Neuropsychologia 133 (2019) 107150

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Neuropsychologia
journal homepage: www.elsevier.com/locate/neuropsychologia

Deficient body structural description contributes to apraxic end-position T

errors in imitation
Hormos Salimi Dafsaria, Anna Doverna, Gereon R. Finka,b, Peter H. Weissa,b,∗
a
Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Center Jülich, Leo-Brandt-Str. 5, 52425, Jülich, Germany
b
Department of Neurology, Faculty of Medicine and University Hospital Cologne, > University of Cologne,, Kerpener Str. 62, 50937, Cologne, Germany

ARTICLE INFO ABSTRACT

Keywords: Apraxia is a common cognitive deficit after left hemisphere (LH) stroke. It has been suggested that a disturbed
Body structural description (BSD) representation of the human body underlies apraxic imitation deficits. Thus, we here tested the hypothesis that a
Apraxia deficient body structural description (BSD), i.e., a deficient representation of a body part's position (relative to a
Imitation standard human body), contributes to apraxic end-position errors in imitation, while controlling for deficits in
Voxel-based lesion-symptom mapping (VLSM)
the semantic representation of the human body (body image, BI) and naming deficits.
Parietal cortex
A quantitative pointing task to assess putative BSD deficits and an apraxia assessment, including imitation and
pantomime tasks, were applied to 27 patients with LH stroke and 19 healthy subjects. While LH stroke patients
without apraxia (n=15) did not differ from control subjects in their pointing performance, patients suffering
from imitation apraxia (n=10) showed a differential deficit when pointing to body parts of other humans
compared to object parts. Voxel-based lesion symptom mapping (VLSM) revealed an association of these dif-
ferential pointing deficits (indicating a deficient BSD) with lesions in the angular gyrus of the left inferior
parietal cortex.
This first quantitative group study of BSD deficits in LH stroke patients supports the notion that apraxic end-
position errors in imitation are – at least in part – due to a deficient coding of the position of human body parts.

1. Introduction
The impairments caused by apraxia, a cognitive motor deficit that is
often observed after left hemisphere (LH) stroke, cannot be fully ac-
counted for by primary sensory and motor deficits, disturbed commu-
nication, or lack of motivation (Dovern et al., 2012). Frequently ob-
served apraxic impairments pertain to the imitation of abstract and
symbolic gestures, pantomiming the use of objects and tools, as well as
actual object use. The underlying pathophysiology of these apraxic
deficits is still debated.
Goldenberg suggested that apraxic patients are unable “to evoke
and represent conceptual knowledge about the human body, which is
necessary for performing the apparently simple task of imitating
[meaningless] gestures.” (Goldenberg, 1995). In the same vein, an in-
fluential account proposes an essential role of “body part coding” in
apraxia (Goldenberg and Karnath, 2006). These authors stated that “the
body parts involved in gestures are categorized” “based on knowledge
about distinctive features and boundaries” of these body parts and that
the “gestures are coded as simple spatial relationships between a
limited set of discrete body parts” (see also (Goldenberg, 2009)).
Therefore, body part coding is considered “an intermediate step be-
tween perception and reproduction of gestures” (Goldenberg, 1999;
Goldenberg and Karnath, 2006). The finding that not only the imitation
but also the matching of gestures is disturbed in LH stroke patients
lends further support to the hypothesis that patients with imitation
apraxia may suffer from a deficient conceptual knowledge about the
human body (Goldenberg, 1999).
However, studies investigating within the same patient population
apraxic deficits and deficits in processing human bodies/body parts are
sparse (Goldenberg, 1995). This is in part because different concepts
have been proposed to capture the neural representation of the human
body (Schwoebel and Coslett, 2005): the body schema (BS), the body
structural description (BSD), and the body image (BI).
Body schema (BS) is a „dynamic representation of the relative
positions of body parts derived from multiple sensory and motor in-
puts“ (Schwoebel and Coslett, 2005). Head and Holmes first described
the BS as a body standard “against which all subsequent changes of
posture are measured before they enter consciousness“ (Head and

∗
Corresponding author. Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Centre Jülich, Leo-Brandt-Str. 5, 52425, Jülich,
Germany.
E-mail address: P.H.Weiss@fz-juelich.de (P.H. Weiss).

https://doi.org/10.1016/j.neuropsychologia.2019.107150
Received 16 June 2017; Received in revised form 24 June 2019; Accepted 26 July 2019
Available online 29 July 2019
0028-3932/ © 2019 Elsevier Ltd. All rights reserved.
H.S. Dafsari, et al.
Holmes, 1911). Note that in many publications “body schema” is used
as an umbrella term for all three terms (body schema, body structural
description, and body image (Le Clec'H et al., 2000)) rather than in its
specific meaning, i.e., a dynamic neural representation of the human
body that allows an online updating of the body part's position during
limb movement. In contrast, the body structural description (BSD) is
a „topological map of locations derived primarily from visual input that
defines body part boundaries and proximity relationships“ (Schwoebel
and Coslett, 2005). Usually, the clinical assessment of the BSD involves
asking the patient to point to a body part on his/her own or another
human body (Semenza and Goodglass, 1985). Finally, the body image
(BI, the alternative term used is “body semantics”) is involved in con-
sciously evaluating human bodies. BI is regarded to be „a lex-
ical–semantic representation of the body, including body part names,
functions, and relations with artefacts“ (Schwoebel and Coslett, 2005).
Again, in the psychiatric context, different use of the term “body image”
is quite common, e.g., body image distortion in anorexia nervosa
(Wagner et al., 2003).
Concerning the body part coding hypothesis of imitation apraxia,
the BSD is the relevant concept (Goldenberg, 1995). Patients with a
deficient BSD are impaired in localizing a body part (and its bound-
aries) on their body or another human's body. Note that many clinical
tests examining imitation deficits in stroke patients (e.g., the Cologne
Apraxia Screening, KAS) concentrate on the end-position of the tested
body part (i.e., limb or face) rather than on the (movement) trajectory
to this position. This also applies to the popular Goldenberg imitation
tests (imitating hand positions or finger configurations, (Goldenberg,
1995)), which were used in Goldenberg and Karnath's study on body
part coding (Goldenberg and Karnath, 2006). However, in patients with
imitation deficits, dissociations concerning the trajectory and end-po-
sition can occur. Some patients show disturbed trajectories but achieve
a proper end-position of the tested effector (e.g., hand), while other
patients exhibit a smooth (movement) trajectory to a wrong end-posi-
tion (Hermsdörfer et al., 1996). Thus, BSD deficits may contribute to
apraxic end-position errors during imitation rather than to deficits in
(movement) trajectories (Reader et al., 2018).
Nevertheless, BSD deficits could also contribute to object use defi-
cits in apraxia. Most likely, a deficient BSD affects both the panto-
miming of object use and the actual use of objects in those cases where
the object is used with a given body part (e.g., brushing one's teeth,
combing one's hair). In contrast, object use that is not directed to the
body but instead to another object (e.g., carving/sawing a piece of
wood, cutting a slice of bread) is probably less affected by BSD deficits.
Since the contribution of body part coding and thus BSD to imitation is
undisputed (in LH stroke patients), we here concentrate on the re-
lationship between BSD deficits and apraxic end-position errors in
imitation. Consequently, we focused on those apraxic patients who
showed end-position errors in imitation in the current apraxia assess-
ment (i.e., the Cologne Apraxia Screening, KAS). Note that the scoring
of the KAS imitation subtests is solely based on end-position errors and
not also on spatiotemporal errors as in other apraxia assessments (e.g.,
the TULIA (Vanbellingen et al., 2009) or the AST (Vanbellingen et al.,
2010)).
Insights into the neural correlate of the BSD can be derived from
imaging studies in healthy populations and clinical studies in neuro-
logical patients.
Functional imaging studies in healthy subjects implicated different
parts of the (left) parietal cortex in the body schema (BS) and the BSD.
In memory-guided reaching movements, a “dynamic representation of
the current postural configuration of the body” (i.e., the BS) was as-
sociated with activity in the superior parietal lobe (SPL, (Parkinson
et al., 2010)). In contrast, a task involving the BSD, i.e., pointing to
human body parts (compared to pointing to body parts of dogs), acti-
vated the inferior parietal cortex, in particular, the (left) angular gyrus
(Felician et al., 2009). Other studies found activations in the left pos-
terior intraparietal sulcus (IPS), when healthy subjects performed tasks
2
Neuropsychologia 133 (2019) 107150
involving the BSD (judging the distance between two body parts
(Corradi-Dell'Acqua et al., 2008) or relating the position of a rotated
arm to a standard body (Corradi-Dell'Acqua et al., 2009)).
Concerning the lesions underlying BSD deficits as investigated in
studies with neurological patients, the current knowledge is largely
derived from case studies (Buxbaum and Coslett, 2001; Felician et al.,
2003). Deficient BSD has oftentimes been associated with left parietal
cortex lesions (Ogden, 1985; Semenza, 1988; Sirigu et al., 1991), a
lesion site that is also related to apraxia (Dovern et al., 2011; Hoeren
et al., 2014; Niessen et al., 2014). While there are some behavioural
group studies in neurological patients (Semenza and Goodglass, 1985),
a quantitative lesion study examining the (differential) lesion patterns
underlying apraxic end-position errors in imitation and deficits of the
BSD is lacking. Therefore, we set out to develop a quantitative assess-
ment of BSD deficits in patients with LH stroke with and without
apraxia. Then, these quantitative behavioural data were subjected to a
statistical lesion analysis adopting voxel-based lesion symptom map-
ping (VLSM) to examine the hypothesis that a deficient BSD contributes
to apraxic end-position errors in imitation.
2. Methods
2.1. Study participants
Nineteen healthy control subjects (mean age of 59.7 years, range
47–61 years) and 27 patients with first-ever LH stroke (mean age of
60.3 years, range 26–81 years) were included in the current in-
vestigation.
Stroke localisation, including the territory of the medial cerebral
artery (MCA) of the LH, was confirmed with the help of clinical brain
imaging by either CT or MRI scans. Imaging was performed within the
first days of hospitalisation. Few patients suffered from a concurrent
stroke in adjacent vascular territories of the LH (e.g., posterior (n=2) or
anterior (n=1) cerebral artery strokes). The exclusion criteria were
alcohol or drug abuse, uncorrected visual impairment, left-handedness,
pre-existing strokes, and inability to give informed consent.
Additionally, patients with clinically relevant depression or dementia
(diagnosed by the treating physicians) were excluded.
Patients and healthy subjects volunteered for the study. The healthy
volunteers received a fixed reimbursement of €15 for the testing
(lasting about an hour).
The ethics committee of the Medical Faculty, University Hospital
Cologne, University of Cologne had approved the study.
2.2. Clinical and neuropsychological assessment
Apraxia was assessed with the Cologne Apraxia Screening (KAS,
(Weiss et al., 2013)). The KAS is a publicly available screening instru-
ment (published by Hogrefe: https://www.testzentrale.de/shop/
koelner-apraxie-screening.html). The KAS comprises four subtests that
are organized in a factorial manner. One factor is task (pantomime
versus imitation) and the other factor is effector (bucco-facial versus
limb gestures). This structure results in the following four subtests: 1.
pantomime of object use (i.e., transitive gestures) involving bucco-fa-
cial movements; 2. pantomime of object use (i.e., transitive gestures)
involving limb movements; 3. imitation of (intransitive) bucco-facial
gestures; 4. imitation of (intransitive) limb gestures. The stimulus ma-
terial consists of photos that either depict the object or a woman
showing the to-be-imitated gesture, minimizing the influence of con-
current aphasic deficits (P. H. Weiss et al., 2016, ). All subtests consist
of five items each. Moreover, both imitation subtests contain two
meaningless items each (and three meaningful gestures).
In the pantomime subtests, one or two points (depending on the
complexity of the pantomime) are awarded for certain predefined fea-
tures of the pantomime. For example, for the item “pantomiming the
use of a toothbrush” the following movement features are scored with
H.S. Dafsari, et al. Neuropsychologia 133 (2019) 107150

Table 1
Demographic and neuropsychological data of the patient groups with left hemisphere (LH) stroke and the healthy controls.
Apraxic LH stroke patients LH stroke patients with imitation Non-apraxic LH stroke patients Healthy controls
(n=12) apraxia (n=10) (n=15) (n=19)

age (years) 60 (15.5) 59.8 (14.4) 60.6 (13.8) 59.7 (7.8)

gender (male/female) 7/5 6/4 10/5 9/10
time post-stroke (days) 8.1 (6.6) 9.1 (6.8) 8.6 (9.3)
stroke aetiology (ischaemic/haemorrhagic) 9/3 7/3 14/1
LQ +93.3 (9.9) +92.0 (10.3) +87.3 (16.8) +85.8 (20.4)
MRC scale (right hand) 3.63 3.45 4.43
(1.2) (1.2) (0.7)*
mRS 2.67 (1.4) 2.7 (1.3) 1.47 (1.2)*
KAS score 66.3 (21.1) 65.0 (23.0) 78.8 (1.2)*
ACL-K score 20.3 (13.5) 19.8 (14.4) 31.7 (7.82)*

Note that the ten LH stroke patients with imitation apraxia are a subgroup of the 12 apraxic LH stroke patients (see also Supplementary Tables).
Given are the means and standard deviations in brackets (SD). LH = left hemisphere.
ACL-K = Aphasia Check List-short version (Kalbe et al., 2005): maximum score 40 points; cut-off < 33 points; mild [26–32 points], moderate [15–25 points], severe
[0–14 points] language impairment.
KAS = Cologne Apraxia Screening (Weiss et al., 2013): maximum score 80 points; cut-off ≤ 76 points).
LQ: Laterality quotient as assessed by the Edinburgh Handedness Inventory (Oldfield, 1971).
MRC = Medical Research Council rating scale for assessing paresis (O'Brien, 2000): Grade 0: No contraction; Grade 1: Flicker or trace of movement; Grade 2: Active
movement, with gravity eliminated; Grade 3: Active movement against gravity; Grade 4: Active movement against gravity and resistance; Grade 5: Normal power.
Grades 4-, 4 and 4+ may be used to indicate movement against slight, moderate, and strong resistance, respectively. Modified Rankin scale (mRS, (Rankin, 1957; van
Swieten et al., 1988)): grades: 0 = No symptoms at all; 1 = No significant disability despite symptoms; 2 = Slight disability; 3 = Moderate disability; 4 = Moder-
ately severe disability; 5 = Severe disability.
∗
Significant difference between the LH stroke patients with imitation apraxia and those without apraxia (p < 0.05).

one point each: (i) the hand is almost closed to a fist, (ii) the hand is
held laterally in front of the mouth, (iii) the mouth is slightly opened
and the teeth are shown, and (iv) circling/pushing movements of the
hand. When a given movement feature is absent, no point is given. For
the evaluation of the imitation subtests (i.e., imitation of bucco-facial
and limb gestures), four points are given for the correct imitation on the
first trial. Note that an imitated gesture is considered correct if the
patient has adequately reproduced the final end-position of the gesture
as depicted on the photos. If the first imitation trial fails, the stimulus
photo is shown for a second time. Two points are given for a successful
second trial or no point for an erroneous second trial. For each of the
twenty KAS items, the patient can maximally achieve four points.
Therefore, a maximum score of 20 points can be achieved in each of the
four subtests. Thus, the KAS total score can be maximally 80 points.
Based on the normative data of the KAS, a psychometric analysis re-
vealed that a patient with a score of 76 or less should be considered
apraxic. More information on the KAS can be found in Dovern et al.
(2012) and (Kusch et al., 2018).
As in previous studies (Binder et al., 2017; Dovern et al., 2017),
aphasic deficits were assessed by the short version of the aphasia
checklist (ACL-K). The ACL-K contains four subtests: a colour-figure
test, a verbal fluency task, a reading task, and a rating of verbal com-
munication (Kalbe et al., 2002). The scores of the ACL-K can amount up
to 40 points. The lower the score, the more severe the aphasic deficits:
14 points or less indicate severe aphasia, scores between 15 and 25
points indicate moderate aphasia, scores between 26 and 32 indicate
mild aphasia, and scores above 33 are within the normal range (i.e., no
aphasia).
(Pre-morbid) handedness was assessed with the help of the
“Edinburgh Handedness Inventory” (EHI, (Oldfield, 1971)) for stroke
patients and healthy subjects. The score of the EHI is a laterality quo-
tient (LQ), indicating the relative proportion of actions performed with
the right versus the left hand. Therefore, positive EHI-scores (i.e., po-
sitive LQs) indicate right-handedness, while negative EHI-scores (i.e.,
negative LQs) indicate left-handedness. The higher the positive LQ, the
stronger the right-handedness. The lower the negative LQ, the stronger
the left-handedness. Note that patient and control groups were matched
for handedness.
Contralesional limb paresis was evaluated using the Medical
Research Council (MRC) scale (O'Brien, 2000). The MRC-scale is a 5-
point-scale indicating the degree of paresis:
➢ Grade 0: No contraction
➢ Grade 1: Flicker or trace of movement
➢ Grade 2: Active movement, with gravity eliminated
➢ Grade 3: Active movement against gravity
➢ Grade 4: Active movement against gravity and resistance
➢ Grade 5: Normal power.
Grades 4-, 4, and 4+ may be used to indicate movement against
slight, moderate, and strong resistance, respectively.
Since the experimental procedures required patients to point with
their index finger, we asked them to use their left, ipsilesional hand to
avoid putative confounding effects of the contralesional, right-sided
paresis. Despite these instructions, two patients who were not severely
paretic (MRC paresis scale of 4+ and 5) decided to use their con-
tralesional, right hand for pointing: one patient (rakl1001m) for both
pointing tasks, the other patient (haed1109w) only for the object
pointing task. Patient haed1109w had a perfect score in the object
pointing (relative score 1.0) and a nearly perfect score in the body
pointing tasks (relative score 0.98).
The degree of handicap after stroke was assessed using the modified
Rankin Scale (mRS; (Rankin, 1957; van Swieten et al., 1988)). The six
grades of this common scale are: 0 = No symptoms at all; 1 = No sig-
nificant disability despite symptoms; able to carry out all usual duties
and activities; 2 = Slight disability; unable to carry out all previous
activities, but able to look after own affairs without assistance;
3 = Moderate disability; requiring some help, but able to walk without
assistance; 4 = Moderately severe disability; unable to walk without
assistance and unable to attend to own bodily needs without assistance;
5 = Severe disability; bedridden, incontinent, and requiring constant
nursing care and attention; 6 = Dead.
Table 1 lists the demographic and neuropsychological data of the
healthy controls (n=19), LH stroke patients without apraxia (n=15),
LH stroke patients with apraxia (n=12), and the subgroup of apraxic
LH stroke patients with imitation apraxia (n=10). As a deficient BSD
contributes mainly to apraxic end-position errors in imitation, we fo-
cused our analyses on those ten apraxic patients with imitation apraxia
in the current apraxia assessment (i.e., Cologne Apraxia Screening,
KAS). Detailed information about the LH stroke patients with apraxia

3
H.S. Dafsari, et al.
Fig. 1. A. Schematic presentation of the body pointing task. B. Schematic presentation of the object pointing task.
can be found in the supplementary tables.
2.3. Experimental design
Our primary research objective was to investigate specific BSD
deficits by assessing pointing to body versus object parts while con-
trolling for naming deficits and deficient body image (BI). We hy-
pothesised that LH stroke patients with apraxic end-position errors in
imitation would obtain significantly lower scores in the body part
pointing tasks (compared to pointing to object parts). Such a beha-
vioural pattern would suggest that a disturbed BSD is a relevant factor
for apraxic end-position errors in imitation.
After the neuropsychological assessment, subjects were comfortably
seated in front of a laptop computer (MacBook Pro), on which the visual
stimuli were presented.
2.3.1. Pointing to body parts
This task aimed to assess the subject's ability to point to parts of the
human body. First, we inquired the sections of the human body, i.e.,
head, trunk, arms, and legs. Then, we inquired in more detail body
parts within these sections (e.g., for the head: ear, eye, nose, mouth).
Fig. 1a depicts a schematic representation of the body part pointing
4
Neuropsychologia 133 (2019) 107150
task. A pre-test aimed at ruling out a body image deficit for the given
body part item. Such a body image deficit was operationalized as the
inability to name that body part. Note that impaired body part naming
may result from either a deficient body image or from aphasic deficits.
Therefore, participants were asked to name a body part item that was
presented on a computer screen, e.g., a thigh.
If the subjects succeeded in naming that item, they then proceeded
to point to the particular item on a picture of a human body (Fig. 1a).
However, if the participant failed to name the shown body part prop-
erly, he/she was told the body part's name. Then, the subject was
presented with three related body parts, one of which was the inquired
body part, e.g., thigh, hips, and upper arms. This intermediate step in
the testing procedure ensured that patients with aphasic naming pro-
blems, who nevertheless recognized the body part, could still partici-
pate in the body part pointing task. If the subject also failed this task,
the given body part item was excluded from the body part pointing
task. In other words, if a patient could not name a body part, she/he
was told the name of this body part and was presented with pictures of
three related body parts. Then, the patient was asked to point to the
particular body part – selecting it from the three presented body parts.
If the patient could accurately point to the previously named body part
indicating that she/he could adequately associate the body part's name
H.S. Dafsari, et al.
Fig. 2. A. Photograph was taken during the body part pointing tasks (item “thigh”), the patient incorrectly points to the shank. B. Photograph was taken during the
object part pointing tasks (item “lampstand”), the patient correctly points to the stand of the lamp.
with the picture of that body part, that body part was included in the
pointing to body part pointing task - although she/he could not name
the body part. In contrast, if the patient also failed to point to the
correct body part picture after being told the body part's name, that
body part was excluded from the body part pointing task (see below for
the description of the resulting relative performance score).
Note that the inability of LH stroke patients to process a given item
that was excluded by the naming pre-test could either result from a
deficient body image or aphasic deficits since both deficits could lead to
impaired body part naming. However, preserved body part naming
excludes a relevant deficit of the body image. Thus, the pre-test ensured
that a failure in pointing to human body parts could be considered to
reflect a deficient BSD (and not a deficient body image), with lower
scores in the body pointing tasks reflecting a more severe BSD deficit.
For illustration purposes, Fig. 2a depicts a patient who was in-
structed to point to the thigh on a picture of a human body displayed on
the monitor. Note that the photo was taken after the patient's response.
Therefore, the red and yellow rectangles used for scoring are already
present to illustrate the task and the scoring procedure (see below)
within the same figure.
2.3.2. Pointing to object parts
This task assessed the participants' ability to point to parts of non-
human objects. The procedure was similar to that for the body part
pointing task. Fig. 1b depicts a schematic representation of the object-
part pointing task. In each trial, the participants were asked to name an
object that was presented to them on the computer monitor, e.g., a
lamp. If the subjects failed to name the object correctly, they were told
the object's name. Then, they were presented with three related objects,
one of which was the inquired object (e.g., lamp, mobile phone, and
binoculars), and were asked to select the proper object. This inter-
mediate step in the testing procedure ensured that patients with aphasic
naming problems, who nevertheless recognized the object, could still
participate in the object part pointing task. If subjects named or selected
the object correctly, they proceeded to name a part of the given object,
e.g., lampstand. If subjects failed in naming the object-part, they were
told the name of the object-part and then instructed to select the given
object-part out of an array of three object parts, e.g., lamp stand, lamp
shade, and lamp holder. If subjects succeeded in naming or selecting the
object part, they proceeded to point to the object part on a picture of
another object of the given type, e.g., lampstand of another lamp.
Fig. 2b demonstrates that when instructed to point to the lamp-
stand, the same patient who failed on the body part pointing task
(Fig. 2a) performed the object pointing task correctly for this test item.
The order of the two pointing tasks was pseudo-randomized, albeit
the corresponding naming tasks always preceded the pointing tasks for
either body or object items.
2.3.3. Scoring procedure
A similar scoring system was adopted for both pointing tasks. For
5
Neuropsychologia 133 (2019) 107150
each item, we developed a scoring sheet: A yellow rectangle was closed
around the body/object part at which the subject should point to (e.g.,
thigh). A red rectangle was closed around the surrounding body parts
(e.g., hip and knee). If the subject correctly pointed to the inquired
body/object part within the yellow rectangle, the subject received full
points. If the subject pointed to the body/object part nearest to the
inquired part, i.e., within the red rectangle, but outside the yellow
rectangle, the subject received half of the points. If the subject had
pointed outside the red rectangle, the subject received no points. The
subjects could score a total of two points for each of the 20 body part
items (in total: 2 × 20=40 points) and a total of four points for each of
the ten object part items (in total: 4 × 10=40 points).
Since some patients could not perform the tasks for all items due to
their naming deficits (see sections 2.3.1 and 2.3.2), a relative perfor-
mance score was computed reflecting the individual performance in
either task (see also Supplementary Table S3). This relative perfor-
mance score was calculated by dividing the score obtained by a given
person by the attainable maximum score for this person in a given task.
Thus, if a subject could correctly name or select only 12 items in the
body part naming task, but performed correctly for these 12 items
(resulting in 2 points for each of these 12 items), this subject received a
relative performance score of 1 (individual obtained score: 2 × 12=24,
individual attainable maximum score: 2 × 12=24, relative perfor-
mance score: 24/24=1). However, if this subject would fail in 3 of the
12 items (resulting in 0 points for these 3 items), then her/his relative
performance score would be 0.75 (individual obtained score:
0 × 3 + 2 × 9=18, individual attainable maximum score:
2 × 12=24, relative performance score: 18/24=0.75).
The subjects were requested to touch the computer screen specifi-
cally on the location of their answer (e.g., thigh) and keep their index
finger in that position until the evaluation was carried out by the ex-
aminer. The evaluation was performed with the help of the yellow and
red rectangles, as described above. The rectangles appeared on the
screen by a button press of the examiner, while the subjects were asked
not to move and to keep their index finger at the location of their an-
swer.
2.4. Data analyses
All statistical analyses were performed with the “Statistical Package
for the Social Sciences” software (IBM SPSS Version 22.0 for Windows).
A repeated-measures ANOVA was calculated to assess the (differential)
effects of the two pointing tasks on the patients' performance. Since the
healthy control subjects performed the task “at ceiling” (i.e., without
any error in either task), the data violated the normal distribution re-
quirements for an ANOVA. Accordingly, the healthy control subjects’
data were not included in the ANOVA. As a deficient BSD contributes
mainly to apraxic end-position errors in imitation, we focused our
analyses on those ten apraxic patients who showed end-position errors
in imitation in the current apraxia assessment (i.e., Cologne Apraxia
H.S. Dafsari, et al.
Screening, KAS). Therefore, we computed a 2 × 2 repeated-measures
ANOVA for the relative performance scores with the within-subject
factor TASK (body versus object part pointing task) and the between-
subject factor GROUP (LH stroke patients with imitation apraxia
[n=10], LH stroke patients without apraxia [n=15]). Results are re-
ported at a significance level of p < 0.05.
Furthermore, correlation analyses between the apraxia test scores
(i.e., KAS total score and sub-scores) and the scores of the two pointing
tasks were performed for the same patient sample included in the
ANOVA (n=25, i.e., the LH stroke patients with imitation apraxia
[n=10] and the LH stroke patients without apraxia [n=15]).
2.5. Lesion mapping and analyses
Lesion mapping was based on clinical imaging by CT (n=6) or MRI
(n=20). For one of the 27 patients (haed1109w) no imaging suitable
for lesion mapping was available since the initial CT scan showed no
infarct demarcation despite persistent neurological/neuropsychological
deficits. Note, however, that the pattern of behavioural results was si-
milar when the patient haed1109w was excluded from the analyses.
Time from symptom onset to clinical imaging was on average 2.7 days
(standard deviation (SD) 5.6; range 0–26 days).
Using the MRIcron software (http://people.cas.sc.edu/rorden/
mricron/index.html), the investigator (HSD) manually copied the le-
sions to a T1-weighted template brain (ch2.nii). The lesion mapping
was double-checked by two further investigators (AD & PHW); all in-
vestigators had to agree on lesion location and extent. At the time of
mapping, the two additional investigators (AD, PHW) were blind re-
garding the test performance of a given patient (P.H. Weiss et al.,
2016a). Neuroanatomic localisation of lesion sites was performed using
the anatomy toolbox in SPM (Eickhoff et al., 2005).
Voxel-based lesion symptom mapping (VLSM) was employed for
statistical lesion analyses (Bates et al., 2003). VLSM was used to analyse
the relationship between lesion site and apraxia severity (oper-
ationalized by the KAS total score) as well as between lesion site and
BSD deficits (operationalized as the individual difference score of the
body versus object pointing task). For this difference score, the relative
performance scores of the object pointing task were subtracted from the
relative performance scores of the body pointing task in each patient.
Only voxels damaged in at least 3 patients (i.e., ≥10% of all patients)
were tested in the VLSM analyses. The statistical threshold was set to
p < 0.05 (corrected for False Discovery Rate, FDR) except when noted
otherwise.
3. Results
3.1. Behavioural data
To investigate the hypothesised link between BSD disturbances and
apraxic end-position errors in imitation, we evaluated the relative
performance scores in the two pointing tasks between the LH stroke
patients with apraxic end-position errors in imitation (as assessed by
the KAS, n=10) and the LH stroke patients without apraxia (i.e., those
patients with an unremarkable KAS score, n=15) using a 2 × 2 re-
peated-measures ANOVA.
For the relative performance scores (see Fig. 3), the 2 × 2 repeated-
measures ANOVA with the within-subject factor TASK (body versus
object part pointing task) and the between-subject factor GROUP re-
vealed a tendency for the main effect of TASK (F(1,23)=3.12, p=0.091,
ηp2=.119), indicating a trend for higher relative performance scores in
the object pointing task (compared to the body part pointing task).
Furthermore, there was a significant main effect of GROUP (F (1,23)
=5.05, p < 0.035, ηp2=.180), with lower relative performance scores
in the LH stroke patients with imitation apraxia (compared to the LH
stroke patients without apraxia).
Importantly, the ANOVA revealed a significant interaction between
6
Neuropsychologia 133 (2019) 107150
Fig. 3. Mean relative performance scores of the three groups (healthy controls
[n=19]: white bars, patients without apraxia [n=15]: grey bars, patients with
imitation apraxia [n=10]: black bars) for the body (left side) and object (right
side) pointing tasks. Error bars indicate standard error of the mean (SEM). Note
that the SEM of the controls was 0.
TASK and GROUP (F (1,23)=5.34, p < 0.031, ηp2=.188). This sig-
nificant TASK by GROUP interaction resulted from the differentially
reduced relative performance score of the LH stroke patients with
imitation apraxia in the body pointing task (0.776, compared to their
relative performance score in the object pointing task: 0.889). In con-
trast, LH stroke patients without apraxia performed similarly in both
pointing tasks (relative performance scores: body part pointing task:
0.966, object part pointing task: 0.951).
Note that the LH stroke patients with imitation apraxia who suffered
from deficits in pointing to another person's body parts did also show
deficits in pointing to their own body parts when clinically assessed by
verbal command (Semenza and Goodglass, 1985). Due to the lack of a
formal assessment of pointing to one's body parts, the current study
could not differentiate BSD deficits related to one's body from those
related to other human bodies and whether these contribute to (imi-
tation) apraxia in a differential manner. In their seminal study,
Semenza and Goodglass (1985) used different conditions, one of which
(i.e., condition B: The subject points to body parts on a drawing of a
human figure on verbal command) resembled the current body part
pointing task. Notably, all examined patient groups of Semenza and
Goodglass performed similarly in condition B as in condition A (see
their Table 2 on page 166), in which the patients were asked to point to
their body parts on verbal command. Semenza and Goodglass collapsed
conditions A and B for the error analysis (see their Table 1 on page
165). Consequently, these authors concluded, “that a common factor
underlies success in identifying body parts under all conditions”.
Therefore, it can be assumed that this “common factor” (here termed
BSD) contributes to apraxic (imitation) deficits. Furthermore, the cur-
rent study adds to the findings of Semenza and Goodglass by including a
task that assessed pointing to object parts allowing for a direct com-
parison between body and object part tasks. Thereby, the current data
revealed a specific impairment in pointing to body parts (i.e., BSD
deficits) in the current LH stroke patients with apraxic end-position
errors in imitation.
Consistent with the more pronounced severity of aphasic deficits (as
assessed by the ACL-K see Table 1) in the apraxic patients, more items
were excluded due to naming deficits, when examining LH stroke pa-
tients with imitation apraxia compared to LH stroke patients without
apraxia. Importantly, the amount of excluded items was similar for both
H.S. Dafsari, et al.
pointing tasks across groups. For the LH stroke patients without
apraxia, the number of patients examined with the full set of items (i.e.,
20 items for the body part pointing task and 10 items for the object
pointing task) versus a reduced set of items due to naming deficits was
13 versus 2 for the body part pointing task and 14 versus 1 for the
object pointing task. Considering all apraxic LH stroke patients (n=12,
i.e., the 10 patients with apraxic end-position errors in imitation and
the two patients with selective pantomime apraxia), 7 apraxic patients
were examined with the full set of items, while 5 apraxic patients were
tested with a reduced item set for both pointing tasks (see
Supplementary Table S3).
The single subject data provided in the Supplementary Tables show
that BSD deficits are associated with apraxia at the group level. How-
ever, at the single patient level, we also observed dissociations between
the performances in the apraxia test and the pointing tasks (e.g., patient
amdi0503m is severely apraxic (and aphasic), but still achieves rea-
sonable relative scores of about 0.6 in both pointing tasks). Concerning
aphasia severity, different result patterns were observed. While patients
orro0324m and rakl1001m were severely aphasic (ACL-K-score of 0 and
9, respectively) and performed poorly in the body pointing task (re-
lative performance score in the body pointing task: 0.32 and 0.4, re-
spectively), patient lado0805w was also severely aphasic (ACL-K score
of 3), but performed well when pointing to body parts (relative per-
formance score in the body pointing task: 0.93). These result patterns
suggest that aphasic deficits observed in our study cannot solely explain
the current BSD deficits.
Correlation analyses (performed for the same patient sample that
was included in the ANOVA (n=25), i.e., the LH stroke patients with
imitation apraxia [n=10] and those without apraxia [n=15]) between
the apraxia test scores (i.e., KAS scores) and the scores of the two
pointing tasks revealed significant correlations between the relative
performance scores of the body part pointing task and the total KAS
score (rho=0.463, p < 0.05) as well as the KAS imitation sub-score
(rho=0.450, p < 0.05). Notably, the correlation between the relative
performance scores of the body part pointing task and the KAS panto-
mime sub-score revealed a non-significant trend only (rho=0.372,
p=0.07). In contrast, there were significant correlations between the
relative performance scores of the object part pointing task and the
total KAS score (rho=0.504, p < 0.05) as well as the KAS pantomime
sub-score (rho=0.552, p < 0.05), while the correlation between the
relative performance scores of the object part pointing task and the KAS
imitation sub-score revealed a non-significant trend (rho=0.381,
p=0.06). Therefore, the correlation pattern rather supports the notion
that BSD deficits (mainly) contribute to apraxic end-position errors in
imitation. However, it should be noted that the correlation results are
relatively weak and thus should be interpreted with caution.
3.2. Lesion analyses
Since the imaging data were available for all but one patient of the
current study, Fig. 4A shows the lesion overlay of the 26 LH stroke
patients included in the lesion analyses. The highest lesion overlap was
observed within the territory of the MCA, especially in the left middle
and superior temporal cortex and the inferior parietal cortex, i.e., an-
gular gyrus and supramarginal gyrus. In contrast, frontal and occipital
regions were affected to a lesser degree.
In Fig. 4B, the lesion analysis using voxel-based lesion-symptom
mapping (VLSM) for the total score of the Cologne Apraxia Screening
(KAS) is presented. Lesions to the middle and superior temporal gyrus,
the operculum, insula, temporal cortex, supramarginal gyrus, angular
gyrus, postcentral gyrus, and the centrally located white matter were
significantly associated with reduced KAS scores and thus the severity
of apraxic (pantomime and imitation) deficits (p < 0.05, FDR-cor-
rected). Notably, a very similar lesion pattern for the KAS was observed
in a recent study for a group of 44 patients with left hemisphere (LH)
stroke (Binder et al., 2017).
7
Neuropsychologia 133 (2019) 107150
The significant interaction between the two pointing tasks and the
factor GROUP (driven by the differentially reduced relative perfor-
mance scores of the apraxic LH stroke patients in the body versus object
part pointing tasks) constitutes the main finding of our study at the
behavioural level. Therefore, a further VLSM analysis was performed
with the individual difference scores that were computed by subtracting
the relative performance scores in the object pointing task from the
relative performance scores in the body pointing task in each patient. In
Fig. 4C, the lesion analysis (VLSM) with these individual difference
scores is presented (p < 0.05, uncorrected). Lesions associated with a
worse performance in the body pointing task (compared to the object
pointing task) were mainly found in the angular gyrus of the left in-
ferior parietal lobe. Further smaller lesion sites that showed a similar
association were located in the superior and middle temporal cortex.
4. Discussion
To examine the hypothesis that a deficient BSD contributes to
apraxic end-position errors in imitation, we developed a test for
quantitatively assessing deficits in pointing to body and object parts
that is clinically applicable to LH stroke patients and minimizes the
confounding effects of comorbid aphasia and a deficient body image
(i.e., “a lexical–semantic representation of the body including body part
names“ (Schwoebel and Coslett, 2005)). This test revealed that patients
with LH stroke and imitation apraxia are specifically impaired in
pointing to body (versus object) parts. Thus, they suffer from a deficient
body structural description (BSD). Within the lesion pattern causing
apraxic deficits, the specific deficits in pointing to body parts (i.e., BSD
deficits) were associated with lesions of the angular gyrus of the left
inferior parietal lobe. Data support the notion that apraxic end-position
errors in imitation are – at least in part – due to a deficient coding of the
position of human body parts, i.e., a deficient BSD.
To our knowledge, quantitative and clinically applicable assess-
ments of the body structural description (BSD, (Semenza, 1988;
Semenza and Goodglass, 1985)) or paradigms assessing the body image
(BI, (Cash et al., 2004)) are scarce. The current test procedure ensured
that the observed pointing deficits are not solely due to aphasic deficits
or a deficient BI since a pre-test for each item ensured that the subject
associated a given body part or object (part) with its name. This al-
lowed using a broad array of body and objects parts.
Regarding the complex definitions of body schema, body image, and
body structural description (BSD), we adopted for the current study the
definitions proposed by Schwoebel and Coslett (Schwoebel and Coslett,
2005). These authors consider body image to be „a lexical–semantic
representation of the body, including body part names, functions, and
relations with artefacts“. Accordingly, we operationalized deficits in the
body image as deficits in the lexical-semantic representation of body
parts assessed by naming the body parts. Thus, the procedure of ex-
cluding body part items from testing (if a given patient was unable to
name a particular body part item AND was unable to correctly point to
this body part after the patient was told the body part's name) mini-
mized the impact of aphasic deficits on the current pointing tasks.
Importantly, it also excluded a relevant influence of body image deficits
(operationalized as deficits in the lexical–semantic representation of the
body parts) on the performance in the body part pointing task.
Furthermore, the procedures for assessing body and object part
pointing were similar so that we could directly compare the respective
relative performance scores for both sub-tests and identify the specific
body part pointing deficits of the LH stroke patients with apraxic end-
position errors in imitation. Importantly, the current study, in which
aphasic deficits and deficits of the BI were controlled for, constitutes
one of the very few quantitative group studies on BSD deficits
(Schwoebel and Coslett, 2005; Semenza and Goodglass, 1985). Most
previous studies that carefully delineated BSD from body image (BI) or
body schema (BS) were case reports (Buxbaum and Coslett, 2001; Sirigu
et al., 1991).
H.S. Dafsari, et al. Neuropsychologia 133 (2019) 107150

Fig. 4. A. Lesion overlay of all studied LH stroke patients for whom suitable imaging data was available (n=26). For one of the tested 27 patients no imaging data
suitable for lesion mapping was available. Colour shades represent the number of overlapping lesions. The highest overlap of stroke lesions was observed for the
territory of the middle cerebral artery (MCA). B. Lesion analysis adopting voxel-based lesion mapping (VLSM) of the KAS total scores (n=26). Lesions to the middle
and superior temporal gyrus, the operculum, insula, Heschl gyrus, supramarginal gyrus, angular gyrus, postcentral gyrus, and the centrally located white matter were
significantly associated with reduced KAS scores and thus the severity of apraxic (pantomime and imitation) deficits. Results are displayed at a threshold of
p < 0.05, corrected for False Discovery Rate (FDR). C. Lesion analysis (VLSM) for the differential scores of the body versus object pointing tasks (n=26, un-
corrected). Lesions associated with a worse performance in the body pointing task (compared to the object pointing task) were mainly found in the angular gyrus of
the left inferior parietal lobe. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

The relative performance scores in the body part pointing tasks al-
lowed us to draw conclusions regarding the severity of the BSD deficit.
Our results showed clear and significant differences in the pointing task
performances between the patient groups: patients with imitation
apraxia scored significantly worse in the body pointing tasks than non-
apraxic patients, while the performances of the two groups were similar
in the object pointing task. Thus, imitation apraxia was a relevant
predictor for the performance in the pointing task involving human
body parts, but not in the pointing task with object parts. Hence, LH
stroke patients with apraxic end-position errors in imitation seem to
have a body-selective pointing deficit. As the performance in the body
part pointing task serves as a measure of the severity of a BSD deficit
(controlled for general task demands by the object part pointing task),
the current data suggest that LH stroke patients with apraxic end-po-
sition errors in imitation have a specific and more severe BSD deficit
than non-apraxic LH stroke patients.
With respect to the lesion analyses with VLSM in the current sample
of LH stroke patients (n=26), apraxic deficits in imitation and panto-
mime (as assessed by the KAS) were mainly caused by lesions of the
inferior parietal cortex (supramarginal gyrus, SMG; angular gyrus, AG),
the temporal cortex, and the postcentral gyrus. This apraxic lesion
pattern is consistent with previous findings (Dovern et al., 2011;
Haaland et al., 2000; Hoeren et al., 2014; Niessen et al., 2014) and very
similar to the lesion pattern reported in a previous study that also used
the KAS to test for apraxia (Binder et al., 2017).
BSD deficits (i.e., differential deficits in pointing to body parts
versus object parts) were predominantly associated with lesions of the
angular gyrus as part of the inferior parietal lobe. Therefore, within the
broader lesions causing apraxia per se, lesions of the angular gyrus led
to specific BSD deficits in the current apraxic LH stroke patients.
However, it should be noted that the VLSM with the difference score
body part versus object part pointing did not survive thresholds cor-
rected for multiple comparisons, while the VLSM with the KAS-scores
did survive correction for False Discovery Rate (FDR).
The angular gyrus has been associated with different deficits, such
as “speech comprehension deficits, finger agnosia, spatial disorienta-
tion, acalculia, agraphia, and dementia” (Seghier, 2013). Note that
Goldenberg and Karnath (2006) found that their patients with selec-
tively disturbed imitation of hand postures exhibited a lesion overlap in
the inferior parietal lobule (IPL). These authors argued that especially
hand posture imitation draws on body part coding, a notion consistent
with the results of the current quantitative lesion analysis. The current
test procedures controlled for the effect of aphasia, which is reflected in
the lesion pattern. While BSD deficits in the current LH stroke patients
are associated with inferior parietal cortex lesions, lesions to the inferior
frontal gyrus (Brodmann Area 44) led to combined apraxic and aphasic
deficits after LH stroke (P. H. Weiss et al., 2016). Consistent with the
results of our structural lesion analysis, a functional imaging study that
investigated the neural mechanisms underlying the BSD by adopting a
task of pointing to human body parts (compared to pointing to body

8
H.S. Dafsari, et al.
parts of dogs) also activated the inferior parietal cortex, in particular
the (left) angular gyrus (Felician et al., 2009).
4.1. Limitations
While there has been considerable progress regarding lesion map-
ping methods (H.-O. Karnath et al., 2018; Rorden and Karnath, 2004),
some limitations remain or are inherent to the method. One confound is
the time since stroke. We used clinical imaging by CT (n=6) or MRI
(n=20) for lesion mapping. As a result, the interval between symptom
onset and the acquisition of the images used was, on average, 2.7 days
(standard deviation (SD) 5.6; range 0–26 days). Thus, we used rather
acute images for lesion mapping (H–O. Karnath and Rennig, 2017).
Notably, CT was only used for lesion mapping when there was a de-
marcated lesion. Nevertheless, the delineation of the exact lesion extent
may have been more difficult than in cases in which MR images were
available. However, the manual tracing technique is still considered to
be best suited for exact lesion delineation (Wilke et al., 2011).
Given the variability in terms of lesion volume, lesion analyses can
be performed with co-varying out lesion volume. However, the dis-
advantage of this method is that it only has low statistical power. In
fact, “there were no significant voxels for the logistic regression ana-
lyses for sub- and total pantomime and imitation scores when lesion
size was added as a covariate” in a lesion mapping study of 96 LH stroke
patients (page 2803 of (Hoeren et al., 2014)). Consistent with this ob-
servation, no voxel was found in the current VSLM analyses when we
included lesion volume as a covariate.
In addition to the above-mentioned aspects, there are also issues
related to diaschisis (e.g., (Carrera and Tononi, 2014), (Grefkes and
Fink, 2014). Therefore, structural lesion mapping only in part captures
the functional consequences of stroke lesions.
5. Future directions
The current study constitutes one of the very few group studies ex-
amining BSD deficits in neurological patients and the first quantitative
lesion study on this topic. Note that our study could not comprehen-
sively address all interesting issues concerning the relationship between
BSD and apraxic deficits. Future studies on this topic should explore in
more detail whether a deficient BSD rather contributes to apraxic def-
icits in movements directed towards the body (e.g., combing one's hair)
than to apraxic deficits in movements directed away from the body
(e.g., cutting a slice of bread). It has been proposed that especially
deficits in imitating meaningless (ML) gestures (compared to mean-
ingful (MF) gestures) are related to deficient “body part coding”
(Goldenberg and Karnath, 2006). Accordingly, it is worth to include the
meaning of a gesture as a further dimension in future studies on the
relationship between BSD and apraxia to elucidate whether the
meaning of a gesture modulates the effect of a deficient BSD on apraxic
imitation deficits (Achilles et al., 2016; Goldenberg and Hagmann,
1997).
6. Conclusion
We have successfully developed a short and clinically applicable test
for quantitatively assessing deficits caused by a disturbed BSD in pa-
tients suffering from LH stroke. LH stroke patients with apraxic end-
position errors in imitation showed a differential deficit in pointing to
body (versus object) parts. The specific body pointing deficits were
mainly associated with angular gyrus lesions. Thus, our data support
the notion that apraxic end-position errors in imitation are – at least in
part – due to a deficient coding of the position of human body parts.
Disclosures
The authors report no disclosures.
9
Neuropsychologia 133 (2019) 107150
CRediT authorship contribution statement
Hormos Salimi Dafsari: Conceptualization, Data curation, Formal
analysis, Writing - original draft. Anna Dovern: Data curation, Formal
analysis. Gereon R. Fink: Conceptualization, Writing - original draft.
Peter H. Weiss: Conceptualization, Formal analysis, Writing - original
draft.
Acknowledgements
The authors would like to thank their colleagues at Cognitive
Neuroscience, Institute of Neuroscience and Medicine (INM-3),
Research Centre Jülich. We also thank Charlotte Schömig for testing
some of the stroke patients and Jan-Michael Werner and Daniel Bettin
for photo-modelling. HSD was supported by the Köln Fortune Program
of the Faculty of Medicine, University of Cologne (107/2012). GRF
gratefully acknowledges financial support by the Marga and Walter Boll
Foundation.
Appendix A. Supplementary data
Supplementary data to this article can be found online at https://
doi.org/10.1016/j.neuropsychologia.2019.107150.
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