Apraxia is defined as a "disorder of skilled movement not caused by weakness, akinesia, deafferentation, abnormal tone or posture, movement disorders such as tremors or chorea, intellectual deterioration, poor comprehension, or uncooperativeness" (Heilman and Rothi, 1993 as cited in Adriani et al., 2007, p. 61). In simple words apraxia can be referred to as motor agnosia (Chawla.J., 2009). Apraxics are not partially paralytic but they lack information about how to perform skilled movements (Chawla.J.,2009). The following essay is structured as follows. It begins with a short description of apraxia , its types, then it views the existing models apraxia which is followed by understanding the laterality of lesions in apraxia. After that it throws light on imitation of gestures in apraxia and finally it argues for a multidisciplinary approach to study apraxia.
Keywords - apraxia , lesions, neuropsychological model , multidisciplinary approach.
Apraxia is a disorder of motor control which can be referred neither to "elemental" motor deficits nor to general cognitive impairment (Geschwind & Damasio, 1985; Heilman & Rothi, 1993).
This definition leaves room for many interpretations, and indeed the term "apraxia" has been applied to a multitude of heterogeneous disturbances (Goldenberg, 2008). There is, however, a core of symptoms which have been in the focus of Liepmann's (1908) original conception of apraxia and which remain to be unanimously recognized as deserving a diagnosis of apraxia. They differ from most other motor symptoms of brain damage by two features:
Firstly, they concern both sides of the body although they are caused by unilateral, predominantly left-sided, brain lesions; and, secondly, the skilfulness of movements depends on the conditions of their elicitation. Movements of similar spatial and biomechanical complexity as those which give rise to awkwardness and spatial errors in testing for apraxia, can be performed swiftly and skilfully in other contexts.
There are three domains of actions which are susceptible to apraxic errors: Imitation of gestures, performance of meaningful gestures on command, and use of tools an objects. Meaningful gestures can be either symbolic gestures with a conventional meaning (emblems) or pantomimes of tool use. All three domains may be impaired after severe brain damage, but more restricted lesions can bring forward selective disturbances of only one or two domains contrasting with preserved performance in the remaining ones (Barbieri & De Renzi, 1988; Cubelli, Marchetti, Boscolo, & Della Sala, 2000; Goldenberg & Hagmann, 1997; Goldenberg, Hentze, & Hermsdrfer, 2004; Motomura & Yamadori, 1994; Tessari, Canessa, Ukmar, & Rumiati, 2007).
Apraxia is a syndrome reflecting motor system dysfunction at the cortical level, exclusive of primary motor cortex. In planning movements, previously learned, stored complex representations of skilled movements are used. These 3-dimensional, supramodal codes, also called representations or movement formulae, are stored in the inferior parietal lobule of the left hemisphere. Diseases that involve this part of the brain, including strokes, dementias, and tumors, can cause loss of knowledge about how to perform skilled movements.
Apraxia can occur with lesions in other locations as well. Information contained in praxis representations is transcoded into innervatory patterns by the premotor cortices, including the supplementary motor area (SMA) and possibly the convexity of the premotor cortex; the information is then transmitted to the primary motor cortex and a movement is performed. Lesions of the SMA or other premotor cortices also can cause apraxia; in this case, knowledge about movement is still present, but the ability to perform movement is absent.
Apraxia also occurs with lesions of the corpus callosum, such as tumors or anterior cerebral artery strokes. Although the corpus callosum is not known to be involved directly in the performance of skilled movements, it contains crossing fibers from the right hemisphere to the premotor cortex. This type of apraxia represents a classic disconnection syndrome; patients with callosal apraxia typically are apractic only with the left hand.
Few data are available regarding the frequency of apraxia; however, it commonly occurs after stroke and in dementia2 of the most frequent neurological illnesses.
Theauthor of this articleasks patients to pantomime hammering a nail into the (imaginary) wall in front of them, screwing a screw into the wall, and using a pair of scissors to cut a piece of paper. Nevertheless, many other pantomimes could be performed, including brushing teeth, cutting with a saw, whipping eggs with an eggbeater, or peeling a potato.
A healthy response to any of these commands is to perform a crisp, well-planned movement. Patients should perform the movement with the hand oriented correctly to hold an imaginary tool, with the tool held at the correct orientation and distance from the target (wall, screw, paper, respectively), and with the motion performed in such a way that the action gets performed. In other words, the author would like to see an action that would successfully cut a piece of paper, as if scissors and paper were really there.
Any type of error in performing the above activities (in the absence of aphasia or lack of comprehension of the command or lack of motor deficit) implies a loss of knowledge about the movement to be performed. If the hand is not oriented to hold the tool correctly, if the action is performed in the wrong plane, if the target (eg, wall) is not located correctly, or if movement is performed incorrectly, the response is scored as an error.
Apraxia has a neurological cause that localizes fairly well to the left inferior parietal lobule, frontal lobes (especially the premotor cortex, supplementary motor area, and convexity), or corpus callosum.Any disease of these areas can cause apraxia, although stroke and dementia are the most common causes. Interestingly, callosal apraxia is rare after callosotomy and is much more common with anterior cerebral artery strokes or tumors. Apraxia can be related to specific neural substrate that causes the disorder, for example following subcortical lesions in corticobasal degeneration (Merrians et al., 1999 as cited in Petreska et al.,2007).
Types of Apraxia
The following types of apraxia has been described in this section.
Ideational Apraxia - It is historically defined as a conceptual organization of actions. It was first assesed by performing purposive sequences of actions that require the use of various objects in correct order (preparing tea) (Poeck .,1983). Ideational apraxia is a larger deficit that concerns the evocation of single actions. In this view , complex sequences of multiple objects are simply more suitable to reveal the deficit , possibly because of the heavier load placed on memory and attentional resources (De Renzi and Lucchelli, 1988).
Conceptual apraxia is defined as the loss of knowledge about tools and movements associated with their use. Patients with parietal lesions may have conceptual apraxia. These patients may be contrasted with patients with SMA (supplementary motor area) lesions or other lesions of the premotor cortex. The latter type of patient would have normal knowledge about how to move, yet be unable to perform the movement correctly because of faulty transcoding of the "innervatory patterns" in the motor cortex (Chawla,J.,2009). This apraxia is often observed in alzheimer's disease.
Ideomotor Apraxia - The concept of ideational apraxia was proposed by Liepmann. Operationally it is defined as "failure to produce the correct movement in response to verbal command, or failure to imitate correctly a movement performed by the examiner" (Liepmann.,1990 as cited in Makuuchi et al., 2005). For instance, individual with this apraxia cannot make correct motor responses when examiner asks them to salute or to waive their hands to express "goodbye". The neural correlates of ideomotor apraxia have been thought to be located in the left parietal lobe but some studies have claimed other region (Makuuchi et al., 2005). Lesion studies have reported defective imitation and movements executed by verbal commands (ideomotor praxis) after left parietal damage (Ghika et al., 1998 as cited in Makuuchi et al.,2005). A recent lesion study found maximum overlap of lesions in patients with ideomotor apraxia in the left intraparietal sulcus (Harrington et al., as cited in Makuuchi et al.,2005).
Conduction Apraxia - It is the syndrome of superior performance on verbal command than on immitation (Ochipa et al.,1994 as cited in Petreska et al.,2007). The opposite pattern has also been observed i.e., very poor performance on verbal command that improved on immitation or when seeing the object (Heilman.,1973 ; Merians et al., 1997 as cited in Petreska et al., 2007). The extreme occurrence of conduction apraxia, namely the selective inability to imitate with normal performance was termed visuo - imitative - apraxia (Merians et al.,1997).
Constructional Apraxia - According to Benton it is "the impairement in combinatory or organizing activity in which details must be clearly perceived and in which the relationship among the component parts of the entity must be apprehended" (Laeng 2006 as cited in Petreska et al.,2007). Constructional apraxics are unable to draw objects, copy figures simultaneously. It is an outcome of damage not only to the dominant but non dominant hemisphere as well. Hence, constructional apraxia appears to reflect the loss of bilaterally distributed components for constructive planning and the perceptual processing of categorical and coordinate spatial relations (Platz and Mauritz., 1995 ; Laeng.,2006 as cited in Petreska et al., 2007).
Apraxia can also be defined in relation to the selectively affected effectors: orofacial/ buccofacial apraxia , oral apraxia , upper and lower face apraxia, lid apraxia, limb apraxia, leg apraxia, trunk apraxia, etc. Motor planning disorders in children are deniminated developmental dyspraxia (Cermak.,1985). Apraxia can also designate a praxic ability impaired in an isolated manner such as : gait apraxia, apraxic agraphia, dressing apraxia, orienting apraxia and mirror apraxia (Petreska et al.,2007).
Callosal apraxia is particularly appropriate for disentangling the specific hemispheric contributions to praxis.
Existing Models of Apraxia
Five diifferent neuropsychological views has been observed for apraxia. They are:
- Liepmann's Model - This model dates back to 100 years ago. Liepmann proposed the idea of existence of "movement formulae" which contains the time space form picture of an action (Rothi et al., 1991 as cited in Petreska et al.,2007).He believed that in right handers, these movement formulae are stored in the left parietal lobe, endorsing the view of left hemispheric dominance of the praxis (Faglioni and Basso .,1995 as cited in Petreska et al., 2007). To execute a movement , the spatio temporal image of the movement is transformed in to "innervatory patterns" that yield "positioning of the limbs according to directional ideas" (Jacobs et al.,1999 as cited in Petreska et al., 2007). Liepmann distinguished between 3 forms of apraxia namely, "ideational" . "ideomotor" and "limb kinetic."
- Disconnection Model by Geschwind - Acoording to this model verbal command for movement is comprehended in Wernicke's area and transferred to the ipsilateral motor and premotor areas that control the movement of the left hand (Clark et al.,1994 as cited in Petreska et al., 2007). For a left hand movement , the information needs to be transmitted to right association cortex via corpus callosum. This model cannot explain impaired immitation or impaired object use since they do not require a verbal command (Rothi et al.,1991 as cited in Petreska et al.,2007).
- Representational Model by Heilman and Rothi (1993) - According to this model apraxia is a gesture production deficit that may result from the destruction of the spatiotemporal representations of learned movements stored in the left parietal lobule. The model attempted to distinguish between dysfunction caused by destruction of parietal lobes and deficit which would result from the disconnection of the parietal areas from the frontal motor areas (Heilman et al.,1982 as cited in Petreska et al.,2007). This explains why patients with a gesture production deficit with anterior and posterior lesions perform differently on tasks of gesture discrimination, gesture recognition and novel gesture learning.
- Cognitive Model of Limb Praxis by Roy and Square (1985) - It basically involves two limb systems namely the conceptual system and production system (Petreska et al.,2007). The "conceptual system" provides an abstract representation of the action and comprises of three kinds of knowledge (Petreska et al.,2007). The "production system" incorporates a sensorimotor representation of the action and mechanisms for movement control (Petreska et al.,2007). This model predicts three patterns of impairement (Heath et al.,2001 as cited in Petreska et al.,2007) namely "pantomime deficit" , "deficit in imitation" and "concurrent impairement" (Petreska , et al., 2007, p.67).
- Multi - modular Model by Rothi (1991) - To address the issue of modality spercific dissociation which was absent in the earlier models Rothi proposed a multi-modular model which reflects the complexity of human praxis more appropriately. This multi modular model has input that is selective according to the modality, a specific "action semantics system" dissociable from other semantivs system, an "action reception lexicon" that communicates with an "action production lexicon" anda separate "non lexical route" for the imitation of novel and meaningless gestures (Rothi et al., 1997 as cited in Petreska et al.,2007,p.67).
This model was extended by Cubelli in 2000 and two new dimensions "visuomotor conversion mechanism and "gestural buffer" were added. Buxbaum and others (2000) further extended the model based on their observation. According to them, a unitary set of representations named "body schema" calculates and updates the dynamic positions of the body parts relative to one another. Importantly, this is a common processing stage between "lexical" and "non lexical route" and hence serves meaningful and meaningless actions.
Existing models of apraxia fail to account for differential performance in imitation of hand postures and finger configuration (Goldenberg and Hagmann.,1997 ac cited in Petreska et al.,2007,p.69). Moreover, in a study of ideomotor apraxia data was provided which was compatible with the influential "mirror neuron hypothesis" (Buxbaum et al.,2005 as cited in Petreska et al.,2007,p.69). Apraxia models cannot easily be reconciled with this hypothesis which is based on the neurophysiological observations from the monkey brain (Rizzolatti and Craighero.,2004 as cited in Petreska et al.,2007,p.69). The representations in "mirror neuron hypothesis" serve action recognition and action production tasks, thus it can be said that perception of movement is constrained by its executional knowledge (Petreska, et al., 2007,p.69). Realated to apraxia, the "mirror neuron hypothesis" questions the seperation of "input" and "output lexicon" (Koski et al.,2002 as cited in Petreska et al.,2007,p.69).