Handbook of Clinical Neurology, Vol.

151 (3rd series)

The Parietal Lobe
G. Vallar and H.B. Coslett, Editors
https://doi.org/10.1016/B978-0-444-63622-5.00016-4
Copyright © 2018 Elsevier B.V. All rights reserved

Chapter 16

Constructional apraxia
GUIDO GAINOTTI1,2 AND LUIGI TROJANO3*
1
Institute of Neurology, Sacred Heart Catholic University, Rome, Italy
2
IRCCS Fondazione Santa Lucia, Department of Clinical and Behavioral Neurology, Rome, Italy
3
Department of Psychology, University of Campania ‘Luigi Vanvitelli’, Caserta, Italy

Abstract
Since the classic papers of Kleist, Mayer Gross, and Critchley, constructional apraxia (CA) has been con-
sidered to be a typical sign of a parietal lobe lesion, and as a precious tool to appreciate the spatial abilities
subserved by this lobe. However, the development of more sophisticated neuropsychologic models and
methods of investigation has revealed several problematic aspects. It has become increasingly clear that
CA is a heterogeneous construct that can be examined with very different tasks, that are only mildly inter-
connected, and tap various kinds of visuospatial, perceptual, attentional, planning, and motor mechanisms.
On the basis of these considerations, the relationships between parietal lobe functions and constructional
activities must be considered, taking into account on the one hand the heterogeneity of the tasks and of the
cognitive functions requested by different kinds of constructional activities and, on the other hand, the
plurality of functions and of processing streams linking different parts of the parietal lobes to the occipital
and frontal lobes.

disorders grouped under the heading of CA and, on the

INTRODUCTION
In his classic book The Parietal Lobes, MacDonald
Critchley (1953) stated that constructional apraxia
(CA), defined as “a difficulty in putting together one-
dimensional units so as to form two-dimensional figures
or patterns,” is one of the most important and commonly
occurring signs of parietal lobe damage. Interest in CA as
a marker of a specific cognitive and pathophysiologic
disturbance has, however, changed with the development
of cognitive neurosciences: CA was first related to the
mechanisms of apraxia (Strauss, 1924), then to hemi-
spheric asymmetries in visuospatial functions (Scheller
and Seideman, 1931) and finally, in recent times, to
the more clinical problems of the etiologic form and
the neuropsychologic staging of dementia (Ajuriaguerra
et al., 1960).
In the present chapter we will summarize the historic
evolution of the construct of CA, stressing on the one
hand the complex and heterogeneous nature of the
other hand, the relationships between CA and mecha-
nisms subsumed by the parietal lobe.
HISTORIC NOTES
The clinical and theoretic usages of the term
“constructional apraxia” (CA) are rather heterogeneous
and have changed over time, being strictly linked to
the models of brain functions and brain pathology that
were pre-eminent in different periods of the history of
the neurosciences. As the term “constructional apraxia”
suggests, this concept was developed in the period of
Liepmann’s (1912) investigations of limb apraxia.
Liepmann (1912) believed that attainment of a skilled
movement requires the acquisition of a “movement
formula” and of an “innervatory pattern” that would
communicate the “formula” information to the appropri-
ate primary motor areas. Liepmann also thought that the
left parietal role was crucial in supporting the movement

*Correspondence to: Luigi Trojano, Department of Psychology, University of Campania ‘Luigi Vanvitelli’, Viale Ellittico 31, 81100
Caserta, Italy. Tel and fax: +39-0823-274784, E-mail: luigi.trojano@unicampania.it
332 G. GAINOTTI AND L. TROJANO
formula, but the precise localization of the relevant neu-
ral centers within the left parietal lobe remained unclear
(Kimura, 1980).
As reported by De Renzi in his seminal book on spa-
tial cognition (1982), Rieger (1909) first described the
inability shown by some brain-damaged patients
(BDPs) to build words with letters, or patterns with
sticks. Rieger (1909), however, did not distinguish this
inability from other aspects of ideomotor apraxia and
was, therefore, unable to stress the specificity of his
observation. A few years later Poppelreuter (1917)
developed the construct of optische Apraxie to identify
impairments in a series of activities requiring careful
control of vision on action, such as drawing, cutting a
shape with scissors, or finding one’s way in familiar
surroundings.
The excessively broad range of activities included by
Poppelreuter (1917) under the heading of optic apraxia
led Kleist (1934) to introduce the term “constructional
apraxia” to designate “a disturbance which appears in for-
mative activities (such as assembling, building, or draw-
ing) in which the spatial form of the task is missed,
although there is no apraxia of the single movements.”
To be sure, Kleist (1934) considered CA proper as resulting
from “an impaired bond between visual-spatial functions
and the kinesthetic engrams which are decisive for manual
activity,” excluding from the field of CA constructive dis-
orders which can be explained in terms of visuoperceptual
impairment or ideomotor apraxia. Kleist (1934) empha-
sized that it can be difficult to disentangle CA from disor-
ders of action related to visual impairments, but a careful
analysis of patients’ errors in drawing tasks (Fig. 16.1)

a
d
e
b

c
Abb. 161. Bitter.

Haus

Nagel Profil
Abb. 165. Otto. Haus
Abb. 166. Ziegel.

Vorlage
Haus aus dem Gedãchtnis

Nachzeichnung Haus nach Vorlage

Abb. 167. Schnell.
Fig. 16.1. Four figures reported in Kleist’s (1934) description of constructional apraxia. Abb. (figure) 161 shows drawings by the
patient Bitter, who sustained a right parietal lesion near to the skull midline, with left hemianopia. a, profile of a human face rotated
by 90°; b–e, four attempts at drawing a house to command. Abb. 165 and Abb. 166 show drawings by the patients Otto and Ziegel,
with bilateral parieto-occipital lesions encroaching upon the angular gyrus, and double hemianopia with spared central vision.
From left, attempts at drawing to command a nail (Nagel), a profile (Profil), and a house (Haus). Abb. 167 shows drawings by
the patient Schnell, who had a left parietal lesion, involving the angular gyrus, and a right posterior lesion and left hemianopia.
Left, a model (Vorlage) and a patient’s attempt to copy it (Nachzeichnung); middle, attempt to draw a house from memory (Haus
€
aus dem Gedachtnis); right, attempt to copy a drawing of a house (Haus nach Vorlage).
 CONSTRUCTIONAL APRAXIA
led him to prefer the term “constructional” to the
term optische Apraxie, since he thought that errors pro-
duced by his patients could not be ascribed to faulty
visual perception. In proposing such a new nosological
entity, Kleist (1934) also suggested that it was fre-
quently associated with lesions in the left posterior pari-
etal lobe, and, more precisely, with damage to
Brodmann area (BA) 39 (angular gyrus) in the left hemi-
sphere, that would serve as a center for linking visual
and kinesthetic functions. However, Kleist (1934) was
quite prudent about this possible localization, as it
was based on postmortem pathologic examination of
a few patients.
In subsequent years, Kleist’s (1934) original defini-
tion, which linked the term CA to a specific pathophys-
iologic mechanism, was substantially neglected, and the
term CA was used to refer to all disturbances observed
during drawing, assembling, and building complex
models. Two main groups of interpretations were
advanced in that period to explain constructive distur-
bances: (1) some authors (e.g., Strauss, 1924; P€ otzl,
1928; Mayer Gross, 1935) regarded CA as an executive
disorder restricted to complex manipulation, in the
absence of visuoperceptive disturbances; (2) other
authors (Scheller and Seideman, 1931; Lange, 1936;
Dide, 1938) considered visuoconstructive disorders as
resulting from a basic visuoperceptive impairment and
often reported right-BDPs in support of their interpreta-
tion. Scheller and Seideman (1931), Lange (1936), and
Dide (1938) went one step further, and hypothesized that
the right hemisphere plays a special role in visuospatial
functions, and that visuoconstructive disorders of right-
BDPs may be the consequence of this basic visuospatial
disorder. This idea was supported, after the second World
War, by a number of systematic clinical studies (Paterson
and Zangwill, 1944; McFie et al., 1950; Hecaen et al.,
1951, 1956; Ettlinger et al., 1957; Piercy et al., 1960),
which emphasized the frequency of CA in right-BDPs
and drew attention to the close relationship observed in
these patients between perceptual and constructional
disabilities.
Hecaen et al. (1951) also suggested that qualitative
differences could exist between the constructive disabil-
ities shown by patients with right- or left-hemisphere
lesions; this issue was developed by Duensing (1953),
Mc Fie and Zangwill (1960), and Piercy et al. (1960),
who strongly contrasted executive with visual-
perceptual forms of CA. Duensing (1953) described
the drawings of left-BDPs as marked by great simplifica-
tion of the outline, and frequent hesitations, whereas
those of right-BDPs were described as characterized
by a failure to reproduce the spatial relationships among
the various parts of the model. Furthermore, the presence
of a model would facilitate the drawings of left-BDPs
333
with apraxia, but would not improve the performance
of right-BDPs.
Subsequently, Mc Fie and Zangwill (1960) compared
the qualitative aspects of the constructive disorders
shown by 8 patients with left parietal damage with those
of 10 right-BDPs previously described by Ettlinger et al.
(1957); they substantially confirmed Duensing’s (1953)
distinction between left executive and right visuospatial
forms of CA. Piercy et al. (1960), on the other hand, car-
ried out the first major systematic survey of the relation-
ships between visuoconstructive disabilities and
hemispheric locus of lesion; they found that CA was sig-
nificantly more frequent and more severe in patients with
right-sided (and in particular with right parietal) lesions
and that qualitative differences similar to those noted by
Duensing (1953), and by Mc Fie and Zangwill (1960),
existed between right- and left-BDPs. On the basis of
the similarities observed in these studies, Mc Fie and
Zangwill (1960) proposed the term CA to designate
the disability shown by left parietal patients and
“spatial agnosia” for the performance of right parietal
patients.
Irrespective of the contrasts concerning the qualitative
differences between the drawings of left- and right-BDPs
and the underlying pathophysiologic mechanisms, Mc
Fie and Zangwill (1960) emphasized the fact that, in most
of these patients, the intrahemispheric locus of lesion
specifically involved the parietal lobes, as previously
highlighted by Mayer Gross (1935), who had considered
CA as mainly related to left parietal lesions, and had
stressed the association of CA with Gerstmann syn-
drome, and by Critchley (1953), who had shown that
the responsible lesions generally encroach upon the pos-
terior parietal areas.
METHODOLOGIC PROBLEMS IN THE
ASSESSMENT OF CONSTRUCTIONAL
APRAXIA
Only 2 years after the publication of the papers by Mc
Fie and Zangwill (1960) and Piercy et al. (1960),
Benton (1962) underlined the limitations of the clinical
approach and the inconsistency of the criteria adopted
by different authors to make the diagnosis of CA.
According to Benton (1962), two factors could account
for the divergence of opinions: (1) the subjective nature
of the clinical method; and (2) the fact that many differ-
ent tasks had been used to study constructive disorders.
The solution suggested by Benton (1962) to improve
the comparability of results obtained by different
authors, namely the use of graded tests with precise
scoring procedures and comparison with a control
group, has been widely accepted and followed by all
subsequent authors.
334 G. GAINOTTI AND L. TROJANO
It has been much more difficult to solve the second
problem, because CA has been used as a single diagnos-
tic category, which operationally identified all distur-
bances observed on very heterogeneous tasks such as
drawing, assembling, and building complex models
(Gainotti, 1985; Trojano and Conson, 2008). However,
drawing and assembling activities cannot be considered
equivalent: some researchers (Arrigoni and De Renzi,
1964) noted a significant correlation between drawing,
three-dimensional object construction, and visuospatial
tasks in right- and left-BDPs, but other studies (Benton
and Fogel, 1962) yielded contrasting data. This heteroge-
neity of methods used to evaluate CA must be stressed. In
the early studies of Rieger (1909) and Kleist (1912),
tasks in which patients were required to assemble sev-
eral elements (e.g., sticks) while reproducing two-
dimensional models were used. Three-dimensional
constructional tasks (Benton and Fogel, 1962;
Trojano et al., 1997) were rarely used, because only a
few researchers recommend testing both two- and three-
dimensional constructional competence (Benton, 1989;
Capruso and Hamsher, 2011).
Drawing tasks have been widely used to assess con-
structional abilities, but, unlike the tests mentioned
above, they rely on graphomotor skills. In fact, dissoci-
ation between drawing and other constructional tasks has
been reported amongst aphasic patients (Kashiwagi
et al., 1994). Furthermore, copying and free drawing can-
not be considered equivalent. We have seen in the section
on historic notes, above, that, according to Duensing
(1953), Mc Fie and Zangwill (1960), and Piercy et al.
(1960), copying is more impaired in right-BDPs,
whereas free drawing is more affected in patients with
left-brain damage. Free drawing – in which the patient
is required to draw a named object (e.g., a clock, a face) –
is apparently the most immediate test of constructional Fig. 16.2. Drawing of a clock face on an empty circle. Top
skills. It reveals information about patients’ ability to row: drawings by left-brain-damaged patients usually show
draw complete shapes, or a tendency to omit parts, and simplifications and distortions, but with relatively spared spa-
tial relationships; on the right, see errors in writing numbers.
their ability to organize the figure as a whole, with its
Second row: drawings by right-brain-damaged patients usu-
component elements in their correct spatial relationships ally show left-sided omissions and frequent visuospatial
(Fig. 16.2). However, this task is not easily standardized defects. Lower rows: drawings by demented patients show
and relies on nonconstructional cognitive abilities. gross spatial distortions, perseverations, and errors reflecting
Regarding the latter point, Gainotti et al. (1983) impaired semantic knowledge; when required to draw hands
demonstrated that drawing from memory was more at the given time (at 2:45 in these instances), patients with
compromised in aphasics than in nonaphasic left-BDPs dementia often refuse, make conceptual errors, or write num-
and in right-BDPs, likely in relation to patients’ bers instead of drawing the hands.
lexical-semantic deficits, rather than to their visual-
constructional disorders. Similarly, Grossman (1988) mechanisms and imagery abilities (see Trojano and
observed that BDPs might fail in associating a shape with Grossi, 1994, for a discussion).
its appropriate size when drawing single objects, reveal- A clear instance of the complexity of free-drawing
ing an associative rather than a purely constructional dis- tasks is clock drawing (for a comprehensive discussion,
order. In the assessment of constructional skills, then, the see Freedman et al., 1994). As classically defined by
complexity of free-drawing tasks should be recognized, Kaplan (1988), clock test administration implies com-
in terms of the role played by lexical-semantic manding patients to “draw the face of a clock with all
 CONSTRUCTIONAL APRAXIA
the numbers and set the two hands to 10 after 11.” The
involvement of several cognitive abilities in clock draw-
ing to command (Fig. 16.2) made this task very popular
as a rapid screening test for general cognitive impairment
and dementia, although there are many proposed admin-
istration procedures and scoring systems. One strategy
for improving diagnostic accuracy is to compare the
drawing to command condition with a copy condition,
in which subjects are required to copy a predrawn clock,
since in the copy condition performance would rely only
on a subset of cognitive functions centered on visuoper-
ceptual and constructional skills (Price et al., 2011).
However, although copying tasks seem to directly
assess the patient’s ability to reproduce simple figures,
such as circles and squares, or complex designs, such
as a clock or the Rey–Osterreith complex figure
(ROCF) (Rey, 1941; Osterreith, 1944), even this task
can involve problem-solving and executive abilities,
and its performance level is related to age, educational
level, and even cultural background (see Rosselli and
Ardila, 2003, for a review). It is therefore crucial for diag-
nosis of CA to adopt a standardized task, with solid nor-
mative data, employing different kinds of stimuli, well-
known or novel, of graded complexity (Figs 16.3–16.5).
INCIDENCE AND QUALITATIVE ASPECTS
OF CONSTRUCTIONAL APRAXIA IN
RELATION TO THE SIDE AND
INTRAHEMISPHERIC LOCUS OF LESION
As previously mentioned in the first major systematic
survey of the relationships between visuoconstructive
disabilities and hemispheric locus of lesion based on
clinical studies, Piercy et al. (1960) had claimed that
quantitative and qualitative differences exist between
the constructional disorders shown by right- or left-
BDPs. Indeed, the former showed a greater incidence
and severity of constructional disturbances that, from
the qualitative point of view, were characterized by a
failure to reproduce spatial relationships among the var-
ious parts of the model, whereas the latter produced
simplified drawings, poor in outline and lacking in
detail, but well organized from a spatial point of view
(Figs 16.3–16.5).
The general inference drawn from these observations
was that the right hemisphere (and in particular the right
parietal lobe) is dominant for visuospatial functions,
and that constructional tasks can be used to assess this
right-hemispheric visuospatial specialization. How-
ever, subsequent more controlled studies of CA, in
which the distinction between apraxic and nonapraxic
patients was made on the basis of an objective cut-off
point (De Renzi and Faglioni, 1967; Gainotti, 1972;
Colombo et al., 1976; Arena and Gainotti, 1978;
335
Kirk and Kertesz, 1989; Carlesimo et al., 1993;
Trojano et al., 2004), have failed to find a greater prev-
alence of CA in right-BDPs and similar results have been
obtained by studies (Arrigoni and De Renzi, 1964;
Warrington et al., 1966; De Renzi and Faglioni, 1967;
Dee, 1970) which have compared the severity of con-
structional disorders shown by right- and left-BDPs.
At variance with these conclusions are results
obtained by Villa et al. (1986) in a study aiming to eval-
uate the influence of the laterality and the intrahemi-
spheric locus of the lesion and the role of the
coexistence of mental deterioration on scores obtained
on two constructive tasks. Regardless of defects attribut-
able to unilateral spatial neglect (see Chapter 14), right-
BDPs showed the highest incidence and severity of
constructive disturbances, and patients with parietal –
and particularly with right parietal – damage obtained
the poorest mean scores and exhibited the highest inci-
dence of apraxic performances (Villa et al., 1986).
The qualitative differences between the constructive
defects in right- and left-BDPs were confirmed by
Gainotti and Tiacci (1970), who contrasted the patterns
of drawing disability in the two groups, and by Kirk
and Kertesz (1989), who noted that performance on a
free-drawing task correlated strongly with scores on a
visual-perceptual task in right-BDPs, but more strongly
with tests of verbal comprehension, and with the severity
of the motor defect in left-BDPs. These authors con-
cluded that CA originates from a visuospatial defect in
right-BDPs, whilst it could be linked to semantic or ele-
mentary motor disorders in left-BDPs. The suggestion
that, on a copying task, a disorder at the elementary
motor level may play a crucial role in left-BDPs has been
confirmed by Carlesimo et al. (1993), whereas Trojano
et al. (2004) have shown that drawing accuracy was sig-
nificantly correlated with some spatial perceptual and
representational tests in right- but not in left-BDPs,
retaining a “weak” version of the spatial lateralization
hypothesis.
Even more controversial is the meaning of the quali-
tative features considered as typical of CA resulting from
left-hemisphere lesions. Warrington et al. (1966) put for-
ward the hypothesis that the constructive disabilities of
left-BDPs may be due to a planning disorder. This
hypothesis was put to the test by Hecaen and Assal
(1970), who required right- and left-BDPs to copy a cube
under two different conditions: (1) simple copy of the
model; and (2) copy with the help of landmarks previ-
ously marked on the paper sheet. The presence of land-
marks significantly improved the copy performance of
left-BDPs, but not of right-BDPs. On the basis of these
findings, Hecaen and Assal (1970) claimed that a plan-
ning disorder underlies constructive disabilities of left-
(but not of right-) BDPs, but Collignon and Rondeaux
336 G. GAINOTTI AND L. TROJANO

Fig. 16.3. Copying of geometric drawings: cube (model on the top). First row: drawings by left brain-damaged patients usually
show simplifications and distortions, but with relatively spared spatial relationships. Second row: drawings by right-brain-
damaged patients usually show left-sided omissions and frequent visuospatial defects. Lower rows: drawings by demented patients
show gross simplifications, spatial distortions, errors of perspective, and closing-in (bottom figure).

(1974), Gainotti et al. (1977), and Pillon (1981) could not
replicate the results obtained by Hecaen and Assal
(1970), administering analogous tests to larger samples
of right- and left-BDPs.
On the contrary, the possibility that some features of
the constructive disabilities shown by left-BDPs may be
due to high-level conceptual-semantic disorders, and
other features to the presence of a right-hand motor
defect, is supported by several data. As for the first point,
Gainotti et al. (1983) showed that the inability to draw
from memory displayed by these patients is strongly
related to the presence of semantic-lexical disorders at
 CONSTRUCTIONAL APRAXIA 337

Fig. 16.4. Copying of geometric drawings: novel figure (model on the top). First row: simplifications, perseverations, and dis-
tortions in drawings by left-brain-damaged patients. Second row: left-sided omissions and gross visuospatial defects in drawings
by right-brain-damaged patients. Lower rows: drawings by demented patients may show gross spatial distortions, perseverations,
simplifications, and closing-in (bottom figure).

the receptive level, and Kirk and Kertesz (1989) noted
that in left-BDPs performance on a free-drawing task
correlated strongly with scores obtained on tests of verbal
comprehension. As for the second point, Kirk and
Kertesz (1989) noted that in left-BDPs the tendency to
produce hesitant and simplified drawings correlated with
the severity of right-sided motor defects.
The hypothesis of different alterations of drawing
abilities depending on the hemispheric side of the lesion
has been renewed in a study in which 30 right- or left-
BDPs with vascular lesions centered upon the parietal
lobes were required to perform a stick assembly test
and several other tests of spatial perception (Laeng,
2006). On the basis of the results, Laeng (2006) proposed
that qualitative differences in CA of right- and left-BDPs
might be explained by a predominant role of the right
hemisphere in computating precise metric spatial (coor-
dinate) relations, and by the major contribution of the left
hemisphere in appreciation of abstract (categoric) spatial
relations, like those usually captured by prepositions or
locatives (e.g., “inside,” “between”), in keeping with
the hypothesis put forward by Kosslyn (1987; see
Trojano et al., 2006).
A specific, but different, impairment in right-BDPs
was postulated by Russell et al. (2010) in a study on 8
patients showing CA compared with 7 right-BDPs
338 G. GAINOTTI AND L. TROJANO

Fig. 16.5. Copying of Rey complex figure (model on the top). Drawings by left-brain-damaged patients (upper row), by right-
brain-damaged patients (second row), with or without hemineglect, and by demented patients (lower row). Note in the right bottom
figure that the reproduction of the single subcomponents is relatively spared, but spatial relationships among them are lost.

without CA. In all CA patients brain lesions involved
frontal and parietal lobes. BDPs with or without CA per-
formed two tasks in which they were required to judge
whether a pattern shifted position (spatial task) or chan-
ged in configuration (nonspatial task) across saccades.
BDPs with CA performed worse than BDPs without
CA and, on this basis, the authors suggested that CA
in right-BDPs might result from impairment in remem-
bering spatial information across fixations, i.e., in remap-
ping stimuli locations across saccades.
Lastly, it has to be mentioned that drawing in right-
BDPs is often affected by unilateral left neglect, and that
in these cases the spatial position and hierarchic structure
of stimuli strongly influence patients’ graphic produc-
tions (Behrmann and Plaut, 2001).
The difficulty of linking CA with the side or the intra-
hemispheric locus of the cerebral lesion was stressed in
an old study by Benson and Barton (1970) in 24 BDPs
with positive radioactive brain scan in one of the four
quadrants of the brain (right anterior, right posterior, left
anterior, and left posterior). In this study, constructional
disabilities differed among patient groups, depending
upon the side and the intrahemispheric locus of lesion,
as well as upon the nature of the task.
More recently, similar conclusions have been reached
in a very well-controlled study, in which the relationships
between drawing performance and brain lesions were
addressed in a large consecutive sample of focal BDPs
by means of voxel-based morphometry (Chechlacz
et al., 2014). The authors required patients to copy a com-
plex figure included in the Birmingham Cognitive
Screen battery (Humphreys et al., 2012) to obtain several
scores expressing different facets of the constructional
task. The results showed that different lesions in the
two hemispheres were significantly correlated with each
score: (1) overall accuracy correlated with lesions of the
subcortical nuclei in the right hemisphere; (2) omissions
of left details of the stimulus correlated with lesions in the
right inferior parietal lobule (angular and supramarginal
gyri) and in the right middle frontal gyrus; (3) spatial
 CONSTRUCTIONAL APRAXIA
errors correlated with a wide range of brain lesions,
including the insula and inferior temporal gyri, in both
the right and the left hemisphere, and the precuneus in
the left hemisphere; (4) errors in reproducing the stimu-
lus details correlated with lesions in the right middle tem-
poral gyrus; and (5) errors in reproducing the overall
configuration of the stimulus correlated with lesions in
the left insula, and the left calcarine cortex. This study
clearly demonstrated that lesions in either hemisphere
can determine different drawing impairments, and, by
implication, that drawing depends on several cognitive
processes based on wide interconnected neuronal net-
works. Furthermore, according to this study, the left infe-
rior parietal region, and above all the left angular gyrus,
would not be included within these neural networks.
Results more consistent with the classic views of the
relationships between CA and (right) parietal lobe have
been obtained by Biesbroek et al. (2014). They adminis-
tered to a large cohort of patients with first-ever ischemic
stroke the ROCF copy test and the judgment of line ori-
entation, (JLOT), in which subjects are requested to iden-
tify among several alternatives the lines that are in the
same orientation as those presented as stimuli (Benton
et al., 1975), because both tests measure visuoperception,
while only the ROCF has a constructional component.
They found large shared anatomic correlates for the
ROCF and JLOT in the right-hemispheric frontal lobe,
superior temporal lobe, and supramarginal gyrus,
whereas lesions in the right superior parietal lobule,
angular gyrus, and middle occipital gyri were associated
with poor performance on the ROCF, but not the JLOT.
Although these findings may be partly explained
by exclusion of patients with right paresis and/or
tool apraxia from the study, they may provide evidence
for a relevant role of the inferior and superior parietal
lobules of the right hemisphere in visuoconstructive
activities proper.
CONSTRUCTIONAL APRAXIA IN
ALZHEIMER DISEASE AND OTHER
FORMS OF DEMENTIA
The observation that many brain regions in both hemi-
spheres are involved in different aspects of drawing,
and by implication of constructional tasks, can provide
an explanation for the classic findings suggesting that
CA is related to poor intellectual abilities in focal BDPs
(Arrigoni and De Renzi, 1964), and can represent an
index of diffuse cognitive deterioration, both in left-
(Borod et al., 1982) and right- (Benowitz et al., 1990;
Lee et al., 2008) BDPs. In the same vein, in patients with
subcortical vascular dementia severity of constructional
impairments has been shown to correlate with extension
of white-matter damage (Price et al., 2005).
339
Indeed, CA is considered one of the most common
behavioural alterations in different types of dementia
(for review, see Trojano and Conson, 2008; Trojano
and Gainotti, 2016). In principle, constructional disor-
ders in dementia may be ascribed to the failure of visuo-
spatial processing, or to an impairment of planning
abilities, since constructional tasks, particularly those
implying new or complex models, can be considered
as a sort of problem-solving task. Therefore, different
degenerative diseases are likely characterized by differ-
ent mechanisms giving rise to CA. However, different
pathogenetic mechanisms can lead to constructional dis-
orders even within a single degenerative disease, such as
Alzheimer disease (AD), which, from its early stages, is
characterized by functional or structural involvement of
the mesial and lateral aspects of the parietal lobes (see
Rapoport, 1991; Herholz, 1995; Mosconi et al., 2004;
Huang et al., 2007, and Schroeter et al., 2009, for
reviews).
CA is not observed in the amnesic forms of mild cog-
nitive impairment (Gainotti et al., 2014) but is present
from early clinical stages of AD, with increasing severity
as the illness progresses (Ajuriaguerra et al., 1960). In
free-drawing tasks AD patients often show simplifica-
tions, spatial alterations, and lack of perspective (Kirk
and Kertesz, 1991) from the early stages of AD, while
copying may deteriorate later (Rouleau et al., 1996).
The reproduction of complex figures is particularly
sensitive to the progression of the disease (Binetti
et al., 1998; Figs 16.3–16.5). For instance, the ROCF
may be reproduced in a simplified way, with single con-
stitutive elements put one after the other, even in early
AD. Here, patients seem to be able to recognize and
reproduce single, well-known elements but are unable
to reproduce complex spatial relationships correctly
(Fig. 16.5). Another “simplification” error may consist
in the reproduction of more familiar or simpler figures
instead of more complex ones (e.g., a square instead of
a diamond). As the disease progresses, patients usually
become unable even to draw simple figures correctly,
as they no have longer access to well-consolidated motor
subroutines. Throughout the disease course, but particu-
larly in advanced stages, the tendency to draw very close
to the model in copying tasks, or to overlap the copy with
the model, or to draw starting from one or more elements
of the model can be observed (Figs 16.3 and 16.4); in late
stages patients can only trace the pencil over the lines of
the model, producing a scrawl. This class of phenomena,
termed “closing-in” (Mayer Gross, 1935), has often been
reported in patients with different kinds of dementia
(De Lucia et al., 2014; Grossi et al., 2015), particularly
AD (Ajuriaguerra et al., 1960; Gainotti, 1972). and in
some patients with selective posterior atrophy (Suzuki
et al., 2003), although most recent interpretations of
340 G. GAINOTTI AND L. TROJANO
this symptom tie it to frontal/executive dysfunctions
(De Lucia et al., 2013).
The constructional impairment in AD patients may
stem from different cognitive mechanisms. Caine and
Hodges (2001) carried out two separate studies to inves-
tigate visuospatial and semantic deficits in a sample of
AD patients in the early stages of the disease, and found
that only a small proportion of patients were impaired on
visuospatial tasks. In the moderate stage of AD, visuo-
spatial impairments would become more evident, and
play a relevant role in the development of constructional
disorders (Binetti et al., 1998). More recently, Guerin
et al. (2002) suggested that constructional impairment
in patients with AD is likely to be related to early phases
of spatial-constructional processing rather than to the late
stage of planning, although other authors have under-
lined the possible contribution of executive impairments
in these patients (Freeman et al., 2000).
In recent years, the different mechanisms giving rise
to CA in AD patients have been tackled by means of mor-
phometric and neurofunctional studies. For instance,
Ahn et al. (2011) reported that impaired performance
on the ROCF copying task was strongly related to atro-
phy in the right hemisphere, with task performance being
primarily correlated with atrophy in the superior tempo-
ral gyrus, middle frontal gyrus, superior parietal lobule,
fusiform gyrus, lingual gyrus, and posterior cingulate
gyrus. However, Serra et al. (2014), comparing AD
patients with or without CA, identified on a clinical diag-
nostic free-hand copying of drawings test, reported a
quite different picture: AD patients with CA showed a
significant reduction of the gray matter bilaterally in
the angular gyrus (BA 39), precuneus (BA 7), posterior
cingulate cortex (BA 23/31), right fusiform (BA 37),
middle temporal gyrus (BA 21), and occipital cortex
(BA 18), as compared with AD patients without CA.
The differences between such studies might originate
from different characteristics of the AD samples, and
from the neuropsychologic measures used to assess con-
structional abilities.
Several recent neurofunctional studies illustrate such
sources of variability. In a large sample of AD patients,
Shon et al. (2013) found that drawing the clock face with-
out a model correlated with regional glucose metabolism
in the bilateral temporoparietal and left middle frontal
regions, whereas copying a clock face correlated with
metabolism in bilateral temporoparietal regions only.
Similarly, in a large sample of drug-naïve AD patients,
Matsuoka et al. (2013) observed that regional blood flow
in bilateral parietal regions correlated with overall perfor-
mance on clock drawing and with the partial score on set-
ting the hands. A positron emission tomography (PET)
study using copying of a simple geometric figure as a
measure of constructional abilities showed, instead, an
exclusive correlation of copying performance with glu-
cose metabolism in the left inferior parietal lobule and
left inferior frontal gyrus (Teipel et al., 2006).
The different role played by visuospatial and execu-
tive disorders in constructive disabilities of demented
patients is illustrated by studies comparing AD patients
with patients affected by frontotemporal dementia
(FTD). For instance, Thompson et al. (2005) observed
that FTD patients outperformed AD patients in copying
geometric figures of different complexity, were charac-
terized by a higher number of perseverative errors and
of poor organization of the copy, but showed a lower
number of spatial errors than AD patients. In the same
vein, Possin et al. (2011), using quantitative morphomet-
ric evaluation of structural magnetic resonance imaging
(MRI), showed that FTD patients performed better than
AD patients in copying drawings, but in AD patients
poor figure copy was associated with defective perfor-
mance on spatial perception and attention tasks and cor-
related significantly with volume in the right parietal
cortex. In contrast, in FTD patients performance on fig-
ure copy was significantly associated with scores on spa-
tial planning and working-memory tasks, and correlated
with right dorsolateral prefrontal cortex volumes. The
apparently paradoxic recent observation that some
patients with FTD can show defective copying abilities
but improve their graphic productions after a delay (when
the model is not in sight) would be compatible with the
idea that defective planning and attentional control abil-
ities can interfere with drawing in these patients, through
mechanisms similar to those giving rise to closing-in
(Roth et al., 2014).
With respect to the relationships between CA and
other forms of dementia, it is also interesting to note that,
according to McKeith et al. (2004) visuospatial difficul-
ties are often early and prominent in dementia with dif-
fuse Lewy bodies disease (LBD) and these defects likely
contribute to the disproportionate impairment in con-
structional tasks in LBD patients (Mori et al., 2000;
Crowell et al., 2007; Nervi et al., 2008). According to
Tiraboschi et al. (2006), visuospatial or constructional
impairments are present in 74% of patients with early-
stage pathologically confirmed LBD dementia compared
with 45% of those with AD and, even if the neuroimag-
ing hallmark of LBD consists of a reduced occipital lobe
metabolism with respect to AD (Filippi et al., 2012), a
loss of parieto-occipital white-matter integrity has been
documented in LBD (Nedelska et al., 2015).
NEURAL AND COGNITIVE BASIS
OF DRAWING
The study of constructional abilities in BDPs has been
complemented in recent years by papers investigating
 CONSTRUCTIONAL APRAXIA
brain–behavior relationships by means of the modern
functional neuroimaging techniques in healthy subjects.
Most functional neuroimaging studies focused on draw-
ing, although functional MRI (fMRI) neuroimaging dur-
ing drawing is constrained by the relevant artefacts
induced by the hand and arm movements. For this rea-
son, the majority of experimental paradigms included
drawing-related tasks, rather than actual drawing, and
it is only recently that fMRI-compatible graphic tablets
(e.g., Hauptmann et al., 2009) have allowed the analysis
of hand movements during drawing.
An fMRI study (Ino et al., 2003) in which subjects had
to move their fingers to trace clock hands at given hours,
compared to a control condition in which subjects had to
perform horizontal and vertical movements with their
fingers, demonstrated the activation of a bilateral fronto-
parietal network, including the superior parietal lobule
(BA 7) and the intraparietal sulcus (BA 39, 40). Such
a network was largely symmetric, and was observed in
most subjects on individual analysis.
In another fMRI study subjects were required to
mimic tracing contours of visually presented objects,
compared with a condition in which subjects had to
observe and name the same objects (Makuuchi et al.,
2003). The results of the group analysis showed cortical
activation in the left sensorimotor and premotor areas
and in the posterior temporal sulcus (BA 37), and,
above all, an almost symmetric bilateral activation in
the superior parietal lobule (BA 7), in the intraparietal
sulcus (BA 7/40), and in the supramarginal gyrus
(BA 40), whereas no activation was found in the angular
gyrus. Individual analysis showed that the superior
parietal lobule and the dorsal premotor areas were acti-
vated in most subjects, with a predominance on the left
hemisphere.
The problem of possible artefacts due to arm and hand
movements was overcome in two studies by Harrington
et al. (2007, 2009) by requiring subjects to imagine them-
selves drawing common objects. In the first study the
authors contrasted drawing and writing (Harrington
et al., 2007), whereas in the second (Harrington et al.,
2009), subjects were required to simulate drawing of
objects or nonsense shapes shown to them before each
trial. Simulated drawing recruited a large, distributed net-
work of frontal, parietal, and temporal structures. In par-
ticular, drawing familiar objects, as compared with
nonobjects, determined activation within the inferior
temporal and anterior inferior frontal cortex in the left
hemisphere. According to the authors the inferior tempo-
ral cortex is involved in visual semantic processing dur-
ing the drawing of familiar objects, while anterior
inferior frontal activation may be related to selection of
specific semantic features of objects. Although based
on a task largely relying on visual imagery, these
341
observations highlight the complex cognitive mecha-
nisms involved in the drawing process.
Ogawa and Inui (2009) employed an experimental
set-up in which subjects were required to trace over
the visually presented model or to copy the model on a
separate space. The results of the contrast between copy-
ing and tracing (aimed to subtract the purely motor per-
formance from the copying condition) showed an
activation of the lingual gyri, superior occipital gyri,
and the inferior parietal lobule bilaterally (intraparietal
sulcus, BA 7/40). On this basis, the authors concluded
that the posterior parietal cortex is crucially involved
in the spatial transformations needed to reproduce a
model in copying tasks, independently from the memory
requirements of the task, and from task difficulty. How-
ever, it is worth mentioning that an fMRI study contrast-
ing time-constrained visuomotor tracking and copying
showed a strong activation in the occipital lobes bilater-
ally, but not in the inferior parietal lobules (Ferber
et al., 2007).
Taking advantage of an fMRI-compatible graphic tab-
let, Miall et al. (2014) required participants to draw faces
or abstract patterns with different levels of visual detail,
while their eye movements were controlled. The results
demonstrated that task difficulty affected eye movements
more than hand movements, and modulated activation
within the wide cortical network, including the right
superior parietal lobule and the precuneus, recruited by
figure copying.
Copying sketchy or naturalistic faces (contrasted with
tracing the contour of the same face stimuli, and with pas-
sive viewing of the stimuli to be copied) was also inves-
tigated in another fMRI study (Schaer et al., 2012). The
results showed that, compared to passive viewing, natu-
ralistic and sketchy drawing recruited predominantly the
dorsal visual pathway, somatosensory and motor areas
and bilateral BA 44, whereas copying compared to trac-
ing involved the precuneus, cuneus, and primary
visual areas.
The fMRI studies reviewed above greatly differed in
the task used for assessing drawing, since most addressed
drawing-related activities, such as imagined drawing or
drawing without seeing one’s own hand. Moreover, stim-
uli varied from sinusoidal lines, to geometric shapes, to
faces, thus being very heterogeneous in their cognitive
requirements.
Last, in some studies drawing or drawing-related
tasks were contrasted with tracing, in others with pas-
sive viewing, and in others with naming objects. These
considerations contribute to explain the divergences
among studies, and suggest caution in deriving a
comprehensive model of the neural and cognitive
underpinnings of the drawing processes on the basis
of the neurofunctional evidence available. Nonetheless,
342 G. GAINOTTI AND L. TROJANO
functional neuroimaging and neuropsychologic data
concur in demonstrating that drawing is a multicompo-
nential process, based on a widely distributed neural
network.
Such observations are compatible with the idea that
the process of drawing involves different cognitive com-
ponents. Several authors have tried to single out such
components within comprehensive models (Roncato
et al., 1987; van Sommers, 1989; Grossi, 1991; Guerin
et al., 1999). All these models share the idea that visuo-
spatial processes, dedicated planning abilities, and gen-
eral control processes are involved in drawing (for a
review, see Grossi and Trojano, 2002), although the
models differ from each other in terms of formal charac-
teristics, depth of analysis, and some theoretic aspects.
It is worth mentioning that Grossi (1991), drawing on
the distinction between lexical and sublexical compo-
nents of language, proposed the existence of two copying
procedures: a lexical route, which predominantly
involves activation of familiar constructional schemata
(for example, in drawing a square or a face) and a line-
by-line procedure, based on a spatial analysis which does
not use constructional representations (activated, for
instance, when copying novel stimuli). Both procedures
may be adopted for copying complex pictures, but some
patients might be constrained to use either one or the
other. For instance, visual agnosic patients might tend
to adopt a slavish line-by-line copying procedure since
they cannot access the lexical route for familiar objects
(Wapner et al., 1978; Trojano and Grossi, 1992). In con-
trast, focal BDPs (Grossi et al., 1996; Trojano and Grossi,
1998) or patients affected by degenerative dementia may
draw simple figures successfully without integrating cor-
rectly shaped simple elements in a coherent whole. Such
errors could be ascribed to planning or visuospatial
defects in the presence of relatively spared abilities to
activate motor subroutines for drawing well-known fig-
ures, a sort of constructional lexicon, which develops as a
result of formal education and personal aptitudes.
The cognitive models for drawing abilities have not
gained general acceptance, because only a few patients
have been described who made consistent errors across
several visuospatial and constructional tasks, allowing
attempts at coherent theoretic explanations (see Grossi
et al., 1996, for the dissociation of vertical and horizontal
space processing; see Roncato et al., 1987; Trojano and
Grossi, 1998, for cognitively oriented diagnosis of CA).
Moreover, it must be acknowledged that the analysis of
constructional errors is not a straightforward proce-
dure and is further complicated by the effect of con-
structional strategies. One can reproduce a figure
through different procedures; for instance, in copying
the ROCF it is possible to reproduce first the main rect-
angle or to draw the model by segmenting it into small
subunits. Such a decision will have a great impact on
the process of drawing and will also influence type and
number of errors.
A clear example of the influence of constructional
strategies on performance comes from neglect literature:
Ishiai et al. (1997) demonstrated that the choice of differ-
ent constructional strategies could even abolish omis-
sions in neglect patients’ drawings. In some cases the
choice of a specific strategy seems to be forced by other
cognitive defects, as in the case of visual agnosic patients
(Wapner et al., 1978; Trojano and Grossi, 1992).
Several studies have aimed to establish whether focal
brain lesions may alter constructional strategies, after the
early formalized observations of Osterreith (1944) on
ROCF copying by BDPs. It has been asserted that obser-
vation of copying strategies in certain patients reveals the
presence of a constructional disability more effectively
than analysis of the final result (Kaplan, 1983, 1988).
Semenza et al. (1978) noted that in copying tasks
right-BDPs and left-nonaphasic BDPs tended to use a
global strategy, similar to that adopted by normal sub-
jects, whereas aphasics used a more analytical (piece-
meal approach) strategy in copying the model. At
variance, Binder (1982) demonstrated that, in copying
the ROCF, both right- and left-BDPs broke the task down
into successive steps, while control subjects tended to use
a global strategy. Similarly, Trojano et al. (1993), in a
study on a sample of focal BDPs without severe CA
observed that, regardless of the lesion locus, patients
tended to adopt a line-by-line procedure in copying the
ROCF, likely in response to the difficulties raised by
the task.
CONCLUDING REMARKS ON THE
RELATIONS BETWEEN
CONSTRUCTIONAL APRAXIA AND
PARIETAL LOBE LESIONS
Even if, since the classic papers of Kleist (1934), Mayer
Gross (1935), and Critchley (1953), CA has been consid-
ered a typical sign of parietal lobe lesion, and as a pre-
cious tool to appreciate the spatial abilities subsumed
by this lobe, the links between parietal lobe damage
and CA have become more and more problematic with
the development of more sophisticated neuropsycholo-
gic models and methods of investigations. On the one
hand, it has become increasingly clear that CA is a
heterogeneous construct that can be examined with very
different tasks, including drawing, assembling, and
building complex models, that are only mildly intercon-
nected and tap various kinds of visuospatial, perceptual,
attentional, planning, and motor mechanisms. On the
other hand, when attempts have been made to correlate
neuroimaging data with specific kinds of constructional
 CONSTRUCTIONAL APRAXIA
disorders in large consecutive samples of focal BDPs,
results have been very scattered and the inferior parietal
region has sometimes (Biesbroek et al., 2014), but at
other times not (Chechlacz et al., 2014), been included
in the range of the widely interconnected neuronal net-
works subsuming constructional abilities.
It must be acknowledged, however, that not only the
kind of task, but also the content of the material to be
reproduced can have contributed to decreasing the links
between parietal lobe and constructive disabilities. The
stimuli used to assess CA by clinical authors, such as
Ettlinger et al. (1957) and Mc Fie and Zangwill
(1960), who stressed the relationships between CA and
parietal lobe lesions, consisted indeed of simple models,
such as geometric figures, or the schematic drawings of a
house or of a man. On the contrary, much more complex
and naturalistic stimuli have often been used in studies in
which no relation between parietal lesions and drawing
performance was observed. For instance, in tasks of free
drawings of naturalistic stimuli, used by Gainotti et al.
(1983), Grossmann (1988), and Kirk and Kertesz
(1989), results obtained by left-BDPs were related to
the presence of aphasia, verbal comprehension disorders,
and semantic-lexical disturbances typical of temporal
lobe lesions. Similar objections can be made to results
of investigations using face stimuli as models (Schaer
et al., 2012; Miall et al., 2014), even if in these studies
the drawing activity recruited the dorsal visual stream
(Schaer et al., 2012) and the right superior parietal lobule
(Miall et al., 2014).
It must also be noted that, although drawing is an
exquisitely human ability, some insights into the neural
basis of drawing have been collected by recording and
analyzing single neuron activity in primates trained to
perform sequential movements resembling drawing with
their hands.
For instance, Averbeck et al. (2002) characterized the
functional roles of different brain areas in coding differ-
ent aspects of drawing. These include higher-level cog-
nitive attributes, such as the shape and serial order of
the segments being drawn, as well as lower-level attri-
butes, such as the direction, position, and speed of draw-
ing. Results obtained in these studies suggest that the
parietal lobes play an important role in basic components
of constructional tasks. Thus, Chafee et al. (2007) per-
formed a study of single-cell recordings, analyzing the
activity of posterior parietal area PG (7a) neurons in
monkeys performing a constructional task. In this task,
a model consisting of a variable arrangement of squares
(one of which was missing) was presented, and monkeys
replaced the missing square to reconstruct the model con-
figuration. Activity of many 7a neurons varied systemat-
ically with the position of the missing square and
predicted where monkeys were going to add parts to
343
the object they were building. These data show that some
parietal neurons participate in neural representations of
space that reflect spatial cognitive as opposed to senso-
rimotor processing, coding the results of spatial compu-
tations performed on visual stimuli to meet the cognitive
objectives.
More recently, Averbeck et al. (2009) examined the
differential contributions of the superior parietal cortex
and the caudal dorsolateral prefrontal cortex in monkeys
trained to draw different geometric shapes (triangles,
squares). The analysis of firing rate in individual neurons
demonstrated that prefrontal neurons carried consider-
able information about hand velocity, a purely motor fac-
tor. Conversely, neurons in the superior parietal cortex
coded both shape and motor factors, suggesting that
the superior parietal cortex plays a role in both the cog-
nitive and motor components of the “drawing” task.
Furthermore, neuropsychologic evidence of parietal
involvement is supported by functional imaging studies
of healthy individuals, which have highlighted parietal
involvement in drawing from copying. For instance,
Makuuchi et al. (2003), on the basis of their fMRI study
(mentioned above), suggested that in copying a visually
presented object, information is mainly transferred to the
parietal lobe via the visual dorsal pathway, and the pari-
etal lobe selects the drawing strokes to construct a repre-
sentation of the object. This representation is transmitted
to the dorsal (BA 6) and ventral (BA 44) premotor areas,
motor areas, and to motor subcortical structures (i.e.,
basal ganglia and cerebellum). In parallel, the ventral
stream processes visual properties of objects and this
information may be implemented in the drawing plan.
On the other hand, Ogawa and Inui (2009) compared
healthy subjects’ drawing brain activities, by tracing over
the visually presented model or by copying the model on
a separate space, and used fMRI to test the hypothesis
that the posterior parietal cortex plays a role in coordinate
transformation. A memory-guided condition was also
introduced, resulting in four drawing conditions; tracing
over or copying a model at different locations (tracing
and copying), with or without an on-screen model (visual
and memory guidance). As hypothesized, the intraparie-
tal sulcus bilaterally in the posterior parietal cortex
showed significantly greater activations in copying than
in tracing, under both visual and memory guidance, with
a distinct activation pattern involving the premotor and
mesial motor regions. This study indicates a role of the
posterior parietal cortex in coordinate transformation
for drawing by copying, which may be important for
the copying deficit observed in CA.
Another important contribution of functional neuro-
imaging to the evaluation of the relationships between
CA and parietal lobe impairment comes from studies
conducted in AD in which PET and other neuroimaging
344 G. GAINOTTI AND L. TROJANO
studies have repeatedly shown a pattern of reduced
metabolism in temporoparietal areas (see reviews in
Rapoport, 1991, Herholz, 1995, and Schroeter et al.,
2009). Several authors have obtained data suggesting
that this pattern of reduced metabolism in temporopar-
ietal areas may be related to impairment on constructive
tasks. For instance, Ahn et al. (2011) found a relation-
ship between ROCF copying scores and atrophy of the
superior parietal lobe, Serra et al. (2014) showed that
AD patients with CA have a reduction of the gray matter
in the angular gyrus, Shon et al. (2013), found that
drawing the clock face correlates with regional glucose
metabolism in bilateral temporoparietal areas, and
Matsuoka et al. (2013) observed that overall perfor-
mance on clock drawing is significantly correlated with
regional blood flow in the bilateral parietal and poste-
rior temporal lobes.
By contrasting findings in AD patients with those
obtained in FTD, in which the parietal lobes are substan-
tially spared, Thompson et al. (2005) and Possin et al.
(2011) suggested that the drawing impairments in the
two patient groups were based on different cognitive
mechanisms and related to different anatomic structures.
In AD the patients’ poor figure copy was associated with
performance on spatial perception and attention tasks,
and correlated significantly with volumes in the right
parietal cortex, whereas in FTD patients performance
on figure copy correlated significantly with scores on
spatial planning and working-memory tasks, and was
related with right dorsolateral prefrontal cortex volumes.
Complementary to the relative integrity of visuospatial
forms of constructive abilities in FTD are the prominent
visuospatial difficulties observed in LBD, in which these
perceptual defects probably contribute to the dispropor-
tionate impairment in constructional tasks remarked in
this disease (McKeith et al., 2004; Tiraboschi et al.,
2006) and the lesions mainly involve the posterior dorsal
portions of the brain.
These interpretations of the role that the parietal lobe
could have in constructive activities are consistent with
the account that a recent review of the organization
and evolution of parietofrontal processing streams in
monkeys and humans (Caminiti et al., 2015) has given
of the activity of neurons in the caudal part of the inferior
parietal lobule (area PG), because, according to these
authors, this area reflects the cognitive process related
to the analysis of object structure necessary to direct a
construction task.
In conclusion, on the basis of the above-mentioned
considerations, the relationships between parietal lobe
functions and constructional activities must be consid-
ered, taking into account on the one hand the heteroge-
neity of tasks and of cognitive functions requested by
different kinds of constructional activities and, on the
other hand, the plurality of functions and of processing
streams linking different parts of the parietal lobes to
the occipital and frontal lobes. According to Caminiti
et al. (2015), we should take into account, among the lat-
ter: (1) the integration of visual and somatic information
accomplished by the dorsal parietal areas and necessary
for visually guided arm movement; (2) the visual control
of hand–object interaction for different forms of hand
action, carried out by the ventral parieto-premotor
stream; and (3) the information more directly related to
arm movement, such as the kinetic and kinematic limb
variables necessary for composing motor commands
for continuous hand movements mimicking hand draw-
ing, performed by the somatomotor stream (somatosen-
sory cluster S1, S2 and medial intraparietal). These
suggestions can be considered as useful hints to guide
further anatomoclinical and experimental investigations,
but much work is certainly needed before the links can be
clarified between functions and processing streams of
different parts of the parietal lobes (see Freud et al.,
2016, for a recent reappraisal of this issue) and related
aspects of constructional abilities.
REFERENCES
Ahn HJ, Seo SW, Chin J et al. (2011). The cortical neuroanat-
omy of neuropsychological deficits in mild cognitive
impairment and Alzheimer’s disease: a surface-based mor-
phometric analysis. Neuropsychologia 49: 3931–3945.
Ajuriaguerra J, Muller M, Tissot R (1960). A propos de quel-
ques problèmes poses par l’apraxie dans les demences.
Encephale 49: 275–401.
Arena R, Gainotti G (1978). Constructional apraxia and visuo-
perceptive disabilities in relation to laterality of cerebral
lesions. Cortex 14: 463–473.
Arrigoni C, De Renzi E (1964). Constructional apraxia and
hemispheric locus of lesion. Cortex 1: 170–197.
Averbeck BB, Chafee MV, Crowe DA et al. (2002). Parallel
processing of serial movements in prefrontal cortex. Proc
Natl Acad Sci USA 99: 13172–13177.
Averbeck BB, Crowe DA, Chafee MV et al. (2009).
Differential contribution of superior parietal and dorsal-
lateral prefrontal cortices in copying. Cortex 45: 432–441.
Behrmann M, Plaut DC (2001). The interaction of spatial ref-
erence frames and hierarchical object representations: evi-
dence from figure copying in hemispatial neglect. Cogn
Affect Behav Neurosci 1: 307–329.
Benowitz LI, Moya KL, Levine DN (1990). Impaired verbal
reasoning and constructional apraxia in subjects with right
hemisphere damage. Neuropsychologia 28: 231–241.
Benson DF, Barton MI (1970). Disturbances in constructional
ability. Cortex 6: 19–46.
Benton AL (1962). The visual retention test as a constructional
praxis task. Confin Neurol 22: 141–155.
Benton AL (1989). Constructional apraxia. In: F Boller,
J Grafman (Eds.), Handbook of neuropsychology. vol. 2.
Elsevier, Amsterdam, pp. 387–394.
 CONSTRUCTIONAL APRAXIA
Benton AL, Fogel ML (1962). Three-dimensional construc-
tional praxis: a clinical test. Arch Neurol 7: 347–354.
Benton AL, Hannay HJ, Varney NR (1975). Visual perception
of line direction in patients with unilateral brain disease.
Neurology 25: 907–910.
Biesbroek JM, van Zandvoort MJ, Kuijf HJ et al. (2014). The
anatomy of visuospatial construction revealed by lesion-
symptom mapping. Neuropsychologia 62: 68–76.
Binder LM (1982). Constructional strategies on complex fig-
ure drawings after unilateral brain damage. J Clin
Neuropsychol 4: 51–58.
Binetti G, Cappa S, Magni E et al. (1998). Visual and spatial
perception in the early phase of Alzheimer’s disease.
Neuropsychology 12: 29–33.
Borod JC, Carper M, Goodglass H (1982). WAIS performance
IQ in aphasia as a function of auditory comprehension and
constructional apraxia. Cortex 18: 212–220.
Caine D, Hodges JR (2001). Heterogeneity of semantic and
visuospatial deficits in early Alzheimer’s disease.
Neuropsychology 15: 155–164.
Caminiti R, Innocenti GM, Battaglia-Mayer A (2015).
Organization and evolution of parieto-frontal processing
streams in macaque monkeys and humans. Neurosci
Biobehav Rev 56: 73–96.
Capruso DX, Hamsher KD (2011). Constructional ability in
two- versus three-dimensions: relationship to spatial
vision and locus of cerebrovascular lesion. Cortex 47:
696–705.
Carlesimo GA, Fadda L, Caltagirone C (1993). Basic mecha-
nisms of constructional apraxia in unilateral brain-
damaged patients: role of visuo-perceptual and executive
disorders. J Clin Exp Neuropsychol 15: 342–358.
Chafee MV, Averbeck BB, Crowe DA (2007). Representing
spatial relationships in posterior parietal cortex: single neu-
rons code object-referenced position. Cereb Cortex 17:
2914–2932.
Chechlacz M, Novick A, Rotshtein P et al. (2014). The neural
substrates of drawing: a voxel-based morphometry analysis
of constructional, hierarchical, and spatial representation
deficits. J Cogn Neurosci 26: 2701–2715.
Collignon R, Rondeaux J (1974). Approche clinique des mod-
alites de l’apraxie constructive secondaire aux lesions cor-
ticales hemispheriques gauches et droites. Acta Neurol
Belg 74: 137–146.
Colombo A, De Renzi E, Faglioni P (1976). The occurrence of
visual neglect in patients with unilateral cerebral disease.
Cortex 12: 221–231.
Critchley M (1953). The parietal lobes, Hafner Press,
New York.
Crowell TA, Luis CA, Cox DE et al. (2007).
Neuropsychological comparison of Alzheimer’s disease
and dementia with Lewy bodies. Dement Geriatr Cogn
Disord 23: 120–125.
Dee HL (1970). Visuoconstructive and visuoperceptive defi-
cits in patients with unilateral cerebral lesions.
Neuropsychologia 8: 305–314.
De Lucia N, Grossi D, Fasanaro AM et al. (2013). Frontal defects
contribute to the genesis of closing-in in Alzheimer’s disease
patients. J Int Neuropsychol Soc 19: 802–808.
345
De Lucia N, Grossi D, Trojano L (2014). The genesis of closing-
in in Alzheimer disease and vascular dementia: a compara-
tive clinical and experimental study. Neuropsychology 28:
312–318.
De Renzi E (1982). Disorders of space exploration and cogni-
tion, Wiley, Chichester.
De Renzi E, Faglioni P (1967). The relationship between
visuo-spatial impairment and constructional apraxia.
Cortex 3: 327–342.
Dide M (1938). Les desorientations temporo-spatiales et la
preponderance de l’hemisphère droit dans les agnoso-
akinesies proprioceptives. Encephale 33: 276–294.
Duensing F (1953). Raumagnostische und ideatorisch-
apraktische Storung der gestaltenden Handelns. Dtsch
Z Nervenheilkd 170: 72–94.
Ettlinger G, Warrington E, Zangwill OL (1957). A further
study of visual-spatial agnosia. Brain 80: 335–361.
Ferber S, Mraz R, Baker N et al. (2007). Shared and differential
neural substrates of copying versus drawing: a functional
magnetic resonance imaging study. Neuroreport 18:
1089–1093.
Filippi M, Agosta F, Barkhof F et al. (2012). EFNS task force:
the use of neuroimaging in the diagnosis of dementia. Eur
J Neurol 19 (e131–140): 1487–1501.
Freedman M, Leach L, Kaplan E et al. (1994). Clock drawing:
a neuropsychological analysis, New York, Oxford.
Freeman RQ, Giovannetti T, Lamar M et al. (2000).
Visuoconstructional problems in dementia: contribution
of executive systems functions. Neuropsychology 14:
415–426.
Freud E, Plaut DC, Behrmann M (2016). ’What’ is happening
in the dorsal visual pathway. Trends Cogn Sci 20: 773–784.
Gainotti G (1972). A quantitative study of the “closing-in”
symptom in normal children and in brain-damaged
patients. Neuropsychologia 10: 429–436.
Gainotti G (1985). Constructional apraxia. In: Fredericks
JAM. Handbook of clinical neurology, 45. Elsevier,
Amsterdam, pp. 491–506.
Gainotti G, Tiacci C (1970). Patterns of drawing disability in
right and left hemispheric patients. Neuropsychologia 8:
379–384.
Gainotti G, Miceli G, Caltagirone C (1977). Constructional
apraxia in left brain-damaged patients: a planning disorder?
Cortex 13: 109–118.
Gainotti G, Silveri MC, Villa G et al. (1983). Drawing objects
from memory in aphasia. Brain 106: 613–622.
Gainotti G, Quaranta D, Vita MG et al. (2014).
Neuropsychological predictors of conversion from mild cog-
nitive impairment to Alzheimer’s disease. J Alzheimers Dis
38: 481–495.
Grossi D (1991). La riabilitazione dei disturbi della cognizione
spaziale. Milan, Masson.
Grossi D, Trojano L (2002). Constructional apraxia. In:
G Denes, L Pizzamiglio (Eds.), Handbook of clinical and
experimental neuropsychology. Psychology Press, Hove.
Grossi D, Calise G, Correra C et al. (1996). Selective drawing
disorders after right subcortical stroke: a neuropsychological
premorbid and follow-up case study. Ital J Neurol Sci 17:
241–248.
346 G. GAINOTTI AND L. TROJANO
Grossi D, De Lucia N, Milan G et al. (2015).
Relationships between environmental dependency and
closing-in in patients with fronto-temporal dementia.
J Int Neuropsychol Soc 21: 1–7.
Grossman M (1988). Drawing deficits in brain-damaged
patients’ freehands pictures. Brain Cogn 8: 189–205.
Guerin F, Ska B, Belleville S (1999). Cognitive processing of
drawing abilities. Brain Cogn 40: 464–478.
Guerin F, Belleville S, Ska B (2002). Characterization of visuo-
constructional disabilities in patients with probable dementia
of Alzheimer’s type. J Clin Exp Neuropsychol 24: 1–17.
Harrington G, Farias D, Davis C et al. (2007). A comparison of
the neural basis for imagined writing and drawing. Hum
Brain Mapp 28: 450–459.
Harrington G, Farias D, Davis C (2009). The neural basis for
simulated drawing and the semantic implications. Cortex
45: 386–393.
Hauptmann B, Sosnik R, Smikt O et al. (2009). A new method
to record and control for 2D movement kinematics during
functional magnetic resonance imaging (fMRI). Cortex 45:
407–417.
Hecaen H, Assal G (1970). A comparison of constructive def-
icits following right and left hemispheric lesions.
Neuropsychologia 8: 289–303.
Hecaen H, Ajuriaguerra J, Massonet J (1951). Les troubles
visuo-constructifs par lesions parieto-occipitales droites.
Role des perturbations vestibulaires. Encephale 46:
122–179.
Hecaen H, Penfield W, Bertrand C et al. (1956). The syndrome
of apractognosia due to lesions of the minor cerebral hemi-
sphere. Arch Neurol Psychiatry 75: 400–434.
Herholz K (1995). FDG PET and differential diagnosis of
dementia. Alzheimer Dis Assoc Disord 9: 6–16.
Huang C, Eidelberg D, Habeck C et al. (2007). Imaging
markers of mild cognitive impairment: multivariate analy-
sis of CBF SPECT. Neurobiol Aging 28: 1062–1069.
Humphreys GW, Bickerton WL, Samson D et al. (2012). The
Birmingham Cognitive Screen (BCoS), Psychology Press,
London.
Ino T, Asada T, Ito J et al. (2003). Parieto-frontal networks for
clock drawing revealed with fMRI. Neurosci Res 45:
71–77.
Ishiai S, Seki K, Koyama Y et al. (1997). Disappearance of
unilateral spatial neglect following a simple instruction.
J Neurol Neurosurg Psychiatry 63: 23–27.
Kaplan E (1983). A process approach to neuropsychological
assessment. In: T Boll, BK Bryant (Eds.), Clinical neuro-
psychology and brain function: research, measurement
and practice. APA, Washington, pp. 129–167.
Kaplan E (1988). The process approach to neuropsychological
assessment. Aphasiology 2: 309–311.
Kashiwagi T, Kashiwagi A, Kunimori Y et al. (1994).
Preserved capacity to copy drawings in severe aphasics
with little premorbid experience. Aphasiology 8: 427–442.
Kimura D (1980). Translations from Liepmann’s essays on
apraxia. In: Research Bulletin 506, London (Ontario):
University of Western Ontario, Department of Psychology.
Kirk A, Kertesz A (1989). Hemispheric contributions to draw-
ing. Neuropsychologia 27: 881–886.
Kirk A, Kertesz A (1991). On drawing impairment in
Alzheimer’s disease. Arch Neurol 48: 73–77.
Kleist K (1912). Der Gang und der gegenwartige Stand der
Apraxie Forschung. Ergebnisse der Neurologie und
Psychiatrie 1: 342–452.
Kleist K (1934). Gehirnpathologie, Barth, Leipzig.
Kosslyn SM (1987). Seeing and imagining in the cerebral
hemispheres: a computational approach. Psychol Rev 94:
48–175.
Laeng B (2006). Constructional apraxia after left or right uni-
lateral stroke. Neuropsychologia 44: 1595–1606.
Lange J (1936). Agnosien und Apraxie. In: O Bumke,
O Foester (Eds.), Handbuch der Neurologie. 6. Springer
Verlag, Berlin, pp. 807–870.
Lee BH, Kim EJ, Ku BD et al. (2008). Cognitive
impairments in patients with hemispatial neglect from
acute right hemisphere stroke. Cogn Behav Neurol 21:
73–76.
Liepmann H (1912). Anatomische Befunden bei Aphasischen
und Apraktischen. Neurologisches Zentralblatt 31:
1524–1529.
Makuuchi M, Kaminaga T, Sugishita M (2003). Both parietal
lobes are involved in drawing: a functional MRI study and
implications for constructional apraxia. Brain Res Cogn
Brain Res 16: 338–347.
Matsuoka T, Narumoto J, Okamura A et al. (2013). Neural cor-
relates of the components of the clock drawing test. Int
Psychogeriatr 25: 1317–1323.
Mayer Gross W (1935). Some observation on apraxia. Proc
R Soc Med 28: 1203–1212.
Mc Fie J, Zangwill OL (1960). Visuoconstructive disabilities
associated with lesions of the left cerebral hemisphere.
Brain 83: 243–260.
McFie J, Piercy MF, Zangwill OL (1950). Visual-spatial agno-
sia associated with lesions of the right cerebral hemisphere.
Brain 73: 167–190.
Mc Keith I, Mintzer J, Aarsland D et al. (2004). Dementia with
Lewy bodies. Lancet Neurol 3: 19–28.
Miall RC, Nam SH, Tchalenko J (2014). The influence of
stimulus format on drawing – a functional imaging study
of decision making in portrait drawing. NeuroImage 102:
608–619.
Mori E, Shimomura T, Fujimori M et al. (2000).
Visuoperceptual impairment in dementia with Lewy bod-
ies. Arch Neurol 57: 489–493.
Mosconi L, Perani D, Sorbi S et al. (2004). MCI conversion to
dementia and the APOE genotype: a prediction study with
FDG-PET. Neurology 63: 2332–2340.
Nedelska Z, Schwarz CG, Boeve BF et al. (2015). White mat-
ter integrity in dementia with Lewy bodies: a voxel-based
analysis of diffusion tensor imaging. Neurobiol Aging 36:
2010–2017.
Nervi A, Reitz C, Tang MX et al. (2008). Comparison of clin-
ical manifestations in Alzheimer disease and dementia with
Lewy bodies. Arch Neurol 65: 1634–1639.
 CONSTRUCTIONAL APRAXIA
Ogawa K, Inui T (2009). The role of the posterior parietal cortex
in drawing by copying. Neuropsychologia 47: 1013–1022.
Osterrieth PA (1944). Le test de copie d’une figure complexe.
Arch Psychol 30: 286–356.
Paterson A, Zangwill OL (1944). Disorders of visual space
perception associated with lesions of the right cerebral
hemisphere. Brain 67: 331–358.
Piercy M, Hecaen H, Ajuriaguerra J (1960). Constructional
apraxia associated with unilateral cerebral lesions – left
and right sided cases compared. Brain 83: 225–242.
Pillon B (1981). Troubles visuo-constructifs et methodes de
compensation: resultats de 85 patients atteints de lesions
cerebrales. Neuropsychologia 19: 375–383.
Poppelreuter W (1917). Die Psychischen Schaedigungen
durch Kopfschuss im Kriege 1914-1916, 1Voss,
Leipzig.
Possin KL, Laluz VR, Alcantar OZ et al. (2011).
Distinct neuroanatomical substrates and cognitive
mechanisms of figure copy performance in Alzheimer’s
disease and behavioral variant frontotemporal dementia.
Neuropsychologia 49: 43–48.
P€
otzl O (1928). Die optischagnostischen St€orungen, Deuticke,
Leipzig.
Price CC, Jefferson AL, Merino JG et al. (2005). Subcortical
vascular dementia: integrating neuropsychological and
neuroradiologic data. Neurology 65: 376–382.
Price CC, Cunningham H, Coronado N et al. (2011). Clock
drawing in the Montreal Cognitive Assessment: recom-
mendations for dementia assessment. Dement Geriatr
Cogn Disord 31: 179–187.
Rapoport SI (1991). Positron emission tomography in
Alzheimer’s disease in relation to disease pathogenesis –
a critical review. Cerebrovasc Brain Metab Rev 3:
297–335.
Rey A (1941). L’examen psychologique dans les cas d’ence-
phalopathie traumatique. Arch Psychol 28: 215–285.
Rieger C (1909). Uber Apparate in dem Hirn. Jena, Fisher.
Roncato S, Sartori G, Rumiati R (1987). Constructional
apraxia: an information processing analysis. Cogn
Neuropsychol 4: 113–129.
Rosselli M, Ardila A (2003). The impact of culture and educa-
tion on non-verbal neuropsychological measurements: a
critical review. Brain Cogn 52: 326–333.
Roth HL, Bauer RM, Crucian GP et al. (2014). Frontal-
executive constructional apraxia: when delayed recall is
better than copying. Neurocase 20: 283–295.
Rouleau I, Salmon DP, Butters N (1996). Longitudinal analy-
sis of clock drawing in Alzheimer’s disease patients. Brain
Cogn 31: 17–34.
Russell C, Deidda C, Malhotra P et al. (2010). A deficit of spa-
tial remapping in constructional apraxia after right-
hemisphere stroke. Brain 133: 1239–1251.
Schaer K, Jahn G, Lotze M (2012). fMRI-activation during
drawing a naturalistic or sketchy portrait. Behav Brain
Res 233: 209–216.
Scheller H, Seideman H (1931). Zur Frage der optisch-
raumlichen Agnosie. Mschr Psychiatr 81: 97–188.
347
Schroeter ML, Stein T, Maslowski N et al. (2009).
Neural correlates of Alzheimer’s disease and mild cog-
nitive impairment: a systematic and quantitative
meta-analysis involving 1351 patients. Neuroimage 47:
1196–1206.
Semenza C, Denes G, D’Urso V et al. (1978). Analytic and
global strategies in copying designs by unilaterally brain-
damaged patients. Cortex 14: 404–410.
Serra L, Fadda L, Perri R et al. (2014). Constructional
apraxia as a distinctive cognitive and structural brain
feature of pre-senile Alzheimer’s disease. J Alzheimer
Dis 38: 391–402.
Shon JM, Lee DY, Seo EH et al. (2013). Functional neuro-
anatomical correlates of the executive clock drawing task
(CLOX) performance in Alzheimer’s disease: a FDG-
PET study. Neuroscience 246: 271–280.
Strauss H (1924). Ueber konstructive Apraxie. Mschr
Psychiatr 56: 65–124.
Suzuki K, Otsuka Y, Endo K et al. (2003). Visuospatial deficits
due to impaired visual attention: investigation of two cases
of slowly progressive visuospatial impairment. Cortex 39:
327–342.
Teipel SJ, Willoch F, Ishii K et al. (2006). Resting state glu-
cose utilization and the CERAD cognitive battery in
patients with Alzheimer’s disease. Neurobiol Aging 27:
681–690.
Thompson JC, Stopford CL, Snowden JS et al. (2005).
Qualitative neuropsychological performance characteris-
tics in frontotemporal dementia and Alzheimer’s disease.
J Neurol Neurosurg Psychiatry 76: 920–927.
Tiraboschi P, Salmon DP, Hansen LA et al. (2006). What best
differentiates Lewy body from Alzheimer’s disease in
early-stage dementia? Brain 129: 729–735.
Trojano L, Conson M (2008). Visuospatial and visuoconstruc-
tive deficits. In: G Goldenberg, BL Miller (Eds.),
Handbook of clinical neurology. 88. Elsevier, Amsterdam,
pp. 373–392.
Trojano L, Gainotti G (2016). Drawing disorders in
Alzheimer’s disease and other forms of dementia.
J Alzheimers Dis 53: 31–52.
Trojano L, Grossi D (1992). Impaired drawing from
memory in a visual agnosic patient. Brain Cogn 20:
327–344.
Trojano L, Grossi D (1994). A critical review of mental imag-
ery defects. Brain Cogn 24: 213–243.
Trojano L, Grossi D (1998). ‘Pure’ constructional apraxia – a
cognitive analysis of a single case. Behav Neurol 11:
43–49.
Trojano L, De Cicco G, Grossi D (1993). Copying procedures
in focal brain-damaged patients. Ital J Neurol Sci 14:
23–33.
Trojano L, Angelini R, Gallo P et al. (1997). An “ecological”
constructional task. Percept Mot Skills 85: 51–57.
Trojano L, Fragassi NA, Chiacchio L et al. (2004).
Relationships between constructional and visuospatial
abilities in normal subjects and in focal brain-damaged
patients. J Clin Exp Neuropsychol 26: 1103–1112.
348 G. GAINOTTI AND L. TROJANO
Trojano L, Conson M, Maffei R et al. (2006). Categorical and of hemispheric side, locus of lesion and coexistent men-
coordinate spatial processing in the imagery domain inves- tal deterioration. Neuropsychologia 24: 497–510.
tigated by rTMS. Neuropsychologia 44: 1569–1574. Wapner W, Judd T, Gardner H (1978). Visual agnosia in an
Van Sommers P (1989). A system for drawing-related neuro- artist. Cortex 14: 343–364.
psychology. Cogn Neuropsychol 6: 117–164. Warrington EK, James M, Kinsbourne M (1966). Drawing dis-
Villa G, Gainotti G, De Bonis C (1986). Constructive ability in relation to laterality of cerebral lesion. Brain 89:
disabilities in focal brain-damaged patients: influence 53–82.