These high-order abnormalities of learned movement patterns have several unique features. Seldom are they evident to the patient himself and therefore they are not sources of complaint, even if they disrupt daily activities such as dressing. Or, if the patient appreciates them, he has difficulty describing the problem except in narrow terms of the activity that is impaired, such as using a phone or dressing. For this reason they are also often overlooked by the examining physician. Obviously, if the patient is confused or aphasic, spoken or written requests to perform an act will not be understood and one must find ways of persuading him to imitate the movements of the examiner. Moreover, the patient must be able to recognize and name the articles that he attempts to manipulate.
In practical terms, as mentioned, the lesion responsible for ideomotor apraxia, which affects both hands, usually resides in the left parietal region. Kertesz and colleagues provided evidence that the lesions responsible for aphasia and apraxia are different, although the two conditions are frequently associated because of their origin in the left hemisphere. The exact location of the parietal lesion, whether in the supramarginal gyrus or in the superior parietal lobe (areas 5 and 7) and whether subcortical or cortical, has been variable.
Although the majority of ideational and ideomotor apraxias occur with lesions in the left cerebral hemisphere, the right hemisphere retains some of these capacities. A small number of apraxic patients have right hemisphere damage. This also explains the preservation of most praxis skills in the left hand following callosal lesions. Geschwind accepted Liepmann’s proposition that a lesion of a subcortical tract (presumably the arcuate fasciculus) can disconnect the parietal from the left frontal cortex, accounting for the ideomotor apraxia of the right limbs. The apraxia in the left limb is the consequence of a functional disconnection of the left and right premotor association cortices. These conceptualizations, while possibly valid, are of more theoretic than practical significance and depend heavily on the disconnection model discussed in Chap. 21. An alternative view is that there is not an actual disconnection of the two frontal lobes as much as there is a failure of the left to activate the right frontal lobe because the right does not receive instructions from the damaged left parietal lobe. It is the dominant parietal lobe that still embodies the property of praxis.
Of a somewhat different nature is an oral-buccal-lingual apraxia, which is probably the most commonly observed of all apraxias in practice. It may occur with lesions that undercut the left supramarginal gyrus or the left motor association cortex and may or may not be associated with the apraxia of the limbs described above. Such patients are unable to carry out facial movements on command (lick the lips, blow out a match, etc.), although they may do better when asked to imitate the examiner or when confronted with a lighted match. With lesions that are restricted to the facial area of the left motor cortex, the apraxia will be limited to the facial musculature bilaterally and may be associated with a verbal apraxia or cortical dysarthria (namely, Broca’s aphasia, see Chap. 22).
The so-called apraxia of gait is considered in
Chap. 6, but strictly speaking, this is not an apraxia since walking is not truly a learned act. The terms dressing apraxia and constructional apraxia are used to describe special manifestations of nondominant parietal lobe disease, in contrast to the above-described forms of apraxia that result from lesions on the dominant side. Although dressing apraxia in many ways resembles an ideomotor apraxia, it probably has a basis in a form of a loss of appreciation of extrapersonal space. These issues are discussed further in Chap. 21.