The term apraxia denotes a disorder in which an attentive patient loses the ability to execute previously learned activities in the absence of weakness, ataxia, sensory loss, or extrapyramidal derangement that would be adequate to explain the deficit. All the elements of the activity may be demonstrated in circumstances other than in response to the command to execute the activity or gesture. This was the meaning given to apraxia by Liepmann, who introduced the term in 1900, and discussed further by Denny-Brown in 1958.
Any explanation of apraxia requires an appreciation of the interplay between cortical areas that create highly complex motor behaviors. On the basis of studies of patients with lesions of different parts of the brain, it appears that the initiating and assembling of the complex motor activities and continuously modifying the components of a motor sequence are directed by the frontal lobes. Lesions of the frontal lobes have the effect of impeding the organization of motor sequences in the contralateral limbs so that a complex activity will not be initiated or sustained long enough to permit its completion, or it may be performed awkwardly. However, clinical and functional imaging data indicate that planned or commanded action is formulated not in the frontal lobe, where the impulse to action arises, but in the parietal lobe of the language-dominant hemisphere, where visual, auditory, and somesthetic information is integrated. The formation of ensembles of skilled movements, which Liepmann called a “space-time plan,” depends on the integrity of the dominant parietal lobe; if this part of the brain is damaged, complex patterns of movement cannot be activated at all or the movements are awkward and inappropriate.
Apraxia has been traditionally divided into three types: ideational, ideomotor, and limb-kinetic. They are described in greater detail in Chap. 21 but a brief account is provided here because of their intimate involvement with motor activity. The failure to conceive or formulate an action to command was referred to by Liepmann as ideational apraxia. Sensory areas 5 and 7 in the dominant parietal lobe, the supplementary and premotor cortices of both cerebral hemispheres and their integral connections are involved collectively to accomplish these actions. In ideomotor apraxia, the patient may know and remember the planned action, but because these areas or their connections are interrupted, he cannot actually execute it with either hand. Certain tasks are said to differentiate ideomotor from ideational apraxia, as discussed further on, but the distinction may be quite subtle. Nonetheless, ideational apraxia has been said to be characterized by difficulty in “what to do,” whereas ideomotor apraxia is a block in “how to do” as a result of an inability to transmit the gesture to executive motor centers.
A third disorder, opaque to many neurologists, is limb-kinetic apraxia (or kinetic-limb apraxia). It is a clumsiness and maladroitness that is the result of an inability to fluidly connect or to isolate individual movements of the hand and arm as described by Kleist. In the originally conceived form, a hand displays awkwardness that is disproportionate to weakness or sensory loss, yet gestures and complex movements can be accomplished, unlike the case in ideomotor apraxia. Central to the disorder is a breakdown of fine fractionated finger movements for which reason the nature of limb kinetic apraxia and its differentiation from a mild corticospinal disorder has been elusive enough that many neurologists do not view it as a true apraxia.
The term limb-kinetic apraxia has also been applied to cases of paralysis that obscures the apraxia on one side but causes a breakdown of fine finger movements on the opposite side. This is more properly termed “sympathetic apraxia.” In particular, in a right-handed person, a lesion in the left frontal lobe that includes Broca’s area, the left motor cortex, and the deep underlying white matter may cause left-limb apraxia. Clinically, there is a nonfluent aphasia, a right hemiparesis, and clumsiness of the nonparalyzed left hand.