BRAIN

AND

COGNITION

6, 412-428 (1987)

Persisting Apraxia in Two Left-Handed, Aphasic Patients with
Right-Hemisphere Lesions
Y. M. ARCHIBALD
Department

of Clinical

Neurosciences, Victoria Hospital, London, Ontario, Canada

Apraxia usually follows a left hemisphere lesion in right-handers with left
hemisphere speech representation. Apraxia following a right hemisphere lesion
in left-handers is rare, however, and not well documented in the literature. Two
left-handed patients are described in whom apraxia and aphasia followed a right
hemisphere lesion. Both the apraxic and the aphasic deficits improved but were
still demonstrable 6 weeks following the infarct. The data are consistent with
those for right-handers with left hemisphere lesions in suggesting some overlap
of anatomical structures for the control of speech and praxis. Q 1987 Academic
Press, Inc.

INTRODUCTION
It is generally agreed that apraxia refers to inability to perform, or
inappropriateness in performing, actions that cannot be attributed to
paralysis, paresis, or other primary motor deficits, nor to impaired comprehension or motivation. Liepmann (1905/1980) originally described three
kinds of apraxia: ideational, ideomotor, and limb kinetic. Ideational apraxia
refers to the inability to carry out the correct sequence of acts necessary
to achieve a specific goal. Ideomotor apraxia refers to difficulty with the
selection, sequencing, and spatial orientation of movements involved in
gestures. Limb kinetic apraxia refers to difficulty making fine, precise
movements with the limbs contralateral to the locus of lesion, although
the sequencing and spatial orientation of the action is correct. There is
by no means universal agreement about types of apraxia, and there will
be no attempt to discuss or further clarify them in this paper. Rather,
I thank Miss Margaret Lenehan and Mrs. Sheelagh Kalman for their valuable help in
assessing the speech and language status of Patient 2 and for their advice in assessing
Patient 1. I also thank Dr. Robert Coates for his patience and help in selecting the appropriate
CT scans for submission and Miss Joanne Lavergne for her helpful critical comments.
Requests for reprints should be sent to Dr. Y. M. Archibald, Department of Clinical
Neuroscience, Victoria Hospital, 395 South Street, London, Ontario, Canada N6A 4G5.
412
0278-2626187$3.00
Copyright
All rights

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

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413

its purpose is to discuss some of the issues arising from the unusual
cases to be presented.
The localization of the brain lesion producing apraxia is less disputed
than the discussion surrounding apraxic types. Left hemispheric lesions
are known to produce apraxia in right-handed people. Liepmann (1905/1980)
originally proposed this locus, and it has since been confirmed by a
number of researchers (Hecaen, 1962; Kimura & Archibald, 1974; Hecaen
& Albert, 1978; De Renzi, Faglioni, Lodesani, & Vecchi, 1983).
A recent study relating locus of lesion, determined by CT scan, to
apraxia found that both large and small left hemisphere lesions appear
to be crucial (Kertesz & Ferro, 1984). The large lesions were deep in
either the parietal area or the frontocentral cortical-subcortical area, the
small lesions mostly in the subcortical frontal area and anterior callosal
fibers.
In left-handed individuals, where language may be bilaterally represented
in the brain, apraxia has been described following a variety of lesions.
Hecaen and De Ajuriaguerra (1964) documented five cases of apraxia in
59 brain-damaged left-handers. The lesion was always left sided or bilateral.
Case reports documenting apraxia following right sided cerebral lesions
in left-handers are rare, however. Most were reported prior to 1935 when
techniques to establish the locus of lesion were far more limited (Poeck
& Kerschensteiner, 1971). More recently, however, Heilman, Coyle,
Gonyea, and Geschwind (1973) and Margolin (1980) have reported apraxia
following a clearly demonstrated right hemisphere lesion.
The combined occurrence of apraxia with aphasia frequently follows
a left hemisphere lesion in right-handers (Kimura, 1983a). In left-handers,
where language representation is more variable, the association of apraxia
with aphasia following a right hemisphere lesion is rare. The patient of
Heilman et al. (1973), for instance, who became apraxic and agraphic in
the right hand (the left was hemiplegic) subsequent to a right hemisphere
lesion, was not aphasic. The authors postulated that their patient was
left hemisphere dominant for language but right hemisphere dominant
for handedness and writing. Margolin (1980) described a similar case.
Recent reports of the combined occurrence of apraxia and aphasia
following a well-documented right hemisphere lesion include the following
three. Poeck and Kerschensteiner (1971) described a 19-year-old, lefthanded girl who developed ideomotor apraxia and a severe, predominantly
motor, aphasia following a right sided cerebral lesion. The EEG showed
generalized slow activity in the right midtemporal area. The apraxia was
bilateral to both verbal command and imitation. Both the apraxia and
the aphasia resolved within about 2 weeks.
Poeck and Lehmkuhl (1980) reported a left-handed woman with a
circumscribed right hemisphere lesion, documented on CT scan, in the
area of the posterior part of the sylvian fissure. She presented with

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Y. M. ARCHIBALD

Wernicke’s aphasia and ideomotor and ideational apraxia. The aphasia
and ideomotor apraxia improved quickly, but the ideational apraxia persisted for at least 17 days, the last reported date of testing. The patient
was unable to execute a series of actions requiring the use of various
objects in the correct sequence necessary to achieve the desired goal,
e.g., preparing a cup of coffee.
More recently a case of reversed hemispheric organization in a lefthander was reported, with CT scan documentation (Delis, Knight, &
Simpson, 1983). A persistent Wernicke’s aphasia and apraxia were prominent features in this patient with a right temporoparietal lesion.
In light of the fact that apraxia occurs only rarely in left-handers with
right hemisphere lesions, it is important to document carefully the nature
and duration of the deficit when it does occur and compare it with
appropriate control groups. By determining what the deficits involve in
such cases, more information can be obtained about brain organization
and neural mechanisms.
Recently, two patients presented at Victoria Hospital, London, Ontario,
with aphasia resulting from right hemisphere lesions. They were both
left-handed except for writing and, in the case of one, racquet sports,
but were apparently forced to use their right hand for writing at school.
Both patients had a right middle cerebral artery infarct involving the
temporoparietal area. In one case, a smaller lesion in the right frontal
lobe was also documented. An opportunity was thus presented to examine
praxic functions in two primarily left-handed aphasic males with a right
hemisphere lesion.’
PATIENT 1

Patient 1, a 50-year-old scrap dealer with a Grade 4 education, was
left-handed except for writing. He was seen following a right middle
cerebral artery infarct, thought to have occurred on January 7th, 1983.
He was initially admitted to his local hospital on January 14th with
complaints of chest pain then transferred to Victoria Hospital on January
27th for further investigation. Neurological examination at the time of
admission revealed confusion and inattentiveness, difliculty with memory,
naming, and repetition. A brain scan showed a right temporoparietal
defect. This was confirmed by a CT scan, both plain and enhanced,
which showed an extensive low-density area in the right temporal region
spreading back to include the inferior parietal region (Figs. 1 and 2). A
low-density area in a comparable part of the left hemisphere in righthanders has been reported to be a prototypical lesion site for a Wernicke’s
aphasia (Naeser & Hayward, 1978; Mazzocchi & Vignolo, 1979).
’ Informed consent was obtained from the two patients to carry out and repeat the
assessments.

PERSISTING APRAXIA

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415

FIG. 1. Patient 1, CT scan, January 1983.

Speech and Language

Patient 1 was administered parts of the Minnesota Test for the Differential
Diagnosis of Aphasia (Schuell, 1965), the Token Test (De Renzi, 1979),
and the Boston Naming Test (Kaplan, Goodglass, & Weintraub, 1976)
on the initial assessment. Conversational and narrative speech were fluent
but conveyed little meaning. Picture description was also fluent with
paraphasic errors. Literal (e.g., ‘ ‘copellor” for ‘ ‘propeller”) and verbal
paraphasias (e.g., “steeple” for “stapler,” “squirt” for “squid”) and
occasional neologisms (e.g., “horntoed horse” for “unicorn”) characterized
his performance on the Boston Naming Test. Repetition for single words
and four-syllable phrases was mildly impaired and sentence repetition
was impaired for 10 syllables or more. Digit span was four forward.
Comprehension was at a chance level for sentences and only 7 of 36
correct responses were made on the Token Test. His aphasia was judged
to be of the Wernicke type.
The extent of the reading and writing deficit was difficult to assess
because of his low educational level. However, he was able to write
single numbers and letters to dictation but made errors with more complex

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Y. M. ARCHIBALD

FIG. 2. Patient I, CT scan, June 1983

numbers and was virtually unable to write a single three-letter word.
Iteration characterized his signature and repetitive writing, for which he
was required to write the letters mn six times. Simple computations (e.g.,
how much is 7 + 3?) could not be done.
Neuropsychological

Assessment

Impaired visual and visuospatial functioning was evident in impersistence
of gaze with difficulty fixating, a lower left and partial upper left field
defect on testing to confrontation, and omission of most of the left half
of the Rey Figure in copying. IQ values were in the defective range with
a Verbal IQ of 59, a Performance IQ of less than 48, and a Full Scale
IQ of 51. The patient was quite unable to do most Performance scale
items, including Block Design. Recall of nonsense figures and the Rey
Figure was consistent with data for patients with right rather than left
hemisphere lesions (Archibald, unpublished data). A left-hand advantage
was obtained on grip strength, consistent with his handedness.

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WITH RH LESIONS

TABLE 1
SCORES
ON TESTSOF TRANSITIVEAND INTRANSITIVEMOVEMENTS
FORPATIENT1 AND FOR
RIGHT-HANDEDPATIENTS WITH LEFT AND RIGHT HEMISPHERE
LESIONS
Intransitive

Transitive
Command
only
(Max = 12)
Patient 1
Left hand
Right hand
Left hemisphere
patients, left handb
Right hemisphere
patients, right hand”

8
8
7.6
(O-12)
11.8
(1 l-12)

Command
&
imitation
(Max = 12)

Command
only
(Max = 6)

Command
&
imitation
(Max = 6)

9
9
8.8
(O-12)”
1I .8’

4
4
3.8
(O-6)”
6”

6
5
4.5
(l-6)”
6

-

a Indicates range.
’ Kimura and Archibald (1974).
‘ Imitation was not done with these patients, since their scores were perfect or near
perfect.
’ No range.

Praxis

Praxic functions were assessed in a variety of ways. Patient 1 was
able to execute a series of actions using objects in the correct sequence
necessary to attain a specific goal, e.g., he was able to fold paper and
put it in an envelope and could insert a piece of paper in a binder, having
first punched it and opened the file appropriately. He did not, therefore,
have a deficit in so-called ideational apraxia.
Performance on tasks of transitive and intransitive movements was
also assessed, first by asking Patient 1 to demonstrate the use of a series
of common objects (transitive) or to execute common actions such as
waving goodbye (intransitive). If he failed to do the action to verbal
command, the examiner then demonstrated it, using the actual object in
the case of the transitive acts. Following this, the patient was asked to
imitate the experimenter, but without the object. A movement-copying
test (Kimura Kz Archibald, 1974)’ was also administered in order to
determine how he could copy unfamiliar, meaningless sequences, to
which he had not already attached a verbal label. Data for the transitive
and intransitive tasks are presented in Table 1. Comparison data on these
* The sample in Kimura and Archibald’s study consisted of 16 left hemisphere patients
with a well-defined unilateral left hemisphere lesion and 14with a unilateral right hemisphere
lesion. Most patients had had a cerebral vascular accident.

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Y. M. ARCHIBALD

TABLE 2
SCORESFOR MULTIPLE
HANDED
HAND

PATIENTS

WITH

MANUAL
MOVEMENTS FOR PATIENT 1 AND FOR LEFT- AND RIGHTLEFT AND RIGHT HEMISPHERE LESIONS, USING THEIR IP~ILATERAL

N
Patient 1
Left hand
Right hand

Multiple manual
movements
(max = 24)

SD

4
6

Right-handed males”
Left anterior (left-hand)
aphasics only
Left posterior (left-hand)
aphasics only
Right anterior (right hand)
Right posterior (right hand)

15
6
34
14
11
16

15.3
12.8
13.1
9.2
18.3
17.9

-b
-

Left-handers, males and
females’
Left lesions (left hand)
Right lesions (right hand)

22
11

17.6
16.4

3.5
3.8

: Kimura (1983a).
-Indicates standard deviation not available.
’ Kimura (1983b).

same tasks are also presented for right-handed patients with unilateral
hemispheric lesions (Kimura & Archibald, 1974).
Relative to Kimura and Archibald’s patients with right hemisphere
lesions, using their ipsilateral hand, Patient 1 was clearly impaired in
both hands on the transitive and intransitive tasks. His scores are, however,
comparable to those of patients with left hemisphere lesions, using the
ipsilateral left hand. On movement copying (multiple manual movements,
Table 2), Patient 1 is also impaired in both hands compared to Kimura’s
right-handed, right hemisphere males, using their ipsilateral right hand
(Kimura, 1983a)3and, more significantly, compared to Kimura’s righthanded, left hemisphere males using their ipsilateral left hand (Kimura,
1983b).4Comparing Patient 1 to Kimura’s left-handers, again he is clearly
inferior to patients with both left and right hemisphere lesions using their
ipsilateral hand.
3 The sample consisted of 81 patients with a unilateral left hemisphere lesion and 53
patients with a unilateral right hemisphere lesion.
4 The sample consisted of 27 left-handed patients with a unilateral left hemisphere lesion
and 11 with a unilateral right hemisphere lesion. In both of these studies, the majority of
the lesions were vascular in origin.

PERSISTING

APRAXIA

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TABLE

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3

FOLLOW-UPSCORES FOR PATIENT1 ON TESTS OF TRANSITIVE,
MANUAL

419

INTRANSITIVE,

AND MULTIPLE

MOVEMENTS

Left hand

Right hand

10
10

7
8

4
5
16

4
6
14

Transitive (max = 12)
Command only
Command & imitation
Intransitive (max = 6)
Command only
Command & imitation
Multiple manual (max = 24)

Follow-Up
Speech and Language

Six weeks following the first assessment, and approximately 10 weeks
postonset, speech and comprehension showed considerable improvement.
Narrative and descriptive speech were more meaningful but still contained
some paraphasic errors, as did naming to confrontation. Speech was
judged to be primarily anemic. The auditory comprehension deficit was
less severe, but remained impaired. For example, the Token Test score
was 18 out of 36 compared to 7 out of 36 on initial assessment.
Neuropsychological

Assessment

Impersistence of gaze and difficulty fixating had cleared, but Patient
1 was still unable to scan visually. The left field defect had resolved to
a mild left lower neglect and the copy of the Rey Figure, while still
below the normal range in score, was not more distorted on the left than
on the right. Verbal IQ was not reassessed, but the Performance IQ was
72. Recall of nonsense figures was within the normal range, and recall
of the Rey Figure remained consistent with data for patients with right
hemisphere lesions. The left-hand advantage was reaffirmed on grip strength
and substantiated further by finger tapping.
Praxis

A test of oral praxis (Mateer & Kimura, 1977; Mateer, 1978), not
previously administered, showed some difficulty with single movements
to imitation. Patient 1 obtained a component score of six out of nine on
multiple movements but was unable to imitate any of the three sequences
of movements. Execution of series of actions, using objects, remained
accurate. Data for the transitive and intransitive tasks and movement
copying are presented in Table 3.
Right-hand scores for the transitive tasks remained impaired relative

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Y. M. ARCHIBALD

to those of Kimura and Archibald’s right-handed patients with a right
hemisphere lesion (Table 1). They also remained comparable, however,
to those of right-handed patients with left hemisphere lesions. Patient
l’s contralateral left-hand scores on the transitive tasks still trail those
of Kimura and Archibald’s right-handed patients with a right hemisphere
lesion using their ipsilateral hand. For the intransitive tasks, Patient l’s
right-hand scores on imitation were comparable to Kimura and Archibald’s
patients with right hemisphere lesions. The movement-copying score for
Patient l’s ipsilateral right hand was substantially higher than before but
comparable to those of Kimura’s right-handed patients with left rather
than right hemisphere lesions (Table 2). Notably his score falls between
that of the left anterior aphasics and the left nonaphasics. This may be
explicable in terms of the fact that Patient 1 was impaired on a variety
of aphasia tests but only minimally on tests comparable to those used
by Kimura. Patient l’s right-hand score is also lower than, but within
the range of, Kimura’s left-handed patients with right-hemisphere lesions.
In summary, then, scores on most tasks had improved by the time of
the follow-up assessment. However, Patient 1 was still aphasic, with a
primarily anemic deficit and some comprehension difficulties. Data for
tasks of oral praxis and for the right hand on tasks of transitive movements
and multiple manual movements were consistent with those of righthanded patients with left hemisphere lesions, using their left hand.
PATIENT 2

Patient 2, a 68-year-old retired auto mechanic with a Grade 12 education,
was also left-handed, except for writing and racquet sports. He was
admitted following the sudden onset of a left hemiparesis, a left facial
droop, and aphasia, with further deterioration of speech and an increase
in weakness following admission. The CT scan showed a relatively large
area of radiolucency extending from the right midtemporal to the posterior
parietal region and a smaller area of radiolucency in the right frontoparietal
region, posterior to, and higher than, Broca’s area. These changes were
judged to be consistent with an infarct in the right middle cerebral artery
territory. Carotid angiography revealed a 95% narrowing of the right
carotid artery. Two days following completion of the first neuropsychological assessment, a right carotid endarterectomy was performed
(see Figs. 3 and 4).
Speech and Language

A speech and language evaluation was carried out by the speech pathologist using a variety of tests, e.g., selected subtests of the Boston
Diagnostic Aphasia Examination and Minnesota Test for the Differential
Diagnosis of Aphasia as well as local Victoria Hospital speech pathology
tests of auditory comprehension. Speech was fluent but severely anemic.

PERSISTING APRAXIA

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421

FIG. 3. Patient 2, CT scan, February 1983.

It was characterized by verbal and literal paraphasic errors, strings of
functors, and incomplete sentences. Auditory comprehension was mildly
impaired for single words but moderately impaired for complex ideational
material, factual material which did not relate to a picture or object, and
lengthy and complex material. Repetition was limited to three- or fourword phrases. Aphasia was judged to be of the Wemicke type, resolving
to an anomia. In view of the severely impaired repetition, however, some
overlap with a conduction type was indicated.
Additionally, the patient was virtually unable to read. Oral reading
was characterized by many verbal paralexic errors and silent reading
was limited to simple picture-to-word and printed-to-spoken-word matching.
Dysgraphia was also severe. Perseverative and paragraphic errors were
made at the level of letters and words. Output to dictation was very low
and was negligible in attempting to formulate written language. Thus,
the Wemicke-anemic aphasia, in conjunction with severe dyslexia and
dysgraphia, is consistent with a comparable lesion site in the left posterior
parietal hemisphere of right-handed patients.

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Y. M. ARCHIBALD

FIG. 4. Patient 2, CT scan, July 1983.

Neuropsychological

Assessment.

Neuropsychological assessment showed impaired visual and visuospatial
functioning. Impersistence of gaze with difficulty fixating, a lower left
field defect, and a partial upper left defect on testing to confrontation
as well as left neglect on a visual search task were documented. The
copy of the Rey Figure did not show obvious evidence of left neglect,
but the right side of the figure was drawn first and one feature was
omitted on the left side. The total score for the Rey Figure was below
the normal range and consistent with that of patients with unilateral
hemispheric damage.
Intellectual functioning was not assessedverbally because of the patient’s
aphasia and lack of physical stamina. However, his Performance IQ was
81. Interestingly, the Block Design scale score of 11, adjusted for age,
is well within the normal range. Impaired recall of the Rey Figure and
nonsense figures is consistent with data for patients with right hemisphere
lesions. Grip strength showed a left-hand advantage. Left-right orientation
was intact on the self but impaired on the mirror image.

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PERSISTING APRAXIA WITH RH LESIONS
TABLE 4

SCORESON TESTS OF TRANSITIVE AND INTRANSITIVE MOVEMENTS FOR PATIENT 2 AND FOR
RIGHT-HANDED PATIENTS WITH LEFT AND RIGHT HEMISPHERELESIONS

Transitive
Command
only
Patient 2
Left hand
Right hand
Left hemisphere
patients, left hand
Right hemisphere
patients, right hand

3
4
(oY2)b
11.8
(11-12)

Intransitive

Command
&
imitation

Command
only

Command
&
imitation

6
7
8.8
(O-12)b
11.8

1
2
3.8
(0-6)b
6’

4
4
4.5
(1-6)b
6’

a Kimura and Archibald (1974).
* Range of scores.
’ Imitation was not done with these patients, since their scores were perfect or near
perfect.
d No range.

Praxis

Oral apraxia was demonstrated for sequences of movements such as
lateralizing the tongue, opening the mouth, and protruding the lips, but
not for single movements. The patient was, however, able to execute
sequential actions such as punching a piece of paper and opening a binder
and inserting the paper correctly, thus showing no evidence of ideational
apraxia. Tasks of transitive and intransitive functions and copying multiple
movements proved more difficult for him. The data for transitive and
intransitive tasks are tabled below, with comparison data for patients
with left and right hemisphere lesions (Table 4). Clearly, Patient 2 was
impaired in both hands on the transitive and intransitive tasks relative
to Kimura and Archibald’s right-handed patients with left hemisphere
lesions using their left hand. He was also, of course, impaired relative
to right hemisphere patients using their right hand.
His scores on multiple manual movements are also comparable to those
of right-handed patients with left hemisphere lesions (Table 5). The score
for Patient 2’s ipsilateral hand falls in the range of the scores for left
anterior patients and left posterior nonaphasic patients. Patient 2’s scores
are clearly inferior to those of Kimura’s right hemisphere males using
their right hand. His right-hand scores are also lower than, but within
the range of, Kimura’s left-handed patients with lesions of the right
hemisphere.

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Y. M. ARCHIBALD
TABLE 5

SCORES M)R MULTIPLE MANUAL MOVEMENTS FOR PATIENT 2 AND FOR LEFT- AND RIGHTHANDED PATIENTS WITH LEFT AND RIGHT HEMISPHERE LESIONS

N
Patient 2
Left hand
Right hand

Multiple manual
movements
(max = 24)
10
14

Right-handed males”
Left anterior (left-hand)
aphasics only
Left posterior (left-hand)
aphasics only
Right anterior (right hand)
Right posterior (right hand)

15
6
34
14
11
16

15.3
12.8
13.1
9.2
18.3
17.9

Left-handers, males and femalesb
Left lesions (left hand)
Right lesions (right hand)

22
11

17.6
16.4

a Kimura (1983a).
’ Kimura (1983b).

Follow Up

Speech and Language
Six weeks later, speech remained predominantly fluent, with minimal
grammatical organization and marked word retrieval problems, literal
paraphasias, and some circumlocutions. Auditory comprehension was
improved but still sensitive to syntactically complex material. Repetition
had increased to six syllable sentences and was characterized by verbal
apraxic struggling. Aphasia was judged to be mixed and mainly compatible
with a parietal locus of lesion. However, the verbal apraxic struggles
which disrupted his grammatical structuring, in conjunction with his
preserved comprehension, were felt to be more typical of an anterior
lesion site. Reading skills improved significantly, but writing remained
severely impaired for letter recall, spelling, and generation of sentences
and paragraphs.
Neuropsychological Assessment
Some of the visual difficulties had improved, although the patient
complained of trouble aligning an object in the left and right fields. He
no longer showed impersistence of gaze or difficulty focusing. However,
he was able to scan only the simple practice items of the scanning task.
Left neglect remained on the visual search task, but search times overall
were much faster. The copy of the alternative Rey Figure was in the
borderline normal range, although again, the right half of the figure was

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TABLE 6
FOLLOW-UP SCORESFOR PATIENT 2 ON TESTS OF TRANSITIVE, INTRANSITIVE, AND MULTIPLE
MANUAL MOVEMENTS

Transitive (max = 12)
Command only
Command & imitation
Intransitive (max = 6)
Command only
Command & imitation
Multiple manual (max = 24)

Left hand

Right hand

11
11

11
11

4
6
14

4
6
12

copied first. Intellectual functioning remained stable with the Performance
IQ at 80. Recall of the Rey Figure was less impaired than before, and
recall of nonsense figures was borderline normal. Grip strength was equal
in the two hands while finger tapping, not done before, showed a small
right-hand advantage. Left-right orientation was now mildly impaired on
the self but intact on the mirror image. Finally, severe left sensory
neglect, particularly of the leg, was documented on double sensory
stimulation.
Follow-up motor and speech data suggested the presence of a more
active anterior lesion, perhaps attributable to changes from the endarterectomy.
Praxis

No difficulty was encountered for single oral movements, but sequences
of movements could still not be performed. Ideational praxis was not
reassessed because of time constraints. Data for the transitive and intransitive tasks and multiple manual movements are presented below
(Table 6).
For transitive and intransitive movements, performance had improved
and was more comparable to that of right hemisphere patients using their
right hand, in other words, performance was close to normal. For multiple
manual movements, however, the pattern of performance in the right
hand remained comparable to that of Kimura’s right-handed, left hemisphere males, both anterior and posterior, using their left hand. His righthand score was also somewhat lower than that of Kimura’s left-handers
with right hemisphere lesions.
Patient 2 showed improvement on some tasks on follow-up, including
speech and language. His score on multiple manual movements, however,
remained essentially unchanged and consistent with those of right-handed
male patients with left hemisphere lesions.
The two left-handed patients described above had clear right hemisphere

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Y. M. ARCHIBALD

lesions producing both apraxia and aphasia. While improvement was
demonstrated on the 6-week follow-up assessment, the apraxia, nevertheless, persisted. Their data for apraxia are comparable to those of
right-handed patients with left hemisphere lesions.
DISCUSSION
Although left hemisphere specialization for bimanual praxic functions
has been demonstrated in right-handers, less is known about the representation of these functions in left-handers. Kimura’s recent data (1983b)
on a consecutive series of brain-damaged patients indicate a more bilateral
organization of praxic functions in left-handers. The two patients in the
current study, however, do not show evidence of such bilateral organization,
since they were severely and persistently apraxic from a clearly demonstrated unilateral right hemisphere lesion.
The corpus callosum is implicated in some cases of apraxia. Typically,
however, the apraxia is unilateral and occurs in the hand ipsilateral to
the hemisphere dominant for speech. The lesion may involve only the
corpus callosum or the corpus callosum in conjunction with the left
frontal cortex, left hemisphere white matter, or subcortical left hemisphere
areas (Heilman, Rothi, & Kertesz, 1983). It is unlikely, however, that
the corpus cahosum was implicated in the two patients presented in this
paper. Both upper limbs were tested, since neither patient suffered a
hemiparesis, and both were clearly apraxic.
The apraxia reported in the current paper was not of the ideational
type, which characterized Poeck and Lehmkuhl’s (1980) patient, but was
comparable to that documented by Kimura in right-handed males following
a left hemisphere lesion (1983a). The scores are a little lower, however,
than those for Kimura’s left-handers (1983b) with right hemisphere lesions,
but the patients in her sample were not rendered aphasic by their lesion.
Hemispheric representation of speech in left-handers is more variable
than in right-handers. One hypothesis is that speech is more bilaterally
organized in left-handers than in right-handers. Data from sodium amytal
studies (Rasmussen & Milner, 1975) and more recently from Kimura’s
study (1983a) suggest that speech is represented in the left hemisphere
in about 70% of left-handers and in the right hemisphere, or bilaterally,
in the remaining 30%. Although the possibility of some left hemisphere
representation of speech cannot entirely be ruled out, the patients in this
study appear to have primarily right hemisphere representation of speech.
In both cases, the lesion locus and the type of aphasia correspond to a
comparable lesion site and aphasia type following a left hemisphere lesion
in right-handed patients (Kimura, 1983a).
While speech and praxis are usually both represented in the same,
i.e., left, hemisphere in right-handers, divergent hemispheric representation
has been documented in some left-handers. Specifically, Heilman et al.

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APRAXIA

WITH

RH LESIONS

427

(1973) and Margolin (1980) each report a case in whom speech was judged
to be in the left hemisphere and praxis in the right. Although left-handed,
each patient had been switched to write with the right hand as a child.
Following a right hemisphere lesion they became apraxic and agraphic
in the right hand. Neither patient was aphasic. The authors reasoned
that callosal pathways were used to transfer the linguistic component of
writing from the left to the right hemisphere in order to arouse the
appropriate motor sequences for writing. These, in turn, had to be transferred back to the left motor area to innervate the right hand. Consequently,
a right hemisphere lesion rendered these patients unable to perform the
motor aspects of writing, while oral spelling, reading, and other language
functions remained intact. The two patients in this paper, however, appear
to have right hemisphere representation of both language and praxis,
since they were both aphasic and apraxic following a right hemisphere
lesion. One patient, at least, was also agraphic in the right hand. Unfortunately, left-hand writing was not tested. Nonetheless, his right-hand
agraphia is consistent with right hemisphere representation of both language
and praxis. In so far as these functions are represented in the same
hemisphere, cerebral organization in Patients 1 and 2 is comparable to
that for right-handers.
The finding that Patients I and 2 displayed similar language and praxic
deficits to the patients of Delis et al. (1983) from a right hemisphere
lesion raises the further question of whether or not they also show other
evidence of reversed hemispheric organization. Consideration of the data,
particularly for Patient 1, does not suggest this, however, since Patient
1 showed severely impaired visuospatial functioning. His initial copy of
the Rey Figure was disorganized and did not bear much resemblance to
the model. Moreover, his percentage recall of the Rey Figure in the delay
condition was more consistent with that for patients with right rather
than left hemisphere lesions. Patient 2 was also impaired on the Rey
copy, but to a much lesser extent. His percentage recall in the delay
condition was also consistent with that for patients with right hemisphere
lesions. Were hemispheric functioning reversed, it would be expected
that the visuospatial and memory deficits would be more in keeping with
those documented following left hemisphere lesions.
In view of the fact that aphasic and apraxic deficits frequently occur
together, the possibility arises that they share the same neural structures.
There has been enough evidence of dissociation (Kertesz, Fen-o, & Shewan,
1984, Kertesz & Ferro, 1984), however, to suggest that in some patients
the representation of language and praxic functions is independent.
Nevertheless, evidence from the current study of left-handers with right
hemisphere lesions is consistent with most of the left hemisphere data
for right-handers which suggest some anatomical and functional overlap
for the control of speech and praxis.

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Y. M. ARCHIBALD

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