Copyright Ó Blackwell Munksgaard 2003

Acta Neurol Scand 2003: 108: 55–59
Printed in UK. All rights reserved

ACTA NEUROLOGICA
SCANDINAVICA
ISSN 0001-6314

Case report

Benign bilateral independent periodic
lateralized epileptiform discharges
Fushimi M, Matsubuchi N, Sekine A, Shimizu T. Benign bilateral
independent periodic lateralized epileptiform discharges.
Acta Neurol Scand 2003: 108: 55–59. Ó Blackwell Munksgaard 2003.
Bilateral independent periodic lateralized epileptiform discharges
(BIPLEDs) usually appear transiently in patients with severe
disturbances of consciousness and are indicative of a poor prognosis.
Recurrent BIPLEDs have not previously been reported in the
literature. We report a 64-year-old patient with bilateral hippocampal
lesions (cerebral infarction) who exhibited persistent periodic
lateralized epileptiform discharges (PLEDs) (chronic PLEDs)
associated with recurrent BIPLEDs. Electroencephalography was
recorded for more than 6 months. Left hemispheric PLEDs appeared
first. Next, PLEDs shifted to the right hemisphere and BIPLEDs
occasionally developed. Brain magnetic resonance imaging and singlephoton emission computed tomography with technetium-99hexamethyl-propyleneamine oxime was performed before and after the
appearance of BIPLEDs. The patient had no remarkable clinical
symptoms aside from mild memory impairment for this period of time.
This is the first case of recurrent ÔbenignÕ BIPLEDs, that is, BIPLEDs
with a positive prognosis.

Periodic lateralized epileptiform discharges
(PLEDs) are a relatively rare phenomenon on
electroencephalography (EEG) caused by events
such as infarcts and encephalitis (1). In general,
PLEDs appear transiently (1), and few reports
have described persistent PLEDs (2–4). Bilateral
independent periodic lateralized epileptiform
discharges (BIPLEDs) are PLEDs occurring
independently in both cerebral hemispheres (5).
BIPLEDs are usually caused by anoxic encephalopathy and central nervous system (CNS) infections (thus the high incidence of coma), and are
typically associated with a poorer prognosis than
PLEDs (5).
PLEDs generally occur transiently, and recurrent BIPLEDs have not been reported previously
in the literature. However, in the present case,
PLEDs represented a chronic condition associated
with recurrent BIPLEDs. Brain magnetic resonance imaging (MRI) and single-photon emission
computed tomography with technetium-99-hexa-

M. Fushimi, N. Matsubuchi,
A. Sekine, T. Shimizu
Department of Neuropsychiatry, Akita University School
of Medicine, Akita, Japan

Key words: periodic lateralized epileptiform
discharges; bilateral independent periodic lateralized
epileptiform discharges; hippocampal lesion; memory
impairment; magnetic resonance imaging;
single-photon emission computed tomography
Masahito Fushimi, Department of Neuropsychiatry,
Akita University School of Medicine, 1-1-1 Hondo,
Akita-city, Akita 010-8543, Japan
Tel.: +81 188 846122
Fax: +81 188 846445
e-mail: fushimi@psy.med.akita-u.ac.jp
Accepted for publication September 10, 2002

methyl-propyleneamine oxime (HMPAO-SPECT)
were performed before and after the appearance of
BIPLEDs. Bilateral hippocampal lesions with
decreased regional cerebral blood flow (rCBF)
were demonstrated. This case illustrates the previously unreported EEG findings of persistent
PLEDs (chronic PLEDs) associated with recurrent
ÔbenignÕ BIPLEDs.
Case report

The patient was a 64-year-old man who had been
treated for the past 3 years at our institution for
diabetes mellitus, hypertension, hyperlipidemia
and nephrotic syndrome. No history of epilepsy
or alcoholism was reported. From about 1 week
before admission, the patient experienced symptoms of upper airway inflammation. While at
home, he suffered a suspected generalized convulsion and was brought to hospital by ambulance.
On arrival, convulsions had already ceased and the
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Fushimi et al.
patient was fully conscious (Glasgow coma scale
14). No abnormal findings were present on neurologic examination. Pyrexia and an elevated leukocyte count were present and pneumonia was
diagnosed following chest radiography. Laboratory
tests revealed hyponatremia (124 mEq/l), elevated
creatine phosphokinase (CPK) levels (252 IU/l),
and mild hyperglycemia and he was admitted to
hospital. No significant abnormalities were demonstrated on brain computed tomography (CT) or
lumbar puncture.
On day 2, CPK values increased further
(5140 IU/l) and myoglobulinuria appeared. By
day 12, CPK values had decreased (557 IU/l)
and myoglobulinuria had disappeared. The
patient recovered from pneumonia shortly after
admission, with temperature returning to normal
on day 2 and abnormal findings on chest radiography disappearing by day 3. Hyponatremia
resolved by day 5 and CPK values normalized
by day 13. From about this time, mild signs of
short-term memory disturbance [Mini-Mental
State Examination (MMSE) 25] were observed.
Brain MRI on day 15 revealed no abnormalities
that could explain these clinical symptoms. However, on day 28, further brain MRI revealed
bilateral abnormalities in the hippocampal regions. Based on the history, examination and
investigations, bilateral infarction of the hippocampal regions was diagnosed. The patient was
discharged on day 80, as memory impairment was
only mild and he was capable of performing
normal daily activities (MMSE 26, WAIS-R 89).
Since his discharge, he has been visiting the
hospital as an outpatient for treatment of his
pre-existing conditions. No further remarkable
abnormalities have been displayed other than mild
memory impairment and mild hyperglycemia.

Results
EEG findings over time

EEGs were based on the International 10–20
system and referential montage was used. EEGs
were recorded 23 times between day 8 and day 226.
In all EEGs, basic rhythm was satisfactory (e.g., no
slowing down). In EEGs from day 8 to day 16, left
hemispheric PLEDs were identified (Fig. 1A). On
days 27 and 30, BIPLEDs were detected (Fig. 1C).
In EEGs from day 31 to day 226, right hemispheric
PLEDs were seen in all EEGs (Fig. 1B) and on
days 115, 136 and 170, left hemispheric PLEDs
were also observed. Additional BIPLEDs were
thus documented on three separate occasions on
days 115, 136 and 170 (Fig. 1D).
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Brain MRI findings

Brain MRI on day 15 was unremarkable. However, MRI on day 28 using a T2-weighted image
and fluid-attenuated inversion recovery revealed
areas of abnormal hyperintensity in bilateral hippocampal regions (Fig. 2A), while T1-weighted
imaging displayed abnormal enhancement in the
right hippocampal region (Fig. 2B). However,
about 2 months later, these findings had almost
completely resolved and subsequent MRI revealed
no additional abnormal findings.
HMPAO-SPECT findings

HMPAO-SPECT was performed before and after
the appearance of BIPLEDs on day 115. Eight
days before the appearance of BIPLEDs (only
right hemispheric PLEDs appeared), rCBF was
decreased in the right fronto-temporal region
(Fig. 3A). Six days after the appearance of BIPLEDs, rCBF in the right fronto-temporal region was
unchanged contrary to slight decrease in rCBF in
the left fronto-temporal region compared to before
the appearance of BIPLEDs (Fig. 3B).
Discussion

In general, PLEDs appear transiently and disappear within 2–3 weeks (1). A small number of
reports have described persistent PLEDs (2–4). In
this case, a relatively rare situation was encountered in which PLEDs occurred persistently for
more than 6 months. Furthermore, a number of
unusual features characterized this case. Generally,
in EEGs with periodic discharges, background
activity is abnormal (e.g. slowing down). In the
present case, however, good basic rhythm appeared
on the EEG when PLEDs or BIPLEDs developed.
This case also differs from chronic epilepsy as
reported by Westmoreland et al. (3). Another form
of chronic PLEDs involves the occurrence of
PLEDs only during synchronized (NREM) sleep,
while the EEG is normal during wakefulness (4).
However, to the best of our knowledge, this is the
first case of recurring BIPLEDs over an extended
period without the development of any remarkable
symptoms other than mild memory impairment. In
previous reports, BIPLEDs are often associated
with severe disturbances of consciousness, such as
coma (5). The present case therefore demonstrates
a new variant of BIPLEDs with a relatively good
prognosis.
The pathogenesis of PLEDs is not entirely
clear. In the present case, lesions on MRI were in
a small, restricted area. In such cases, metabolic

Benign BIPLEDs

Figure 1. EEGs based on the International 10–20 system and referential montage. EEG day 9, left hemispheric PLEDs (A) and EEG
day 226, right hemispheric PLEDs (B). BIPLEDs detected in EEGs on day 27 (C) and day 115 (D).

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Fushimi et al.

Figure 2. MRI on day 28 (coronal view) with fluid-attenuated inversion recovery reveals high intensity lesions in bilateral hippocampal regions (A) and a T1-weighted coronal image shows abnormal enhancement in the right hippocampal region (B).

Figure 3. HMPAO-SPECT images 8 days before the appearance of BIPLEDs (only right hemispheric PLEDs had appeared),
showing decreased rCBF in the right fronto-temporal region (A). Six days after the appearance of BIPLEDs, rCBF decreased slightly
in the left fronto-temporal region in addition to the right fronto-temporal region (B).

abnormalities are frequently involved (6–8).
Hyperglycemia probably exerted an influence in
the present case.
Regarding the laterality, left hemispheric PLEDs
appeared at first. PLEDs then shifted to the right
hemisphere, with the occasional development of
BIPLEDs. Our explanation of this pattern is based
on differing levels of rCBF and differing thresholds
for triggering PLEDs. Initially, ischemia may have
been more severe in the left hemisphere. However,
when lesions developed into infarcts, they were
more severe in the right hemisphere. As a result,
subsequent EEGs displayed the gradual shift of
58

PLEDs from left to right hemisphere. BIPLEDs
probably developed during this period of transition. As a lesion was also present in the left
hippocampal region, any factor (probably metabolic) inducing PLEDs would probably lead to
their occurrence in both hemispheres. We therefore
suspect the threshold for triggering PLEDs may
have been higher in the left hemisphere than in the
right. This hypothesis is based on changes in rCBF
seen on HMPAO-SPECT: before BIPLEDs developed (appearance of right hemispheric PLEDs),
rCBF was decreased in the right hemisphere. After
had BIPLEDs developed, rCBF was also decreased

Benign BIPLEDs
in the left hemisphere. However, whether rCBF
decreases or increases at the site at which PLEDs
appear remains controversial (9, 10). Further study
of similar cases in the future is needed to provide
firm support for this hypothesis.
Acknowledgements
The authors would like to thank Dr K. Kato and Dr I. Sakuma
of the Department of Radiology, Akita University School of
Medicine, Akita, for conducting the neuroimaging studies.

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