JOURNAL

OF THE

NEUROLOGICAL
SCIENCES
ELSEVIER

Journal of the Neurological Sciences139(I 996) 58-65

Akinetic mutism with bithalamic infarction. Neurophysiological
correlates
Peter H.M.F. van Domburg a2* , Hans J. ten Donkelaar b, Servaes L.H. Notermans ’
’ Department of Neurology, Unir:ersi@ Hospital Nijmegen, Rein&r Postlaan 4, P.O. Box 9101 6500 HB Nijmegen,, The Netherlands
b Department of Anatomy and Embryology, Faculty of Medical Sciences, Unil~ersity Hospital, Nijmegen, The Netherlands
’ Department of Clinical Neurophysiology, LInkersi@ Hospital, Nijmegen, The Netherlands

Received 5 June 1995;revised 5 December 1995; accepted 19 December 1995

Abstract
A 42-year-old man presented with akinetic mutism, caused by bilateral thalamic infarction, resulting in a temporary amnesic syndrome
and, finally, selective downgaze palsy. Electroencephalographic recording in the initial phase showed generalized spike-and-wave
discharges, similar to those found in animal studies after lesion or stimulation of specific thalamic nuclei. Analysis of magnetic resonance
images (MRI) of the head showed that the centre of ischemic necrosis particularly involved the intralaminar thalamic nuclei and a small
part of the rostra1 mesencephalon. The findings support the previously suggested involvement of cortico-thalamo-mesencephalic circuitry
in the initiation of motor responses, and the association of the non-specific thalamic nuclei with the appearance of generalized
epileptiform phenomena in cases of reduced vigilance.
Keywords: Thalamus; Thalamopeduncularartery; Spike-and-wave discharges;Akinetic mutism

1. Introduction
The uncommon ischaemic vascular disorders of the
thalamus can be classified into four clinical syndromes,
depending on the vascular territory involved (Percheron,
1973; Graff-Radford et al., 1985; Bogousslavsky et al.,
1988). Obstruction of the so-called thalamopeduncular
(perforant or paramedian) artery (PTA, see Fig. 1) results
in a bilateral (meso-)thalamic lesion, generally including
parts of the nonspecific intralaminar as well as of the
dorsomedial nuclei (Castaigne et al., 198 1; Bogousslavsky
et al., 1988). The clinical symptoms include varying
changes of consciousness, supra-nuclear ophthalmoplegia,
apathetic behavior and an amnesic syndrome, generally
with a rather favourable prognosis (Castaigne et al., 1981;
Guberman and Stuss, 1983; Tatemichi et al., 1992).
Clinical experience suggests a linkage of arousal state
with the occurrence of epileptiform changes in certain
cases. The association of this phenomenon with the suggested thalamic control of neocortical activation, mainly
based on animal studies, has been the subject of much

* Correspondingauthor.Tel: + 3 1 (24) 611111;Fax: + 3 I (24) 541122.
0022-510X/96/$15.00 0 1996 Elsevier Science B.V. All rights reserved
PII SOO22-5 10X(96)00026-3

dispute (Steriade and Llinh, 1988; Vanderwolf and Stewart, 1988; Gloor et al., 1990). The clinicoanatomical and
electrophysiological findings in our case provide further
evidence for this association in man.

2. Case report
A 42-year-old man was admitted to hospital, after he
could not be woken up normally in the morning. The
preceding time he worked as a public servant and was in
good health with normal intelligence. His medical history
was inconspicuous and he had no predisposition to epilepsia. On admission he presented with a sleep-like state, with
double incontinence, sometimes alternated by short periods
of restlessness. His blood pressure was 150/90, and he
had normal regular pulsations of carotid arteries, normal
body temperature and ECG findings. On neurological examination there were no signs of meningeal irritation, he
had narrow pupils that did not react to light and the eyes
remaining in mid-position. The reactions to painful stimuli
were predominantly stretching of extremities and some
facial pain expression. Examination of blood and cerebrospinal fluid (including metabolites of monoamines)

P.H.M.F.

mn Dornhurg

et al. / Journal

of the Neurological

A

IiAS

,,
\

Fig. I. Schematic representation of the vascular supply of thalamic
subdivisions (mainly based on Percheron, 1973 and Schlesinger, 1976). 1
= Anterior choroidal artery; 2 = polar artery (inaccurate: tuberothalamic artery); 3 = thalamopeduncular (thalamo-subthalamic or interpeduncular) artery (TPA): 4 = inferolateral choroidal artery (geniculothalamic
artery); 5 = posterolateral choroidal artery: ACA = anterior cerebra1
artery; AC1 = internal carotid artery: ACM = medial cerebral artery;
ACP = posterior cerebral artery: ANT = anterior thalamic nucleus;
BAS = basilar artery: CA = anterior commissure; C(e)M = centre
median (central medial thalamic nucleus): cc = corpus callosum; CI =
colliculus inferior; CMA = corpus mamillare; COMP = posterior
communicating artery; CP = posterior commissure; CS = colliculus
superior.

showed no abnormalities. From the third day onward there
was a gradually restoring gaze: The patient thus seemed to
pay attention to his immediate surroundings, yet there was
not any response to various stimuli. One week after admission the patient still showed this akinetic and mute state,
with a normal sleep-waking-cycle, double incontinence
and without particular signs of motor or sensory impairment. A symmetrically ring-shaped paramedian bilateral
thalamic lesion with contrast enhanced surrounding
(penumbra) was shown on the CT scan (Fig. 2). No source
of septic or thrombotic embolization could be found by
cranial angiography, but trans-esophageal echocardiogram
was not performed. There were normal peak serum levels
of homocysteine after a standard methionine loading test.
During the second and third week of recovery spontaneous body movements gradually returned. There was still
no adequate response to stimulation, however, and a tendency to automatisms or stereotypic movements: He managed to handle his guitar (he used to play at home), in a
manner suggestive of playing, without evidence of conscious participation and continuing the movements when
the instrument was taken away. At other times he rubbed
his belly aimlessly for a long period without signs of

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139 (1996158-65

59

discomfort. During the third week the mute state changed
into a hypokinetic state, with incidental inadequate emotional expressions. He gradually began to talk excessively,
though largely unintelligibly, often slurred and indistinctly,
sometimes with delusional or annoying expressions. What
struck his wife and the nursing staff was a growing lability
of affect without evidence of conscious participation. The
twenty-third day after the onset of illness he walked away
from the ward, without clear purpose, fearing that the
nursing staff intended to keep him confined indefinitely.
Although disoriented and confused, he gradually began to
answer simple questions, such as “where do you live?“,
correctly although with few words. Yet the cooperation in
clinical or neuropsychological tests remained wanting.
During the fourth week the conditions of the Raven Progressive Matrices and the Hooper test (visual organization)
were partially met with. He appeared incapable to settle a
simple block pattern. He showed constructional apraxia
and could not retain a simple story. Performance on the
Trail Making Test was very poor. During the fifth week
semantic paraphasias and word-finding disturbances were
recognizable. The amnesic syndrome was reflected in a
poor Wechsler Memory Scale (WMS) score of 74 in the
fourth week, recovering to estimated premorbid level of
135 at fifteen months. After a clinical revalidation period,
he had become independent for daily activities, although
very slow, after three quarters of a year. There was still
poor performance on the Trail Making Test then, suggesting lack of concentration. Wechsler Adult Intelligence

Fig. 2. CT-scan image (transversal section) obtained at the 9th day of
admission.

60

P.H.M.F. ran Domburg et al./Joumal

of the Neurological Sciences I39 (1996) 58-65

P.H.M.F. van Domburg et al. /Journal qf the Neurological

Score (WAIS) was reliably calculated 118/94 (for verbal
and performance score, respectively) at twelve months and
125 at fifteen months after admission. Selective downgaze
palsy, with incapacity to read or write, loss of initiative,
absent-mindedness, slightly disturbed balance and difficulty in performing combined tasks or precise movements
were the remaining signs. After one year he resumed his
former job partially under adapted circumstances. Two
years after admission there was only selective downgaze
paresis, slight inertia and complete recovery of overall
intelligence, learning capability and retention.
2.1. Electrophysiological

findings

Electroencephalographic (EEG) recordings were performed at the day of admission (day 11, days 2 and 8 and
about 1 month later. The initial registration showed generalized slowing of background activity, loss of differentiation and some varying activity, diffusely spread, in the
alpha range (8-9 Hz). A tendency to dys-regulation of
irregular delta bursts was most pronounced fronto-centrotemporally. As shown in Fig. 3 there were some repeated
bursts of generalized slow-wave and spike-and-wave (SW)
discharges of 6/s, interrupted by desynchronisation of
about 2 s, at the initial recording. The patient clinically
remained in an unchanged akinetic mute state. Follow-up
recordings gradually showed recurrence of normal background activity, gradual decline of centrotemporal dysregulation and no further signs of epileptiform activity or
hypersynchronization.
Somatosensory evoked potentials (SSEP) of the median
and sural nerve, recorded on Neuropack Four mini (Nihon
Kohden) apparatus, at day 13, revealed symmetric normally shaped early components, normal peak latencies and
inter-peak intervals, but atypically shaped later (cortical)
components. These SSEP findings provided further evidence for the more ventrolaterally located sensory relay
thalamic nuclei not being involved in an early phase
(Graff-Radford et al., 1985; Moriaka et al., 1989).
2.2. Magnetic resonance imaging
ical localization

(MRI) and neuroanatom-

A Philips 1,5 tesla MRI scanner was used to obtain
5-mm thick horizontal, coronal and sagittal Tl and T2weighted inversion recovery MRI cuts. This examination
was performed two months after admission in order to
establish an eventual necrotic area. The initial hypofunctional penumbra (shown as a contrast enhanced area on CT
in Fig. 2) probably has been somewhat more extensive,
particularly involving a larger central thalamic region. The
(intercommissural) line connecting anterior and posterior
commissure (APC) was used as a reference for the stereotaxical demarcation of the hypodense area on MRI cuts
(Fig. 4). The centre of the hypodense area in the right
thalamus was located at about 10 mm laterally from the

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139 (19961 58-65

61

median sagittal plane and between 7 and 15 mm behind
the anterior commissure. On the transversal cuts it is
identifiable at the level of the APC-line and at the slice 9
mm higher. Using the stereotaxic atlas of Talairach and
Toumoux (1988; Figs. 45-46, 82-83 and 117-l 19) as a
reference, the thalamic nuclei involved were identified,
including the antero-medial part of the ventral lateral
nucleus, the lateral part of the dorsomedial nucleus and
intralaminar nuclei, extending ventrally over the centre
mkdian (CeM) and parafascicular (Pf) nuclear complex
(Fig. 4. A-C). Th e mamillothalamic tract and some other
traversing fibres may have been involved. Similarly the,
somewhat smaller, lesion on the left side has its centre at
the intralaminar level. At the mesencephalic level a very
small hypodense area was located subthalamically in the
pretectal ventral tegmental area, as is shown on the sagittal
representation.

3. Discussion
Our patient did not seem to have special risk factors for
vascular lesions. His rather young age is remarkable and
this was also noteworthy for similar cases in other studies.
We could trace 75 cases with thalamic paramedian infarction from the literature and counted a mean age of 58 years
and, more specifically, 53 (19-81) years when the infarct
was bilateral (52 cases>.Because of their strategic localization, with otherwise intact cortical function, these lacunar
infarcts may result in a particular transient dementia syndrome (Stuss et al., 19881, but generally show a mild
outcome (Castaigne et al., 1981; Guberman and Stuss,
1983; Tatemichi et al., 1992). Cases of selective downgaze
paralysis, as appeared in our patient (after temporary more
extensive disconjugate ophthalmoplegia
with narrow
pupils), are rarely seen, and reflect the involvement of a
small rostra1 mesencephalic midline area, supplied by small
TPA branches (Halmagyi et al., 1978; Trojanowski and
LaFontaine, 198 1; Biittner-Ennever et al., 1982).
Apart from short coma, the particular changes of consciousness, reported in the initial stage of cases with
bilateral (meso-)thalamic infarction included hypersomnia
(Graff-Radford et al., 1985), pseudo-hypersomnia or presleep behavior (Guilleminault et al., 1993), and akinetic
mutism (Segarra, 1970; Castaigne et al., 1981). The clinical picture in our patient, particularly during the first week,
meets the criteria of akinetic mutism, as originally drafted
by Cairns (Cairns et al., 1941): ‘a condition in which the
patient appears to be awake and may follow the examiner
with his eyes, but spontaneous motor and verbal responses
are lacking; he is doubly incontinent and responds incompletely to noxious stimuli, although not paralysed’. Apart
from small lesions of the posterior diencephalon and adjacent midbrain, interrupting the paramedian reticular formation (MRF), akinetic mutism may be caused by large,
bilateral, basal medial frontal lobe lesions, involving the

P.H.M.F. wzn Domhurg et al./ Journal of the Neurological Sciences 139 (1996) 58-65

62

The clinical impression, characteristically shown in our
patient, is that of an early reappearance of arousal, suggested by permanently open eyes, normal blinking and
recovering gaze, yet without evidence of adequate psychomotor response. There was neither a tendency to take a
sleep posture (Guilleminault et al., 19931, nor could the
patient be pulled out of his hypokinetic and mute state

orbital cortex, septal area and cingulate gyri (Plum and
Posner, 1982; Kurtz et al., 1988; Ntmeth, 1988). The
concept of a diffuse cortical dysfunction from reduced
‘non-specific’ MRF-thalamocortical activation, is mainly
based on older literature (Cairns, 1952; Klee, 1961; Segarra,
1970), and may seem to be corroborated by PET-scan
(Levasseur et al., 1992) and EEG studies (NCmeth, 1988).

4-

D.10

mm

sI
7654

3

2

1

0

I
1

23456

,
54321012345

Fig. 4. MRI of the final necrotic area with corresponding schematic representations, drawn to scale. (a) Transversal section. (b) Paramedian sagittal section.
(c) Frontal section.

P.H.M.F. ~‘an Domburg et al. /Journal

Bogousslavsky et al., 1991). Therefore, the concept of
thalamic neglect with hypokinesia, i.e. the failure to respond to relevant stimuli, although not paralysed (Valenstein and Heilman, 1981; Watson et al., 1981) seems more
appropriate, and was further consolidated in other studies
(Waxman et al., 1986; Heilman et al., 1987; Fleet et al.,
1987). This akinetic mute state can be distinguished from
athymhormia or ‘loss of psychic self-activation’, presented
in some cases of small bilateral thalamic infarction, more
antero-median located, particularly involving dorsomedial
nuclei (Bogousslavsky et al., 1991). Patients with
athymhormia, originally reported after bilateral lesions of
the striatum and generally with less tendency to full recov-

-12-16

mm

654321012345

Fig. 4. (continued).

of the Neurological Sciences 139 (1996) 58-65

63

ery, suffer from a flat affect and loss of drive (lack of
interest in things of life), but they may respond if only
adequately stimulated (Habib and Poncet, 1988). The slight
anatomic variations in vascular supply and thalamic nuclei
involved might account for these subtle differences in
clinical manifestations (Stuss et al., 1988; Tatemichi et al.,
1992).
In our patient the central part of the thalamus was most
severely affected, with involvement of intralaminar and
midline nuclei. These structures, including intralaminar
central medial (centre median; CeM) en parafascicular (Pf)
nuclei, are known to have rather diffusely spread projections to the cortex, and are closely linked to the motor
system (Groenewegen and Berendse, 1994). However, they
are not the pre-eminent source of diffuse neocortical activation and arousal, as was the conventional view
(Vanderwolf and Stewart, 1988; Gloor et al., 1990). The
circuitry from intralaminar thalamic (CeM-Pf) nuclei to
frontocortical and back to the thalamic enfolding nucleus
reticularis (NRT), has been suggested to serve as a kind of
gate control, selectively preparing the aroused organism
for responses to meaningful stimuli (Skinner and Yingling,
1976; Watson et al., 198 1; Crick, 1984). Whereas intralaminar, particularly CeM-Pf, thalamic nuclei seem to control
the firing threshold of cortical neurons (Miller, 1992;
Steriade and Deschenes, 1984) their activity partly depends on reciprocal connections with the NRT and MRF,
which are involved in tonic arousal (Skinner and Yingling,
1976; Watson et al., 1981; Steriade and Llinas, 1988;
Miller, 1992). More caudally located thalamic structures,
involved in the regulation of gaze, appear to function
independently (Waxman et al., 1986; Groenewegen and
Berendse, 1994) as was evident in our patient from the
early reappearance of the primitive orienting response.
The electroencephalographic findings on the day of
admission, showing repeated bursts of 6/set slow wave
and spike-and-wave (SW) discharges (Fig. 3) must result
from the initial elimination of the ‘non-specific’ intralaminar thalamic structures. The EEG pattern was similar,
although with double frequency, to that reported in experimental stimulation studies of the massa intermedia in the
cat (Jasper and Droogleever-Fortuyn, 1947) and in cases
of absence epilepsy (Snead, 1995). Based on both stimulation and ablation studies of selective thalamic structures in
animals, the thalamus-enfolding nucleus reticularis thalami
(NRT) has been proposed to be either the driving force
(Avanzini et al., 1992; Vergnes and Marescaux, 1992) or
at least involved in both EEG spindle rhythmicity and the
absence-like SW and slow wave discharges, associated
with a decreased level of vigilance (Yingling and Skinner,
1975; Gloor et al., 1990; Miller, 1992). Bilateral thalamic
lesions, such as in the present study, therefore may be
responsible for both the akinetic mute state and dysinhibition of NRT-related SW and slow wave discharge activity,
by interruption of thalamocortical and intrathalamic connections. Interestingly, similar changes have been reported

64

P.H.M. F. can Domhurg et al. / Journal of the Neurological Sciences 139 (1996) 58-65

in a case with bilateral deep frontally located infarcts
(Kurtz et al., 1988). The EEG findings in our case confirm
experimental evidence on the involvement of intralaminar
thalamic nuclei in the promotion of absence-like phenomena in man (Snead, 1995) and its association with behavioural inertia or decreased vigilance, so far only
demonstrated in animal experiments.

Acknowledgements
We wish to thank J. Jansen for assistance in the preparation of the manuscript, A. Richt, speech therapist, for
advice on interpretation of speech disturbances; G. Cho
Chia Yuen, for neuropsychological investigation, and Dr.
H. Schoonderwaldt for the clinical support during admission.

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