BRAIN

AND

COGNITION

6, 450-463 (1987)

Apraxia in a Patient with Atypical Cerebral Dominance
STEVEN Z. RAPCSAK, LESLIE J. GONZALEZ ROTHI,
AND KENNETH M. HEILMAN
Veterans Administration
Medical Center and Department
Universiry of Florida, College of Medicine

of Neurology,

Liepmann postulated that the left hemisphere of right-handed persons contains
the “movement formulas” that control purposeful skilled movements of the limbs
on both sides of the body. Accordingly, in right-handers apraxia should follow
damage to the left hemisphere, whereas right hemisphere damage should not
lead to apraxia. Although this is generally true, we recently examined a righthanded man who after a right hemispheric stroke became aphasic and apraxic
with his nonparalyzed right hand. Our observations suggestthat the right hemisphere
of this right-handed man made a critical contribution to the planning and execution
of skilled movements. This case provides evidence that right-handers should not
be considered a homogeneous group in terms of cerebral motor dominance and
that contrary to Liepmann’s postulate, hemispheric dominance for the control
of skilled movements does not entirely determine handedness. 0 1987 Academic
Press, Inc.

INTRODUCTION
Apraxia is a disorder of skilled movement not caused by weakness,
akinesia, deafferentation, abnormal tone or posture, movement disorders,
intellectual deterioration, poor comprehension, or uncooperativeness
(Heilman & Gonzalez Rothi, 1985). According to Liepmann, abnormalities
of skilled movement in apraxic patients are caused by a destruction of
motor engrams or by a disconnection of these engrams from the motor
areas that control movements of the extremities. Since in right-handers
the left hemisphere contains these engrams, apraxia should follow damage
to the left hemisphere, whereas right hemisphere damage should not lead
to any appreciable impairment in performing gestures. Liepmann’s own
study provides support for this theory. He tested 41 patients with right
This work was supported by Grant NS-20204 from the National Institutes of Health and
by the Medical Research Service of the Veterans Administration. Address correspondence
and requests for reprints to Kenneth M. Heilman, MD, Department of Neurology, Box
5236, J. Hillis Miller Health Center, University of Florida, Gainesville, FL 32610.
450
0278-2626187$3.00
Copyright
All rights

0 1987 by Academic Press, Inc.
of reproduction
in any form reserved.

APRAXIA

451

hemiparesis and 42 patients with left hemiparesis and found 20 patients
in the former group who were apraxic, whereas no patient in the latter
group showed this deficit (Liepmann, 1905). Liepmann’s hypothesis of
left hemisphere dominance for motor skills in right-handers received
almost unanimous support from subsequent investigators as well (Ajuriaguerra, Hecaen, & Angelergues, 1960; Geschwind, 1965; Goodglass
& Kaplan, 1963).
In the present study we describe a right-handed patient who became
severely impaired in his ability to perform skilled movements with his
dominant hand after a right hemispheric stroke. Detailed study of his
gestural abilities allowed us to define better the nature of his disorder
and to examine the relationship between motor dominance and handedness.
Case Report

A 61-year-old man was originally admitted to his local hospital for
elective surgical repair of a hydrocele. The operation was uneventful,
but the day after surgery he suddenly became mute and left-sided weakness
developed.
He was transferred to the Gainesville Veterans Administration Medical
Center the same day. The patient had had three myocardial infarctions
in the past and has a documented ventricular aneurysm. He has also
had coronary bypass surgery and has a mitral valve prosthesis. He has
had three previous episodes of left-sided weakness, each of which occurred
in association with the heart attacks, and the neurological deficits cleared
within 24 to 48 hr. None of these episodes was associated with language
disturbance. He sustained head injury while in the Navy in 1951 and a
post-traumatic seizure disorder developed. The seizures were described
as tonic-clonic convulsions without any obvious focality. The patient had
had normal electroencephalographic findings several times in the past
and has been maintained on phenytoin and phenobarbital with reasonably
good seizure control. He has no history of birth trauma or early brain
damage.
On admission, the patient was awake and alert, but was mute and
could follow only simple midline commands. He could not follow written
commands, but could write. Writing posture of the right hand was normal,
and he produced well-formed letters. His writing, however, was linguistically incorrect, with only a few recognizable closed-class words. Perseverations were also evident. He wrote obliquely and tended to leave
a wide margin on the left side of the page. His writing could be characterized
as “jargonagraphia” with features of spatial agraphia as well.
He had a right gaze preference and oriented to visual and auditory
stimuli better when presented on the right than on the left. Extinction
on bilateral simultaneous stimulation was present in the visual and auditory
modalities.

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RAPCSAK, GONZALEZ ROTHI, AND HEILMAN

The patient had a dense left hemiparesis with a flaccid plegic left arm
and only minimal movements of the left leg. Left central facial weakness
was pronounced. Muscle tone was diminished on the left, and all deep
tendon reflexes were brisker on that side as well. Sensation was diminished
to all modalities on the left. Strength, tone, and sensation were all normal
on the right side.
The admission diagnosis was infarction in the distribution of the right
middle cerebral artery probably due to embolization from the heart. This
was confirmed by computerized tomogram (CT) that showed a large right
frontotemporoparietal infarct with slight shift of the midline structures
and compression of the lateral ventricle on the right. Contrast CT showed
luxury perfusion and gyral enhancement in the same regions (Fig. 1).
No lesions in the left hemisphere were seen.
The CT measurements of the width and length of the left occipital and
right frontal regions showed the pattern of asymmetry typical for righthanded males (Naeser, 1984).

FIG. I. Contrast-enhanced CT scan showing large right-sided frontotemporoparieta
infarction.

FIG.

I-Continued.
453

FIG. I-Confinued.
454

APRAXIA

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Neuropsychological Studies
1. Assessment of handedness. Handedness was assessed both by selfreport and by the information obtained from the patient’s wife. He always
used his right hand for all the activities on a modified version of Annett’s
(1967) handedness questionnaire. Because the patient grew up in an
orphanage and has no living relatives, a family history of handedness is
not available to us.
2. Language assessment. Language functions were serially evaluated
with the Western Aphasia Battery (Kertesz, 1982).
Although the patient was globally aphasic initially with an aphasia
quotient (AQ) of 2, evaluations between the third and sixth weeks of his
hospital course documented rapid improvements in language abilities.
The AQ increased to 58 when last tested 48 days after the stroke. Figure
2 shows language recovery as measured by AQ over time. Auditory
comprehension showed the most improvement, but spontaneous speech
remained nonfluent and agrammatical. Writing has remained essentially
unchanged. He can match single written words to pictures, and he occasionally follows simple written commands but often fails in reading
comprehension at the sentence level.
3. Emotional prosody and processing of emotional information. Our
patient’s spontaneous emotional prosody was normal, and he could comprehend the emotional prosody of the examiner. He had some difficulty,
however, with repeating emotionally intoned but semantically neutral
sentences spoken by the examiner. On the repetition task he occasionally
reproduced the propositional message without the appropriate emotional
intonation and then verbally denoted the affect. For example, instead of
sounding sad, he repeated: “The boy went to the store, and he was
sad.”
He displayed a large variety of spontaneous and appropriate facial
expressions. He also gesticulated freely with his right hand. He could
produce different emotional facial expressions on command and on imitation. When shown photographs of faces expressing different emotions,
he named the affect appropriately. He could also point to the appropriate
face when the affect was named by the examiner.
4. Visuospatial and visuoconstructional functions. Spontaneous drawings
were oversimplified, lacking spatial perspective and detail. This was more
pronounced on the left side of his drawings. His performance improved
somewhat on copying, except for the Rey figure that was very poorly
done.
He bisected lines slightly to the right of the midline and tended to
ignore objects on his left side. Conversely, he crossed out all the lines
on the cancellation task.
5. Testing of praxis: Rationale. Patients with apraxia from left hemisphere

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RAPCSAK, GONZALEZ ROTHI, AND HEILMAN
90
60
70

I

60
6

50

i

40
30
20
10
Lc
10

20

30

40

50

DAYS

FIG. 2. Language recovery as measured by AQ on the Western Aphasia Battery.

lesions typically make temporospatial errors or use a body part as the
object. According to the classical theory of apraxia, these movement
errors either result from the destruction of the motor engrams or represent
a disconnection of the primary motor areas from these engrams. Without
these visuokinesthetic motor engrams, the motor system cannot adopt
the appropriate spatial positions of the relevant body parts over time
(Heilman & Gonzalez Rothi, 1985). If our patient made predominantly
temporospatial and body-part-as-object (BPO) errors, we may invoke a
mechanism similar to the one described to account for them.
However, because this patient is apraxic from a right hemispheric
lesion, we may find that his errors are qualitatively different from the
type of errors made by patients who are apraxic from left hemispheric
lesions. Therefore, his apraxia may be related to different neuropsychological mechanisms. A qualitative analysis of errors may also provide
clues to the nature of the right hemisphere’s contribution to the learning
and execution of skilled movements in this unusual case.
Finally, after acute brain injury patients may have severe behavioral
disorders that obscure more subtle defects. Observing this patient over
a period of time therefore may help uncover behavioral abnormalities
not seen immediately after the injury.
METHODS
The patient’s ability to perform transitive limb gestures was evaluated by asking him to
demonstrate the use of 15 common household objects. He performed all tasks with his
nonparalyzed right upper extremity. He was given this task once a week for the first 6
weeks of his hospital course (Sessions l-6), and another evaluation was performed at
8 weeks after the stroke (Session 7).
To circumvent our patient’s language comprehension deficit, during Testing Sessions
l-5 we first asked him to show how he would use an object that he was allowed to see
but not handle (Visual Command). He was then asked to imitate the examiner who was
pantomiming the use of an object (Imitation). Finally, he was to demonstrate the use of
objects by handling them (Object Use). During the last two testing sessions (6 and 7) he
was also asked to perform to commands given in the verbal mode (Verbal Command). BV

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APRAXIA

1

2

3

4

5

6

7

SESSIONS

FIG. 3. Number of perseverative errors on Testing Sessions l-7.

this time the patient adequately comprehended yes-no questions and could follow simple
commands. He also had no difficulty pointing to objects named by the examiner and could
verbally describe the task he was asked to perform.
Each testing session was videotaped. The tapes were subsequently reviewed by four
judges who scored the types of errors committed by the patient. Three of four judges had
to reach agreement on the error type before it was used in our final analysis. The operational
definitions used to score the movement errors are provided in the appendix.
We also tested buccofacial and intransitive movements on verbal command and imitation,
but since the patient’s performance on these tasks was similar to his performance with
transitive movements, we included only the latter in our analysis.

RESULTS

The results of our study of transitive movements show that the most
common error types were perseverative, spatial, and BP0 errors. Temporal
errors were so infrequent that we did not include these in our analysis.
Spatial and BP0 errors are typical in apraxia, so these are considered
together and contrasted with perseverative errors.
Figure 3 shows the number of perseverative errors on each testing
session, and Fig. 4 illustrates the number of spatial and BP0 errors.

l1

2

3

4

5

6

7

SESSIONS

FIG. 4. Number of spatial and BP0 errors on Testing Sessions l-7.

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GONZALEZ

ROTHI,

AND HEILMAN

DISCUSSION

The motor perseveration demonstrated by this patient initially was
dramatic. That apraxic patients make some perseverative errors is wellknown. Liepmann (1900) noted perseverations in the patient he described
in his first case report; he was careful to point out, however, that these
perseverative errors did not dominate the clinical picture. He contrasted
his patient’s performance with that of another case described by Pick
(1892). Pick’s patient showed severe motor perseverations, and these
seemed to cause all the faulty responses in demonstrating the use of
objects. Pick proposed to call this disorder “pseudo-apraxia.”
Perseverations on tasks that require cognitive flexibility are characteristic
of frontal lobe damage. In fact, qualitatively our patient’s motor perseverations were very similar to the “stuck-in-set” type of motor
perseveration in patients with massive frontal lobe lesions described by
Luria (1977). This is characterized by an inability to switch from one
action to another and to control recurrent but no longer appropriate
motor responses. To Luria (1965) it meant that “the program of action
once initiated becomes inert and the patient having once performed the
required task is incapable of switching to the fulfillment of any other
task, but continues to perform the first task on which he is stuck.” Such
patients cannot change their way of responding in accordance with varying
environmental signals.
The inflexibility of the patient with a frontal lobe lesion is most pronounced when the programs to be executed are complex or abstract,
while more concrete and automatic sequences can still be performed.
This may explain why our patient, whose infarct damaged large areas
of the frotal lobe, had more perseverative errors on the more complex
tasks of performing to verbal and visual command and imitation, although
he could still perform quite well on the more automatic and concrete
task of handling objects.
He was also aphasic, and perseverations are commonly seen in aphasics.
Perseverative responses can be observed on a variety of verbal and
nonverbal tasks and most often in cases of global aphasia (Allison &
Hurwitz, 1967; Helmick & Berg, 1976; Mateer, 1978; Yamadori, 1981;
Sandson & Albert, 1984). Since globally aphasic patients usually have
large lesions that involve the language-dominant frontal lobe, their perseverative behavior may represent examples of the stuck-in-set type of
perseveration described by Luria. However, several of Luria’s cases
were not aphasic, and therefore the presence of aphasia does not appear
to be the sine qua non for this syndrome.
We believe that the severe perseverative responses of our patient
during the early testing sessions indicate his general inability to develop
the cognitive sets necessary to respond adequately to environmental

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stimuli. This represents a loss of cognitive flexibility that is probably
due to severe frontal lobe damage. The presence of this cognitive disorder
precludes classification of his initial performance as ideomotor apraxia.
As recovery took place, these perseverative errors became less and
less prominent (Fig. 3). The decrease of perseverative responses was
paralleled by the emergence and gradual increase of spatial and BP0
errors (Fig. 4). Although conceivably BP0 errors in aphasics may be
related to an inability to develop the correct cognitive set due to a failure
to comprehend the exact nature of the instructions for the pantomime
task, the patient’s predominant errors were spatial. These errors were
especially prominent during the last three testing sessions and were qualitatively similar to the errors of apraxic patients who have left hemispheric
lesions. We conclude that our patient’s inability to perform skilled movements at this stage was due to apraxia. The emergence of these “classical”
apraxic errors suggests that the right hemisphere contributed significantly
to the performance of skilled movements and that without this contribution,
the left hemisphere could not program these movements on verbal command, visual command, or imitation.
Although decidedly unusual, there have been other reports of defective
limb praxis in right-handers after right hemisphere lesions. Assal, Perentes,
and Deruaz (1981) reported the case of a 32-year-old right-handed man
with no family history of left-handedness who became globally aphasic
after a right hemispheric stroke. Limb apraxia was noted both on verbal
command and on imitiation. Unfortunately, the authors did not describe
the types of errors made by their patient on these tasks. His language
functions improved rapidly, perhaps indicative of bilateral language representations. Limb apraxia was no longer present on a repeat evaluation
3 weeks later. This patient subsequently died, and postmortem examination
of the brain showed an extensive right hemispheric subcortical infarct.
The left hemisphere was intact.
In a recent publication, Basso, Capitani, Laiacona, and Zanobio (1985)
described another right-handed patient with no family history of lefthandedness who developed fluent aphasia after a right hemispheric stroke.
This patient showed severe ideomotor apraxia when tested on a 24gesture imitation task. Detailed analysis of his movement errors is not
provided, but generally they were due to perseverations of previous
gestures.
There are also a few reports in the literature of right-handed persons
who became apraxic but not aphasic after damage to the right hemisphere.
Studies by Italian investigators have shown that when praxis is assessed
with a quantitative procedure and apraxia is diagnosed on an objective
basis, with reference to the performance of a control group, one can find
a few right-handers with right hemisphere lesions who will perform in
the apraxic range (Faglioni & Basso, 1985). The incidence of apraxia in

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GONZALEZ

ROTHI,

AND

HEILMAN

these patients is related to the thoroughness of the testing methods. De
Renzi, Pieczuro, and Vignolo (1968) used a lo-gesture imitation test and
found apraxia to be present in 2% of 45 patients with right hemisphere
damage. Pieczuro and Vignolo (1%7) found it in 9% of 35 right-hemispheredamaged patients using a 20-gesture test. With a 24-gesture imitation test
20% of 80 right-hemisphere-damaged patients were found to be apraxic
by De Renzi, Motti, and Nichelli (1980). The patients in the last study
did not appear impaired on verbal command. Their errors on imitation
tasks were not qualitatively different from the errors of the left-hemispheredamaged group, although a detailed analysis of the types of movement
errors is not provided by the authors. De Renzi (unpublished data, cited
by Faglioni & Basso, 1985) recently confirmed his findings in a sample
of 110 right-hemisphere-damaged patients, 12% of whom performed in
the apraxic range. Some of these patients also failed when performing
on verbal command or on visual presentation of the object, and some
made errors even when the objects were handled.
In a smaller sample of patients Haaland and Flaherty (1984) also found
right-handed, right-hemisphere-damaged patients who were apraxic. When
the errors made by these patients were compared with the errors of
apraxic patients who had left hemisphere damage, some qualitative differences were noted. However, unlike Haaland and Flaherty’s righthanded patients with right hemisphere damage, our patient made errors
qualitatively similar to those made by the left-hemisphere-damaged group
in that study, in that the errors reflected a deficit in integrating intrapersonal
space with a representation of extrapersonal space.
Our case is unusual and appears to contradict Liepmann’s hypothesis
that handedness reflects the greater capacity of one cerebral hemisphere
to learn the execution of skilled movements (Liepmann, 1908; Geschwind
& Galaburda, 1985). According to that theory, the greater skill of the
dominant hand reflects the superiority of the hemisphere controlling that
hand in learning the “movement formulas” necessary to program these
movements. Right-handedness therefore implies that the left hemisphere,
which is directly controlling the right hand, is more capable of acquiring
programs for motor skills than is the right hemisphere. Because, according
to Liepmann, the movement formulas are contained in one hemisphere
(e.g., the left hemisphere in right-handers), when called on to carry out
skilled movements with the hand ipsilateral to the movement formulas,
one must use a transcallosal route. Evidence for this callosal hypothesis
has been provided by Liepmann and Maas (1907) and more recently by
Watson and Heilman (1983). Because our patient became apraxic after
damage to the right hemisphere, we suspect that before the stroke he
was using a transcallosal route when performing skilled movements with
his right hand.
There is no ideal measure of handedness. However, both by self-report

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and a handedness questionnaire, our patient was a right-hander. Since
we could not obtain a family history of handedness, “familial sinistrality”
cannot be rule out.
Annett (1985) postulates that there is a genetically determined “rightshift” factor, that biases its carriers toward right-handedness. In those
persons without this factor, handedness is randomly determined by accidental factors and they may be right-, left-, or mixed-handers. The
observation that our right-handed patient became apraxic after a right
hemisphere lesion suggests that right-handers should not be considered
a homogeneous group in terms of cerebral motor dominance and therefore
provides support for Annett’s hypothesis. Perhaps those right-handers
that have the right-shift factor have left hemispheric motor dominance
but those without this factor may be either left or right hemisphere
dominant or have bilateral representations.
APPENDIX: CLASSIFICATION SYSTEM FOR MOVEMENT ERRORS
1. Content. The pantomime has incorrect content. There are several
subtypes of errors:
a. Perseverative-the subject is pantomiming the content of a
prior command.
the content is wrong, it is related
b. Refuted content-Although
to the target (e.g., same category).
c. Nonrelated, nonperseverative.
2. Temporal.
a. Movement sequencing errors.-A

correctly performed pantomime may have a sequence of movements. For example,
when the subject is asked to use a key to open a door, first
there should be adduction of the thumb against the flexed
index finger (holding the key), then extension at the elbow
(putting the key into the door) followed by rotation at the
elbow (turning the key).
b. Movement timing and speed-Each movement of a pantomime
has characteristic timing and speed. For example, in hitting
a ball with a bat or tennis racquet, the hitting movement
accelerates more rapidly than the preparatory movement. There
is also a delay after the bat or racquet is brought back.
c. Movement occurrence-Single or repetitive movement cycles.
For example, scissors and pliers or door knob opening and
screwdriver.

3. Spatial.
a. Movement

amplitude-Each
movement of a pantomime has
a characteristic amplitude. For example, while brushing one’s
teeth, the movement amplitude is small, while when using an
ax the movements have a large amplitude.
b. Znternal conjiguration (posture)-When pantomiming, the fin-

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RAPCSAK, GONZALEZ ROTHI, AND HEILMAN

gers, hand, and arm must be in specific spatial relationships
to one another. Usually there is an (a) initial posture when
one begins the act and (b) a final posture when the act is
completed. Usually the body parts make an orderly transition
from initial to final posture. For example, when flipping a coin
all the fingers are flexed at both the MP and IP joints. The
index finger is less flexed at the MP joint. The wrist is in a
neutral position (neither extended nor flexed) with neither
ulnar nor radial deviation. The arm is adducted and the elbow
is flexed usually not more than 50” or 60”. The thumb is held
by the index finger. In the final posture, the thumb is extended
at the IP and MP joints. The elbow may be further flexed.
All other parts remain unchanged.
c. External configuration-When pantomiming, the fingers, hand,
and arm must be in specific spatial relationship to the object
being acted upon in the environment (for example, hammering
on the wall vs hammering a nail on the floor.
4. Body part as object (BPO)-Instead of pantomiming, the subject
uses body parts as objects.
REFERENCES
Ajuriaguerra, de F., Hecaen, H., & Angelergues, R. 1960. Les apraxies. Varietes cliniques
et lateralization lesionelle. Revue Neurologique, 102, 566-594.
Allison, R., & Hurwitz, L. 1967. On perseveration in aphasics. Brain, 90, 429-448.
Annett, M. 1967. The binomial distribution of right, mixed and left handedness. Quarter/y
Journal

of Experimental

Psychology,

19, 327-333.

Annett, M. 1985. Left. right hand and brain: The right shift theory. London: Erlbaum.
Assal, G., Perentes, E., & Deruaz, J. P. 1981. Crossed aphasia in a right handed patient.
Postmortem findings. Archieves of Neurology, 38, 455-458.
Basso, A., Capitani, E., Laiacona, M., & Zanobio, M. E. 1985. Crossed aphasia: One or
more syndromes? Cortex, 21, 25-45.
De Renzi, E., Motti, F., & Nichelli, P. 1980. Imitating gestures. A quantitative approach
to ideomotor apraxia. Archives of Neurology, 37, 6-10.
De Renzi, E., Pieczuro, A., & Vignolo, L. A. 1968. Ideational apraxia: A quantitative
study. Neuropsychologia,
6, 41-52.
Faglioni, P., & Basso, A. 1985. Historical perspectives on neuronatomical correlates of
limb apraxia. In E. A. Roy (Ed.), Neuropsychological
studies on apraxia and related
disorders. Amsterdam: North-Holland/Elsevier.
Geschwind, N. 1965. Disconnexion syndromes in animal and man. Brain, 88, 237-294.
Geschwind, N., & Galaburda, A. M. 1985. Cerebral lateralization: Biological mechanisms,
associations, and pathology: I. A hypothesis and a program for research. Archives of
Neurology,

42, 428-459.

Goodglass, H., & Kaplan, E. 1963. Disturbance of gesture and pantomime in aphasia.
Brain, 86, 703-720.

Haaland, K. Y., & Flaherty, D. 1984. The different types of limb apraxia errors made by
patients with left versus right hemisphere damage. Brain and Cognition, 3, 370-384.
Heilman, K. M., &Gonzalez Rothi, L. J. 1985.Apraxia. In K. M. Heilman & E. Valenstein
(Eds.), Clinical neuropsychology.
London/New York: Oxford Univ. Press. 2nd ed.

APRAXIA

463

Helmick, J., & Berg. C. 1976.Perseverations in brain injured adults. Journal of Communication
Disorders, 9, 571-582.
Kertesz, A. 1982. The Western Aphasia Battery. New York: Grune & Stratton.
Liepmann, H. 1900.Das Krankheitsbild der Apraxie (Motorischen Asymbolie). Monatsschrift
fur Psychiatric and Neurologie,
8, 15-44, 102-132, 182-197.
Liepmann, H. 1905. Die linke Hemisphare und das Handeln. Muenchner Medizinische
Wochenschrifr,

49, 2322-2326, 2375-2378.

Liepmann, H. 1908. Drei Aufsatze aus dem Apraxiegebiet.
Berlin: Karger.
Liepmann, H., & Maas, 0. 1907.Fall von linksseitiger Agraphie und Apraxie bei rechtsseitiger
Lahmung. Zeitschriji fir Psychologie und Neurologie, 10, 214-227.
Luria, A. R. 1965. Two kinds of motor perseverations in massive injury to the frontal
lobes. Bruin, 88, l-10.
Luria, A. R. 1977. Higher cortical functions in man. New York: Basic Books. 2nd. ed.
Mateer, C. 1978. Impairments of nonverbal oral movements after left hemisphere damage:
A follow-up analysis of errors. Brain and Language, 6, 334-341.
Naeser, M. A. 1984.Relationship between hemispheric asymmetries on computed tomography
scan and recovery from aphasia. In Seminars in Neurology, 4(2), Thieme-Stratton,
New York.
Pick, A. 1892. Beitrage zur Lehre von den Storungen der Sprache. Archiv fiir Psychiatric
und Nervenkrankheiten,
23, 896-918.
Pieczuro, A., & Vignolo, L. A. 1967. Studio sperimentale sulla aprassia ideomotoria.
Sistema Nervoso, 19, 131-143.
Sandson, J., & Albert, M. L. 1984. Varieties of perseveration. Neuropsychologia,
22,715732.
Watson, R. T., & Heilman, K. M. 1983. Callosal apraxia. Brain, 106, 391-403.
Yamadori, A. 1981. Verbal perseveration in aphasia. Neuropsychologia,
19, 591-594.