145

Behavioural Neurology 19 (2008) 145–151
IOS Press

Clinical Note

Disrupted auto-activation, dysexecutive and
confabulating syndrome following bilateral
thalamic and right putaminal stroke
Lieve De Wittea , Sebastiaan Engelborghs b,c,d, Jo Verhoeven e, Peter P. De Deynb,c and Peter Mariëna,b,∗
a

Department of Linguistics, Vrije Universiteit Brussel, Brussels, Belgium
Department of Neurology, ZNA Middelheim Hospital, Antwerp and Laboratory of Neurochemistry and Behaviour,
Institute Born-Bunge, University of Antwerp, Antwerp, Belgium
c
Department of Health Care Sciences, University College Antwerp, Antwerp, Belgium
d
Department of Nursing Sciences, Faculty of Medicine, University of Antwerp, Antwerp, Belgium
e
Department of Language and Communication Sciences, City University, London, UK
b

Abstract. Objective: Clinical, neuropsychological, structural and functional neuroimaging results are reported in a patient
who developed a unique combination of symptoms after a bi-thalamic and right putaminal stroke. The symptoms consisted of
dysexecutive disturbances associated with confabulating behavior and auto-activation deficits.
Background: Basal ganglia and thalamic lesions may result in a variety of motor, sensory, neuropsychological and behavioral
syndromes. However, the combination of a dysexecutive syndrome complicated at the behavioral level with an auto-activation
and confabulatory syndrome has never been reported.
Methods: Besides clinical and neuroradiological investigations, an extensive set of standardized neuropsychological tests was
carried out.
Results: In the post-acute phase of the stroke, a dysexecutive syndrome was found in association with confabulating behavior and
auto-activation deficits. MRI showed focal destruction of both thalami and the right putamen. Quantified ECD SPECT revealed
bilateral hypoperfusions in the basal ganglia and thalamus but no perfusion deficits were found at the cortical level.
Conclusion: The combination of disrupted auto-activation, dysexecutive and confabulating syndrome in a single patient following
isolated subcortical damage renders this case exceptional. Although these findings do not reveal a functional disruption of the
striato-ventral pallidal-thalamic-frontomesial limbic circuitry, they add to the understanding of the functional role of the basal
ganglia in cognitive and behavioral syndromes.
Keywords: Putamen, bithalamic stroke, confabulatory syndrome, dysexecutive syndrome, psychic akinesia

1. Introduction
Ischemic lesions of the basal ganglia and the thalamus may result in clinical syndromes characterized by
∗ Corresponding

author: Prof Dr. P. Mariën, ZNA Middelheim Hospital, Department of Neurology, Lindendreef 1, BE-2020
Antwerp, Belgium. Tel.: +32 3 2803136; E-mail: peter.marien5@
telenet.be.

a wide range of symptoms varying from pure motor
deficits to complex sensory, neuropsychological and
behavioral alterations [5,52,67]. There is ample evidence that ischemic lesions of the basal ganglia result in motor and neurobehavioral syndromes in which
dystonia and apathy are common [6,14,21,28,32,52,54,
71]. Bilateral vascular thalamic lesions may induce a
wide range of neurobehavioral symptoms such as: 1)
transient vigilance disorders, 2) hypersomnia, 3) verti-

ISSN 0953-4180/08/$17.00  2008 – IOS Press and the authors. All rights reserved

146

L. De Witte et al. / Disrupted auto-activation, dysexecutive and confabulating syndrome

cal gaze palsy, 4) anterograde amnesia, 5) speech and
language disturbances and 6) apathy [3,20,24,30,31,
35,38,49,50,57,59,61,73]. A typical syndrome of apathy which has been documented in association with
uni- or bilateral lesions of the thalamus and/or the basal
ganglia [10–12,14,15,19,23,31,68,70,72] is known as
‘athymhormia’, ‘psychic akinesia’, or ‘loss of psychic
self-activation’ (LPSA), of which two distinct subtypes
can be distinguished. The first variant is a condition
of extreme loss of activity and motivation resulting in
apathy, motor and verbal aspontaneity with subjacent
‘mental emptiness’. Remarkable in this condition is
the sharp contrast between impaired self-activation and
intact heteroactivation of behavior. The second behavioral condition consists of an apparent flatness or
poor expressiveness of affect and the disappearance of
psychic life [11,13,23,39,42,45].
Levy and Dubois [62] define apathy as an ‘observable pathologic behavioral syndrome consisting of a
quantitative reduction of self-generated voluntary and
purposeful behaviors’ and distinguish three subtypes
in the underlying mechanisms of apathy: ‘emotionalaffective’, ‘cognitive’ and ‘auto-activation’. Apathy
related to a disruption of ‘emotional-affective’ processing refers to a reduction of goal-directed behavior due
to an inability to associate affective and emotional signals with ongoing and forthcoming behaviors, whereas
apathy related to a disruption of ‘cognitive’ processing is related to cognitive deficits in elaborating plans
of action. The third and most severe form of apathy consists of a disruption of auto-activation processing which refers to the inability of self-activating and
self-initiating thoughts and activities: this affects both
cognitive and emotional responses. This behavioral
syndrome is similar to ‘athymhormia’, ‘psychic akinesia’ and ‘loss of psychic self-activation’. The ‘autoactivation’ deficit mostly involves bilateral lesions of
the thalamus, the pallidal globe, the caudate nucleus
or the striato-pallidal region. Although the condition
most commonly occurs after bilateral lesions, patients
with unilateral lesions have been reported [1,4,8,11,23,
26,29,31,33,37,45,46,51,53,65,66,68,69,71]. Besides
psychic akinesia, impairments in executive functioning
and confabulations are also associated with bi-thalamic
lesions [20,22,38,40,70,73] .
This article reports the clinical, neuropsychological,
structural and functional neuroimaging results in a patient who developed a unique set of symptoms consisting of a dysexecutive syndrome in association with confabulating behavior and auto-activation deficits after a
bi-thalamic and right putaminal stroke.

Fig. 1. Brain MRI axial FLAIR carried out five days after stroke
revealing focal ischemic damage to both thalami and the right putamen.

2. Case report
A 78-year-old right-handed woman was admitted to
hospital after a sudden onset of incoherent speech and
confusion. Medical history was unremarkable. Apart
from mild disorientation, clinical neurological examination on admission was normal. Tests of eye movements and other cranial nerve functions were normal.
Brain magnetic resonance imaging (MRI) in the acute
phase (5 days post-onset) revealed ischemic lesions in
both thalami and the right putamen (Fig. 1). Comparison of the MRI-images with an atlas of neuro-imaging
and neuroanatomy [27] showed unilateral involvement
of the left medial and anterior thalamic nucleus, unilateral involvement of the right dorsal anterior nucleus,
bilateral involvement of the intralaminar nuclei, unilateral involvement of the right putamen and bilateral
involvement of the frontal subcortical white matter.
In the post-acute phase of the stroke (2 weeks postonset), anomic language disturbances, concentration
and memory deficits were found in combination with a
dysexecutive syndrome. At the behavioral level, a combination of inhibitory and disinhibitory symptoms were
found. Seven months post-onset, repeat neurolinguistic and neuropsychological investigations revealed severe frontal dysexecutive dysfunctions in combination
with a unique neurobehavioral syndrome characterized
by a severe loss of psychic self-activation and the presence of a confabulatory syndrome. 99 m Tc ECD single
photon emission computed tomography (SPECT) scan
was carried out eight months post-onset. Trans-axial
images with a pixel size of 3.56 mm were anatomically standardized using SPM and compared to a stan-

L. De Witte et al. / Disrupted auto-activation, dysexecutive and confabulating syndrome

Fig. 2. Quantified ECD SPECT eight months after stroke disclosing
hypoperfusions in the thalamus, both caudate nuclei and the left
lentiform nucleus.

dard normal and SD image obtained from 15 normal
ECD perfusion studies. Using a 31 ROI template the
z-scores (SD) were then calculated for each region. A
regional z-score of > 2.0 was considered significant.
In comparison to normal database findings the quantified baseline ECD SPECT at eight months post-stroke
showed a significant decrease of perfusion in both thalami (left: −1.96 SD; right: −2.47 SD), both caudate
nuclei (left: −5.24 SD; right: −3.92 SD) and the left
lentiform nucleus (−4.97 SD). No deficits were found
at the cortical level (Fig. 2).

3. Methods
Formal neuropsychological investigations were carried out two weeks (acute phase) and seven months
(late phase) after the stroke. Language was assessed
by means of subtests of the Boston Diagnostic Aphasia Examination (BDAE) [25], subtests of the Aachen
Aphasia Test (AAT) [56], the Boston Naming Test
(BNT) [18,58], subtests of the Hierarchic Dementia
Scale (HDS) [41] and a semantic verbal fluency task
(unpublished norms). Cognitive functions were examined by means of the Mini Mental State Examination (MMSE) [43], the Colored Progressive Matrices (CPM) [35], the Hierarchic Dementia Scale
(HDS) [41], the Trail Making Test (TMT) [63,64], the
Stroop Color Word Test (SCWT) [36] and the Wisconsin Card Sorting Test (WCST) [7].

4. Results
Neurolinguistic and neurocognitive test results are
summarized in Table 1. In the acute phase of the stroke,

147

the patient obtained normal scores for auditory comprehension, written comprehension, repetition, reading
and writing. Similar results were obtained in the late
phase of the stroke. Two weeks post-onset, the visual
confrontation naming subtest of the HDS (4/10) and
the BNT (22/60; −3.91 SD) showed severe anomia.
Most naming errors were semantic paraphasias (14/38)
(e.g. tree for cactus), followed by perseverations (9/38),
semantic neologisms (7/38) (e.g. “freezing pencil” for
igloo), inadequate circumlocutions (4/38) (e.g. parts of
a throw for domino) and visual errors (4/38) (e.g. cup
for mask). Seven months post-onset a remission of
naming errors was found (HDS: 10/10; BNT: 51/60
(+1.41 SD)). In a semantic verbal fluency task the patient was asked to name as many animals, means of
transport, vegetables and clothes as possible within one
minute for each semantic field. In the acute phase
the patient produced 22 items (−1.82 SD). Her performance had improved considerably in the late phase
(39 items; −0.37 SD). In the acute phase of the stroke
spontaneous speech was characterized by incidences of
neologistic and semantic jargon. Seven months later
jargon had resolved completely. Despite normal oral
language skills, the patient did not take any initiative to
speak spontaneously.
At a neurocognitive level, the MMSE revealed a deficient score of 22/30 (−3.33 SD) two weeks post-onset
neurological symptoms. A normalization of the total score was found seven months post-onset (26/30;
−0.66 SD) [60]. As shown by the HDS subtest results, recent memory and concentration were disrupted
in the acute phase. Seven months later, recent memory
defects and concentration disturbances had resolved.
Praxis, orientation, visual perception, gnosis and arithmetics were normal as assessed by the HDS. On the
CPM, the patient obtained normal results in the acute
and late phase of the stroke. Executive dysfunctions
were found at both the psychometric and behavioral
level. As demonstrated by a severely deficient score
on the Stroop Color-Word Test (card III = percentile
1) the ability of resistance to interference in more automatic stimuli was severely disturbed in the acute phase.
Seven months later performance had improved (card
III = percentile 30). A severely defective result on
the WCST (zero categories in 64 trials) indicated that
mental flexibility, abstract reasoning, frontal planning
and organization were severely impaired in both the
acute and lesion phase of the stroke. Disturbed mental
flexibility was also evidenced by a defective result on
the TMT (part B: percentile 10).
At the behavioral level a range of frontal-like disturbances were observed such as apathy, disconcern,

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L. De Witte et al. / Disrupted auto-activation, dysexecutive and confabulating syndrome
Table 1
Neuropsychological test results obtained two weeks and seven months post-onset
Neuropsychological tests
Mini Mental State Examination
Intelligence
Raven Coloured Progressive Matrices
Memory
Hierarchic Dementia Scale (HDS)
registration (item 8)
recent memory (item 20)
remote memory (item 17)
Language
Boston Diagnostic Aphasia Examination (BDAE)
complex auditory language comprehension
Akense Aphasia Test (AAT)
repetition total
Boston Naming Test (BNT)
Hierarchic Dementia Scale (HDS)
naming (item 6)
comprehension (item 7)
reading (item 10)
writing (item 18)
Verbal fluency – semantic
animals
vegetables
clothing
means of transport
Concentration
Hierarchic Dementia Scale (HDS)
concentration (item 13)
Frontal functions
Trail Making Test
version A
version B
Stroop Color-Word Test
card I
card II
card III
Wisconsin Card Sorting Test (WCST)
Praxis – Orientation – Visual Perception & Gnosis Calculation
ideomotor praxis (HDS, item 3)
ideational praxis (HDS, item 5)
construction (HDS, item 12)
drawing (HDS, item 15)
orientation (HDS, item 11)
visual perception (HDS, item 4)
gnosis (HDS, item 9)
calculation (item 14)

Week
2
22

Month
7
26

Percentile
2/7

Max

Mean

SD

30

27

1.5

23

31

75/95

8
2
10

10
8
10

9.17
8.51
9.62

0.94
1.64
0.80

14

15

93/100

15

150
22

150
51

100/100

150
60

144.1
43.3

8.07
5.45

4
10
10
10
22
6
5
5
6

10
10
10
10
39
11
12
10
6

10
10
10
10

9.87
9.85
9.83
9.06
43.4

0.34
0.42
0.56
1.26
11.76

1 min
1 min
1 min
1 min

7

10

10

8.94

0.87

–
–

49 sec
> 450 sec

−/80
−/< 10

46 sec
106 sec
> 197 sec
0

36 sec
55 sec
107 sec
0

60/95
3/75
1/30
0/0

10
10
10
10
10
10
10
10

10
10
10
10
8
10
10
10

9.45
9.81
8.33
8.72
9.45
9.87
9.47
8.83

0.80
0.45
1.88
0.97
1.02
0.49
0.50
1.26

36

10
10
10

64
10
10
10
10
10
10
10
10

Legend: max = maximumscore; SD = standard deviation; sec = seconds.

indifference, loss of interest, loss of critical attitude,
poor motivation, flattened affect and abusive language
(cursing). In addition the patient often confabulated. In
spontaneous conversations, for example, she said that
her husband, who died 18 years ago, did not accompany her because he dislikes hospitals. When she was
asked to describe a script, such as a typical morning
routine, a bizarre mix of confabulations disrupted the
content of her speech. Some of these confabulations
were based on true habits in the past while others were

false beliefs. Although she was a resident in a nursing
home, she claimed to wake up at six o’clock to prepare
breakfast for both her children. She insisted that her
son lives with her on the second floor of her house and
that he leaves the house every morning at seven o’clock
to catch the train to go to work. She further claimed
that her daughter has a room on the first floor of her
house and that she leaves at eight to work in a sheltered
workshop (= true but 28 years ago). The reality is that
both her son and daughter had left the house a long time

L. De Witte et al. / Disrupted auto-activation, dysexecutive and confabulating syndrome

ago. At the moment of the examination, she claimed
that her husband stayed at home with her daughter (=
false). When the examiner told the patient that she
stayed in a nursing home, she said that her daughter
lives with her husband now (= false).
The frontal-like inhibition disturbances and the confabulatory syndrome have remained unchanged. Her
son considers the behavioral alterations as the most
striking consequence of the stroke. Instead of the active, talkative woman she used to be before the stroke,
she remains apathetic, passive and confabulatory. Because of these changes, she was admitted to a nursing
home where she avoids contact with other residents.
She hardly speaks and takes no initiative to communicate. Nevertheless, minimal levels of speech are punctuated with spontaneous and provoked confabulations.
When no strong external stimulation is given, she does
not do anything spontaneously. On the Middelheim
Frontality Scale (MFS), she scored 7/10 [55]. The Beck
Depression Inventory (BDI) did not show evidence in
favor of a depressive syndrome [2].

5. Discussion
This paper reports a patient with a unique combination of cognitive and behavioral symptoms due to a bilateral thalamic and right putaminal stroke. The patient
developed a dysexecutive syndrome that persisted during follow-up. In addition to impaired performance on
frontal tasks evaluating mental flexibility, frontal planning and organization, loss of psychic self-activation
and a confabulatory syndrome are found. Loss of psychic self-activation is characterized by apathy, loss of
initiative, loss of concern, loss of critical attitude, motor
and verbal aspontaneity, mental emptiness and flattened
affect. This behavioral syndrome shares clear semiological similarities with syndromes caused by lesions of
the dorso-medial prefrontal cortex and corresponds to
the third subtype of the apathetic syndrome described
by Stuss et al. [16] and Levy and Dubois [62] as a ‘behavioral apathetic syndrome’ and an ‘auto-activation
deficit’. The confabulatory syndrome in this patient
consists of a mix of spontaneous as well as provoked
confabulations. Most impressive are the spontaneous
confabulations in which the patient shows a definite
certainty about the veracity of her assertions. Most
of these spontaneous confabulations are based on true
events or on habits in the past while the provoked confabulations mainly reflect false beliefs. These findings
provide additional evidence for a positive correlation

149

between the degree of mental flexibility and the degree of spontaneous confabulation and are in agreement
with the hypothesis of Nys et al. [22]. In this patient,
a long-term coexistence of spontaneous confabulations
and mental a-flexibility is observed as evidenced by the
poor scores on the WCST and the TMT.
From an anatomo-clinical point of view, the persistence of executive dysfunctions may be attributed to the lesion in the medial thalamic nucleus, the
intralaminar thalamic nuclei or any combination of
these nuclei. Our findings are consistent with previous studies demonstrating an association between
a lesion consisting of a combination of thalamic
nuclei damage and a persistent dysexecutive syndrome [47–49,73]. Regarding the possible pathophysiological mechanisms underlying the neurobehavioral syndrome of psychic akinesia and/or confabulation, most research suggests disruption of the striatoventral pallidal-thalamic-frontomesial limbic loop [9,
17,22,31,44,50,62,67]. Quantified SPECT in this patient does not support this view since no perfusion
deficits were found in the anatomo-clinically suspected
frontal brain regions. The lack of SPECT evidence for a
functional disruption of this circuitry may indicate that
bilateral involvement of the thalamus associated with
putaminal damage is sufficient to induce the observed
cognitive and behavioral symptoms. However, further
research is necessary to clarify the role of combined lesions of the basal ganglia and thalami in dysexecutive,
auto-activation and confabulatory syndromes.
6. Conclusion
A patient is reported who developed a persistent
dysexecutive syndrome with confabulations and autoactivation deficits after ischemic damage to both thalami and the right putamen. There appears to be
no SPECT evidence for a functional disruption of
the striato-ventral pallidal-thalamic-frontomesial limbic loop. At the behavioral level the unique semiological association of the ‘auto-activation deficit’ and a
confabulatory syndrome has – to the best of our knowledge – never been described before.
Acknowledgements
We are grateful to Mrs. Inge Bats (Institute BornBunge, University of Antwerp) for the photographic
work. This research was supported by the Research
Foundation – Flanders (FWO–F). S.E. is a postdoctoral
fellow of the FWO-F.

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L. De Witte et al. / Disrupted auto-activation, dysexecutive and confabulating syndrome

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