Clinical Neurophysiology 112 (2001) 1726±1728

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BIPLEDs in akinetic mutism caused by bilateral anterior
cerebral artery infarction
Joost Nicolai*, Michael J.A.M. van Putten, DeÂnes L.J. Tavy
Department of Neurology and Clinical Neurophysiology, Ziekenhuis Leyenburg, Leyweg 275, 2545 CH Den Haag, The Netherlands
Accepted 17 May 2001

Abstract
Introduction: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA)
territory is reported rarely, however, often leading to akinetic mutism.
Case report: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24 h after
admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and
polymorphic delta activity.
Discussion: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs.
However, BIPLEDs may occur in bilateral ACA territory infarction. q 2001 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Akinetic mutism; Anterior cerebral artery; Bilateral independent periodic lateralized epileptiform discharges; Brain infarct; Electroencephalography; Periodic lateralized epileptiform discharges

1. Introduction
Akinetic mutism is described as a condition of silent,
alert-appearing immobility that characterizes certain subacute or chronic states of altered consciousness in which
sleep±wake cycles have returned but externally obtainable
evidence for mental activity remains almost entirely absent
and spontaneous motor activity is lacking (Plum and
Posner, 1980).
Several disorders have been described to cause akinetic
mutism, such as vascular, toxic, degenerative and infectious
disorders. Vascular causes include bilateral occlusions of
the anterior cerebral artery (ACA), vasospasm due to subarachnoid haemorrhage from anterior communicating aneurysms and paramedian thalamic or thalamo-mesencephalic
strokes (Bassetti and Bogousslavsky, 1995). We describe a
70 year-old man suffering from akinetic mutism due to a
bilateral ACA territory infarction with rather uncommon
electroencephalography (EEG) ®ndings.
2. Description of a case
On 26 October 2000, a 70 year-old man was admitted to
our hospital. A few hours before admission, he experienced

acute dif®culty in walking. During transportation to our
hospital he started vomiting, lost consciousness and developed bradycardia and hypotension. Examination on admission showed a blood pressure of 130/75 mmHg. There was
eye opening to speech only, without limb movements on
demand or to pain; verbal responses were absent. The pupils
were equal and reactive. Corneal and oculocephalic re¯exes
were present. Plantar re¯ex was extensor on both sides. One
hour later, consciousness was regained and no paresis was
noticed. No metabolic disturbances were found. Computerized tomography (CT) of the brain showed no abnormalities, besides leucoaraiosis.
The differential diagnosis included a non-convulsive
status epilepticus and a metabolic or postanoxic encephalopathy. Subsequent EEG, recorded 24 h after admission (Fig.
1), showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs). On re-examination, there was
eye opening and limb movement to pain, indicating a
worsening of his clinical condition. The diagnosis of
akinetic mutism was subsequently made, supposed to be
due to a bilateral ACA territory infarction. This was
con®rmed by magnetic resonance imaging (MRI) on the
®fth day after admission (Fig. 2). Three weeks later, he
suddenly died. Autopsy was not allowed.

* Corresponding author.
E-mail address: jnicolaidenhaag@hotmail.com (J. Nicolai).
1388-2457/01/$ - see front matter q 2001 Elsevier Science Ireland Ltd. All rights reserved.
PII: S13 88-2457(01)0060 2-2

CLINPH 2001548

J. Nicolai et al. / Clinical Neurophysiology 112 (2001) 1726±1728

1727

Fig. 2. Transverse T2-weighted MRI image obtained 4 days after admission, demonstrates bilateral infarction in the ACA territory.

Fig. 1. (A) EEG recording performed approximately 24 h after admission.
Shown are PLEDS over the right hemisphere during the ®rst 3 s, indicated
by the solid arrows (1) and over the left frontal area in the remaining 3 s,
indicated by the dashed arrows (2). Longitudinal bipolar montage. (B).
Shown are PLEDS over the left frontal area, indicated by the dashed arrows
(2). Initially, periodic discharges are present over the right hemisphere, as
well, indicated by the solid arrows (1). Note that the frequency of the
PLEDS over the left frontal area changes from about 1.2 to 0.6 Hz.
These lower-frequency PLEDS are not present over the contralateral hemisphere.

3. Discussion
Bilateral infarction in the ACA distribution is presumably
rare. In a series of 413 patients with ischaemic infarction,
only one case was described (Gacs et al., 1983). In a study of
1490 patients admitted for a ®rst stroke over a period of 7
years, only two cases were found (Bogousslavsky and Regli,
1990). In the period 1930±1999, Minagar found detailed
reports of 8 patients with a bilateral ACA infarction causing
akinetic mutism in 7 (Minagar and David, 1999). The one
exception had no reduction of motor or speech activities but
showed complex behavioural changes and a lack of attention (Laplane et al., 1981). Mutism caused by unilateral

infarction of the ACA territory is described as well; 8 out
of 16 patients with a left-sided and two out of 9 patients with
a right-sided ACA infarction had initial mutism (Bogousslavsky and Regli, 1990).
Bassetti and Bogousslavsky state that akinetic mutism
caused by bilateral infarction in the ACA distribution is
characterized by bifrontal or generalized EEG slowing,
with lack of desynchronization following external stimuli
(Bassetti and Bogousslavsky, 1995). Ingvar described two
cases of akinetic mutism with a normal EEG. However, the
precise cause of the akinetic mutism in these two cases is not
clear from his description, which makes a comparison dif®cult (Ingvar, 1971). Only in 4 case reports on akinetic
mutism due to bilateral ACA infarction are EEG ®ndings
discussed, as shown in Table 1.
The clinical diagnosis of bilateral ACA infarction can be
dif®cult, which is probably due to the presence of reduced
consciousness in the initial stage. Coma is reported due to
bilateral ACA territory infarction lasting from 1 day
(Oomman and Madhusudhanan, 1999) to even 4 weeks
(Lipschutz et al., 1991). Coma due to the combination of
diabetic ketoacidosis and bilateral ACA infarction lasting
for 2 days, resulting in akinetic mutism, is described as well
(Freemon, 1971). In several cases reported, the initial diagnosis was brainstem infarction (Minagar and David, 1999)
or basilar artery occlusion (Ferbert and Thron, 1992). As in
our patient, initial CT scan or MRI scan can be normal. In
many reported cases a lumbar puncture was performed
(Freemon, 1971; Gugliotta et al., 1989; Lipschutz et al.,
1991; Borggreve et al., 1994) on the day of admission,
indicating that the clinical picture had not been immediately
recognized. In our patient the initial diagnosis was not clear
either, the EEG performed 24 h after admission showed a
rather unexpected ®nding, i.e. BIPLEDs.
BIPLEDs are de®ned as independent, asynchronous periodic lateralized epileptiform discharges (PLEDs) (Pohlmann-Eden et al., 1996) and can be distinguished from

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J. Nicolai et al. / Clinical Neurophysiology 112 (2001) 1726±1728

Table 1
EEG ®ndings reported in akinetic mutism due to bilateral anterior cerebri artery infarction
Reference

Sex/age

Clinical picture

EEG made after

Main EEG ®ndings

Freemon (1971)
Gugliotta et al. (1989)

M/62 (case 3)
M/65

Akinetic mutism
Akinetic mutism

Not mentioned
At admission
5 days
10 days

Diffuse theta and delta
Sporadic 4±7 Hz theta right occipital region
Diffuse slow activity, delta right rolandic region
Diffuse 7±8 Hz theta, multifocal, intermittent,
polymorphic delta
Sharp wave and spike and wave complexes,
bilaterally central regions
Bilateral sharp 4±7 Hz theta, disseminated
polymorphic 1±3 Hz delta
Diffuse slowing

Spontaneous nocturnal sleep
Borggreve et al. (1994)

M/73

Minagar and David (1999)

M/63

Akinetic mutism, almost
complete quadriplegia
Akinetic mutism

ipsilateral independent PLEDs (Silbert et al., 1996), alternating PLEDs or cerebral bigeminy (Bertolucci and Silva,
1992) and multifocal PLEDs (Lawn et al., 2000). In case of
BIPLEDs the complexes are asynchronous and usually
differ in morphology, amplitude, repetition rate and the
site of maximal involvement (de la Paz and Brenner, 1981).
The complexes in BIPLEDs are similar to those that
occur with PLEDs: surface-negative bi-, tri-, or polyphasic
spike and sharp waves, with an amplitude ranging from 50
to 300 mV, duration ranging from 60 up to 800±1000 ms
and periodicity ranging from 0.3 to 4 s (Pohlmann-Eden et
al., 1996). Postanoxic encephalopathy, central nervous
system (CNS) infection (encephalitis or meningitis) and
chronic seizure disorders are reported to be the major causes
of BIPLEDs (de la Paz and Brenner, 1981).
Thirteen out of 18 patients with BIPLEDs were comatose
and mortality was high (61%) in the series described by de
la Paz and Brenner. In a series of 5 children with BIPLEDs,
3 had suffered from anoxia and two had a CNS infection
(Raroque et al., 1993).
Multifocal PLEDs occur independently in 3 or more locations and involve both hemispheres (Lawn et al., 2000).
Multifocal PLEDs are associated with vascular lesions,
CNS infections, metabolic/toxic disorders, chronic seizure
disorders and hypoxic ischaemic insults. Twenty-six out of
35 patients with multifocal PLEDS were comatose and the
mortality was high (57%) (Lawn et al., 2000).
To our knowledge, this is the ®rst description of a patient
with akinetic mutism due to bilateral ACA infarction, showing BIPLEDs on the EEG.
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