-ergamon Neuropsycholo~lia,Vol. 33, No. t, pp. 63-72, 1995
1-" Elsevier Science Ltd
Printed in Great Britain
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IMITATING GESTURES AND MANIPULATING A MANNIKIN--
THE REPRESENTATION OF THE HUMAN BODY IN
IDEOMOTOR APRAXIA
GEORG GOLDENBERG
Neurologisches Krankenhaus Rosenhiigel, Riedelgasse 5, A-1130 Wien, Austria
(Received 17 June 1994; accepted 20 August 1994)
Abstract--Imitation of meaningless gestures was examined in patients with left brain damage (LBD),
right brain damage (RBD) and controls. In addition to imitation on the own body, patients were
asked to replicate the gestures on a life-sized mannikin. Manual dexterity was assessed by
manipulation of beads, and general visuospatial abilities by block-design. LBD patients who
displayed apraxia when imitating gestures on their own bodies scored dramatically worse than any
other group when imitation was assessed on the mannikin. By contrast, on block-design and
manipulation of beads patients with RBD were inferior not only to LBD patients without apraxia but
also to apractic patients. Analysis of CT scans revealed that apraxia occurred with frontal, parietal
and deep lesions, and that the impairment on the manipulation of the mannikin was present
regardless of lesion site. The results support the contention that the basic deficit underlying impaired
imitation of meaningless gestures in apraxia is to be sought at a conceptual level. Possibly, patients
with apraxia are not able to evoke and represent conceptual knowledge about the human body which
is necessary for performing the apparently simple task of imitating gestures.
INTRODUCTION
Around the turn of the century Liepmann conducted the first systematicgroup study of limb
apraxia 1,-21].He examined performance of symbolic gestures in normal controls, patients
with left brain damage and patients with right brain damage. Patients with brain damage
demonstrated the gestures with the hand ipsilateral to the lesion. Only patients with left
hemispheric lesions committed apractic errors. Most patients with apraxia had aphasia too,
but performance of gestures was faulty even when the correct gestures were demonstrated
and the patients were only required to imitate them. To Liepmann, impaired imitation of
gestures proved that apraxia cannot be referred to being a sequel of aphasia or "asymbolia"
[9]. He stated that errors at the imitation ofgestures testify"that there is not only a weakness
of memory in its common sense, that is, an inexactness of the spatial-temporal image (ofthe
movement), but a difficultyor inability to direct the members of the left hand according to
certain spatial conceptions" I-21,p. 26]. Liepmann introduced the term "ideomotor apraxia"
to denote the inability to translate a correct idea of the intended movement into an
appropriate motor act. The view that the basic deficit in ideomotor apraxia concerns the
execution rather than the evocation of gestures received support later studies which
demonstrated that in patients with ideomotor apraxia imitation of meaningless and novel
movements is as faulty as that of symbolic gestures I-7,20, 23, 28].
The straightforward conclusion that the left hemisphere is dominant for the control of any
63
64 G. GOLDENBERG
skilled movements of either hand is, however, contradicted by the clinical experience that
there is no general clumsiness of the left hand in patients with apraxia. On the contrary, a
striking dissociation between grossly impaired performance in apraxia testing and
apparently normal skill in many other situations is a hallmark of the clinical presentation of
ideomotor apraxia [10, 13, 14, 17, 21, 24, 25]. The widely accepted definition of apraxia as a
disorder of skilled movement not caused by weakness, akinesia, deafferentation, abnormal
tone or posture, and movement disorders such as tremors or chorea [11, 14] implies that
there are situations in which the apractic hand is moved with completely normal skill.
Otherwise, the exclusion ofother motor disorders which is crucial to the diagnosis ofapraxia
could never be verified.
An idea which could account for deficient imitation of meaningless gestures without
postulating a general motor dominance of the left hemisphere is, that the basic deficit in
ideomotor apraxia concerns the ability to code and comprehend movements in relation to
own body [4, 23, 29]. Both symbolic and meaningless gestures are aimed at producing
explicitly defined positions or movements of body parts. By contrast, most movements
outside the testing situation are aimed at and determined by external targets and are
therefore spared from ideomotor apraxia, although they may be vulnerable to ideational
apraxia. The terms "'dyssomatognosiespatiale"[4, 23] and "reflexive apraxia" [29] have been
proposed to characterize this conception of ideomotor apraxia.
The purpose ofthe present study was to test the hypothesis that faultyapprehension ofthe
movements and configuration of body parts underlies impaired imitation of meaningless
movements in ideomotor apraxia. Implicit in the experimental design is the assumption that
the basic disorder affects a general concept of the human body whose validity does not
depend on whether a person's own body is concerned or not. It was hypothesizedthat such a
conceptual disturbance would show up when postures of the hand are to be replicated with
the hand of a mannikin rather than with one's own hand, although the motor demands of
manipulating a mannikin are fundamentallydifferentfrom those of performing the postures
on oneself. To rule out the possibility that a general deficiency ofmotor execution affects any
skilled motor performance, a test of motor skill which required the manipulation of beads
was included in the experimental design. It was hypothesized that a disorder of motor
execution, which manifests itselfin tasks posing motor demands as differing in imitation of
gestures and manipulation of a mannikin, would also show up in another test of manual
dexterity. To explore whether a faulty apprehension of spatial relationships between body
parts might be an expression of a more general disturbance of visuospatial processing, the
comprehension and manipulation of spatial relationships outside the human body was
assessed by block design. As block design demands motor manipulation of blocks, this test
served as a further control for a general disturbance of motor execution.
METHOD
Imitation of meaningless gestures
(a) On oneself: The patients were asked to imitate l0 meaningless gestures of the hand (see Fig. 1) The examiner
sat in front of the patient and demonstrated the gesture "like a mirror", that is, ifthe patients used their left hand, the
examiner demonstrated with the right hand and vice versa. Imitation started immediately after each presentation.
For each posture, 2 points were credited when imitation was correct after the first presentation. Otherwise, the
demonstration was repeated and 1 point was given for a correct imitation on second trial.
(b) On a mannikin: The patients were seated opposite a life-sized wooden mannikin whose arms and hands could
be moved like that of a human being. They were asked to replicate with one hand of the mannikin gestures
demonstrated by the examiner. The examiner sat besides the mannikin and demonstrated the gestures "like the
THE HUMAN BODY IN IDEOMOTOR APRAXIA 65
Fig. 1. Ten meaningless gestures of the hand for imitation.
mannikin", that is, if the patient manipulated the mannikin's left hand, the examiner demonstrated with the left hand
and vice versa. The gestures used, the course of examination and the criteria for scoring were the same as with the
imitation on one's own body. To ensure understanding of the instruction, imitation of a gesture not used in the
examination was demonstrated in the instruction, and if the first item of the examination was failed on both trials,
correct performance of this gesture was demonstrated too.
Manipulation of beads
Patients were asked to take with one hand three beads from three vertical rods and to stick them on three other
rods. They were not allowed to collect and transpose the beads one after another, but had to collect all three beads in
the hand before beginning to stick them on the target rods. The rods were aligned in a frontal plane. Patients who
used their left hand moved the beads from the left set of three sticks to the right one, and vice versa. Between trials,
the hand rested on a mark in front of the middle of the device. After two successful practice trials, 10 trials were run,
and the time from leaving the starting point until the delivery of the last bead was measured with a stopwatch. Ifa
bead fell out of the hand, the trial was repeated. The mean time of the 10 trials was taken for the statistical evaluation.
In this task, manual dexterity is challenged when one bead has to be transferred between hand and rod while at the
same time one or two beads are carried within the hand. The hand has to be divided into two functional
compartments, one for carrying beads and one for moving beads from and to the rod and the beads have to be moved
between these two compartments. As a further difficulty, the boring of the beads has to be aligned exactly with the
position and the direction of the rod when the bead is stuck on the rod.
Block design
The WAIS--R subtest block design was administered in the usual way. As a modification, testing was not
interrupted when the prescribed time limits had expired. If a patient arrived at the correct solution after that time.
one point was subtracted from the minumum score. Raw scores were used for statistical evaluation.
Token-test
All patients with left hemisphere damage were administered the German version of the Token Test [16]. The raw
number of correct responses was scored.
Procedureof testing
Patients with brain damage used the hand ipsilateral to the lesion for imitation of gestures, pantomime of object
use and manipulation of beads. They moved the same hand of the mannikin, but were allowed to use both of their
hands for the manipulation of the mannikin ifthis was not prevented by hemiplegia. Controls used either the right or
the left hand for all tests including the manipulation of the mannikin.
Subjects
Eighty-five right-handed subjects were examined. There were 35 patients with left brain damage (LBD), 20
patients with right brain damage (RBD), and 30 controls without any evidence for brain damage. All patients with
brain damage had suffered a single, unilateral cerebrovascular accident (CVA), and all LBD patients had aphasia.
66 G. GOLDENBERG
RESULTS
No significant differences on any measure were found between controls who had used their
left hand and those who had used their right hand. These two groups were therefore brought
together to make one control group.
Figure 2 shows the scores on imitiation of meaningless gestures. In controls, there was a
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Fig. 2. Resultsof apraxia testing.
clear ceiling effect. Ninety per cent of the control patients obtained the maximum score of 20
and only one control scored as low as 2 points below the maximum. The distribution of
scores of RBD patients had a similar but somewhat less steep bias and the worst score was 16.
Patients with LBD can be divided into two groups: 20 of them scored within a range of 17-20,
that is, as well as RBD patients and very similar to controls, while 15 scored between 2 and
14. The latter group was considered as being apractic, and further comparisons were
conducted between apractic patients, LBD patients without apraxia. RBD patients, and
controls. By this division, apraxia was distinguished from the mild impairment of imitation
which can also be found in some patients with RBD [7] and was investigated as an exclusive
symptom of LBD damage.
Table 1 shows the clinical and demographic data of the four groups. While the mean age of
the whole LBD group was very similar to that of the other groups (57.8 + 14.7), the division
of LBD patients in those with and without apraxia resulted in a significant difference of age
across groups, as patients with apraxia were on average older than those without. Analyses of
covariance with group as main factor and age as covariate showed a significant effect of age
only on the speed of manipulation of beads I-F (1, 68)= 15.0, P<0.0005].
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Table 2 presents the results of the analysis of covariance for manipulation of beads and of
analyses of variance or t-tests, respectively, for the remainder of the experimental tests.
Apractic patients scored dramatically worse than any other group when imitation of
postures was assessed on the mannikin. Compared to LBD patients without apraxia, they
also did less well on block design and on the Token Test and were slower in the manipulation
of beads. However, with block design and the manipulation of beads, RBD patients had the
greatest difficulty. On block design, RBD patients scored significantly lower than LBD
patients with or without apraxia. On manipulation of beads RBD patients were slower than
any of the other groups, although on post-hoctesting they differed only from controls. From
observation oftheir performance it appeared that the RBD patients had particular problems
with the exact alignment ofthe bead's boring to the direction of the rods. When imitation on
the mannikin was compared among LBD patients with and without apraxia in an analysis of
covariance with results of the Token Test, there was a significant effect of the Token Test
[F(1, 31)=4.29, P=0.047] but the difference between both groups remained highly
significant [F (1, 31) = 24.77, P < 0.0005].
CT scans were available from all but one brain damaged patients. Lesions were classified
as to whether they encroached upon the frontal, the insular, the temporal or the parietal
cortex, the basal ganglia, the thalamus, and the subcortical white matter. As an index of
lesion size, the number of affected regions was summed up (Table 3).
The number of affected regions was larger in patients with apraxia than in both other
groups. Furthermore, there were significant differences in the frequency of frontal and
parietal lesions. The frequency of frontal lesions was lower in LBD patients without apraxia
but did not markedly differ between apractic patients and patients with RBD. Parietal
lesions were more common in apractic patients than in both other groups. There were only
two apractic patients in whom neither the parietal nor the frontal cortex was damaged. Both
had deep lesions which affected the basal ganglia and white matter in one, and white matter
only in the other. These patients scored 4 and 7 which is in the severely defective range, with
the mannikin. There were three apractic patients in whom the lesion affected the frontal
cortex and spared the parietal cortex, and seven patients with the reverse dissociation. The
mean score on the mannikin was 10.7 (S.D. 5.9) for the patients with frontal lesions and 7.3
(S.D. 4.0) for those with parietal lesions. This difference is statistically insignificant (t = 1.1,
d.f. = 8, P > 0.2). A similar slight difference in favour of the patients with frontal lesions was
present for imitation on own body (patients with frontallesions: mean 11.7,S.D. 2.5; patients
with parietal lesions: mean 9.6, S.D. 3.5).
DISCUSSION
The hypothesis that motivated that study predicted that faulty apprehension of spatial
relationships between body parts would manifest itselfnot only in imitation on oneself but
also in imitation on a mannikin. The results are in accordance with this prediction. However,
the associated occurrence of two deficits does not prove that they result from a common
functional disturbance. Alternatively, the association may stem from anatomical contiguity
of brain regions responsible for each of the functions and from the effect of lesion size. A
larger lesion within an area devoted to one of the functions will not only cause a more severe
deficitofthis function but also have a greater chance to encroach upon neighbouring regions
subserving basically different functions. In the present study, this caveat certainly applies to
the comparison between LBD patients with and without apraxia. Patients with apraxia had
THE HUMAN BODY IN IDEOMOTOR APRAXIA 69
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larger lesions, and they did worse than patients without apraxia not only on imitation on the
mannikin, but also on the Token Test, block design and manipulation of beads, even iffor the
latter two measures the differences were not statistically significant.
The analysis of the apractic patients' lesions did, however, not disclose any evidence that
extension of the lesion into a critical region of the left hemisphere caused impaired imitation on
the mannikin. In accord with previous studies we found apraxia to be present in patients with
parietal lesions, frontal lesions and deep lesions [2, 19]. Imitation on the mannikin was equally
defectivein all three groups of patients. To sustain the assumption that the association between
impaired imitation on the body and on the mannikin was caused by anatomical contiguity of
the cerebral systems supporting both tasks, one would have to assume that both systems are
distributed in a very similar fashion throughout the left hemisphere. A common basic
functional disturbance is a more convincing explanation for the associated occurrence of
impaired imitation on the mannikin and on the patient's own body.
If we accept a common basic disturbance as the source of errors in imitation on the
patient's own body and on the mannikin, this does not necessarily prove that the disturbance
concerns the apprehension of spatial relationships between body parts. Alternatively, it may
stem from a disorder of motor execution which affects the execution of any skilled movement
or from a pervasive visuospatial impairment which affects the apprehension of any spatial
relationships. Both of these possibilities are made unlikely by a comparison between apractic
patients and patients with RBD.
Although the lesions of RBD patients happened to be on average smaller than those of
apractic patients, RBD patients did worse than apractic patients on block design and were
slower in the manipulation of beads. The latter difference failed to reach statistical
significance, but is nonetheless in unequivocal contrast to the superior performance of RBD
patients on both imitation tasks. Imitation of the mannikin, block design and manipulation
of beads require the manipulation of external objects under visual feedback control. It would
appear that the demands on motor execution are more similar among them than between
imitation on the mannikin and imitation on own body, where no external object is involved,
and where the target positions are largely hidden from view (see Fig. 1). At the same time, the
opposite group differences of block design and imitation on the mannikin speak against a
general weakness of visuospatial processing as being the cause of impaired imitation on the
mannikin.
In sum, it does appear that impaired imitation of movements on a mannikin by apractic
patients can neither be dismissed as being due to a spurious association of deficits caused by
anatomical contiguity, nor to a general disturbance of the execution of any skilled motor
action, nor to a pervasive impairment of visuospatial processing. It does seem worthwhile to
consider in more detail the hypothesis that defective apprehension of the configuration of
body parts underlies impaired imitation of movements in apraxia.
Defective imitation of gestures on oneself and on a mannikin cannot be ascribed to the
disturbance of a personal "body schema" which integrates information about the extension
and position of one's own body [5, 29]. The need to evaluate the position and configuration
of one's own body is implicit in the planning of any goal directed motor action [3, 18]. Body
parts are moved relative to other body parts, and external targets could not be reached ifthe
initial position of the body and its parts were not taken into account. A disturbance of the
implicit calculation of the position and configuration of one's own body would manifest itself
in misreaching and insecurity of all movements to external objects, and would have affected
not only manipulation of the mannikin but also manipulation of the beads and the blocks.
THE HUMAN BODY IN IDEOMOTOR APRAXIA 71
The common disturbance of imitation on oneself and on the mannikin can neither be
explained by a lack of explicit awareness of the position and configuration of one's body.
Explicit awareness of the position and configuration of oneself is rarely called on when
movements are directed to external objects. Consequently, if awareness is defective of only
one's own body's configuration, this would lead to errors when gestures are demonstrated on
oneself but not when they are demonstrated on a mannikin. If there is a common source to
errors in imitation on oneself and on the mannikin, it must reside in the evocation and
application of a general concept of the human body which applies regardless of whether one's
own body is concerned or not.
The need to conceive one's own body asjust one instance of a general concept of the human
body is inherent to the task of imitating gestures, even if probed on oneself. Imitation of
gestures has been said to test the integrity of a direct route from visual perception to motor
control 1-26, 27], but on closer scrutiny it involves intermediate steps of considerable
complexity. If the examiner sits opposite to the patient, the required movement is a mirror
image of the perceived one. If, for another example, the examiner is taller than the patient,
exact reproduction of their movement would overshoot the target on the patient's body.
Studies in the physiology of motor control I-3, 18] have demonstrated that planning of limb
movements specifies target positions rather than movement paths. When gestures are to be
imitated the target positions are not indicated directly but have to be inferred from a mental
transposition of the demonstrated movement to oneself, and this transposition has to
abstract from accidental determinants of the perceived movements as are, for example, the
size or position of the demonstrating person. A feasible way to achieve this translation would
be to conceptualize the perceived movements in their relationship to a general concept of the
human body which applies irrespectively of the size and position of the body and
irrespectively of whether the body belongs to the examiner, the patient, or a mannikin. In a
way, the patient's body is then used as a mannikin on which the generally valid features of the
movement are demonstrated. The apparently meaningless movements do have meaning
insofar as they represent conceptual knowledge about the human body.
This interpretation does not necessarily imply that conceptual knowledge about the
human body is a distinct category of knowledge which is affected selectively in ideomotor
apraxia. It may be that the human body isjust one instance of a multi-part mechanical object,
and that the basic disorder concerns the apprehension of relationships between the
functionally significant parts of such objects. Possibly, the crucial similarity between the
wooden mannikin and the patient's body does not reside in their human shape but in the fact
that both are multi-part mechanical objects. The present study did not test the manipulation
of other objects with a mechanical complexity comparable to that of the human body. It may
be that apractic patients would have had as many difficulties with them as they had with the
mannikin.
Regardless of whether the basic disturbance concerns the spatial relationships between
body parts or, more generally, the relationships between significant parts of multi-part
objects, it resides at a conceptual level. The inability to evoke conceptual knowledge
necessary for the planning of certain motor tasks has already been recognized as underlying
other manifestations of limb apraxia. Faulty use of tools and simple objects has been related
to the unavailability of knowledge about their appropriate use I-6, 22, 23, 26-1, and faulty
demonstration of symbolic gestures to the inability to evoke the appropriate shape of
gestures when given their meaning [1, 8, 9, 12, 15,1. If faulty imitation of movements is
accepted as a conceptual disturbance too, none of the manifestations of limb apraxia is left to
72 G. GOLDENBERG
correspond to a deficit of motor execution, that is, to the inability to translate a correct
concept of the intended movement into an appropriate motor act.
Acknowledoements--The study was supported by project 8910M of the Austrian Science Foundation. Sonja
Hagman and Joseph Spatt assisted in the examination of patients. Marie-Noel Metz-Lutz kindly provided a copy of
Moorlaas' thesis on apraxia. I want to thank two anonymous reviewers for perspicacious comments on a previous
version of the paper.
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