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Apraxia is a higher level motor disorder that patients exhibit when they perform voluntary movements. In right-handed individuals, lesions of the left parietal cortex produce apraxia of both limbs and buccofacial musculature (which includes the muscles of pharynx, larynx, jaw, velum, tongue, and lips). Less frequently, lesions of the premotor cortex and subcortical structures may also give rise to apraxia. There are a few cases of right-handed patients with apraxia following right-brain damage; however, the role of this hemisphere in higher motor control is not yet clear. In left-handers, apraxia is usually caused by lesions of the right hemisphere, may or may not be associated with aphasia—depending on whether language in these individuals has migrated to this hemisphere—and occurs more rarely following lesions in the left hemisphere.

Apraxia is often but not always associated with aphasia—an acquired language disorder—as both action and language systems are predominantly lateralized in the left hemisphere. The fact that patients may have apraxia without aphasia, and vice versa, reinforced the view that these two deficits are not due to damage to a single mechanism. The anatomical contiguity of the cerebral regions in the left hemisphere that underlie action and language explains why lesions of these regions often impair both functions.

Types of Apraxia

According to Functions

The investigation of apraxia began over a century ago. The first to study this disorder systematically was Hugo Liepmann, who developed a model of how voluntary gestures are organized in the brain and how the ability to evoke and produce them can be affected by brain damage. Liepmann distinguished three different types of apraxia, according to the function that he hypothesized to be affected: ideational, ideomotor, and melokinetic. This clinical classification is based on the type of function or process that is believed to be damaged. Thus, ideational apraxia (IA) corresponds to a deficit in formulating an action plan (or movement formula); it manifests itself when patients are engaged in complex action sequences (as in preparing breakfast) but also when they use one object at a time (such as drinking from a glass). The ideational deficit has been attributed to different causes. Arnold Pick described patients with dementia who suffered from IA, making gross mistakes in using objects that they were able to identify. Subsequently, Joseph Morlaas suggested that IA was due to a faulty recognition of objects (i.e., agnosia of usage), and Klaus Poeck believed it reflected the disintegration of the sequence organization of object-related actions. According to this latter interpretation, patients should be impaired in all tasks tapping the representation of an action sequence (e.g., everyday activities and sequencing photographs of those activities), sparing the use of single objects.

Poeck's interpretation was challenged by the work of Ennio De Renzi and collaborators who reported patients who made mistakes, such as omissions, object misuse, and mislocations of objects, when they performed complex everyday activities as well as when they used individual objects. De Renzi interpreted IA as a conceptual disorder, caused by “amnesia” for object use that prevents patients from adequately accessing the functional characteristics of objects. However, the impaired ability to use objects is not necessarily caused by damage to semantic memory, as patients with tool use impairment and preserved knowledge about objects have been documented. Tool use deficits are prevalently associated with lesions of the posterior regions of the left hemisphere and, in particular, of the parietal cortex, a region that has been identified in imaging studies with healthy individuals as involved in tool use. IA is often caused by focal lesions of vascular etiology, but it can also be observed in patients with dementia.

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