last for hours, days
or even years [1]. Any muscle group can be affected but
because of anatomical and physio-pathological reasons
(wider topographic representation on the motor cortex and
lower epileptic threshold), face and distal limb are more frequently involved compared to proximal limb, trunk or abdomen [1–7]. Whereas vascular lesions are one of the common causes of classic EPC [1], they are rarely considered as
the origin of abdominal involvement [4, 5]. We report here
a new case of abdominal EPC due to acute focal cerebral
ischemia and make a review of abdominal EPC causes.

Case report
A left-handed 76-year-old man was admitted to the hospital
because of persistent non-painful leg and abdominal myoclonus. Three days before, he had suffered from violent jerks
in his left leg during a few minutes and, the evening before,
he suddenly fell on the ground due to acute left hemiplegia. His medical history was notable for arterial hypertension, dyslipidaemia, coronary artery stenting, paroxysmal
atrial fibrillation, radiofrequency catheter ablation. He did

not take any drug reported to induce myoclonus. In addition to continuous jerky movements in abdomen and inner
thigh muscles visible on the left side (video 1), neurological
examination revealed mild left leg weakness. Brain magnetic resonance imaging (MRI) revealed mild hypersignal
on sB 1000 diffusion and T2-weighted FLAIR sequences,
with a corresponding low apparent diffusion coefficient, circumscribed to the central zone in the right parasagittal area
(Fig. 1a). Leptomeningeal enhancement appeared on postcontrast MRI in the same area. MR angiography showed a
severe post-ostial stenosis of the right internal carotid artery.
Routine biochemistry analysis was normal, as well as routine EEG, 24-h EEG recording and FDG brain PET. The
myoclonic jerks persisted the next days, with some fluctuations, increasing with stress and decreasing with rest. Needle
electromyography of abdominal recti muscles demonstrated
that myoclonic jerks were present exclusively in the left side.
A thoracic video fluoroscopy revealed no diaphragmatic
flutter. Despite the absence of convincing EEG and brain
PET anomaly, the diagnosis of EPC affecting abdominal
and thigh muscles was made, and an anti-epileptic medication was started (levetiracetam 1 g twice daily). Abnormal
movements decreased after a few hours and completely disappeared within 3 days. Follow-up brain MRI, performed
3 weeks after admission, showed mild ischemic sequelae in
the right parasagittal central zone (Fig. 1b).

Discussion
Electronic supplementary material The online version of this
article (https​://doi.org/10.1007/s1376​0-020-01466​-4) contains
supplementary material, which is available to authorized users.
* Roger Denays
roger.denays@chrsm.be
1

Department of Neurology, CHR NAMUR, 185, Avenue
Albert Ier, 5000 Namur, Belgium

In unusual clinical presentations such as abdominal myoclonus, EEG is determinant for the diagnosis of EPC. Unfortunately, epileptiform activity is visible in only two-thirds
of cases and EEG is strictly normal in about one-fifth of
patients with EPC [1]. In our case, despite the absence of
EEG anomaly, the diagnosis of EPC was suspected due

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Acta Neurologica Belgica

Fig. 1  Axial images of brain MRI at the time of admission (a) and
3 weeks later (b). a Mild increased signal on sB1000 diffusion
sequences can be seen in the right parasagittal area, circumscribed to

the central zone. b Hypersignal on T2-weighted FLAIR sequences in
the same area, consistent with focal ischemic sequelae

to the coexistence of jerks in left abdomen and thigh, and
reinforced by MRI findings and by the rapid response to
anti-epileptic therapy. Moreover, other causes of abnormal
abdominal or leg movements (such as diaphragmatic flutter, “belly dancer’s” dyskinesia, drug-induced myoclonus,
“limb-shaking transient ischemic attacks”) were readily
excluded.
Abdominal EPC is a rare clinical entity previously
described, to the best of our knowledge, in only 16 cases
in association with brain tumours (4 cases) [6], focal infections (3 cases) [2, 6], cerebrovascular sequelae (2 cases) [5],
cryptococcal meningitis (1 case) [6], focal cortical dysplasia
(1 case) [6], acute ischemic stroke (1 case) [4], subdural
hematoma (1 case) [7], brain tumour surgery (1 case) [3];
two “idiopathic” cases have also been reported [6]. Including
our case, 4 of the 17 cases of abdominal EPC reported in the
literature seem, therefore, having a vascular cause, a proportion that is in the range of 10–27% reported in large retrospective series of patients with classic forms of EPC [1]. In
most previous reports as in our case, the lesion underlying
abdominal EPC was localized in the parasagittal frontal and/
or parietal areas around the central zone, in agreement with
the somatotopic representation of abdominal musculature
[2, 6, 7]. However, other anatomical localizations (such as
the occipital cortex) have also been reported [5], possibly

reflecting complex organization of the homunculus and individual variability, reorganization of the motor cortex due to a
dysplastic area or a cerebrovascular sequelae, or propagation
of discharges through the deep layers instead of the surface
[5, 6].

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Conclusions
We report a new case of abdominal EPC occurring in a context of acute focal cerebral ischemia, suggesting that a cerebrovascular cause may be more frequent than previously
thought. Therefore, cardiovascular investigations are mandatory in abdominal EPC with no other evident etiological
explanation.

Compliance with ethical standards
Conflict of interest The authors declare that they have no competing
interests.
Ethical approval All the procedures performed in the case study were
in accordance with the ethical standards of the institutional research
committee and with the 1964 Helsinki declaration and its later amend-

Acta Neurologica Belgica
ments or comparable ethical standards. This article doesn’t contain any
studies with animals performed by any of the authors.
Informed consent Written informed consent was obtained from the
patient for the publication of this case report.

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