Apraxia

Victor W Mark MD (Dr. Mark of the University of Alabama at Birmingham has no relevant financial relationships to disclose.)
Originally released November 4, 2002; last updated November 16, 2016; expires November 16, 2019

This article includes discussion of apraxia, limb apraxia, callosal apraxia, conceptual apraxia, dissociation apraxia, ideational apraxia, ideokinetic apraxia, and motor kinetic apraxia. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Apraxia refers to the loss of ability to produce skilled movements as the result of brain damage when exclusion of motor disorder that affects unskilled movements could be considered contributing. Apraxia can be observed in diverse conditions, including stroke, brain tumors, head injury, corticobasal syndrome, progressive supranuclear palsy, and other degenerative illnesses. Apraxia has usually been associated with left parietal pathology. However, evidence has associated cerebellar damage to a specific form of apraxia, apraxic agraphia. If further study associates cerebellar damage with other forms of apraxia, then the cerebellum may be recognized as a component of a system linked with the parietal cortex involved with planning movements.

Key points

 

• Apraxia as impairment in the production of learned (or skilled) movements not caused by weakness, paralysis, incoordination, or sensory loss.

 

• Apraxia is usually associated with left parietal pathology.

 

• Three major subtypes of apraxia are frequently distinguished: (1) limb kinetic apraxia, (2) ideokinetic or ideomotor, and (3) ideational apraxia.

 

• Treatment of apraxia has been focused on compensating for the disorder and managing the environment of the apraxic patient.

Historical note and terminology

Apraxia is defined as the loss of the ability to produce purposeful, skilled movements as the result of brain damage (McClain and Foundas 2004; Heilman and Watson 2008). Liepmann defined apraxia as impairment in the production of learned (or skilled) movements not caused by weakness, paralysis, incoordination, or sensory loss (Liepmann 1920). Apraxia is manifested in a person's inability to "move the moveable parts of the body in a purposeful manner even though motility is preserved" (Liepmann 1900; Liepmann 1977). The term apraxia widely pertains to a single action (eg, turning a screwdriver, sewing with a needle, hitchhiking, kicking a ball, sucking on a straw) as opposed to series of movements (eg, putting together a meal, changing a tire). In some instances, examiners evaluate simple actions that require 2 limbs (eg, playing a guitar, boxing, operating a steering wheel, putting on eyeglasses, riding a bicycle).

This article will focus on apraxia as generally defined as failure to carry out skilled (for the most part culturally learned) movements. This article will not discuss disorders of basic, largely unskilled movements such as walking, breathing, eye opening, reaching, self-scratching, etc. Therefore, this review will not address gait apraxia, eye opening apraxia, or respiratory inhibitory apraxia. Additionally, other disorders that are termed “apraxia” will be excluded because they do not reflect disturbances of skilled movement. Thus, constructional apraxia appears to be more of a conceptual and visuoperceptual disorder than a skilled motor disorder; dressing apraxia with regard to putting on garments by inserting one's own limbs and trunk appears to be more closely related to a spatial planning disorder or neglect; and apraxia of speech is a specific impairment in talking. Descriptions of these disorders may be found in other MedLink Neurology clinical summaries.

In the late 1800s Steinthal was the first used the term "apraxia" in describing a disturbance in skilled limb movements as the result of brain damage. Steinthal wrote that apraxia consisted of a disturbance in the relationship between movements and the objects on which the movements were enacted (Steinthal 1871). Subsequently, there was a lack of consensus concerning the mechanism for and definition of apraxia. For example, other researchers had observed the disturbances of object related movements in aphasic patients but attributed both deficits to asymbolia, a generalized disturbance in the comprehension or production of symbols in any modality, including language and gesture (Critchley 1939; Duffy and Liles 1979). Goldstein also related disorders of action to the patient's aphasia and included skilled movement problems within a definition of aphasia (Goldstein 1948). Pick, however, defined apraxia as an asymbolia that was not included within a definition of aphasia (Pick 1905). Another mechanism proposed to explain apraxia was posited by Kussmaul, who defined apraxia as an agnosia, an impairment in the recognition of tools, which then affects the movements produced with tools (Hecaen and Rondot 1985). In 1905, Liepmann described a patient who presented with a severe inability to produce volitional movements with the left hand as well as profound aphasia. Liepmann's point in describing this case was that a disorder of language or gnosis (knowledge) could not explain apraxia of only 1 hand. Movement failures created by language or gnosis deficits would affect both hands. This would later be considered an early description of callosal apraxia (Goldenberg 2003). Thus, Liepmann was the first to describe the mechanism of apraxia as a disorder of movement planning (Liepmann 1905a; Liepmann 1905b; Liepmann 1907; Liepmann 1920; Liepmann 1977).

Liepmann (Liepmann 1905b) studied 89 brain-damaged patients, 42 with left hemiplegia (thus, suspected to have right hemisphere lesions), 41 with right hemiplegia (thus, suspected to have left hemisphere lesions), 5 nonhemiplegic with aphasia (left hemisphere lesions), and 1 who was neither hemiparetic nor aphasic but was apraxic. The patients were asked to produce 3 types of movements: (1) expressive movements such as waving and saluting; (2) transitive (tool-based) and intransitive (non-tool-based) movements to command from memory, such as playing an organ grinder and snapping the fingers; and (3) manipulations of actual tools such as combing hair with a comb and writing with a pen. Liepmann found that the patients with right hemisphere damage rarely made errors on these tasks, whereas the patients with left hemisphere damage made frequent errors. Within the groups of patients with left hemisphere damage, approximately half showed evidence of apraxia; of these, 25% showed impairments when manipulating the actual tools (Liepmann 1905b). Based on these observations, Liepmann proposed that the left hemisphere, specifically the parietal region, was responsible for the skilled production of both hands (Liepmann 1905b). He argued that the right hemisphere is dependent on the plans and directives of the left hemisphere for learned movement and that the right hemisphere receives movement planning information from the left hemisphere via the corpus callosum. Liepmann proposed the existence of movement formulae, which he defined as knowledge of the course of action (time-space sequences) required to complete an action goal as well as the semantic information about the tool and object used. The movement formulae may be implemented by retrieval of innervatory patterns (configurations of neural connections specialized for particular movement patterns) that communicate directly with the motor system for movement production (Liepmann 1905b).

Additionally, further support for Liepmann's proposal that the left hemisphere was responsible for the skilled movements of both hands was found in the case described by Liepmann and Maas of a patient with a lesion of the corpus callosum who was unable to produce skilled movements with his nonparalyzed left hand (Liepmann and Maas 1907). He was unable to write and could not even bring his hand into the writing position. The patient also showed deficits in using actual tools and objects. Liepmann hypothesized that the effect of the corpus callosum lesion in this case was to disconnect the movement formulae of the left hemisphere from the primary motor cortex of the right hemisphere (Liepmann and Maas 1907).

Subsequently, Liepmann (Liepmann 1905a; Liepmann 1905b) described 3 subtypes of apraxia: (1) limb kinetic apraxia, (2) ideokinetic or motor apraxia, and (3) ideational apraxia. Limb kinetic apraxia was described as a loss of the kinetic components of engrams resulting in coarse or unrefined movements with movements that no longer have the appearance of being practiced over time. Ideokinetic or ideomotor apraxia was described as a loss of ability to perform learned movements. Ideational apraxia was described as an impairment of ideational (conceptual) knowledge resulting in loss of the conceptual linkage between tools and their respective actions as well as the ability to sequence correctly produced movements (Liepmann 1905a; Liepmann 1905b). Integral movements may be left out of a series or produced in the wrong order, or correct movements may be produced with the wrong tools. By describing these praxis subtypes, Liepmann proposed that praxis is supported by a multicomponential system that can be differentially impaired (Liepmann 1905a; Liepmann 1905b). Because Liepmann had used the term ideational apraxia for either the incorrect selection of a tool for a desired action or the incorrect sequencing of actions for a multi-step task, inconsistent use of the term continues to the present (Hanna-Pladdy and Gonzalez Rothi 2001).

Other subtypes of motor apraxia were subsequently described in the 20th century and include:

 

• callosal apraxia
• conceptual apraxia
conduction apraxia
• dissociation or disconnection apraxia

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