1. 29 Journal of Neurological Physical Therapy Vol. 28 • No. 1 • 2004
ABSTRACT
Pusher syndrome in patients post-stroke is characterized
by leaning and active pushing toward the hemiplegic side
with no compensation for the instability, and resistance to
passive correction toward midline. Patients with pusher
syndrome post-stroke have been found to require longer
than average to reach independence in activities of daily liv-
ing and ambulation. This behavior is found to be present
primarily in patients with right hemispheric lesions cen-
tered in the area of the posterolateral thalamus. Patients
with this disorder misperceive body orientation in space,
believing that the upright position is approximately 18°
tilted toward the ipsilesional side. This could be the result
of ‘graviceptive neglect’ of signals originating in the con-
tralesional trunk and pelvis. The ability to use visual infor-
mation for the correction of body posture continues to
exist in this population, allowing for the use of visual cues
and cognitive strategies as potential rehabilitation tools.
Key Words: pusher syndrome, stroke, hemiplegia
INTRODUCTION
Pushing is one of the most perplexing perceptual-motor
behaviors encountered in the rehabilitation of patients
post-stroke. It is clinically displayed in 5% of all patients
post-stroke, and in approximately 10% of patients with
stroke referred for neurologic rehabilitation.1
These tend to
be the most severely impaired patients with profound func-
tional limitations in performing transfers,standing,and gait.
Individuals with pusher syndrome also take a longer than
average time to recover independence post-stroke.1,2
Evidence for the suspected nature and type of stroke
responsible for this unusual behavioral disorder has been
published, and may contribute to our knowledge of how to
best treat these patients to facilitate more independent
function.3-5
The purpose of this review is to describe the
characteristics of the pusher syndrome in patients post-
stroke, present current information related to the location
of the stroke lesion and cause of this behavioral disorder,
and to discuss physical therapy interventions for this
patient population.
Patients with hemiparesis post-stroke are known to
demonstrate some postural imbalance, and may lose bal-
ance in the lateral direction, typically falling toward the
weaker side.2,5-8
These patients usually attempt to compen-
sate for this imbalance by shifting body weight across mid-
line, onto the ipsilesional side and away from the hemi-
plegic side. A small percentage of patients post-stroke
demonstrate a behavioral phenomenon characterized by
leaning and active pushing toward the hemiplegic side in
all positions using the nonparetic arm and leg, and resis-
tance to any attempt at passive correction of posture
towards midline or across the body toward the nonaffected
side. These patients subjectively report the impression of
lateral instability and the fear of falling toward the non-
paretic side.3
This behavior has been called the“pusher syn-
drome” by Davies,9
Bailey and Leivseth,10
and Premoselli et
al.11
It also has been referred to as ‘ipsilateral pushing,’1,7
‘contraversive pushing,’2,4
and ‘pusher behavior.’5
CHARACTERISTICS OF PATIENTS WITH PUSHER
SYNDROME
Observations of the clinical behaviors of patients with
pusher syndrome were documented by Davies in her book
entitled Steps to Follow.9
Davies categorized the typical
body systems impairments of these patients into a syn-
drome that included left hemiplegia, spatial and sensory
neglect of the hemiplegic side, postural asymmetries, and
the characteristic shift of body weight toward the hemi-
plegic side with no attempt to support or compensate for
the resultant imbalance.9
These patients typically show no
protective responses when active pushing leads to postural
instability in sitting and standing, and are therefore at high
risk for falls.3,9
Davies clinically observed that sensory
neglect can be severe and include an impaired ability to
perceive any sensory afferent information on the hemi-
plegic side including tactile, proprioceptive, visual, and
auditory stimuli.9
Other investigators have found sensory
impairments to be commonly associated with pushing syn-
drome.12,13
The associated characteristics of patients who display
this phenomenon have been a topic of debate from the
time Davies defined it as ‘the pusher syndrome.’9
Davies
observed that neglect of the physical and environmental
space on the hemiplegic side, and the predominance of
right brain lesion characterized this ‘syndrome.’9
Several
investigators since that time have consistently found an
association of neglect with impaired balance and particu-
larly with pusher syndrome.3-5,14,15
In a study by Karnath and
colleagues3
involving 23 patients with pusher behavior,80%
of 15 patients with right brain lesions and pushing dis-
played spatial neglect and somatosensory impairment.
SPECIAL INTEREST PAPERS
The ‘Pusher Syndrome’
Margaret L. Roller, DPT, MS
Assistant Professor in the Department of Physical Therapy, California State University, Northridge, Northridge, CA
(peggy.roller@csun.edu), and Physical Therapist, UCLA Medical Center Department of Rehabilitation Services, Los Angeles, CA

2. Vol. 28 • No. 1 • 2004 Journal of Neurological Physical Therapy 30
Neglect was determined to be severe in approximately 90%
of these patients. Neglect was not present in 8 patients
with left-sided lesions and pushing, however, aphasia was
often present.3
Perennou et al5
found that 3 patients with
pushing and left hemiplegia due to right hemispheric
stroke also showed severe spatial neglect that included
severe bodily and nonbodily neglect, tactile extinction, and
hypoesthesia. These 3 patients also did not fear falling
toward the hemiparetic side despite pronounced postural
impairment.5
Pedersen et al1
compared characteristics of
34 patients with pusher syndrome post-stroke to patients
post-stroke without the behavior. These investigators found
no significant difference in the presence of neglect and
aphasia in patients with pusher syndrome. Also, no signifi-
cant difference was found between the two groups for
symptoms of anosognosia or apraxia. These authors deter-
mined the results of this study to be contrary to the exis-
tence of a pusher syndrome that encompasses both physi-
cal and neuropsychological symptoms.
Pedersen et al1
also observed no significant association
between the side of stroke lesion and the incidence of
pushing. However other authors have shown a significantly
greater incidence among patients with right brain
lesions.3,11,12
In the study by Karnath et al3
, 65% of the sam-
ple of 23 patients with pusher behavior experienced a right
hemispheric lesion. Regardless of the side of the lesion,the
directional bias of pushing appears to be predominantly
toward the side contralateral to the lesion.1,4,5,11-13
A related
but weaker tendency to fall posteriorly also can exist in this
population.12,13,15
The severity of paresis of the hemiplegic extremities has
not been shown to directly influence the presence of push-
ing or body orientation with respect to gravity while
seated.8
However all 23 of the patients with contraversive
pushing in the study by Karnath et al3
displayed severe pare-
sis of both the upper and lower contralesional extremities.
Perennou et al5
noted that the presence of a mild pelvic
tilt toward the contralesional side occurred in some non-
pushers and concluded that a continuum in pushing behav-
ior must exist, rather than a distinct occurrence of the
behavior. If this assumption is true, then pusher syndrome
is perhaps not simply an entity, but an extreme form of this
disorder of postural misrepresentation that includes visual-
spatial impairment and neglect.5
DISTINGUISHING PATIENTS WITH PUSHER SYNDROME
FROM PATIENTS WITH OTHER SIMILAR DISORDERS
Active pushing with the nonparetic extremities helps to
distinguish patients with pusher syndrome from patients
with thalamic astasia13
and those with lateropulsion in
Wallenberg’s syndrome.15,16
The ability of patients with
pusher syndrome to maintain correct head orientation
toward vertical in the presence of a severe lateral lean helps
to distinguish these patients from those with cerebral
lesions in the ‘vestibular cortex.’17
Thalamic astasia, or the inability to stand unsupported,
has been found to be a result of lesions of the posterolateral
thalamus.13
In a study by Masdeu and Gorelick,13
8 patients
with unilateral thalamic lesions could not sit independently,
demonstrated obvious truncal instability, and fell backward
or to the affected side from a sitting position when unsup-
ported. When asked to sit up,patients with astasia typically
grasp the side rail of the bed with the unaffected hand or
with both hands and pull themselves up, rather than using
the available power of the trunk.13
This behavior is differ-
ent from pusher syndrome.5,13
When patients with pusher
syndrome are asked to sit up they do the exact opposite by
extending the unaffected arm and using it to actively push
away from the nonparetic side. Another difference in these
two types of patients is the severity of hemiparesis. Patients
post-stroke who push have been found to have severe pare-
sis of the contralateral arm and leg,3
whereas patients with
thalamic astasia characteristically have very mild or no
motor weakness.13
Wallenberg’s syndrome can be found in patients with
acute unilateral brainstem infarctions in the area of the
medulla. These patients display a tilt of the subjective visual
vertical (visual perception of the upright position), lat-
eropulsion (a tendency to fall sideways) without active
pushing or resistance to passive correction, and a deviation
of the center of gravity toward the ipsilesional, nonparetic
side. The tendency of patients with Wallenberg’s syndrome
is to fall sideways toward the side of the lesion, or ipsiver-
sively,compared to patients with pusher syndrome who fall
to the side opposite the lesion, or contraversively.15,16
Patients with pusher syndrome post-stroke have been
shown to display an intact perception of subjective visual
vertical, indicating that their processing of visual and
vestibular inputs for perception and orientation of the
visual world is undisturbed.3,17
However, they display an
impaired perception of subjective postural vertical by
demonstrating a severe tilt of the pelvis with active pushing
toward the hemiplegic side,leading to a contraversive tilt of
the body toward the side opposite to the lesion and falling
to that side.3,17
Patients with pusher syndrome are generally
able to keep a correct head orientation toward vertical even
in the presence of a severe lateral lean. This perceptual
characteristic helps to differentiate this population from
patients with cerebral lesions in the posterior insula, also
called the ‘vestibular cortex,’ who commonly experience a
perceived tilt of the subjective visual vertical.17
However,
patients with lesions of this area of the cerebral cortex do
not tend to produce impairments of postural control such
as falling to one side, indicating intact perception and per-
formance of the subjective postural vertical4,17-19
(Table 1).
LOCATION OF STROKE LESION AND CAUSE OF
PUSHER SYNDROME
An examination of MRI scans of the infarcted brain
regions of 23 patients with severe contraversive pushing
was conducted by Karnath et al.3
The overlapping area of

3. 31 Journal of Neurological Physical Therapy Vol. 28 • No. 1 • 2004
these infarctions clearly centered on the posterolateral thal-
amus, an area that is anatomically distinct from the ‘vestibu-
lar cortex’ in the posterior insula,3,17
yet similar to that of
patients with thalamic astasia.13
Karnath et al3
proposed
that the posterolateral thalamus, including the ventral pos-
terior nucleus, lateral posterior nucleus, and probably its
cortical projections, seems to be fundamentally involved in
the neural representation of the graviceptive system in
humans that is critical for our control of upright body pos-
ture. This area extended from the posterolateral thalamus
into the posterior crus of the internal capsule, which helps
to explain the severe hemiparesis present in all 23 of the
patients with contraversive pushing in the Karnath study.3
It is yet unclear whether slightly differing lesion locations in
the posterolateral thalamus may result in different clinical
syndromes due to the disturbance of different functional
systems represented in this structure.3
It is thought that the occurrence of pusher syndrome in
patients post-stroke may be associated with a disturbed
neural representation of the truncal graviceptive system,
which contributes to the control of upright posture of the
body in space.4,5
A kinematic analysis performed by
Perennou et al5
showed that pusher syndrome is not the
result of disrupted processing of vestibular information,but
rather results from a high-order disruption in the process-
ing of somesthetic information originating in the contrale-
sional hemibody. It was suspected that this could be gravi-
ceptive neglect,defined as extinction of graviceptive signals
originating in the contralesional part of the trunk and
pelvis.5
This disruption then leads patients who push to
actively adjust their body posture to a behavioral vertical
biased to the side opposite the cerebral lesion.5
Researchers tend to agree that, whatever the cause of
pusher syndrome, patients who demonstrate the behavior
misperceive their body position in space.4,7,8,17
Evidence for
this misperception can be observed clinically when a
patient complains of a feeling of falling as a therapist moves
the patient’s body to a midline position over the base of
support. When asked which direction they perceive to be
falling, the patient will indicate toward the nonparetic side.
If the therapist were to let go,the patient would instead fall
to the hemiplegic side. The patient perceives and believes
that the appropriate, upright position in space is located
somewhere to the ipsilesional side of true center.4
It has
been demonstrated in a laboratory environment without
visual cues from the surroundings (with eyes closed, blind-
folded,or wearing Frenzel lenses) that patients with pusher
syndrome subjectively perceive their body as oriented
‘upright’ when it is tilted an average of 18° to the ipsile-
sional side.4
This experiment was strong evidence that the
underlying cause of pusher behavior may be a severe mis-
perception of body orientation in relation to gravity.4
Patients with pusher syndrome do not align their body with
the visual vertical (which is intact and upright), with their
perceived postural vertical (which is impaired at an average
of 18˚ to the ipsilesional side),or with an intermediate pos-
ture. Instead, they move the body into the opposite direc-
tion, toward the hemiplegic side. Karnath et al4
expressed
that they cannot definitively clarify this discrepancy. These
investigators speculated that by pushing the longitudinal
body axis toward the contralesional (hemiplegic) side these
patients try to actively compensate for the mismatch
between the intact visual vertical and the‘tilted’orientation
of subjective body verticality. A therapist’s attempt to cor-
rect a patient’s body posture toward the objective upright
position with eyes open seems to contradict the patient’s
effort to ‘compensate,’ which induces the feeling of lateral
instability, fear of falling, and provokes active resistance to
such attempts.4
Generally, a conflict between 2 sensory-
perceptual reference systems is resolved either by sup-
pressing one or both of them, or by a compromise (eg, by
weighted summation).4
However, neither happens in the
case of pusher syndrome.4
It is also possible that pushing is a secondary response
to the patients’unexpected experience of loss of lateral bal-
ance when trying to get up and sit upright in a vertically ori-
ented room.4
As a patient tries to get up and orient the
body (subjectively) upright,they experience lateral instabil-
ity because the center of mass is shifted too far to the ipsile-
sional side. Pushing the body to the contralesional side
might be the reaction to this experience.4
MEASURING CONTRAVERSIVE PUSHING
Only recently has a clinical tool been developed to mea-
sure the degree of pushing behavior that is present in
patients post-stroke. The Standardized Scale for Contra-
versive Pushing (SCP) was designed by Karnath et al4,20
to
classify patients based on the severity of behavioral and
clinical impairments (Table 2). This scale is based on crite-
ria established by Davies4,9
and assesses the following: (1)
Characteristic Pusher Syndrome Thalamic Astasia Wallenberg’s Syndrome Vestibular Cortex Stroke
Direction of pushing or loss of balance Push sideways toward the Fall backward or to the Fall sideways toward the Lean and lose balance
paretic side paretic side without pushing non-paretic side without pushing toward the paretic side
without pushing
Location of lesion Posterolateral thalamus Posterolateral thalamus Medulla of brainstem Posterior insula, AKA
vestibular cortex
Severity of hemiparesis Severe Mild to none Mild Mild
Subjective visual vertical Intact Intact Impaired Impaired
Subjective postural vertical Impaired Not stated Not stated Intact
Table 1. A Comparison of the Characteristics of Different Related Disorders13,15-17

4. Vol. 28 • No. 1 • 2004 Journal of Neurological Physical Therapy 32
posture: symmetry of spontaneous posture while sitting
and standing, (2) extension: the use of the ipsilesional arm
or leg to extend the area of physical contact to the ground
while sitting and standing, and (3) resistance: resistance to
passive correction of posture while sitting and standing.
One point for sitting ability and one point for standing abil-
ity are attainable in each of the 3 sections for a maximum of
2 points for each section and 6 points total. Patients are
scored as possessing contraversive pushing if all 3 criteria
are present, reaching a total score of at least 1 for each cri-
terion.4,20
This scale has not been studied to determine its
psychometric properties, therefore clinicians are cautioned
to use this tool as a guideline only until further investigation
of its reliability and validity is performed with this popula-
tion.
PHYSICAL THERAPY INTERVENTIONS AND RECOV-
ERY OF FUNCTION FOR PATIENTS WITH PUSHER
SYNDROME
Bohannon7
found that some patients with pusher syn-
drome can ‘learn’ to balance in standing with their feet
apart within a half-hour session. After the patients’ posi-
tional misperception was made apparent to them by intro-
ducing them to the appropriate position over their feet,and
providing them with practice and feedback, these patients
typically achieved a short duration of independent static
standing – first with their backs against a wall, and later
without support and during movement.7
The type of prac-
tice and feedback supplied during these training sessions
was not specified.
Both Karnath et al4
and Perennou and associates5
noted
a preserved ability of patients with contraversive pushing
to align the body axis to earth-vertical with the help of
visual cues from the environment and speculated that this
might be a useful rehabilitation tool. In the study by
Karnath et al4
, when patients with contraversive pushing
and suspected impaired truncal graviception visually
explored a structured laboratory environment, they were
able to correctly align their longitudinal body axis to earth-
vertical. This indicates that seeing upright orientation of
surrounding objects and persons helped their impaired
graviceptive system. This experiment was performed under
controlled laboratory conditions in which the body was
immobilized by lateral stabilization, the legs were hanging
freely, and the patients were explicitly instructed to con-
centrate on visual information available in the laboratory
environment. With the help of visual cues, these patients
could only temporarily align their body axis to earth-verti-
cal. It was concluded that visual input does not suffice to
continuously control upright body posture in patients with
pusher behavior.4
Although patients with pusher syndrome
are typically unable to spontaneously use visual input to
control upright body posture, the use of visual cues from
the environment may be an effective training tool when
combined with conscious strategies for the achievement of
postural control.4
In a study of patients with hemispheric cerebral lesions,
contralesional tilt of the pelvis, and impaired perception of
postural vertical without pushing behavior by Perennou et
al,8
transcutaneous electrical nerve stimulation (TENS) of
short pulse duration, with intensity below motor threshold
applied to the skin on the contralesional side of the neck
reduced the bias of the perception of postural vertical. This
effect was greater in patients who showed sensory loss or
neglect and more severe contralesional bias of the postural
vertical, which was defined as being greater than 3.0° off
true vertical. It is believed that this method of applying
TENS works by activating various afferent nerve fibers in
the neck that convey stimuli to the contralateral cerebral
hemisphere, thus unmasking the patients’ latent postural
capabilities. These authors believe that TENS probably acts
as a powerful substitution stimulus that reactivates or reor-
(A) Posture: symmetry of spontaneous posture. Sitting Standing
Score: 1.00 = severe contraversive tilt with falling to the contralesional side ______ ______
0.75 = severe contraversive tilt without falling ______ ______
0.25 = mild contraversive tilt without falling ______ ______
0 = no tilt / upright body orientation ______ ______
Total (max = 2) ______
(B) Extension: use of the ipsilesional arm/leg to extend the area of physical contact to the ground.
Score: 1.00 = performed already in rest ______ ______
0.50 = performed not until position is changed ______ ______
0 = no extension ______ ______
Total (max = 2) ______
(C) Resistance: resistance to passive correction of posture to an upright position.
Score: 1.00 = resistance is shown ______ ______
0 = no resistance is shown ______ ______
Total (max = 2) ______
TOTAL SCORE /6
*Adapted with permission from Neurology.4
Copyright 2000, Lippincott, Williams & Wilkins.
Table 2. Clinical Assessment Scale for Contraversive Pushing (SCP)*

5. 33 Journal of Neurological Physical Therapy Vol. 28 • No. 1 • 2004
ganizes the damaged neural network devoted to body ori-
entation with respect to gravity.8
This intervention may
show promise for patients with pusher behavior who also
demonstrate significant contralesional tilt of the pelvis and
impairment in the perception of postural vertical.
Pedersen and colleagues1
speculated that pushing in dif-
ferent postures represented the degree of severity of the
disorder. If this is accurate, then during remission post-
stroke,pushing should first diminish in the supine position,
then in the sitting position, and finally in the standing posi-
tion. No studies have been done to support this con-
tention.1
Pedersen et al1
determined that, upon admission to a
stroke rehabilitation unit, subjects with pusher syndrome
had more severe strokes as expressed by lower neurologi-
cal scores on the Scandinavian Stroke Scale, and lower ini-
tial activities of daily living (ADL) function scores as mea-
sured by the Barthel Index. The presence of pusher
syndrome was found to slow the recovery process post-
stroke,1,2
requiring an average of 3.6 weeks (63%) longer for
subjects with pushing behavior to reach their highest ADL
function scores on the Barthel Index upon discharge from
a rehabilitation facility.1
Ultimate functional outcome was
not found to be influenced by pusher syndrome;1,2
how-
ever, since patients with this disorder have difficulty and
take longer to achieve any level of independence in activi-
ties of daily living (ADL) and ambulation they have, in the
past, been erroneously regarded as unsuitable for formal
rehabilitation.1
CONCLUSIONS
Pusher syndrome in patients post-stroke is characterized
by leaning and active pushing toward the hemiplegic side
in all positions with no attempt to compensate for the
imbalance, and resistance to any attempt at passive correc-
tion toward the ipsilesional side.3,9
Several authors agree
that hemisensory impairments and severe neglect also char-
acterize this syndrome.3,5,9
This perceptual-motor behavior
is found to be present primarily in patients with right hemi-
spheric lesions centered in the area of the posterolateral
thalamus.3,11,12
Patients with pusher syndrome display a mis-
perception of body orientation in space, believing that the
upright position is approximately 18° tilted toward the
ipsilesional side.4
It is suspected that this could be the
result of ‘graviceptive neglect’ of signals originating in the
contralesional trunk and pelvis.5
Pushing toward the con-
tralesional side may be an attempt to compensate for a mis-
match between an intact perception of the visual vertical
and an impaired perception of postural vertical.4
Since the
ability to use visual information for the correction of body
posture continues to exist in this population, the use of
visual cues,along with cognitive strategies,is recommended
as a rehabilitation tool.4,5
The recovery process for patients
with pusher syndrome post-stroke has been found to be
slow, requiring longer than average to reach a level of inde-
pendence in activities of daily living and ambulation.1
UNANSWERED QUESTIONS AND DIRECTIONS FOR
FUTURE STUDIES
There are still many unanswered questions regarding the
examination and treatment of patients post-stroke with
pusher syndrome. Several suggestions for future research
have been identified based on the findings of this review.
First, the examination tool called the ‘Clinical Assessment
Scale for Contraversive Pushing’ is yet to be investigated to
determine its psychometric properties. This tool demon-
strates the potential to identify the presence and severity of
pushing in patients post-stroke and should be studied to
establish its utility in the clinical setting. It is also unclear
exactly what practice activities, parameters, and feedback
are necessary to create long-term learning of vertical pos-
tures in patients with contraversive pushing. Visual feed-
back training has shown promise in the laboratory setting
and should be studied in patients with pusher syndrome to
determine whether it will decrease the amount of time it
takes to reach a level of independent function in sitting abil-
ity, transfers, and ambulation. Lastly, the length of time to
recover ADL and gross motor function was noted to be
longer for patients with pusher syndrome, yet no studies
were found that analyzed the cost of rehabilitation for these
patients compared to other patients with post-stroke hemi-
plegia. Future research in these areas would greatly add to
our ability to best provide physical therapy management for
patients with this disorder.
REFERENCES
1
Pedersen PM, Wandel A, Jorgensen HS, et al. Ipsilateral
pushing in stroke: incidence, relation to neuropsycho-
logical symptoms, and impact on rehabilitation. The
Copenhagen Stroke Study. Arch Phys Med Rehabil.
1996;77:25-28.
2
Karnath HO, Johannsen L, Broetz D, et al. Prognosis of
contraversive pushing. J Neurol. 2002;249:1250-1253.
3
Karnath HO, Ferber S, Dichgans J.The neural represen-
tation of postural control in humans. Proceedings of
the National Academy of Sciences of the United States
of America. 2000;97:13931-13936.
4
Karnath HO, Ferber S, Dichgans J.The origin of contra-
versive pushing:evidence for a second graviceptive sys-
tem in humans. Neurology. 2000;55:1298-1304.
5
Perennou DA,Amblard B,Laassel el M,et al.Understand-
ing the pusher behavior of some stroke patients with
spatial deficits: a pilot study. Arch Phys Med Rehabil.
2002;83:570-575.
6
Rode G,Tiliket C, Boisson D. Predominance of postural
imbalance in left hemiparetic patients.Scand J Rehabil
Med. 1997;29:11-16.
7
Bohannon RW. Ipsilateral pushing in stroke. Arch Phys
Med Rehabil. 1996;77:524-525.
8
Perennou DA,Amblard B, Leblond C, et al. Biased pos-
tural vertical in humans with hemispheric cerebral
lesions. Neurosci Lett. 1998;252:75-78.

6. Vol. 28 • No. 1 • 2004 Journal of Neurological Physical Therapy 34
9
Davies PM. Steps to Follow: A Guide to Treatment of
Adult Hemiplegia. New York, NY: Springer-Verlag;
1985.
10
Bailey MJ, Leivseth L.The ‘pusher’ syndrome in elderly
stroke patients... symposium on stroke. Br J Ther
Rehabil. 2000;7:11-16.
11
Premoselli S, Cesana L, Cerri C. Pusher syndrome in
stroke: clinical, neuropsychological and neurophysio-
logical investigation. Europa Medicophysica. 2001;
37:143-151.
12
Bohannon RW,Cook AC,Larkin PA,et al.The listing phe-
nomenon of hemiplegic patients. Neurol Report. 1986;
10:43-44.
13
Masdeu JC, Gorelick PB. Thalamic astasia: inability to
stand after unilateral thalamic lesions. Ann Neurol.
1988;23:596-603.
14
Bohannon RW, Smith MB, Larkin PA. Relationship
between independent sitting balance and side of hemi-
paresis. Phys Ther. 1986;66:944-945.
15
Dieterich M, Brandt T. Wallenberg’s syndrome: lat-
eropulsion, cyclorotation, and subjective visual vertical
in thirty-six patients. Ann Neurol. 1992;31:399-408.
16
Bjerver K,Silfverskiold BP.Lateropulsion and imbalance
in Wallenberg’s syndrome. Acta Neurol Scand. 1968;
44:91-100.
17
BrandtT,Dieterich M,Danek A.Vestibular cortex lesions
affect the perception of verticality. Ann Neurol. 1994;
35:403-412.
18
Bisdorff AR,Wolsley CJ,Anastasopoulos D,et al.The per-
ception of body verticality (subjective postural vertical)
in peripheral and central vestibular disorders. Brain.
1996;119(Pt 5):1523-1534.
19
Anastasopoulos D, Haslwanter T, Bronstein A, et al.
Dissociation between the perception of body vertical-
ity and the visual vertical in acute peripheral vestibular
disorder in humans. Neurosci Lett. 1997;233:151-153.
20
Karnath HO,Brotz D,GotzA.[Clinical symptoms,origin,
and therapy of the “pusher syndrome”]. Nervenarzt.
2001;72:86-92.