Exp Brain Res (2004) 156: 399–408
DOI 10.1007/s00221-003-1746-4

RESEARCH ARTICLES

L. Pisella . C. Michel . H. Gréa . C. Tilikete .
A. Vighetto . Y. Rossetti

Preserved prism adaptation in bilateral optic ataxia: strategic
versus adaptive reaction to prisms
Received: 20 June 2002 / Accepted: 30 September 2003 / Published online: 5 May 2004
# Springer-Verlag 2004

Abstract To date the anatomical substrate(s) of prism
adaptation remain(s) particularly debated, with two main
candidates emerging from the literature: the posterior
parietal cortex (PPC) and the cerebellum. The functional
processes involved in the acquisition of the adaptive
aftereffects also remain largely unknown. The main result
shown here is that a patient with a bilateral optic ataxia can
adapt to an optical deviation, which allows us to make a
step forward on these two issues. First, it demonstrates that
the corresponding part of the PPC is not a necessary
substrate for prism adaptation. Second, since this patient
exhibits deficit for fast visuo-motor guidance, it provides
direct evidence for a dissociation between on-line visuomotor control and visuo-motor plasticity. Since the
intermanual transfer rate of adaptation is larger in this
patient than in control subjects, the PPC may still have an
influence on adaptation under normal conditions. We
propose a model of the relative contribution of the PPC
and the cerebellum during prism exposure, associating
these two structures with the two interacting behavioural
components of prism adaptation described by previous
psychophysical experiments: the strategic component
would be linked to the PPC and the adaptive component
to the cerebellum. In this model, the strategic component
enters in conflict with the development and the generalisation of the adaptive aftereffects. This idea is compatible
with the fact that a lesion of the PPC increases the transfer
rate and the generalisation of the adaptation, as is also
observed in unilateral neglect.
Keywords Prism adaptation . Optic ataxia . Posterior
parietal cortex . Cerebellum . Intermanual transfer . Visuomotor control
L. Pisella . C. Michel . H. Gréa . C. Tilikete . A. Vighetto .
Y. Rossetti (*)
Espace et Action, Institut National de la Santé et de la
Recherche Médicale, Unité 534,
16 avenue Lépine, Case 13,
69676 Bron, France
e-mail: rossetti@lyon.inserm.fr

Introduction
Prism adaptation has been widely used since the end of the
nineteenth century as a paradigm of visuo-motor shortterm plasticity. But there have been recent developments
in four main domains of investigation: the decalibration of
visual and proprioceptive inputs (e.g. Rossetti et al. 1993);
the distinction between strategic control vs. realignment
components of adaptation (e.g. Redding and Wallace
1996; Clower and Boussaoud 2000); the generalisation
capacity of the adaptive system (Welch et al. 1993;
Bedford 1993; Imamizu and Shimojo 1995; Imamizu et al.
1995; Ghahramani et al. 1996; Ghahramani and Wolpert
1997); and neurological rehabilitation (Rossetti et al.
1998; Tilikete et al. 2001; Pisella et al. 2002; reviews:
Rossetti and Rode 2002; Rode et al. 2003; Mattingley
2002). These recent results have raised an interest in the
mechanisms and the structures involved in prism adaptation.
Wedge-prisms produce a lateral shift of the visual field
so that any visual target appears at a displaced position.
Adaptation to such an optical shift is acquired during a set
of successive pointing movements. The initial movement
approaches the virtual position of the target, but within
approximately ten subsequent pointing movements, the
pointing error rapidly decreases so that subjects can
already point towards the actual target position (e.g.
Weiner et al. 1983; Rossetti et al. 1993; Welch et al. 1993).
However, this does not mean that plasticity has been
developed at this stage: flexibility of motor execution
allows subjects to point precisely towards the target by
making corrective movements. In the case of an obvious
prismatic shift, a strategic modification of the initial
direction of the pointing movement (Rossetti et al. 1993)
also allows subjects to reach precisely the actual target
position. This contribution to error reduction has been
initially ascribed to a strategic component of the adaptation process by Weiner et al. (1983) (“cognitive correction”), and then by Redding and Wallace (1996) (“strategic
perceptual-motor control”). Further pointing movements
are required to reinforce the adaptation and obtain robust

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negative aftereffects after removal of the prisms, that are
characteristic of the adaptive component (“true adaptation”: Weiner et al. 1983; “adaptive spatial alignment”:
Redding and Wallace 1996). The global reaction to the
visual displacement consists of strategic corrections
(contributing to error reduction) and adaptive realignment
(contributing to both error reduction and aftereffects)
developing simultaneously and interacting between each
other (Redding and Wallace 1993, 1996, 2002).
Strikingly, the literature still remains controversial about
the neural structures involved in prism adaptation. On the
one hand, neuropsychological evidence historically suggested that only cerebellar patients are impaired in prism
adaptation (e.g. Weiner et al. 1983; review: Jeannerod and
Rossetti 1993). A recent lesion study in monkeys (Baizer
et al. 1999) confirmed that a focal lesion of the cerebellum
(especially of the vermis) can abolish the ability to adapt to
prisms. On the other hand, recent imaging data (Clower et
al. 1996) have suggested that the human posterior parietal
cortex (contralateral to the adapted arm) is the only area
activated during prism exposure.1There is no obvious
reason why one of these two structures should play an
exclusive role in the reaction to wearing prismatic goggles.
One may rather propose that each structure is specialised
for a given aspect of prism adaptation, with their
interconnections accounting for the functional interactions
described between the two components of prism adaptation. In the following, therefore, we will describe (1) the
possible role of the cerebellum, (2) the possible role of the
PPC and (3) a simple model integrating the respective
roles of these two structures in the two behavioural
components of prism adaptation.
1. Let us first summarise the functional properties of the
cerebellar system. Studies involving human brain
lesion, imaging and neural modelling have stressed
the importance of the cerebellum for short-term and
long-term visuo-motor learning (e.g. Gilbert and Thach
1977; Ito 1989; Friston et al 1992; Martin et al. 1996;
Imamizu et al. 2000), reflex adaptation (Kawato and
Gomi 1992) and saccadic adaptation (Desmurget et al.
1998). In addition, the cerebellum is also known to be
implicated in visually directed movement (deficit of
visuo-motor guidance called Cerebellar ataxia: Stein
1986; Hallett et al. 1991) and eye-hand coordination
(Miall et al. 2000). All these arguments suggest that the
cerebellum is implicated in the processing and integration of visual errors and hence is candidate to be crucial
in prism adaptation processes (Jeannerod and Rossetti
1 Clower et al. (1996) identified their activation site as area PEG,
which is along the intraparietal sulcus in the angular gyrus (upper
part of Brodmann area 39, see Fig. 1) according to the classification
of Eidelberg and Galaburda (1984) and whose lesion leads to optic
ataxia referring to the lesion superimposition work of Perenin and
Vighetto (1988). However, re-plotting of the Talairach coordinates
of the Clower et al. (1996) study led to rather locate the activation
within Brodmann area 40 (supramarginal gyrus), which does not
pertain to the focus of lesion leading to optic ataxia (Perenin and
Vighetto 1988). We wish to thank an anonymous referee, Isabelle
Faillenot and Christine Baleydier for raising and discussing this
issue.

1993). As suggested by Weiner et al. (1983), the
cerebellum may be the structure that realises the central
recalibration of sensori-motor correspondences. Recalibration involves a global topological realignment
likely to generalise to untrained regions and produces
robust aftereffects, indicating a difficulty in returning to
the original visuo-motor mapping even with cognitive
awareness of the change (Bedford 1993). The cerebellum is known to be a major site for plasticity (Ito 1991,
2000; Armano et al. 2000). It is conceived as a
“sensori-motor correlation storage area” that integrates
the previous motor outputs (efferences) and the visual
error resulting from this output (visual reafference).
2. The other relevant structure, the posterior parietal
cortex (PPC) is implicated in sensorimotor and multisensory integration (Mountcastle et al. 1975; Andersen
et al 1997; Xing and Andersen 2000) and thus is likely
to be involved in the management of some visuo-motor
reorganisation and the spatial re-alignment between
visual and proprioceptive coordinates. In addition,
single-neuron recording (McKay 1992), brain lesion
(monkeys: Faugier-Grimaud et al. 1985; Rushworth et
al. 1998; deficit of visuo-motor guidance called Optic
Ataxia: Perenin and Vighetto 1988; Pisella et al. 2000)
and imaging studies (Grafton et al. 1992; Kertzman et
al. 1997) indicate that the PPC is critically involved in
visually directed movements. The classical prism
adaptation procedure precisely involves manual pointing toward visual targets with the hand and the targets
visible through displacing prisms (hand exposure).
These arguments, together with the result of Clower et
al. (1996), suggest that the PPC may participate in
prism adaptation processes. A study from Meier (1970)
suggested that lesions of the right parieto-frontal
network affect the ability to manage a visuo-motor
task with reversal or inversion of visual feedback.
Numerous imaging studies have confirmed the involvement of the PPC in such cognitive monitoring of new
visuo-motor correspondences linked to mental rotation
processes (Bonda et al. 1996; Inoue et al. 1997; Sugio
et al. 1999). These strategic corrections of visuo-motor
discrepancies are unlikely to generalise to untrained
regions and tasks, and they rarely lead to substantial
aftereffects as opposed to prism adaptation. For
example, after learning a new visuo-motor mapping
in which the direction of a cursor movement is rotated
compared with the hand movement, subjects were able
to revert to normal performance when they knowledgeably attempted to operate under the standard
visuo-motor condition, with only minimal aftereffects
(Cunningham and Welch 1994). In case of prism
exposure, the change is made known by the removal of
the goggles.
3. The functional and anatomical distinctions made above
leads us to speculate that the adaptive realignment
depends on the integrity of the cerebellum, whereas the
cognitive strategies contributing to the compensation of
the prismatic deviation rely on the PPC. Both structures
would collaborate in compensating for the visuo-motor

401
Fig. 1 a Schematised mapping
of the lesion of patient I.G. with
respect to subdivisions of the
posterior parietal lobe in Brodmann areas (1909). b Schematised mapping of the lesion of
patient I.G. with respect to
subdivisions of the posterior
parietal lobe in areas defined by
Eidelberg and Galaburda
(1984). c Horizontal section
through I.G.’s brain, visualised
with structural MRI. Focal damage is present bilaterally in the
posterior parietal lobes, including part of extrastriate areas
(areas 18 and 19), superior parietal lobule (area 7), intraparietal sulcus and upper part of the
angular gyrus (area 39)

conflict introduced by the prisms. When one of the two
structures is lesioned, then the other one would be more
strongly activated and have to produce by itself the
reaction to the visual distorsion in the form of either
strategic compensation or adaptive realignment. Specifically, according to this hypothesis the PPC participates in adaptation without being necessarily involved

in the production of aftereffects. There are two
necessary conditions for this hypothesis to be valid.
First, patients with cerebellar lesion should exhibit
decreased or absent abilities to adapt to prisms. As
mentioned above, several case reports or group studies
already support this prediction (review: Jeannerod and
Rossetti 1993). Second, patients with PPC lesion

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should exhibit normal or even increased adaptation
rates as assessed by the measurement of negative
aftereffects. In addition, they may possibly show a
relative lengthening of their error reduction phase.
It has been shown that prism adaptation can be used as a
technique for rehabilitation of hemineglect patients,
irrespective of the site of their lesion (Rossetti et al.
1998). Individual data from this initial study showed that
each of the eight tested patients were able to adapt to rightdeviating prisms, as revealed by the aftereffect observed
on the manual straight-ahead demonstration. Five of these
patients exhibited a lesion involving the parietal lobe (at
least partially). For two of these patients (J.J.L. and M.C.),
the lesion involved a large portion of the PPC. These
results therefore suggested that patients with a lesion of the
PPC can easily adapt to a prismatic deviation. Note,
however, that first, neglect patients have unilateral lesions,
so it can still be argued that the left (intact) parietal lobe is
responsible for adaptation. Second, two main functional
regions can be distinguished within the PPC based on
neuropsychological data. The right inferior parietal lobule
and the temporo-parietal junction are generally acknowledged as the common intersection site of the lesions
producing unilateral neglect (Vallar and Perani 1986;
Karnath et al. 2000). The superior parietal lobule
symmetrically, and the region including and surrounding
the intraparietal sulcus, represents the focus of the lesions
producing the visuo-motor deficits known as ‘optic ataxia’
(Perenin and Vighetto 1988). Therefore, the present study
tests whether a bilateral lesion of the PPC leading to
bilateral optic ataxia affects prism adaptation. To this aim,
patient I.G. was tested for adaptive aftereffects after
performing a standard visuo-motor pointing procedure
with prismatic goggles. Interestingly, this patient has been
previously shown to be unable to perform automatic
corrective movements (Pisella et al. 2000; Gréa et al.
2002). If on-line visuo-motor corrections during the
pointing procedure are important to acquire visuo-motor
adaptation to prisms, then this lack of on-line flexibility
should prevent our patient from showing adaptive aftereffects.

mainly Brodmann’s areas 19, 18, 7, a limited part of area 39 and the
intraparietal sulcus.
Visual fields showed a partial right inferior homonymous
quadrantanopia with temporal crescent sparing. Pattern-visual
evoked potentials generated for each eye and for each visual
hemifield were normal. Recordings of saccades and smooth pursuit
eye movements elicited by a LED in the dark showed normal gain,
direction and velocities. However, when she was asked to search for
an object presented in the real world she often had wandering
exploratory eye movements for a few seconds before fixating at the
target. She had no hemineglect syndrome during conventional
testing but demonstrated bilateral optic ataxia. Reaching and
grasping inaccuracy predominated for her right hand in her right
peripheral hemifield. During reaching, her hand posture was often
inappropriate in terms of aperture and orientation, and she usually
corrected her grip only through tactile reafferences after she had
completed the movement. However, visually elicited hand movements were generally accurate when performed in foveal vision.
Note that IG initially showed simultanagnosia, which prevented
her to see the target and her hand at the same time and thus to adapt
to prisms. This could account for contradictory result (Newport et al.
2004). The present experiment was conducted when the bilateral
optic ataxia persisted without associated simultanagnosia.

Control subjects
Four naive control subjects (two males and two females 24, 23, 26
and 36 years of age, respectively ) participated in the experiment.
They were right-handed medical undergraduate volunteers from the
Neurology Unit. They had self-reported normal vision and proprioception with no history of neurological disorder.

Design
The testing procedure consisted of a pre-test session, followed by
the prism adaptation procedure, and then by a post-test session. The
pre-test and post-test sessions consisted of an open-loop pointing
task performed without goggles.
The comparison of the performance obtained in the pre-test and
post-test sessions with the open-loop pointing task performed with
the (right) exposed arm attested for the presence and the magnitude
of adaptive aftereffects (Fig. 3).
The comparison of the performances between pre-test and posttest sessions on the open-loop pointing task performed with the (left)
unexposed arm allowed us to investigate the presence and the
magnitude of intermanual transfer of adaptation (Fig. 4).

Apparatus

Methods
This study was conducted with the informed consent of the patient,
in agreement with the French law (4 March 2002) and the Helsinki
declaration relative to patients’ rights.

Case report
I.G. is a 29-year-old woman who suffered from an ischemic stroke
related to acute vasospastic angiopathy in the posterior cerebral
arteries established with an angiogram. Magnetic resonance imaging
revealed a hyperintense signal on T2 sequencing that was fairly
symmetrically, located in the posterior parietal and upper and lateral
occipital cortico-subcortical regions (Fig. 1). Reconstruction of the
lesion (Talairach and Tournoux 1988) indicated that it involved

The apparatus used in this experiment is similar to that employed by
Redding and Wallace (1996). Specifically, this structure consisted of
a two-layer rectangular black wooden box-like frame (30 cm high,
80 cm wide and 80 cm deep) placed on a table and opened on the
side facing the subject. Throughout the experiment, subjects were
seated in front of the structure and placed their arms within the
structure. Their head was kept aligned with the body sagittal axis
using a chin rest situated on the top of the box. A piece of foam
placed on the lower layer of the box near the sternum of the subjects
indicated the hand starting position. Sight of the starting hand
position and of the first approximately 15 cm of the pointing surface
was not permitted by the structure. The last part of their pointing
trajectory remained visible throughout the adaptation session. The
area between the starting position and the targets was totally
occluded during the testing phase. Indeed, two upper horizontal
plywood covers of two different sizes were designed for the prism
adaptation procedure and the open-loop target pointing task.
Throughout the experiment, subjects were required to point on the

403
Fig. 2 Error reduction during
prism exposure. These graphs
show the progressive reduction
of pointing errors in degrees
when performing the pointing
procedure toward the two targets
with prisms goggles for patient
I.G. and the group of control
subjects

lower surface of the box and return to the starting position after each
trial. The lower horizontal surface of the box was covered by
electrosensitive paper that allowed the movement endpoints to be
recorded via a metallic thimble attached to the tip of a subject’s
index finger. This apparatus produced measurements with an
accuracy of 0.1°.

Prism adaptation procedure
The right-based wedge prisms used in the adaptation procedure were
wide field glasses inserted into light glacier goggles and afforded a
wide binocular vision (the total visual field was 105° constituted by
the two monocular visual fields (30° each) and a binocular visual
field of 45°). With these goggles on, the visual field is uniformly
displaced to the left side with minimal visual distortion. During the
exposure period, the subjects wore prismatic goggles producing a
15° leftward visual shift and performed pointing trials during 20 min
with the right index finger (exposed arm). The two visual targets
were coloured dots situated at 10° to the right and to the left of the
body midline at reaching distance (30 cm away from the starting
point) on the lower surface of the box. Subject’s head was held
vertical with a chin rest such that the eyes were downward toward
the targets. During this pointing session, patients were asked to point
under a light speed constraint, alternating towards the two visual
targets. The pointing speed was constrained by the experimenter
indicating where (“right” or “left” target) to direct the next pointing
following a random order list; 80 pointing movements were
performed in a session of 10-min duration, with small breaks after
each series of 20 pointings. During this adaptation procedure, the
upper surface of the box was a narrow plywood that occluded the
first part of the pointing trajectory. Subjects therefore could see only
the targets and the second half of their pointing trajectory, as well as
their terminal error. The progressive reduction of the pointing errors
during the prism adaptation procedure was recorded for each
subject.

Open-loop target pointing
In this visually directed pointing test, subjects were required to point
on the lower surface in alignment with a single visual target, from
the hand starting position located near their sternum. For these
periods (pre-test and post-test), the upper cover consisted in a
plywood just shorter than the box length, allowing the subjects to
see the white target bar positioned at eye level on the back vertical
surface without allowing them to see their moving arm or their
terminal errors. The visual target was situated straight-ahead of the
subjects, and out of reach of the pointing limb (80 cm). The pointing
error was measured as the distance between the pointing position
and the target position and carried a minus sign for leftward errors
and a plus sign for rightward errors. Six trials were successively
performed, first with the right arm (exposed arm) and then with the
left arm (unexposed arm) in order to obtain a reliable average for
each arm in the pre-test session. The task was identically repeated
just after the prism adaptation procedure (post-test session).
This task is generally considered as a measure of the total shift
(TS) of the adaptive aftereffects produced by prism manual
adaptation (e.g. Redding and Wallace 1996).

Statistics
In order to test the existence of aftereffects in the patient a factorial
analysis of variance was performed with trials (n=6) as the random
factor. An identical one-way ANOVA was also performed for each
normal individual in order to assess the patient and the healthy
controls in the same way. In addition, a repeated measure ANOVA
was performed for the group of control subjects (n=4) between the
pre-test and the post-test sessions in order to assess the presence of
adaptive aftereffects (open-loop target pointing movements with
exposed hand) and the presence of intermanual transfer (open-loop
target pointing movements with unexposed hand) at the group scale.

404
Table 1 Adaptation (exposed
hand)

Task

Subjects

Mean shift (deg)

F-value

p

Visual pointing (open-loop)

I.G.
Controls
Control 1
Control 2
Control 3
Control 4

5.0
6.8
7.2
2.7
7.3
10.2

F(1,10)=28.01
F(1,3)=19.85
F(1,10)=24.65
F(1,10)=217.80
F(1,10)=307.70
F(1,10)=476.70

<0.01
<0.05
<0.01
<0.01
<0.01
<0.01

Results

Adaptation

Error reduction

The four control subjects showed significant negative
aftereffects as assessed by the pointing errors in the openloop target pointing task performed with the exposed
(right) hand after prisms removal (one-way ANOVA
p<0.01 for each subject, repeated measures ANOVA
p<0.05 for the group, see Table 1, Fig. 3). Similarly, the
patient I.G. exhibited a significant rightward deviation of
her pointing errors between the pre-test and the post-test
sessions in the same task (one-way ANOVA p<0.01, see
Table 1, Fig. 3).
This compensatory aftereffect demonstrates that the
patient adapted to the optical deviation. The magnitude of
the adaptive aftereffect observed for the patient I.G.
(5.0 deg) was somewhat less than the average for the
control subjects’ group (6.5 deg) but comparable in
magnitude to that usually obtained in prism adaptation

Figure 2 shows the progressive reduction of the pointing
errors during the prism adaptation procedure for patient I.
G. and the group of control subjects. At first pointing,
patient I.G. exhibited a larger error than control subjects
with a magnitude closed to the total prismatic deviation
(11 deg). Patient I.G. then maintained this pointing error
until the fifth trial. Control subjects exhibited an initial
pointing error of about 8 deg in mean. As early as at the
second trial, the error was reduced to the level of pointing
variability (within 3 deg).

Fig. 3 Checking adaptation by open-loop target pointing with the
exposed (right) hand. Columns represent the means and standard
deviations of the errors observed for each subject before (pre) and
after (post) the prism adaptation procedure with the right hand. In
the top left panel, the mean values and inter-individual standard
deviations of the group of four control subjects’ performance are

illustrated (broken line) for a comparison, in addition to the patient’s
performance (continuous line). For all the four control subjects and
the patient, the mean pointing values are significantly modified
between the pre-test and the post-test sessions (see Table 1). The
data in the top left panel show a parallel aftereffect for the control
subjects and the patient

405
Table 2 Transfer (unexposed
hand)

Task

Subjects

Mean shift (deg)

Transfer rate

F-value

p

Visual pointing (open-loop)

I.G.
Controls
Control 1
Control 2
Control 3
Control 4

2.7
0.9
1.7
0.5
0.6
1.1

54%
13%
23%
18%
8%
10%

F(1,10)=19.13
F(1,3)=11.85
F(1,10)=10.64
F(1,10)=0.98
F(1,10)=1.67
F(1,10)=5.60

<0.01
<0.05
<0.01
0.35
0.23
<0.05

studies (Redding and Wallace 1993, 1996). Therefore the
visuo-manual adaptive processes of I.G. can be considered
as normal despite patient I.G.’s bilateral lesion of the PPC.
Transfer
Individual data showed that only control subjects 1 and 4
exhibited a significant rightward shift in the open-loop
target pointing task with the unexposed left hand after
prisms one-way ANOVA (p<0.01 for control 1 and p<0.05
for control 4; see Table 2, Fig. 4) corresponding to 23 and
10% of intermanual transfer, respectively. Control subjects
2 and 3 did not exhibit any significant prismatic aftereffect
with the left hand (p>0.2; see Table 2, Fig. 4). The group
of control subjects thus exhibited a low mean rate of 13%
intermanual transfer, which did, however, reach significance (p<0.05 repeated measures ANOVA; see Table 2,

Fig. 4 Checking intermanual transfer by open-loop target pointing
with the unexposed (left) hand. Columns represent the means and
standard deviations of the pointing errors observed for each subject
before (pre) and after (post) the prism adaptation procedure with the
left hand. In the first panel, the mean values and inter-individual
standard deviations of the group of four control subjects’

Fig. 4). Surprisingly, a high intermanual transfer of 54%
was observed in patient I.G., which was highly significant
(one-way ANOVA p<0.01; see Table 2, Fig. 4). After
prism removal, pointing performance with patient I.G.’s
left hand was shifted by an average of 2.7 deg to the right
(p<0.01; see Table 2, Fig. 4).
This result shows that the intermanual transfer rate of
prism adaptation is strikingly large for the patient with a
bilateral lesion of the PPC.

Discussion
The present paper raises the issue of the processes and the
neural substrates involved in prism adaptation. We had the
opportunity to test the adaptation ability of patient I.G.
who suffered from an impairment of on-line automatic

performance are illustrated (broken line) for a comparison, in
addition to the patient’s performance (continuous line). A significant
transfer was observed for patient I.G. and control subject 1 and 4
(see Table 2). The top left panel shows a larger rate of intermanual
transfer for patient I.G. (54%) than for the control subjects (only
15%)

406

visuo-motor guidance (bilateral optic ataxia) following
bilateral lesion of the PPC.
In the hypothesis presented in the introduction, we
proposed that the PPC and the cerebellum are responsible
for the strategic and adaptive components involved in
reaction to a prism, respectively. Both components
contribute to the error reduction, but the strategic component is not involved in the development of adaptive
aftereffects. In addition, the strategic component involved
in the error reduction seems to share the same mechanisms
as those involved in the cognitive monitoring of other
types of optical deviations and has been shown to activate
the PPC in recent imaging studies (Bonda et al. 1996;
Inoue et al. 1997; Sugio et al. 1999). Therefore, we
predicted that the lesion of the PPC may partially affect the
pattern of error reduction. However, the integrity of the
PPC should not be crucial to observe negative aftereffects
and hence an intact adaptation rate should be observed in
patient I.G.
Three aspects of the present results that support our
hypothesis should be summarised here. First, the pattern of
pointing errors appeared slightly affected in patient I.G.
Second, the patient significantly adapted to prisms despite
a bilateral lesion of the PPC. Her amount of adaptation, as
measured by the open-loop pointing task, did not differ
significantly from that of healthy subjects. Third, the
amount of transfer to the unexposed hand was about three
times that of healthy subjects.
First, the initial pointing error of patient I.G. was close
to the total optical displacement produced by the prisms,
which confirms a reduced ability to modify her pointing
movement on-line (Pisella et al. 2000; Gréa et al. 2002).
She could, however, compensate for the prismatic deviation from the fifth pointing trial. Further studies should
specifically investigate the contribution to this error
compensation of the strategic modification of initial
movement direction, the slow intentional feedback control
and the adaptive realignment.
Second, patient I.G. significantly adapted to prisms
despite a bilateral lesion of the PPC. The amount of
aftereffect found in I.G. is about one third of the optical
deviation, which is within the classical range of prism
adaptation aftereffects (e.g. Redding and Wallace 1993,
1996; Rossetti et al. 1998). This result confirms previous
reports made on patients with unilateral lesion of the
parietal lobe (Weiner et al. 1983; Rossetti et al. 1998).
Weiner et al. (1983) reported that patients with a right
parietal lesion showed a normal negative aftereffect (using
right prisms and right hand exposure). In these previous
studies, it could be argued that the preserved contralateral
parietal lobe of these patients was responsible for the
normal visuo-motor adaptation. With a bilateral damage,
the present case therefore provides a stronger demonstration that areas of the PPC included in the lesion are not
crucial for prism adaptation. Most of the patient’s lesioned
areas are damaged symmetrically in both hemispheres:
areas 19, 18 and the posterior part of the intraparietal
sulcus, as well as areas 7 and 39 (in terms of Brodmann
(1909); see Fig. 1a) or areas PEp and PEG (in terms of

Eidelberg and Galaburda (1984); see Fig. 1b). However,
the current data are not sufficient to exclude a putative role
in the adaptation of the supramarginal gyrus and of the
anterior part of the intraparietal sulcus remaining intact in
patient I.G. (see Fig. 1c).
With respect to these two first results, it is interesting to
note that I.G. has been previously shown to exhibit a
specific impairment in automatic corrective processes
(Pisella et al. 2000). When asked to perform corrections in
response to visual targets that were displaced at the onset
of her movement, she failed to produce the fast corrections
found in normal subjects and instead performed slow
intentional corrections (Pisella et al. 2000). According to
theories of feedforward modeling (Desmurget and Grafton
2000), this suggested that the PPC was crucially involved
in comparing on-line predicted and observed events. We
showed elsewhere that this patient is still able to plan and
execute movements with a quasi-normal kinematic pattern
(Gréa et al. 2002). In addition, we show here that she is
also able to integrate error signals and modify her visuomotor correspondences off-line in order to adapt to prisms,
probably by using proactive visuo-motor control. The
present results therefore provide direct neuropsychological
evidence for a dissociation between the processes involved
in on-line visuo-motor control (flexibility of the pointing
movement) and the processes involved in visuo-motor
adaptation (short-term plasticity of the sensory-motor
system). Both these processes are involved in accuracy
maintenance, though they operate on two different time
scales. This further confirms that the impairment of
cerebellar ataxic patients in sensori-motor adaptation is
not due to their inaccuracy (Martin et al. 1996).
Third, the rate of intermanual transfer showed by I.G.
appears abnormally increased. In the literature, intermanual transfer has been described in two main situations (see
Redding and Wallace 1988). First, intermanual transfer is
reported when realignment is localised in the head-neck
proprioceptive system; this type of adaptation is especially
obvious when the head is free to move. Since we used a
chin rest for all subjects, there is no basis in the present
method to suppose more head shift for the patient than for
controls. Second, intermanual transfer should be theoretically observed when realignment is visual rather than
proprioceptive, as a consequence of subjects, and
particularly patients, adopting different strategies of
sensori-motor guidance, thus solving the task with
different neural circuits. However, Redding and Wallace
(1988) showed that visual aftereffects and intermanual
transfer were unrelated.
Therefore, an alternative hypothesis must be proposed.
The observation of adaptive aftereffects in patient I.G.
provides a strong argument against a necessary involvement of the PPC in prism adaptation and indirectly
suggests that the cerebellum is more likely to be the main
substrate of adaptation. However, the second main result
of our study shows that I.G. unexpectedly transferred more
than 50% of the adaptation to the unexposed hand, while
the group of healthy subjects exhibited low transfer (13%
on average), as classically reported in the literature (Taub

407

and Goldberg 1973; Choe and Welch 1974). This abnormal transfer in patient I.G. suggests in turn that the PPC
may participate in the adaptation. If the lesion of the PPC
reduces the strategic component in this patient, adaptation
would consequently be mostly achieved by recalibration
processes (true adaptive component), hence more likely to
be generalised. A large generalisation of the aftereffects
was also suggested by results obtained in hemineglect
patients where adaptation has been observed to improve
neuropsychological testings (Rossetti et al. 1998), postural
balance (Tilikete et al. 2001), wheel-chair locomotion
(Rode et al. 2003) and even mental imagery (Rode et al.
1999, 2001). Both sensori-motor and perceptual aftereffects are observed after prism adaptation in neglect
patients and these effects are more robust and durable than
in normals (Pisella et al. 2002; McIntosh et al. 2002; Farnè
et al. 2002). Strikingly, hemineglect patients do not notice
the alteration resulting from the optical deviation. In
normal subjects, when the deviation is not noticeable (e.g.
about 3 deg) or when subjects are not informed of its
direction, larger adaptive aftereffects are observed (Jakobson and Goodale 1989). These two results suggest that the
lack of cognitive compensation facilitates the development
of the true adaptive component (see Redding and Wallace
1993, 1997). The lack of strategic component would also
be responsible for the important generalisation found in
neglect patients. An important challenge for future prism
adaptation research will be to determine whether spatial
generalisation (e.g. Bedford 1993), inter-manual-transfer
(Redding and Wallace 1988), and the cognitive effects of
prism adaptation found in patients (Rossetti et al. 1998;
Rode et al. 1999, 2001) and in normals (Colent et al. 2000;
Berberovic and Mattingley 2003; Michel et al. 2003) all
belong to an heterogenous group of unexposed conditions,
possibly extending the aftereffects of a prism adaptation
mostly achieved by recalibration processes.
Finally, recent imaging data showing an involvement of
the PPC in the processes of adaptation (either exclusively:
Clower et al. 1996; or in addition to a cerebellar activation:
Hallett et al. 1997) also support our hypothesis. In these
studies, the optical deviation was reversed (left to right)
every five trials. It can therefore be argued that this
paradigm did not involve the two components of adaptation in the usual way. Rather, this procedure would have
selectively activated, or at least favoured, the main
involvement of the strategic component (the subjects
were continuously kept in an error reduction phase). It is
thus not surprising that in these conditions the parietal lobe
was shown to be activated exclusively or at least partially.
This interpretation would also account for the lack of (or
the non-exclusive) cerebellum activation found in these
studies.
Acknowledgements The authors wish to thank patient I.G. for her
kind participation and Isabelle Faillenot for her help in the
neuroanatomical reading of the MRI scans of the patient. This
work was supported by INSERM (Progrès) and ACI plasticité.

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