Brain (1973) 96, 861-864
I
I
IDEATIONAL APRAXIA—A RE-DEFINITION
BY
K. M. HEILMAN
(From the University of Florida, College of Medicine, Division of Neurology, Gainesville, Florida)
LIEPMANN described ideomotor apraxia (IMA) as a movement disorder where
there was a disconnexion between the idea of the movement and its motor
execution (Liepmann, 1908). The patient with IMA has greatest difficulty with
movement to commands. Imitation may help a little but frequently not at all,
whereas with manipulation of the object there is usually a significant improvement
(Geschwind, 1965). Ideational apraxia (LA) has been defined by several authors as a
defect in the actual handling of objects (De Renzi et al., 1968; Morlaas, 1928).
Several investigators have raised questions as to whether a separate classification
is justified (Geschwind, 1965; Zangwill, 1960; Brown, 1972) or whether LA might
simply represent such a severe stage of IMA as to involve even the easiest gestures,
i.e. use of actual objects (De Renzi et al, 1968; Zangwill, 1960). A recent study
demonstrated that although patients with IMA showed improvement with
actual handling of objects, these patients nevertheless show a defect of their nonparetic
hand in more sensitive tests for actual object handling, i.e. rapid tapping
with their left hand (Heilman, 1973). Is there then an ideational apraxia?
To better understand the nature of apractic problems the following 3 patients were
intensively evaluated and appear to exhibit features definable as LA.
CASE REPORTS
Case 1.—A 34-year-old right-handed woman had sudden loss of consciousness and when she
awoke she noted a transient language disturbance. EEG and brain scan performed at another
hospital showed questionable abnormalities of the left parietal region. She was treated with
diphenylhydantoin and phenobarbital; because of urticaria, however, the former had to be
discontinued and the patient had several other episodes of loss of consciousness followed by
language disturbances. She was referred to the University of Florida Teaching Hospital
and on examination it was noted that the patient was aphasic. She used frequent circumlocutions
in her spontaneous speech and upon attempts to name on confrontation the patient showed a
severe anomia which was not modality specific or unilateral. She was, however, able to describe
what objects were used for and could always select the correct object in a multiple choice type
question. The patient's comprehension was intact as was series speech. She had difficulty with
repetition of highly grammatic sentences, i.e. no if, ands or buts. In addition, the patient had
Supported by Grant NIH-NS-10408.
59 BRAIN—VOL. XCVI
byguestonOctober18,2011brain.oxfordjournals.orgDownloadedfrom
862 K. M. HEU-MAN
dyslexia, dysgraphia, dyscalculia, and constructional apraxia but did not demonstrate finger
agnosia or right-left confusion.
On apraxia testing, when asked to pantomime certain motions with either her right or left arm
(i.e. "Show me how you would use a key") the patient looked at her outstretched hand, then asked
the examiner to repeat the question. When the question was repeated the patient would look down
at her hand and say, "I can't do it." When asked if she understood the question, the patient
would verbally demonstrate comprehension, i.e. "Keys are used for opening locks." When the
correct movement was shown to this patient in a multiple choice fashion, she was always able to
select the correct movement. She was able to imitate in a flawless manner even with minimal
cuing and she performed extremely well with the actual object. She had no difficulty with multiple
object sequencing (i.e. taking a cigarette out of a pack, putting it in her mouth, lighting it, and then
smoking).
Motor and sensory examinations were normal except for mild right-sided hyperrefiexia with
bilateral flexor plantars. A Technetium 99 brain scan showed an abnormal uptake in the left
parietal lobe and a left carotid arteriogram revealed a mass lesion with abnormal vascularity in the
left parietal lobe which on craniotomy was found to be metastatic carcinoma. The patient was
treated with corticosteroids and radiation therapy in a hospital in her home city. Despite treatment
the patient rapidly deteriorated and died. A post-mortem examination was not obtained.
Case 2.—A 64-year-old right-handed diabetic hypertensive female had sudden onset of aphasia.
Examination on admission was unremarkable except for some signs of mild cardiac failure. On
neurological examination the patient had an anomic aphasia, a mild recent memory defect, finger
agnosia, dyscalculia, right-left confusion, constructional dyspraxia, with dysgraphia without
dyslexia. In addition, the patient demonstrated an apraxia which was quite similar to Case 1.
When asked to perform movements to commands with her non-paretic limb, she would make either
irrelevant movements or look perplexed and would ask the examiner to show her how to do it.
She would, however, be able to demonstrate verbally that she understood the command and her
imitation of movement and use of actual object was excellent. The remainder of neurological
examination revealed a very mild hemiparesis with hyperrefiexia. An EEG showed left posterior
hemispheric slowing and a brain scan was normal. The patient's condition remained stable and
she was discharged.
Case 3.—A 56-year-old right-handed female with a history of rheumatic fever at age 18. Because
of progressive heart disease she had a commissurotomy six years previously followed by a mitral
valve prosthesis three years before admission. She had chronic atrial fibrillation and two years ago
following a fall while on anticoagulants, she had a small left subdural haematoma which was
evacuated. Post-operatively, she had a mild transient anomia. On the night of admission the
patient had sudden onset of a right hemiparesis and aphasia. Although she initially had a mild
comprehension difficulty, she gradually improved except for a persistent anomic aphasia, an
agraphia, and a constructional apraxia. She also demonstrated a severe apraxia which was similar
to Cases 1 and 2. Although she had intact comprehension of language, she was unable to perform
useful movements to command with either limb. Her imitation of movements and her ability to use
objects was excellent. The remainder of her neurological examination revealed a right hemiparesis,
a right hemianopsia, right-sided hyperrefiexia with a right-sided extensor plantar response. Her
EEG showed left-sided slowing and Te" scan was within normal limits. She was given
anticoagulants and when seen one year after her ictus had no residual symptoms.
DISCUSSION
Unlike the errors made by patients with IMA (Goodglass and Kaplan, 1963) (i.e.
body part as object, clumsy movements, gestural enhancement, vocal overflow and
pantomimed context), the patients described herein demonstrated movements which
were often irrelevant and appeared as if they did not understand the command.
I
I
I
I
byguestonOctober18,2011brain.oxfordjournals.orgDownloadedfrom
I
I
I
IDEATIONAL APRAXIA—A RE-DEFINITION 863
These patients did show both verbally and by picking the correct movement from a
multiple choice that they did understand the command. The disorder was present
with intransitive as well as transitive movements and involved the face as well as the
extremities. Unlike patients with IMA who frequently fail to improve on imitation,
imitation here was flawless. Furthermore, in contrast with descriptions of other
patients presumed to demonstrate IA because they were unable to handle actual
objects (De Renzi et ah, 1968), in the patients described here actual object handling
was flawless.
Two of these patients had infarction, one from thrombosis and the other from
embolism. The third patient had a neoplastic lesion in the left parietal lobe. Although
the anatomical locus of the lesion was not pathologically identified in the two patients
with infarction, these patients had many of the signs frequently associated with
dominant parietal lobe disease.
While the anatomical locus for the production of this apraxia appears to be the
dominant parietal lobe, the mechanism responsible for this apraxia remains unclear.
Another form of IA was described by Pick (1905) and Marcuse (1904) in which
patients could not perform a series of complex separate movements to commands.
Marcuse (1904) suggested that the defect in this apraxia was a memory defect with
loss of "goal concept." This mechanism (i.e. loss of goal concept) does not appear
to be important in our cases. Although our cases had mild memory disturbances
and anomia, they had difficulty not with series of movements but with isolated
movements, and they could always verbally demonstrate the goal concept. In
addition, it is felt that although the aphasic disturbance is similar to the apraxic
disturbance, neither can be completely explained as a simple memory defect because
when these patients were given multiple choice type questions, they always produced
the correct answer.
It appears then that these patients can verbally understand commands for
movements and that they can adequately maintain these commands in their
immediate memory. In addition, their excellent imitation and use of actual objects
suggests that the engrams for motor sequences are intact. What may be at fault in
this form of IA is the process or processes which occur between language
comprehension and motor encoding. After the command is understood there could
be a mechanism which helps select the motor engram which best fulfils the command.
Wernicke (1895) stipulated that before performing willed movement the goal is
imaginatively anticipated and that the anticipation of the movement produces the
desired kinetic effect by evoking the proper kinaesthetic engram. One may consider
that the defect in these cases of LA is a defect in the verbal mediated motor sequence
selector which is responsible for choosing the correct motor sequences or the
connexions from language decoding areas to this selector or from this selector to the
motor engrams. The loss of memory for motor sequences or the inability of these
memories to reach the motor cortex would then cause IMA.
Another perhaps less mechanistic and hierarchical explanation may be similar to
Goldstein's explanation of anomic aphasia, with which these cases of IA were
byguestonOctober18,2011brain.oxfordjournals.orgDownloadedfrom
864 K. M. HHLMAN
associated. Goldstein (1948) recognized that naming to confrontation was a symbolic
act and that patients require an abstract attitude to perform this act. In a similar
manner, the loss of the ability to pantomime and gesture are also symbolic acts and
may be caused by loss of the abstract attitude. Unfortunately, however, this
explanation does not help us understand the defect in neural processing which occurs
in this disorder.
SUMMARY
Ideational apraxia (IA) has been denned by certain authorities as a defect in the
actual handling of objects. Others have felt that a defect in actual handling may
represent a severe form of ideomotor apraxia (IMA) and a recent investigation
supports the latter hypothesis. IA has been considered by some as a defect in the
performance of a series movement; this is considered by others, however, to be a
defect in memory.
Three anomic aphasia patients had what is probably a true IA because unlike the
patients with IMA who perform to command poorly but with appropriate motions,
these three patients responded to command by looking down at their hands, appearing
perplexed and either saying they could not do it or else making a completely irrelevant
movement. They could, however, demonstrate verbally that they understood and
also would choose the correct movement when presented in a multiple choice fashion.
Unlike the patients with IMA who improve slightly on imitation, these patients
performed flawlessly. The evidence is that all these patients had a lesion in the
dominant parietal lobe. They were able to use actual objects well and perform a
series of movements with these objects.
REFERENCES
BROWN, J. W. (1972) "Aphasia, Apraxia and Agnosia." Springfield: Thomas.
DE RENZI, E., PIECZURO, A., and VIGNOLO, L. A. (1968) Ideational apraxia: a quantitative study.
Newopsychologia, 6, 41-52.
GESCHWIND, N. (1965) Disconnexion syndromes in animals and man. n . Brain, 88, 585-644.
GOLDSTEIN, K. (1948) "Language and Language Disturbances." New York: Grune and Stratton.
GOODOLASS, H., and KAPLAN, E. (1963) Disturbance of gesture and pantomime in aphasia. Brain, 86,
703-720.
HEILMAN, K. M. (1973) A tapping test in apraxia. Neurology, Minneap., 23, 400.
LJEPMANN, H. (1908) "Drei Aufsatze aus dem Apraxiegebiet." Berlin: Karger.
MARCUSE, H. (1904) Apraktische Symptome bei einem Fail von seniler Demenz. Zentbl. NervHeilk.
Psychiat.,n,mi-lS\.
MORLAAS, J. (1928) "Contribution a l'Etudc de rApraxie." Paris: Legrand.
PICK, A. (1905) "Studien fiber motorische Apraxie und ihre nahestehende Erscheinungen." Leipzig:
Deuticke.
WERNICKE, C. (1895) Zweifalle von Rindenlasion. Arb. psychiat. Klin. Breslau. Heft II.
ZANQWILL, O. L. (1960) Le probleme de l'apraxie ideatoire. Revue neurol., 102, 595-603.
{Received July 18, 1973)
I
I
I
I
byguestonOctober18,2011brain.oxfordjournals.orgDownloadedfrom