J Neurol (2006) 253 : 455–463

DOI 10.1007/s00415-005-0025-7 ORIGINAL COMMUNICATION

Leif Johannsen “Pusher syndrome” following cortical

Doris Broetz
Thomas Naegele lesions that spare the thalamus
Hans-Otto Karnath

■ Abstract Stroke patients with
“pusher syndrome” show severe
misperception of their own upright
body orientation although visual-
vestibular processing is almost in-
tact. This dissociation argues for a
Received: 14 April 2005
Received in revised form: 15 August 2005
Accepted: 22 August 2005
Published online: 3 February 2006
L. Johannsen · D. Broetz · H.-O. Karnath (
)
Center of Neurology
University of Tübingen
Hoppe-Seyler-Str. 3
72076 Tübingen, Germany
Fax: +49-7071/295957
E-Mail: Karnath@uni-tuebingen.de
T. Naegele
Dept. of Neuroradiology
University of Tübingen
Tübingen, Germany
second graviceptive system in hu-
mans for the perception of body
orientation. Recent studies revealed
that the posterior thalamus is an
important part of this system. The
present investigation aimed to
study the cortical representation of
this system beyond the thalamus.
We evaluated 45 acute patients with
and without contraversive pushing
following left- or right-sided corti-
cal lesions sparing the thalamus. In
both hemispheres, the simple le-
sion overlap associated with con-
traversive pushing typically cen-
tered on the insular cortex and
parts of the postcentral gyrus. The
comparison between pusher pa-
tients and controls who were
matched with respect to age, lesion
size, and the frequency of spatial
neglect, aphasia and visual field de-
fects revealed only very small re-
gions that were specific for the
pusher patients with cortical dam-
age sparing the thalamus. Obvi-
ously, the cortical structures repre-
senting our control of upright body
orientation are in close anatomical
proximity to those areas that in-
duce aphasia in the left hemisphere
and spatial neglect in the right
hemisphere when lesioned. We
conclude that in addition to the
subcortical area previously identi-
fied in the posterior thalamus,
parts of the insula and postcentral
gyrus appear to contribute at corti-
cal level to the processing of the
afferent signals mediating the
graviceptive information about
upright body orientation.
■ Key words pusher syndrome ·
insula · somatosensory cortex ·
thalamus · gravity · vestibular ·
posture · brain-damage · human

with hemiparesis range from 10 % up to 55 % [2, 3]. Spa-

Introduction
Unilateral stroke can lead to a very specific disorder of
postural orientation. Such patients use their non-paretic
arm and/or leg to actively push from the non-paralysed
towards the paralysed side. This active “contraversive
pushing” leads to loss of balance and falling towards the
paralysed side. Davies [1] termed this disorder “pusher
syndrome”. The patients resist any attempt to correct
passively their tilted body posture towards the earth-
tial neglect and other neuropsychological deficits such
as anosognosia, or apraxia have been ruled out as possi-
ble causes underlying contraversive pushing [2, 4]. Nev-
ertheless, because of the close anatomical relationships
between the relevant neural structures, there is a
high frequency of concurrent severe hemiparesis,
somatosensory loss, aphasia, and spatial neglect with
pushing behaviour [3, 5].
Patients with pusher syndrome experience their
body as oriented “upright” when actually tilted about
JON 2025

vertical upright orientation. Estimates of the frequency 20° to the ipsilesional side [6]. Surprisingly, these pa-
of severe contraversive pushing in acute stroke patients tients showed almost undisturbed processing of visual
456
and vestibular inputs. Thus, in contrast to their
markedly disturbed perception of upright body posture,
orientation perception of the visual world was nearly
unaffected [6]. In other words, pusher patients have a
severe tilt of body posture, in spite of almost normal
visual-vestibular functioning. The opposite has been
observed in patients with acute and chronic vestibular
defects. These patients showed disturbed visual-
vestibular functioning with an ipsilesional tilt of the
subjective visual vertical (SVV), while their perception
of own body orientation (subjective postural vertical,
SPV) was unimpaired [7]. These findings have argued
for a neural pathway in humans for sensing the orienta-
tion of gravity and controlling upright body posture,
separate from the one for orientation perception of the
visual world [6].
Also in healthy subjects, a dissociation between the
perceived orientation of the visual world and of the own
body position has been suggested. Mittelstaedt and Mit-
telstaedt [8] assessed the subjective horizontal posture
(SHP) on a rotating sled centrifuge in normal subjects,
patients with vestibular disorders, and patients with
paraplegia. They concluded that somatic graviceptors
exist in the human trunk for the perception of own body
orientation, in addition to the well-known visual-
vestibular system for the perception of both the orienta-
tion of the visual world and the head in space [9]. Simi-
lar conclusions were drawn by Jarchow et al. [10].
Further evidence was reported by Kaptein and van Gis-
bergen [11], who observed a sudden discontinuity in
normal subjects’ perception of the SVV for body tilts
larger than 135°. The authors suggested the presence of
an automatic response system tied to the properties of
the otoliths according to the formula of the idiotropic
vector model [12] and a second system more demand-
ing in terms of cognitive resources and relying on per-
ceived body tilt as a basis for the perception of the SVV.
The neuroanatomy of the system sensing the orienta-
tion of the visual world – the visual-vestibular system –
has been well established so far. Cortical areas process-
ing vestibular information have been localized in the
monkey at the intraparietal sulcus (area 2v), in the cen-
tral sulcus (area 3aNv), at the posterior sylvian sulcus
(VPS) and the posterior insula region (PIVC) [13–15]. In
humans, such regions have been identified in the poste-
rior insula, the inferior parietal lobule and the superior
temporal gyrus [16–26]. The question thus arises
whether or not there are brain areas beyond those rep-
resenting the visual-vestibular system that are related to
the control of upright body orientation.
Lesion studies in patients with pusher syndrome of-
fer the opportunity to study the neuroanatomy of that
latter system. Karnath et al. [4] investigated a sample of
46 patients with and without contraversive pushing suf-
fering from unselected cortical and/or subcortical le-
sions. The analysis revealed that the posterolateral thal-
amus was typically damaged in left as well as in right
brain damaged patients with pusher syndrome. This
finding suggested a fundamental role of the posterior
thalamus for our control of upright body posture. This
conclusion was corroborated by a recent study carried
out with thalamic stroke patients only [5]. The authors
found a clear anatomo-functional dissociation within
the thalamus. While haemorrhage in the left as well as
the right posterior thalamus provoked pusher syn-
drome, infarction of the anterior thalamus did not cause
the disorder.
Clinical observations suggest that the posterior thal-
amus is not the only neural substrate for our perception
of upright body orientation. Although less frequently,
pusher syndrome also is observed in patients with brain
lesions sparing the thalamus. The aim of the present
study was to investigate the cortical substrates of this
system. Therefore, we studied the lesion location in
pusher patients showing cortical brain damage not in-
volving the thalamus.
Subjects and methods
We prospectively investigated 21 acute stroke patients with pusher
syndrome and unilateral cortical lesions sparing the thalamus who
were consecutively admitted over a long 6-year period to the Neurol-
ogy Department of the University Hospital in Tubingen (cf. Table 1).
The lesions were demonstrated by magnetic resonance imaging
(MRI) or by computed tomography (Spiral CT).All patients showed a
first, unilateral cortical lesion with or without involvement of under-
lying white matter and the basal ganglia. Ten patients had left-sided,
11 had right-sided brain lesions. Sparing of the thalamus was deter-
mined independently by two investigators (TN, H-OK). Patients with
diffuse or bilateral brain lesions or patients with tumours were ex-
cluded.
Two groups of control patients – 12 subjects with acute left-sided
and 12 with acute right-sided cortical lesions sparing the thalamus –
were matched to the groups of pusher patients (cf. Table 1). The con-
trol subjects were admitted in the same time period as the pusher pa-
tients and were matched with respect to age (left-sided lesions:
t = 0.56, p = 0.585; right-sided lesions: t = 1.55, p = 0.137), time since
stroke onset (both t ≤ 0.75, both p ≥ 0.462), the frequency of spatial ne-
glect (left-sided lesions: χ2 = 0.21; right-sided lesions: χ2 = 0.00, both
p > 0.05), the frequency of aphasia (left-sided lesions: χ2 = 0.08; right-
sided lesions: χ2 = 0.00, both p > 0.05), and the frequency of visual
field defects (left-sided lesions: χ2 = 0.02; right-sided lesions:
χ2 = 0.02, both p > 0.05). Moreover, lesion size (left-sided lesions:
U = 49.0, p = 0.468; right-sided lesions: U = 51.5, p = 0.372) and the fre-
quency of contralateral somatosensory loss (left-sided lesions:
χ2 = 2.64; right-sided lesions: χ2 = 0.51, both p > 0.05) were compara-
ble between the pusher patients and the control groups. Contrale-
sional paresis was more frequent in pusher patients with left-sided le-
sions (χ2 = 4.49, p < 0.05), but not in the right brain damaged pusher
patients (χ2 = 1.98, p > 0.05). It was more severe in the left brain dam-
aged pusher patients for the arm and the leg (both U ≥ 21.5, both
p ≤ 0.039), while in the right brain damaged pusher patients it was
more severe for the contralateral arm (U = 15.5, p = 0.002) and only
tended to be more severe for the leg (U = 38.0, p = 0.081).
All patients gave their informed consent to participate in the
study which has been performed in accordance with the ethical stan-
dards laid down in the 1964 Declaration of Helsinki.
 457

Table 1 Demographic and clinical data of the patients with left (L) or right (R) brain lesions showing or not showing contraversive pushing

R-Pusher R-Controls L-Pusher L-Controls

Number 11 12 10 12
Sex 3 f, 8 m 6 f, 6 m 1 f, 9 m 2 f, 10 m
Age Years Mean (SD) 68.0 (9.4) 60.6 (13.2) 67.8 (8.3) 65.7 (9.0)
Etiology 7 Infarct 11 Infarct 9 Infarct 11 Infarct
4 Haemorrhage 1 Haemorrhage 1 Haemorrhage 1 Haemorrhage
Lesion volume (% Hemisphere) Mean (SD) 10.8 (8.3) 13.3 (8.1) 12.4 (6.7) 10.3 (6.4)
Time since lesion-clinical exam (d) Mean (SD) 5.7 (4.2) 4.8 (3.8) 6.5 (5.4) 5.0 (3.7)
SCP-Posture Sitting Median (range) 1 0 1 (0.75–1) 0
Standing Median (range) 1 0 1 0
SCP-Extension Sitting Median (range) 1 (0.5–1) 0 1 (0.5–1) 0
Standing Median (range) 1 (0.5–1) 0 1 0
SCP-Resistance Sitting Median (range) 1 0 1 0
Standing Median (range) 1 0 1 0
Visual field defect % present 18 25 10 8
% t. n. p. 18 0 10 8
Paresis of contralesional side % present 91 67 100 67
Arm Median (range) 0.5 (0–5) 4.25 (1–5) 0 (0–5) 3.75 (0–5)
Leg Median (range) 2.0 (0–5) 4.25 (1.5–5) 1.5 (0–4) 4 (0–5)
Somatosensory deficit of % present 73 67 90 50
contralesional side (touch)
% t. n. p. 9 0 0 17
Aphasia % present 0 0 80 75
Spatial Neglect % present 100 100 10 8

SCP Scale for Contraversive Pushing [6, 27]; t. n. p. testing not possible

■ Clinical investigation
Contraversive pushing was assessed by using the stan-
dardized ‘Scale for Contraversive Pushing’ (SCP) [6, 27].
The SCP assesses (i) symmetry of spontaneous posture,
(ii) the use of the non-paretic arm and/or leg to increase
pushing force by abduction and extension of extremi-
ties, and (iii) resistance to passive correction of posture.
Pusher syndrome was diagnosed when the patients
showed at least a total score of 1 (max. = 2, sitting plus
standing) with respect to their spontaneous posture, at
least a score of 1 (max. = 2, sitting plus standing) con-
cerning the use of the non-paretic arm and/or leg to in-
crease pushing force by abduction and extension, and
when they showed resistance to passive correction of
posture. (In 11 patients, pushing behaviour while stand-
ing could not be quantified with SCP owing to a com-
plete inability to reach a standing position at the time of
the present investigation).
Visual field defects were assessed by standard neuro-
logical examination. The degree of paresis of the upper
and lower limbs was scored with the usual clinical ordi-
nal scale, where ‘0’ stands for no trace of movement and
‘5’ for normal movement. Spatial neglect was diagnosed
when the patients showed the characteristic clinical be-
haviour such as orienting towards the ipsilesional side
when addressed from the front or the left and/or ignor-
ing of contralesionally located people or objects. In ad-
dition, all patients were further assessed with the fol-
lowing four clinical tests: the “Letter cancellation” task
[28], the “Bells test” [29], the “Baking tray task” [30], and
a copying task [31]. Neglect patients had to fulfill the cri-
terion for spatial neglect in at least two of these four clin-
ical tests [cf, 32]. The presence of aphasia was assessed
conducting a bedside examination that evaluated spon-
taneous speech, auditory and reading comprehension,
picture naming, reading, and oral repetition.
■ Lesion analysis
Using two standard protocols, MRI was carried out in 19
and spiral CT imaging in 26 of the stroke patients. Un-
der both protocols the initial scanning optionally was
repeated during the following days until a firm diagno-
sis could be made and the affected area became clearly
demarcated. These final scans were used for the present
study. In those patients who underwent the MRI proto-
col, we used diffusion-weighted imaging (DWI) within
the first 48 hours post stroke and T2-weighted fluid-at-
tenuated inversion-recovery (FLAIR) sequences when
imaging was conducted 48 hours or later after the stroke.
458
While FLAIR images provide high sensitivity for acute
cerebral infarcts, DWI has proved to be particularly sen-
sitive for the detection of hyperacute infarcts and shows
high accuracy in predicting final infarct size [33–36].
Scans were obtained on a 1.5-T echo planar imaging
(EPI) capable system (Magnetom Sonata, Siemens, Er-
langen, Germany). The FLAIR sequence was acquired
with 20 axial slices (thickness 5 mm) with an interslice
gap of 1 mm, a field of view (FOV) of 175
220 mm2, a
repetition time (TR) of 9000 ms and an echo time (TE)
of 118 ms. DWI was performed with a single-shot EPI
spin echo sequence (TR 3200 ms, TE 87 ms, FOV 230

230 mm2, matrix 64
64, slice thickness 5 mm, gap
1 mm). The mean time between lesion and the MRI used
for the present study was 3.3 days (SD 3.9). The bound-
ary of the lesion was delineated directly on the individ-
ual MRI image for every single transversal slice using
MRIcro software [37] (http://www.mricro.com). Both
the scan and lesion shape were then transferred into
stereotaxic space using the spatial normalisation algo-
rithm provided by SPM2 (http://www.fil.ion.ucl.ac.uk/
spm/). For determination of the transformation para-
meters, cost-function masking was employed [38].
To fit approximately the canonical AC-PC orienta-
tion of the MRI scans, the CT imaging protocol used the
line drawn between the occiput and the lower margin
of the orbita to orient the scans in each individual.
Scans were obtained on a spiral CT scanning system
(Somatom Sensation 16, Siemens, Erlangen, Germany)
providing clearer pictures with more anatomical
details and in less time than previous generations of
CT systems [39]. Spiral CT scanning was performed
with a slice thickness of 3 mm infratentorial and 8 mm
supratentorial. MRIcro software was used to map the
lesion on transversal slices of the T1-template MRI from
the Montreal Neurological Institute (www.bic.mni.
mcgill.ca/cgi/icbm_view) that is distributed with MRI-
cro. The template scan is aligned with stereotaxic space
and provides various anatomical landmarks for pre-
cisely plotting size and localization of the lesion. The
mean time since lesion and the CT used for the present
study was 3.4 days (SD 3.4) when the affected area be-
came clearly demarcated. Lesions were mapped onto the
slices that correspond to Talairach Z-coordinates –40,
–32, –24, –16, –8, 0, 8, 16, 24, 32, 40, and 50 mm in Ta-
lairach space by using the identical or the closest match-
ing transversal slices of each individual.
Lesion location in stroke patients with and without
pusher syndrome was compared using the subtraction
technique (for review [39]). This analysis illustrates the
centre of overlap in the patients with pusher syndrome
in direct visual contrast to those areas that do not induce
the disorder when lesioned. The resulting subtraction
image specifically highlights regions that are both fre-
quently damaged in patients with pusher syndrome as
well as being typically spared in patients without that
disorder. Since the two patient groups differed in sample
size, we used proportional values for the MRIcro sub-
traction analysis.
Results
Figs. 1a and 2a show simple overlay plots for the groups
of pusher patients with right-sided lesions (R-Pusher)
and with left-sided lesions (L-Pusher). The lesion over-
lap was comparable between the two groups. The centre
of lesion overlap for the right-hemisphere pusher pa-
tients affected the posterior insula, the postcentral
gyrus, and surrounding white matter, extending from
Talairach coordinates (x, 44; y, –23; z, 16) and (x, 59; y,
–23; z, 16) to (x, 56; y, –22; z, 24) and (x, 40; y, –41; z, 24).
Likewise, the centre of lesion overlap in the pusher pa-
tients with left-hemisphere lesions affected the poste-
rior insula, the postcentral gyrus, and the surrounding
white matter, extending from Talairach coordinates (x,
–38; y, –3; z, 0) and (x, –38; y, –1; z, 8) over (x, –36; y, –7;
z, 16) and (x, –43; y, –15; z, 24) to (x, –38; y, –30; z, 32).
To identify the cortical structures that were com-
monly damaged in patients with contraversive pushing
but are typically spared in patients not showing pushing
behaviour, we subtracted the superimposed lesions of
the control groups (R-Controls, L-Controls; Figs. 1a and
2a) from the overlap images of the groups with pusher
syndrome. The control groups were comparable with re-
spect to age, lesion size, frequency of additional spatial
neglect, aphasia, and visual field defects to the patients
with pusher syndrome. This method creates an image
that shows regions that are commonly damaged in pa-
tients with pusher syndrome but are typically spared in
control patients (coded as positive values), as well as re-
gions specifically damaged in the control patients but
typically spared in pusher patients (coded as negative
values). The subtraction images use progressively
brighter shades of orange to highlight positive values
and progressively brighter shades of blue to illustrate
negative values (Figs. 1b and 2b). We only found very
small regions at the left posterior insula and superior
temporal gyrus (x, –40; y, –27; z, 16), the left inferior
parietal lobule (x, –63; y, –23; z, 24), and the right post-
central gyrus (x, 58; y, –23; z, 16; and x, 53; y, –18; z, 24)
that were specific for pusher patients when subtracted
from the matched controls (Figs. 1b and 2b). Obviously,
the pattern of cortical lesion overlap in pusher patients
largely corresponded to the pattern in stroke patients
without contraversive pushing but with comparable fre-
quency of additional spatial neglect, aphasia, visual field
defects, lesion size and age.
 459

Fig. 1 (A) Overlay lesion plots of the right brain damaged patients with pusher syndrome (R-Pusher; n = 11) and control patients (R-Controls; n = 12). The number of over-
lapping lesions is illustrated by different colours coding increasing frequencies from violet (n = 1) to red (n = max. number of subjects in the respective group). (B) Overlay
plots of the subtracted superimposed lesions of the right brain damaged groups with and without pusher syndrome. The percentage of overlapping lesions of the pusher
patients after subtraction of controls is illustrated by 5 different colours coding increasing frequencies from dark red (difference = 1 % to 20 %) to white (difference = 81 %
to 100 %). They mark those regions damaged more frequently in pusher patients than in control patients. The different colours from dark blue (difference = –1 % to –20 %)
to light blue (difference = –81 % to –100 %) indicate regions damaged more frequently in control patients than in pusher patients. Talairach z-coordinates [55] of each trans-
verse section are given. PoCG postcentral gyrus; Ins insula; Wh.mat. white matter
460

Fig. 2 (A) Overlay lesion plots of the left brain damaged patients with pusher syndrome (L-Pusher; n = 10) and control patients (L-Controls; n = 12). The number of over-
lapping lesions is illustrated by different colours coding increasing frequencies from violet (n = 1) to red (n = max. number of subjects in the respective group). (B) Overlay
plots of the subtracted superimposed lesions of the left brain damaged groups with and without pusher syndrome. Colour coding of the percentage of overlapping lesions
is identical with that in Fig. 1. Talairach z-coordinates [55] of each transverse section are given. PoCG postcentral gyrus; Ins insula; IPL inferior parietal lobule; STG superior
temporal gyrus; Wh.mat. white matter

Discussion
The present study investigated the cortical structures
that contribute – beyond the thalamus [4, 5] – to our
control of upright body orientation. Acute stroke pa-
tients with and without severe contraversive pushing
following left- or right-sided cortical lesions that spared
the thalamus were investigated. In both hemispheres,
the simple lesion overlap of the pusher patients centered
at the insular cortex and the postcentral gyrus. In addi-
tion to the subcortical area previously identified in the
posterior thalamus [4, 5], parts of these cortical struc-
tures seem to be involved in the perception and control
of body orientation. Interestingly, anatomical findings
in the macaque monkey argued for a direct relationship
between the posterior thalamus and the cortical sub-
strates identified in the present study. Thalamocortical
axons arising in the ventral posterolateral and postero-
medial nuclei project to the primary somatosensory
cortex in the postcentral gyrus (Brodmann areas 3a, 3b,
1, and 2), to the secondary somatosensory cortex in the
parietal operculum, and to the insula [40, 41].
The contrast between the lesion pattern of pusher pa-
tients and of control patients without pushing behav-
iour but with comparable age, lesion size, and frequency
of spatial neglect, aphasia and visual field defects re-
vealed only very small regions at the left posterior insula
and superior temporal gyrus, the left inferior parietal
lobule, and the right postcentral gyrus that were specific
for the pusher patients. Obviously, pushing behaviour
largely correlates with damage of cortical structures in
close proximity to those typically causing aphasia in the
left hemisphere and spatial neglect in the right hemi-
sphere. However, this conclusion should be treated with
caution. The number of patients showing contraversive
pushing following a cortical lesion without thalamic in-
volvement was small. Although the collection period for
the present study was already quite long – covering an
interval of 6 years – we only found 21 cases, while many
more pusher patients had thalamic damage (see refs. [4,
5]). It is possible that more patients are required to ob-
tain reliable anatomical differences at the cortical level
between pusher patients and controls.
Kahane et al. [26] investigated the anatomical sites at
which vestibular sensations can be induced in the hu-
man brain by electrical cortical stimulation. Out of 44
anatomical sites in 28 epileptic patients, illusions of tilt
or displacement in the roll plane could be elicited in the
right hemisphere at the postcentral gyrus, the parietal
operculum, and the superior temporal gyrus. In addi-
tion, sensations of displacement and tilt in the pitch
plane were provoked by stimulation at the right-hemi-
sphere parietal operculum, at the middle temporal
gyrus and at the anterior cingulate gyrus. These findings
correspond well with our present results showing that
the posterior insula and postcentral gyrus are typically
461
lesioned in patients showing contraversive pushing after
cortical damage sparing the thalamus.
Following the hypothesis of Mittelstaedt [9] that the
human nervous system uses somatic graviceptors in the
trunk to determine the orientation of own body in
space, it might be speculated that the areas identified in
the present and in the previous studies [4, 5] might be
the structures, in which the afferent information from
these postulated sensors are processed in the human
brain. Mittelstaedt [9] assumed two afferent sensory
pathways that deliver information from the trunk grav-
iceptors to the brain. First, the renal nerve was assumed
to transmit information from mechanoreceptors lo-
cated at the kidneys, such that the kidneys might func-
tion as statoliths indicating the direction of gravita-
tional vertical. Second, it was suggested that the vagus
nerve relayed information concerning the distribution
of blood in the large vessels of the trunk, that might be
influenced by the orientation of the body with respect to
gravity.Vaitl et al. [42, 43] tested this latter possibility by
applying negative and positive pressure (LBNP/LBPP)
to the lower body of healthy subjects, thereby changing
the distribution of body fluids within the trunk. In fact,
LBNP resulted in a subjective perception of head-up
body tilt, while LBPP induced sensations of apparent
head-down body tilt.
Recent studies investigated directly the effects of vis-
ceral afferent nerve stimulation on the activity of the
brain in animals and in human subjects. In cats, stimu-
lation of the renal nerve resulted in responses of neu-
rons in the periphery of the ventral posterolateral nu-
cleus and the dorsal and lateral posterior complex of the
thalamus indicating that these sites process afferent in-
formation from the kidneys [44]. Stimulation of the va-
gus nerve resulted in activity modulation in the lateral
primary somatosensory and insular cortices of rats and
in the primary somatosensory cortex of cats [45–48]. In
humans,functional imaging techniques have shown that
stimulation of the vagus nerve in epileptic patients in-
fluences neural activity in the thalamus, the insular cor-
tex and the postcentral gyrus, among other brain re-
gions [49–51]. Thus, one may speculate that the insular
cortex and the postcentral gyrus found to provoke a dis-
turbance of controlling upright body orientation in the
present study, may be involved in processing afferent
sensory signals from the human trunk (via the vagus
and renal nerves) related to the orientation of the sub-
ject’s body with respect to gravity.
An alternative view contrasting with Mittelstaedt’s
hypothesis has been suggested by Bisdorff et al. [7] and
Anastasopoulos et al. [52]. They have argued that the
proprioceptive, and more generally the somatosensory
systems could mediate a non-vestibular sense of body
uprightness. Their finding of veridical perception of
postural upright (SPV) in patients with acute peripheral
and various central vestibular disorders demonstrated
462

that vestibular information is not necessary for the per-
ception of own body orientation. However, experimen-
tal observations indicated that the contribution of so-
matosensory input for the perception of body posture
might only be of modulatory character. Proprioceptive
input from the lower extremities were found to affect the
perception and control of posture only indirectly by im-
plementing or modulating the output of the truncal
graviceptors [9, 53]. Moreover, Karnath et al. [6] were
able to investigate postural upright perception in one
patient with complete left-sided sensory loss due to a
right thalamic lesion (patient C5 in ref. [6]). Interest-
ingly, this patient did not show any difficulties adjusting
the SPV veridical. Further research is required address-
ing this issue. However, Karnath et al.’s finding made
clear that complete somatosensory loss does not auto-
matically result in an impaired SPV and that it can not
explain the ipsiversively tilted SPV in patients with
pusher syndrome.
To summarize, we examined the lesions of acute pa-
tients with pushing behaviour following cortical/sub-
cortical lesions that spared the thalamus. In both hemi-
spheres, we found the simple lesion overlap of the
pusher patients centering on the insular cortex and
parts of the postcentral gyrus. When subtracted from
the matched controls, we only found very small regions
that were specific for the pusher patients. Obviously, the
cortical structures representing our control of upright
body orientation are in close anatomical proximity to
those typically inducing aphasia in the left hemisphere
and spatial neglect in the right hemisphere. Owing to the
close anatomical connection between posterior thala-
mus and both the insular cortex and the postcentral
gyrus, it is possible that such lesions lead to disruption
or functional alteration [54] of thalamocortical and/or
corticothalamic processing loops related to the control
of upright body posture.
■ Acknowledgement This work was supported by the Deutsche
Forschungsgemeinschaft (Graduiertenkolleg Kognitive Neurobiolo-
gie). We are grateful to the team of physiotherapists at the Centre of
Neurology for their valuable support with the clinical investigation of
the patients.

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