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What is apraxia? The clinician'sdilemmaRobyn L. Tate a & Skye McDonald ba University of Sydney , Australiab University of New South Wales , AustraliaPublished online: 14 May 2010.
To cite this article: Robyn L. Tate & Skye McDonald (1995) What is apraxia? The clinician'sdilemma, Neuropsychological Rehabilitation: An International Journal, 5:4, 273-297, DOI:10.1080/09602019508401473
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NEUROPSYCHOLOGICAL REHABILITATION, 1995.5 (4), 273-297
What is Apraxia? The Clinician’s Dilemma
Robyn L. Tate University of Sydney, Australia
Skye McDonald University of New South Wales, Australia
The study of apraxia has a long history and a large body of empirical data has accumulated. In spite of this, an understanding of apraxia is made difficult in that the literature is characterised by poorly defined concepts, inconsist- encies in terminology and classification systems and limited attempts to integ- rate new research with previous studies or other new information. Short- comings are also evident in the available clinical examination methods, which do not enable a comprehensive evaluation of apraxia. This paper reviews the empirical literature on limb apraxia from three perspectives: definitions of apraxia, taxonomies, and examination procedures. Commonly used clinical batteries are briefly described and it is argued that these instruments need improvement. In particular, a battery is required which has reliable diagnostic criteria and is capable of eliciting the dissociations reported in the research literature on limb apraxia.
INTRODUCTION Historically, the apraxias, along with the aphasias, agnosias, and amnesias, comprise the foundation of the classical neuropsychological syndromes. There is general agreement that apraxia refers to “disorders of the execution of learned movement which cannot be accounted for by either weakness, incoordination, or sensory loss, or by incomprehension of or inattention to commands” (Geschwind, 1975, p. 188). It usually occurs following left hemisphere (especially the supramarginal gyrus area) and callosal lesions, but has also been reported, albeit infrequently, with right hemisphere as well as deep subcortical lesions. The occurrence of apraxia following left hemisphere lesions is common, as evidenced by Liepmann’s
Requests for reprints should be sent to Robyn Tate, Department of Psychology, University of Sydney, Sydney 2006 NSW, Australia.
The dilemmas described in this paper were those the authors faced whilst practising clinical neuropsychologists at Lidcombe Hospital. We acknowledge the theoretical and case dis- cussions on apraxia held over many years with our neuropsychological colleagues working at Lidcombe Hospital.
0 1995 Lawrence Erlbaum Associates Limited
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(1905A980b) original study in which 50% of 41 subjects with right-sided hemiplegia suffered the disorder. This was later confirmed in the series of De Renzi, Motti, and Nichelli (1980) and it is now accepted that the left hemisphere is dominant not only for language, but also for movement. The posterior parietal region of the dominant hemisphere is purported to contain the space-time motor engrams (also called visuokinaesthetic motor engrams by Heilman, Rothi, & Valenstein [I9821 and more recently Heilman & Rothi [1993] refer to them as praxicons). This postulate, how- ever, is not new. Liepmann (translations in Brown, 1988; Kimura, 1980; Rottenberg & Hochberg, 1977) had introduced it at the turn of the century, referring to the dominant hemisphere as the Action Hcmisphere as well as the Speech Hemisphere. Although aphasia frequently coexists with apraxia, the relationship is not causal, the contiguity of the lesions in both disorders being the instrumental factor.
In spite of their central position in clinical neuropsychology, the apraxias remain a somewhat enigmatic group of disorders. Limb apraxias, in par- ticuIar, are poorly delineated in functional terms and lack clear strategies for diagnosis and classification, even though a range of clinical batteries and research instruments is available (e.g. De Renzi & L,ucchelli, 1988; Goodglass & Kaplan, 1983; Kertesz, 1982; Poeck, 1986). The functional significance of limb apraxia is even more poorly understood and, with some exceptions, has been an ignored area of empirical study. Clinicians wishing to base their assessment of limb apraxia on sound, empirically and theoret- ically based principles are soon daunted by the diverse, poorly integrated, sometimes contradictory nature of apraxia research. The aim of this paper is to examine some of the apparent inconsistencies in the literature and to explore their likely causes as these pertain to clinical practice. In a more positive direction we aim to reconcile some of the issues in theoretical accounts of apraxia and to discuss some directions for better clinical assess- ment tools.
THE PROBLEM AREAS
From a perusal of the literature it is apparent that the clinician’s quandry in identifying apraxia is not insignificant: McCarthy and Warrington (1990) comment that the terminology regarding these disorders of voluntary action “has been particularly inconsistent if not confusing” (p. 99), which, as Hecaen and Albert (1978) note, was already the case at the turn of the century when Liepmann, Kleist, Pick and others were describing their cases. And referring to examination procedures for motor apraxia, Poeck (1986) concludes that “the diagnosis is made mainly on the basis of personal experience and intuition” (p. 130). These interrelated sources of confusion pervade the literature on apraxia and are addressed under three headings: definitions, taxonomies, and examination procedures.
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Definition of Apraxia
As a number of authors have observed, the very definition of apraxia introduces the first difficulty confronting the clinician in evaluating the disorder; for the definition is essentially one of exclusion, describing apraxia by what it is not. The identification of apraxia is made all the more obscure for, as Kimura and Archibald (1974) note, the learned movements (also referred to as purposeful or voluntary) are never objectively defined. Moreover, those patients who are likely candidates for apraxia (e.g. from a left cerebrovascular accident [CVA]) often in fact have significant coexisting motor, sensory, and language deficits. The task of determining the degree to which such impairments contribute to the disordered execu- tion of learned movements is, in clinical practice, far from easy. This problem is compounded in cases where the lesion is not de novo or where the condition is progressive and the impairment widespread. Additionally, it is frequently said that identification of (ideomotor) apraxia is often over- looked because the deficit is generally only apparent under examination conditions (De Renzi, 1985; Geschwind & Damasio, 1985; Poeck, 1985). It is widely assumed that the patient can perform such movements normally in everyday behaviours (e.g. although unable to pantomime the use of a toothbrush when requested, the patient is able to perform the task as part of the normal toilet routine). A final difficulty in the identification of apraxia has been attributed to its rapid resolution; although Basso et al. (1987) have demonstrated that recovery from apraxia can be protracted, with 50% of their series with de novo left CVA still apraxic five or more months post-onset and 20% at one year or more.
Taxonomies of Apraxia
Unlike other neuropsychological disorders, an accepted taxonomy for the apraxias is not available. Indeed, the curious situation exists where some disorders with the label apraxia (such as dressing apraxia, apraxia of gait, constructional apraxia) are considered by some authorities (e.g. Geschwind & Damasio, 1985; Poeck, 1986) to be misnomers, because they arise from dysfunctions that are not germane to apraxia as originally described. According to Geschwind and Damasio (1985), this situation arose historic- ally, perhaps as a function of national language barriers. Although the German literature continued to define apraxia in keeping with the disorders displayed in Liepmann’s original cases, this did not occur in the later English and French literature on apraxia, where the label came to include a much wider variety of higher order motor disorders. Geschwind’s (1975) position is that the term “apraxia” should be applied only to the types of disorders consistent with Liepmann’s cases. Nonetheless, it must be said that other authors (e.g. Hecaen & Albert, 1978) argue for the inclusion of at least some cases of, for example, dressing apraxia, as true apraxias,
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depending upon the underlying mechanisms responsible for the breakdown of the ability in the individual case.
The traditional classification of apraxia, following Liepmann’s original formulation, is available in a number of reviews on the topic (e.g. Gesch- wind & Damasio, 1985; Hecaen & Albert, 1978; Heilman & Rothi, 1993; Miller, 1986; Poeck, 1986). Two major types of apraxia are identified: motor apraxia (comprising two varieties of apraxia, limbkinetic and ideomotor) and ideational apraxia. There is some question as to the status of limb-kinetic apraxia, which has been described as a motor disorder intermediate between paralysis and apraxia. Here, movements are per- formed in an awkward and clumsy manner, with a loss of kinetic melody (Goldberg, 1985; Freund & Hummelsheim, 1985; Luria, 1980). Ideomotor and ideational apraxia therefore remain the two classical forms of apraxia. Despite major problems in nosology the “ideomotor” and “ideational” labels are entrenched in the apraxia literature and their usage is difficult to avoid.
In an attempt to operationalise apraxia, Geschwind and Damasio (1985) stipulate any of four conditions in which apraxia may be observed in clinical situations: (1) Failure to produce the correct movement in response to verbal command; (2) failure to imitate correctly a movement performed by the examiner; (3) failure to perform a movement correctly in response to a seen object; or (4) failure to handle an object correctly. The clinician faces a particular difficulty in the evaluation of apraxia, however, in that exactly what constitutes a failure has not been clearly defined.
Ideomotor Apraxia
With respect to ideomotor apraxia (IMA), Geschwind and Damasio (1985) simply define it as “the failure to carry out a requested movement properly’’ (p. 425). Heilman and Rothi (1985) provide a more precise definition, as a difficulty “with the selection, sequencing and spatial orientation of movements” (p. 134). Their subsequent definition (Heilman & Rothi, 1993) focuses on these error types, but although five main types are described in detail, it remains unclear whether such errors are definitive of IMA, or are equally applicable to other types of apraxia. Ideomotor apraxia occurs in upper and lower limbs (either unilateral [left hand] or bilateral) as well as the orofacial musculature (cf. buccofacial apraxia) and, at a more controversial level (see Howes, 1988; Poeck, Lehmkuhl, & Willmes, 1982), the axial or midline body structures. A classical clinical feature of IMA is that it differentially affects the intentionality of a move- ment, with automatic movements being spared. According to Faglioni and Basso (1985), Liepmann’s original position was that IMA was not dis- ruptive to everyday life but only apparent on special testing; the patient with IMA being able to use the objects in the normal routine without
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difficulty. Although this viewpoint is still generally accepted, it is chal- lenged by mounting evidence. De Renzi and Lucchelli (1988) have argued that a severe IMA will disrupt normal functioning by resulting in clumsy and awkward behaviour. Studies by Norwegian workers have demon- strated significant group differences with respect to level of competency in everyday activities and performance on tests of praxis, including imitation of meaningless hand postures (Bjorneby & Reinvang, 1985). Sundet, Finset, and Reinvang (1988) further demonstrated that of a range of neuro- psychological variables (including tests of aphasia), measures of ideomotor apraxia had the most predictive value regarding competency in everyday activities in a group of left hemisphere stroke patients.
Ideational Apraxia
Ideational apraxia (IA) has been variously defined, and in particular there have been two distinct camps regarding its core features according to Poeck and Lehmkuhl (1980). First, many investigators follow Liepmann’s original concept of IA being “a disturbance in the performance of complex actions involving the serial ordering of simple movements, which, in isola- tion, could be executed correctly” (Poeck & Lehmkuhl, 1980, p. 273, emphasis added). On the other hand, some contemporary workers, most notably De Renzi and colleagues, adopt Morlaas’ early definition, wherein IA refers to a disturbance in “the use of real objects, simple as well as complex serial movements” (Poeck & Lehmkuhl, 1980, p. 273, emphasis added). In this latter sense, IA has been interpreted as an “agnosia of usage”, although De Renzi and Lucchelli (1988) consider that ‘‘amnesia of usage” is probably a more accurate description; IA being a form of semantic amnesia (Barbieri & De Renzi, 1988). This concept of action semantics, i.e. knowledge of object use (and related systems) has recently been extended by Ochipa, Rothi, and Heilman (1992), who aim to distin- guish types of apraxia on the basis of error patterns depending on whether they reflect a loss of object knowledge or not.
Distinctions Between IA and /MA
The consequence of these varying criteria of IA is that some subjects may be classified as having IMA by one set of criteria, but classified as having IA by the other. There is general agreement that, in practice, inability to pantomime and/or imitate (e.g. salute, brush teeth, copy a movement) is characteristic of IMA, and inability to use multiple objects in a serial order (e.g. place a candlestick in a holder and light it) defines IA; the controversy surrounds the classification of impairment of the actual use of single objects. The inconsistency in nomenclature would not present undue difficulty if IA were considered a severe form of IMA, but on that issue currently there is general consensus that these two forms of limb
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apraxia represent separate disorders. It has been argued that IMA is clearly distinguishable from IA (De Renzi & Lucchelli, 1988; De Renzi, Pieczuro, & Vignolo, 1968; Poeck, 1986). De Renzi and Lucchelli (1988) reported a substantial correlation ( r = 0.85) between impaired multiple object use and impaired single object use, whereas no significant correlation ( r = 0.31) was found in the same subjects in their capacity to imitate (IMA) and their ability to use multiple objects (IA). Nonetheless, the clinical picture is obscured by dissociations occurring in single cases reported in the literature: Pilgrim and Humphreys (1991) described a patient they classified as having a pure IMA who was normal on bimanual complex tasks but who was impaired with single object use. Similarly, De Renzi and Lucchelli (1988) described a number of their subjects with pure IMA (impaired capacity to imitate and normal ability with complex sequential [multiple object] tasks) who were unable to use single objects.
Alternative Taxonomies The varieties of apraxias covered in many reviews are frequently pre-
sented at a descriptive level. Such accounts invariably comprise a confusing combination of both the fypes of apraxia (viz. limb-kinetic, ideomotor, ideational) as well as their functional effects upon particular body structures (viz. limb, buccofacial, axial). Although the classification based on type of apraxia (regardless of body part), arguably has stronger theoretical implica- tions than that based on the functional effects upon particular body struc- tures, the view of a number of authors (e.g. Geschwind, 1965; Kimura & Archibald, 1974), is that the classical distinctions of IMA and IA have not been helpful either; a position which is amply demonstrated by this review.
Gcschwind (1965) argued for a classification based on neuroanatomical mechanisms (cf. callosal apraxia, sympathetic apraxia, supramargina1 apraxia), and descriptions of these variations in limb apraxia are available (Geschwind, 1965; Geschwind & Damasio, 1985; Heilman & Rothi, 1993; Miller, 1986). 111 brief, callosal and sympathetic apraxia result in a uni- lateral (left-sided) apraxia, hypothesised to occur due to disconnection of the right motor cortex from the language and motor areas in the left hemisphere. Movement to verbal command is impaired in both types of apraxia, and with callosal lesions (especially the anterior portions), performance may improve under conditions of imitation and object use. This dissociation is not seen to such an extent in sympathetic apraxia (i.e. a pairing of left-sided apraxia with right hemiplegia) which is associated with an anterior left hemisphere lesion (located deep to Broca’s area). In this case, performance is reported as poor under all conditions: verbal command, imitation, and object use. Moreover, in contrast to callosal apraxia, sympathetic apraxia is often accompanied by buccofacial apraxia. Heilman et al. (1982) surmised, on the basis of the type of aphasia, that
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patients with apraxias from purported anterior lesions can discriminate correct from incorrect performances. By contrast, apraxia associated with posterior lesions located in the white matter deep to the supramarginal gyms in the parietal lobe, results in bilateral apraxia, generally under all conditions including discrimination. This last disturbance is hypothesised to occur because the visuokinaesthetic motor engrams or praxicons are destroyed.
The last decade has also seen reports of apraxia occurring with circum- scribed deep subcortical lesions, most notably in the left basal ganglia and thalamus (Agostoni, Coletti, Orlando, & Tredici, 1983; Basso, Luzatti, & Spinnler, 1980; De Renzi, Faglioni, Scarpa, & Crisi, 1986) and clinical dis- orders where the pathology is primarily subcortical, such as Huntington’s Disease (Shelton & Knopman, 1991). The severity of the clinical presenta- tion varies; while the seven cases reported by Agostoni and coworkers (three of which had right hemisphere lesions) were mild, the five cases identified by De Renzi and colleagues were much more severe, with impaired performance on both verbal command and imitation. The fre- quency of apraxia with circumscribed subcortical lesions (4 of the 26 patients in the series of Basso et al., 1980) is considered sufficient for De Renzi et al. (1986) to suggest that the classical neuroanatomical sub- strate for lesions causing apraxia should be enlarged to encompass a basal ganglia-thalamus-cortical loop. While apraxia has been consistently demonstrated after lesions in localised areas of the cortex and subcortex, as described above, the studies of Basso et al. (1980) and Alexander et al. (1992) serve as a reminder that dysfunction in such areas does not neces- sarily produce apraxia.
Examination Procedures Tasks
The literature on tests of apraxia is overwhelming with respect to the range of tasks and conditions used by different groups to assess apraxia. The types of tasks include transitive and intransitive gestures, nonsymbolic movements, finger and hand movements, dynamic movements and post- ures. Again it is questionable whether the various synonyms used by different research groups (cf. emblems vs. gestures vs. meaningful vs. rep- resentational vs. symbolic movements) serve any purpose and they have certainly contributed to unnecessary reduplication in terminology. There is more agreement as to the conditions under which movements should be studied: verbal command, imitation, and object use. Although apraxia is reported to have differential impact depending on the movement task used, there is relatively little consistency within the literature regarding these differences in performance profiles.
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Verbal Command (Pantomime) and Imitation. Incapacity to produce the correct movement to verbal command (using pantomime) and/or imita- tion is considered universally as the hallmark of IMA. Nevertheless there is considerable variability between reports on the ability of individual IMA patients to perform these two tasks, suggesting that the disorder as reported is not a homogeneous one. Quantification of the performance of IMA patients on pantomime and imitation tasks has found significant correla- tions (ranging from 0.44 to 0.80) between the inability to pantomime the movement and the incapacity to imitate (De Renzi & Lucchelli, 1998; De Renzi et al., 1980; Kimura & Archibald, 1974). On the whole, imitation of meaningful gestures has been found to be an easier task than pantomime (Alexander et al., 1992; Lehmkuhl, Poeck, & Willmes, 1983; Poeck et al., 1982; Roy, Square-Storer, Hogg, & Adams, 1991; Watson, Fleet, Rothi, & Heilman, 1986) and is frequently used as a second measure after the patient fails to pantomime correctly (Borod, Fitzpatrick, Helm-Estabrooks, & Goodglass, 1989; Goodglass & Kaplan, 1983; Kertsz & Ferro, 1984; Kertesz & Hooper, 1982).
De Renzi et al. (1980) argued, on the basis of previous research, that apraxia may be more easily elicited by using nonmeaningful movements and as a consequence of this they developed an imitation task incorporating both meaningful and meaningless movements. This task also has the dis- tinct advantage of permitting an examination of praxis in severely aphasic subjects who may not otherwise comprehend the requirements of items administered by verbal command. The inclusion of meaningless move- ments increases the level of difficulty of the imitation task and under these conditions, normal subjects perform the pantomime of meaningful gestures slightly better than imitation of movements (both meaningful and meaning- less) (De Renzi, Faglioni, & Sorgato, 1982). So too do some IMA patients, although a double dissociation has been reported: Some subjects are impaired on imitation but not pantomime as well as vice versa (Barbieri & De Renzi, 1988; De Renzi et al., 1982). If conditions of verbal command and imitation include both meaningful and meaningless movements IMA subjects are reported to perform at relatively similar levels on both (Lehmkuhl et al., 1983; Roy et al., 1991), although the study of Alexander e t al. (1992) does not support these findings. Using tasks of two levels of meaningfulness or representation, which were carefully matched for motor complexity, they found that less representational tasks were performed consistently better than more representational tasks.
It may be anticipated that differential performances on pantomime versus imitation tasks would distinguish IMA and I A but there is little solace in this arena either, much of the inconsistency originating from the operational definitions of IMA and IA used by different research groups. Poeck and Lehmkuhl (1980) have implied that patients with IA should be capable of pantomiming object use while Barbieri and De Renzi (1988) argue that inability to pantomime is characteristic of an ideational rather
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than ideomotor apraxia. Empirical studies further compound the issue. Only 4 of the 20 subjects tested for IA by De Renzi and Lucchelli (1988) were able to imitate and all subjects performed below their cut-off score for pantomime. Other studies of subjects with IA also report failure on tasks of both pantomime and imitation (Schwartz et al., 1991; Ochipa, Rothi, & Heilman, 1989).
Similarly, the conventional view that the patient with IMA can use actual objects normally is not upheld by empirical studies. Actual object use is rarely reported in studies of IMA; though when it has, the subject frequently has difficulty. For example, of five studies reporting actual object use in IMA subjects, only one (Agostoni et al., 1983) found that all (seven) subjects could use the actual objects normally. In the other studies (De Renzi et al., 1982,1986; Pilgrim & Humphreys, 1991; Watson et al., 1986) a substantial number of subjects with IMA (21% in the study of De Renzi et al., 1982) had difficulty manipulating actual objects too.
Object Use.
Scoring Methods
A further problem in the assessment of apraxia is that there are no consistent scoring criteria by which a failure on various tasks can be identi-. fied, although numerous quantitative and qualitative approaches have been reported.
Quantitative Measures. The majority of studies of IMA have used quantitative scales. For example, De Renzi and his colleagues have a Movement Imitation Test which is scored 3 (correct on the first trial), 2 (correct second trial), 1 (correct third trial), 0 (not correct on the third trial). This had been used in a number of studies (e.g. Barbieri & De Renzi, 1988; Basso et al., 1987; De Renzi & Lucchelli, 1988; De Renzi et al., 1980, 1982, 1986; Faglioni & Scarpa, 1989). Other studies have used scales estimating relative competence on the tasks of imitation, pantomime and/or actual object use. These have included ranges from 2 (correct) to 0 (incorrect) (Agostoni et al., 1983; Basso et al., 1980; Goodglass & Kaplan, 1963; Kolb & Milner, 1981; Mozaz et al., 1993); 3 (good) to 0 (incorrect/incomplete) (Barbieri & De Renzi, 1988; Borod et al., 1989; De Renzi & Lucchelli, 1988; Kertesz & Ferro, 1984); and 7 (good) to 1 (poor) (Pilgrim & Humphreys, 1991). These scoring methods are useful for com- paring performances of apraxic patients across tasks and expedite the col- lection of data for research purposes. Although they provide an index of severity, the quantitative approach is limited in that no information is provided about the way in which the execution of the movement breaks down. Moreover, there is no indication that these scales are reliable measurement tools-very few of the studies cited (exceptions being Borod et al., 1989; Goodglass & Kaplan, 1963) reported an estimate of interrater reliability.
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Qualitative Measures. In addition to the quantitative approach there have been attempts to characterise the quality of the apraxic performance in terms of the types of errors made. Liepmann emphasised the importance of such errors in the analysis of apraxia, referring to them as parapraxic movements. This approach will undoubtedly prove to be more theoretically and clinically useful as evidenced by recent studies undertaking refined analyses of the sequential and spatio-temporal factors involved in the execution of movements (e.g. Harrington & Haaland, 1992; Poizner et al., 1990; Schwartz et al., 1991). To date, however, studies of the qualitative features of apraxic errors have produced a bewildering array of classifica- tions (see Table 1) that are mainly untested in terms of clinical reliability. The common qualitative errors that have been identified include movement-
TABLE 1 Qualitative Error Types Described in Limb Apraxia
Different Coarsel Muscle
Aurhor(s) Amorphous CIurnsy Suhstitufion Sequence Prrsrvrrufion Groups
Liepmann (in Brown, 1988) Goodglass & Kapliin (1963)
Lehmkuhl et al (1983) Haaland & Flaherty (1984)
Roy & Square ( 1985)
Dc Renzi & Lucchelli (1988)
(a) single object pantomime
(b) multiplc object use
Rothi et al. ( 1988) Shelton & Knopman (1991)
+ + ? Exchanged
- - -
+ + + - - -
__ -
? Hand
movement
-
- + - + + + 2 types
? 1 - Unrecognisable imprecise
+ ? - Misuse
+ - ? Unrecognisable 2 types
~ > + Imprecise Symbolic
content Schwartz et al. (1991) Alexander et al. - - + ( 1992) McDonald et al. + + + (1994) Incl. with Classified as
omission inaccuracy
NB: Error types do not fit these categories
+ + + Movement
+ + -
+ indicates that this error type is described; - indicates that this error type is not described; ? indicates that
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related errors, such as the sequencing and timing of the movement, the spatial orientation of the hands during performance, clumsiness in execu- tion, unsustained and fragmented movements, acoustic or verbal embellish- ments to the movements (augmentation) and use of the body part as the object itself (referred to as BPO). Other types of errors may be classified as movement-unrelated errors, including substitution (i.e. movements which are definite, but do not bear any relationship to the correct move- ment), perseveration of a previous movement or part of a movement, and amorphous movements.
Reports of qualitative features of error performance in IMA have pro- duced contradictory results (see Table 2). Rothi et al. (1988) studied nine left brain-damaged subjects and concluded that the movements produced by their subjects always reflected some relationship to the correct move- ment but were either spatially distorted or performed using different
Unsustainedl Augmentation Partiall Body Part Gesturall Omissionl
No Response IncompleIe as Object Spatial Timing Verbal Other
+ - - - - - -
+ + - - - - + 2 types Pantomimed
context + - + +
Fragmentary Not specified - - -
+ - - - + + -
2 types 3 types
+ ? + + + + + 2 types Initiation Context
2 types
+ + ?
+ ? + + + + +
- - - - Mislocation Perplexity
- Occurrence 3 types 2 types
+ - ? - - - 2 types Onomatopoeic
- + - + + - +
+ - + - + + + Classified as Classified as inaccuracy inaccuracy
the label used in the original study to describe this error type is the one shown under the question mark
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TABLE 2 Findings of Empirical Studies Comparing Error Types in Limb Apraxia
Different Coarsel Muscle
Authorfs) Amorphous Clumsy Substitution Sequence Perseveration Groups
Lehmkuhl et al. NT NT NT NT + NT (1983) Haaland & NT + NT NT NT NT Flaherty (1984) De Renzi & Lucchelli (1988)
object use (b) multiple NT i i - NT NT
+ Rothi et al. - NT +I- - - (1988) Shelton & NT - + - No information NT Knopman (1991) McDonald et al. - + + NT + NT (1994)
+ indicates that this error type was present; - indicates that this error type was rare or not present; +/- NT indicates that this error type was not tested.
muscle groups. Body part as object was a common error. They did not find any errors of sequencing and nor was perseveration or substitution type errors a feature of their IMA subjects. This description of error type with object use conforms approximately with those reported by De Renzi and Lucchelli (1988), Haaland and Flaherty (1984), and Shelton and Knopman (1991).
Poeck and his colleagues, however, have taken a contradictory position. As a result of clinical and empirical studies Poeck determined that BPO errors never occur in isolation. Poeck also defined errors in perseveration as an invariant feature of IMA (Lehmkuhl et al., 1983; Poeck, 1982,1986), substitution errors as characteristic of IMA (Poeck, 1982) and described other errors of fragmentation, augmentation, and omission (Lehmkuhl et al., 1983); these may or may not be synonymous with movement-related errors described by other authors. McDonald, Tate, and Rigby (1994) found two subgroups of apraxic subjects who could be differentiated on the basis of error profile. One group had mainly movement-related errors such as those described by Rothi and colleagues. Subjects in the other group made these errors too but also made movement-unrelated errors more in line with the pattern of apraxic errors described by Poeck and his colleagues. It would appear that apraxic patients are not homogeneous with respect to quality of parapraxic movement. This study also raised the question of the significance of BPO errors as these errors were made by
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Unsustainedl Augmentation Omission/ Partial/ Body Part Gestural/
No Response Incomplete as Object Spatial Timing Verbal Other
NT - NT NT NT + + NT + +I- +!- NT NT NT
+ NT NT + NT NT + - + + +I- - NT NT
NT NT + + NT - NT
NT - + + + NT -
-~ ~ ~
indicates that this error type was not consistently observed, or variations occurred within the same error category;
all apraxic patients, though more frequently than controls. Other studies have also found that BPO errors are not pathognomonic in that they occur in non-brain-damaged people (Mozaz et al., 1993; Ska & Nespoulous, 1987). Moreover, Duffy and Duffy (1989) found no difference between left brain-damaged subjects and normal controls on the frequency of BPO errors nor any correlation between frequency of BPO errors and perform- ance on imitation and pantomime tasks.
Again, with respect to differentiating IMA and IA on the basis of the type of errors, results have been ambiguous. As described above, there is little agreement regarding characteristic errors in IMA and this confusion also extends to attempts to discern the qualitative difference between errors in IMA and IA. For example, substitution-type errors have been reported as characteristic of IMA but not IA (Poeck, 1982) and vice versa (De Renzi & Lucchelli, 1988). Sequencing errors are considered a feature of IMA (Heilman & Rothi, 1985), IA (Poeck, 1985) and neither (De Renzi & Lucchelli, 1988), while perseverative errors have been considered char- acteristic of both (Poeck, 1982, 1986) as well as not characteristic at all (De Renzi & Lucchelli, 1988; Rothi et al., 1988).
The foregoing review has highlighted the problems in the definitions, classifications, and measurement of apraxia, and in particular its most frequent form IMA. Ideomotor apraxia may or may not be apparent in everyday life, may or may not disrupt the ability to use actual objects, may be better on pantomime than imitation and vice versa and may be manifest in qualitatively different constellations of error types. Until there is some
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agreement reached in the literature as to the invariant features of the disorder, further research will continue to confound the issue. Thus while we await better integration of apraxia research it is worth considering some theoretical and practical directions which may prove fruitful in the develop- ment of an adequate clinical assessment of apraxia.
TOWARDS AN IMPROVED CLINICAL APPROACH
Reconciling Theoretical Models of Apraxia An early theoretical explanation of the underlying mechanisms involved in the breakdown of praxis, that of an impairment of symbolic processing, has been unproductive, at least in its original form. According to Liepmann (1905/1980b), Finkelnburg introduced the concept of asymbolia, a loss of the ability to understand and express concepts by means of conventional signs. If apraxia were due to asymbolia then it should be manifest on verbal command but not on imitation, since the latter condition merely requires the copy of a movement, its symbolic content being irrelevant. Liepmann’s studies, however, did not support an explanation of apraxia as a loss of symbolic capacity, “the aphasia of the extremities”. His patients’ imitations of movements were often disturbed and many could demonstrate that they understood the gestures by providing explanations of the movements or naming them. Nonetheless the hypothesis persisted.
In more recent times empirical study of apraxia as a form of asymbolia has centred around the performance of aphasic patients. The landmark study was undertaken by Goodglass and Kaplan (1963) who studied 20 aphasic and 19 nonaphasic brain-damaged subjects. While gesture was more impaired in aphasic subjects, the correlations between severity of aphasia and both gesture production and simple pantomime were low (r < 0.4), and their performance to imitation following failure to verbal command did not improve to the same degree as the nonaphasic subjects. The authors suggested their findings supported Liepmann’s original con- tention that apraxia was not due to a central communication disorder. With a more severely aphasic sample of 230 subjects, Kertesz and Hooper (1982) found somewhat higher correlations between severity of aphasia and upper limb apraxia for intransitive (r = 0.63) and transitive ( r = 0.65) gestures. The scoring system in this study, however, did not distinguish between verbal command and imitation, so that the crucial analysis regarding the symbolic component (viz. improvement on imitation) could not be under- taken. Other compelling evidence against the notion that a symbolic processing disorder is central to apraxia has been noted from Liepmann’s studies to the present day: the existence of patients with unilateral apraxia, the fact that meaningless movements are also generally impaired in apraxia, and the existence of patients who are apraxic but not aphasic.
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Papagno, Della Sala, and Basso (1993) demonstrated double dissociations in 159 of 699 patients with left hemisphere lesions: 10 were apraxic (classi- fied by an imitation test) but not aphasic and 149 were aphasic (classified by the Token Test) but not apraxic. Parenthetically, the authors suggest that the different frequencies of these dissociations are a referral artefact.
Traditionally, the other major conceptual framework regarding the underlying mechanism of apraxia emphasises a neuroanatomical formula- tion, with disconnection being a principal causal mechanism. Increasingly, this approach is being integrated with a cognitive perspective. Kelso and Tuller (1981), for example, suggest that a neuroanatomical model alone has limited applicability, given that such formulation arises from a model based on the hierarchical organisation of brain function. Within this per- spective, function is compartmentalised and transfer of information is unidirectional. Kelso and Tuller propose a more interactive model in which there are reciprocal interconnections between functional elements and function itself is distributed rather than compartmentalised. They describe this model as heterarchical.
Contemporary analysis of the cognitive mechanisms involved in praxis is reminiscent of the behavioural analysis of apraxia characterised by Liepmann’s pioneering work. The model of Roy (1983; Roy & Square, 1985) proposes that the control of an action or movement depends on two systems: a conceptual system (involving an abstract representation or knowledge base for action) and a production system (responsible for gener- alised action programmes and mechanisms for their implementation). Three types of knowledge relate to the conceptual praxis system: (1) Know- ledge of objects and tools and their uses; (2) knowledge of actions and the environmental and contextual variables surrounding object use; and (3) knowledge of action sequences. These components draw upon internal- ised linguistic descriptions (e.g. this is an object which is pushed), as well as externalised descriptions regarding perceptual attributes. Thus an action (e.g. hammering) may be performed with an unconventional object (e.g. a shoe) because it shares perceptual attributes with the conventional object (i.e. a hammer) normally used for the action. The production system involves a number of action programmes at different levels which operate interdependently, in that control may shift from one level to another throughout the course of an action sequence. Higher order levels require conscious attention to maintain the action directed towards the goal. Action sequences contain a number of critical time periods. Failure to attend to or verify progress of the sequence at key choice points may result in error, such as a sequence being diverted to a similar but more familiar action (cf. substitution) or a more recently performed action (cf. persevera- tion). At lower levels the action sequence is more automatic and demands minimal attention. Roy and Square suggest that such programmes may represent action of ecological significance, such as hammering or stirring.
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The distinction between conceptual and production systems has been substantiated clinically. Similar stages of processing in the model developed by De Renzi and colleagues are labelled “evocation” and “execution” respectively. Evocation requires recalling the visual configuration of the movement, which, in Roy’s terms would arise from the conceptual system. Execution of the motor programme, which involves implementation of the temporospatial organisation, calls upon the production system. The model predicts that subjects whose difficulties in praxis originated at the evocation stage should have difficulties in performing a movement to verbal command but not to imitation, as under the latter conditions the evocation stage is bypassed, a model being provided for the subject to copy. By contrast, subjects with difficulties at the execution stage should demonstrate impaired performance both to verbal command and imitation. De Renzi et al. (1982) have demonstrated such dissociations: Of 149 patients with left hemisphere lesions, 35 were impaired on both the imitation of intrans- itive (both meaningful and meaningless) movements as well as use of objects when presented visually (implying a problem with execution), and 15 patients were not impaired on imitation but had difficulty demonstrating the use of objects when presented visually (indicating a problem with evocation).
In a similar vein, Benke (1993) showed that a group of 12 Alzheimer subjects were impaired both on tests of production (imitation of meaning- less movements, which did not require semantic or conceptual knowledge) as well as tasks examining conceptual knowledge of praxis. The correla- tions between the two types of tasks, however, were nonsignificant, which lends support to the separateness of the two systems. De Renzi and col- leagues suggest that disorders in evocation and execution underlie IA and IMA respectively, a position also adopted by Ochipa et al. (1989). The disorders have been shown to be dissociable and are not significantly cor- related. The data of De Renzi and Lucchelli (1988), however, also demon- strate the frequent co-occurence of IMA in subjects with IA, as classified by the Movement Imitation Test and Multiple Objects Test respectively: 13 of the 16 subjects classified with IA also had IMA. It is to be expected, therefore, that in clinical practice IMA will be frequently present in patients with IA.
Recent work, focusing on the more detailed analysis of the conceptual system, has added to the development of a neuropsychological model of apraxia. Evidence from other areas of neuropsychology suggests that the semantic system may comprise distinct components. Riddoch and Humphreys’ (1987) patient with optic aphasia, JB, showed sparing of access to knowledge about the structure of objects (as assessed by a dis- crimination task involving line drawings of known objects and novel non- objects), but impaired conceptual knowledge (tested with an association matching task). This type of detailed analysis is now being applied to the
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study of apraxia with respect to types of knowledge of objects and actions (e.g. Benke, 1993; Ochipa et al., 1992; Riddoch, Humphreys, & Price, 1989). Based on the work of Ochipa et al. (1992), Heilman and Rothi (1993) suggest that the label “conceptual apraxia” be applied to those subjects who cannot evoke the movement configuration, and the label “ideational apraxia” should be reserved for subjects with difficulty per- forming motor sequences. This is consistent with Benke’s (1993) use of the term “conceptual apraxia”.
Returning to the production system, Roy drew attention to different levels of processing, in particular, the distinction between automatic and effortful processing. McCarthy and Warrington (1990) suggest that the knowledge about the uses of objects and the store of well established skilled actions represent automatic processing. At this level, action is run off in sequences, and failure occurs due to a breakdown in linking knowledge of object use with a central representation, which may be consistent with IA. By contrast, the performance of other actions, such as unfamiliar move- ments or familiar movements out of their context, require conscious effort in the performance. These types of movements are argued to be very different from automatic movements, in that they affect a stage at which programmes for action must be selected, assembled and/or maintained prior to implementation. Hence, a disturbance at this level may result in IMA.
Cognitive neuropsychological models of IMA are at an early stage of development. Those put forward by Riddoch et al. (1989) and Rothi, Ochipa, and Heilman (1991) are broadly similar in orientation and build upon Roy’s framework with a focus on accounting for dissociations reported in the clinical literature. Both models propose a knowledge system for objects and actions, with input and output components, and different modalities contributing to the input system. A direct route which bypasses the knowledge system is included for the visual modality input. Such a route is necessary to account for two groups of findings. First, Rothi and colleagues drew attention to the ability of some apraxic subjects to imitate movements which are meaningless and hence do not require access to a knowledge system for their production. Additionally, the patient CD, of Riddoch et al. (1989), was unable to demonstrate the use of objects with his right hand under conditions of visual (but not auditory) input, while at the same time demonstrating that access to conceptual and struc- tural knowledge via visual processing was intact.
Cognitive models of praxis anticipate a wide variety of apraxic symptoms which, to some extent, vindicate the confusion in the literature regarding the features of the disorder. The finer discriminations and anaIyses per- mitted by cognitive models of praxis will enable a clearer delineation of limb apraxia and resolution of apparent inconsistencies found among various tasks and conditions used in the study of apraxia. If fractionation
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of praxis appears, as it does, to be the most fruitful avenue for invest- igation, then clinical batteries in current use need to be refined in order to reflect the current theoretical status of apraxia. Of equal importance is the need to ensure that such clinical tools are practical, sensitive and reli- able in their measures of praxis in both quantitative (i.e. degree of failure) and qualitative (i.e. type of failure) terms and unequivocal in their criteria for determining impairment. There are numerous instruments available in the clinical and research literature and the relative merits of a sample of these batteries are discussed in terms of their ability to meet these clinical requirements.
Apraxia Batteries
Clinical Batteries
The Luria-Nebraska Neuropsychological Battery (Golden, Hammeke, & Purisch, 1980) has a Motor Scale comprising 51 items, but these examine a heterogeneous group of functions, ranging from simple motor movements (both limb and buccofacial) to constructional ability and speed of perform- ance. Only a small number of items are appropriate for the examination of limb apraxia. Although scoring of the Scale is standardised, the praxis items are classified only on a pass (0) or fail (2) basis. Failures are opera- tionally defined but there are no criteria regarding how many failures constitute apraxia.
Testing for limb and buccofacial apraxia is included as a supplementary examination in the Boston Diagnostic Aphasia Examination (BDAE) (Goodglass & Kaplan, 1983). Ten items, evenly divided between transitive and intransitive and all of which are meaningful, are used for limb apraxia. Testing is undertaken under three conditions: verbal command, imitation (if verbal command is failed), and for the five transitive items, object use (if verbal command is failed). An additional three items, using real objects, assess sequential actions. No criteria are provided to define the adequacy of response, although based on earlier work (Goodglass & Kaplan, 1963), the authors recommend that three levels of response (normal, partially adequate, failed) can be reliably identified. No information is provided as to what pattern or degree of failure constitutes the presence of apraxia.
The items of the Western Aphasia Battery (WAB) (Kertesz, 1982) are similar in content and format to the BDAE, as are those of Heilman and Rothi (1993) who recommend testing under the conditions of imitation and object use on all appropriate items, irrespective of whether the patient passes on verbal command. Again, however, both the scoring criteria and the classification of apraxia are vague and ill-defined (however Rothi and Heilman, 1984, provide a cut-off score [<lo] for the Florida Apraxia Screening Test, a 15 item test of 12 transitive and 3 intransitive gestures). Heilman and Rothi also draw attention to the qualitative errors accom-
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panying performance, including body part as object and clumsiness. The WAB subtest scores responses on a quantitative 0-2 scale, and although examples for scoring are provided, they are not sufficiently detailed to allow reliable discrimination, which is of particular concern for borderline performances (e.g. the instruction is given to “allow for variations in normal performance” without further elaboration). A criterion for the diagnosis of apraxia is not provided.
Research Batteries
Research batteries are generally more lengthy than clinical instruments and therefore have sufficient items in each category to ensure adequate reliability and enable the elucidation of dissociations, reasonable guidelines for (quantitative) scoring purposes and adequate normative data to enable classifications. The original battery used by Poeck and colleagues (Lehmkuhl et al., 1983; Poeck et al., 1982) comprised 200 items (for move- ments of buccofacial musculature, each limb and bilateral hand move- ments, all under conditions of verbal command and imitation), requiring some 45-60 minutes to administer. On the basis of their research findings, the authors (Lehmkuhl et al., 1983; Poeck, 1986) recommended a shorter version suitable for clinical practice comprising 20 items for limb apraxia. By and large, the items resemble those of the BDAE, except that addi- tional items are included examining meaningless movements, but there are no items assessing sequences of movements. In contrast to Heilman and Rothi (1993) who recommend that both hands be examined, Poeck and colleagues suggest that only the left (nonparetic) hand need be examined, given that both bilateral and unilateral apraxia will be detected in the hand ipsilateral to the lesion. They further recommend that the lower limbs need not be examined for apraxia, unless the territory of the anterior cerebral artery is involved. Poeck and colleagues’ analysis of apraxia has consist- ently emphasised the significance of qualitative errors. In contrast to the findings of some other investigators, their studies have found that these errors do not occur in normals and only very infrequently in right brain- damaged subjects. Consequently, the classification of apraxia is made on a presence/absence basis using four error types (see Lehmkuhl et al., 1983, Table 1). No data regarding interrater reliability for these error classifica- tions are provided.
The batteries of De Renzi and colleagues provide a range of measures for both ideomotor and ideational components of praxis. Earlier work comprised a Movement Imitation Test and Use of Objects test adminis- tered under three conditions (visual, verbal command, and tactile); the two tests requiring 3 0 4 0 minutes to administer (De Renzi et al., 1982). Subsequent work (De Renzi & Lucchelli, 1988) included a Multiple Objects Test. The Movement Imitation Test has the advantages of enabling
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precise measures of performance to be obtained and bypassing difficulties in the examination of patients with impaired language comprehension. The 24 item Movement Imitation Test is similar to that of Kimura and Archibald (1974), with the items evenly distributed over meaningful versus meaningless, hand postures versus sequences, and fingers versus hand movements. The last two distinctions have resulted in a test able to provide sensitive discriminations: With respect to hand postures versus sequences De Renzi et al. (1980) found some 50% were apraxic on both tasks, 18% on postures but not sequences and 8% on sequences but not postures. Performance is rated on a 0-3 scale and the provision of good normative data, collected over a number of studies facilitates the diagnosis of apraxia. A qualitative error analysis is provided for the Multiple Objects Test (see Table l), but again data regarding interrater reliability are not provided.
The battery of De Renzi and colleagues most closely conforms to five areas of examination described by Liepmann (1905/1980a) as necessary for a comprehensive examination of limb apraxia, which include conditions of verbal command, imitation and object use: (1) Elementary motions, i.e. intransitive meaningless hand movements, e.g. making a fist; (2) move- ments of expression, i.e. intransitive meaningful gestures, e.g. waving; (3) simulation of purposive movements, i.e. transitive movements, e.g. knocking on a door; (4) purposeful movements with an object, i.e. trans- itive movements, e.g. using a key; (5) copying motions, both simple and complicated, i.e. imitating meaningless movements. Additionally, reflexive movements, e.g. movements directed to a part of the body, such as scratching oneself, are also described.
It is clear that while a number of research batteries enable a compre- hensive examination of various aspects of praxis, the development of reli- able criteria to diagnose the presence of apraxia continues to be an area of pressing need. The quantitative systems (such as that of De Renzi and colleagues) do not fully address the continuing and fundamental problem in this area; that is, how correct does a movement need to be in order that it is scored as correct? In order to classify performance, even on a present/ absent basis, those features that constitute a failure need to be described in operational terms. This underscores the importance of developing a qualitative, standardised and reliable system of error analysis. Although this issue is now being addressed in the current research literature, it is far from resolved.
Poeck and colleagues have long been persistent advocates of a qualita- tive analysis of error types in apraxia, but at present there is little consensus as to the range of errors that should be included. As previously described, a number of investigators have identified a range of error types in apraxia (see Table 1). By and large, these go beyond the seven types identified by Liepmann, as described in Brown (1988). Roy and Square (1985) suggested that there are three major error patterns, and within this framework they
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identify some 13 error types. This is a similar framework to that advocated by Rothi et al. (1988). The question remains, however, whether such a large number of error types have clinical (and research) utility if they are unable to be reliably rated. Our own group (McDonald et al., 1994) was unable to classify errors made on each individual item into eight categories with sufficient interrater reliability, even using experienced neuro- psychologists as raters who were trained on pilot videos. Yet very few workers have reported on interrater reliability with their categories, excep- tions being Alexander et al. (1992) and Haaland and Flaherty (1984) and our experience would lead us to expect that it could be quite low when a large number of categories are used. We found that by reducing the number of categories to six we were able to obtain acceptable interrater reliability (89Y0 for subjects with brain damage, 91% for controls). These six categories take account of most of the error types consistently reported in the literature: inaccuracy errors (errors of spatial orientation, unsustained actions and clumsy or awkward execution); substitutions (definite discrete movements that bore no resemblance to the movement required); per- severation (repetition of a previously performed movement or parts of that movement); BPO (using part of the body as the object); augmentation (verbal or acoustic embellishment of a movement); and no response/ amorphous movements. The scoring method used by Alexander et al. (1992) holds much promise, in that it quantifies a qualitative scoring system of demonstrated reliability. They identified six error types (no movement, perseveration, undifferentiated movement, spatial error, BPO, verbalisa- tiodself cue), which were arranged hierarchically in order of increased disruption of the movement.
Recommendations
It is apparent that greater integration is required between empirical and clinical study of limb apraxia. Clinical apraxia batteries need improvement to enable delineation of the types of detailed analyses and dissociations reported in the empirical literature. To date, tests of apraxia for clinical purposes are often found as a brief, supplementary examination in aphasia batteries (cf. BDAE, WAB), As such, most apraxia batteries are hardly comparable with the detailed clinical evaluation of aphasia, which the BDAE, WAB, and other aphasia batteries afford. A comprehensive clinical battery for the examination of apraxia in its own right is required.
While examination procedures for modality-specific deficits (in auditory, visual, and tactile modalities) are easily developed by modifying adminis- tration procedures in current apraxia batteries, the focus of these batteries is mainly on transitive movements. Batteries used in experimental studies provide a pool of items appropriate for a comprehensive evaluation of intransitive (both meaningful and meaningless) movements, the signific-
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ance of this distinction originally being emphasised in Liepmann’s (19051 1980) papers. But most importantly, both clinical and experimental studies of apraxia have, on the whole, failed to provide positive, reliable guidelines by which an apraxic movement can be identified. This issue would be less important if it was agreed that the way in which the apraxic patient fails was invariant, but this is not the case. It would appear that different apraxic syndromes are manifested not only in the kinds of tasks the patient fails but also in the kinds of errors they make. Precise scoring criteria of the executed movements are required to enable a reliable and discriminative diagnosis of both the presence and severity of apraxia, such diagnosis being based on normative data from an appropriate standardisation sample.
Until such a standardised battery is available, the clinician is probably better advised to utilise a research battery for the in-depth examination of the nature and extent of apraxia, such as those developed by De Renzi and colleagues. Moreover, as strongly advocated by Poeck, the clinical examination should also take account of the qualitative nature of errors and a number of instruments with demonstrated reliability have been described in this paper (e.g. Alexander et al., 1992; McDonald et al., 1994). Clinical batteries currently available can only be considered as crude, albeit useful, screening measures.
CONCLUSION In conclusion, this review has highlighted the problems facing clinicians in their attempts to explore the phenomena associated with apraxia. It is apparent that the disorder itself is a heterogeneous one. However, clear elucidation of the boundaries of different apraxic conditions and the mech- anisms underlying these is currently hampered by a lack of agreed defini- tions, the mushrooming of terminology without consideration of contem- porary or historical developments in the broader research community, and the absence of unequivocal diagnostic criteria by which to identify a failure of praxis. In terms of definition it would appear that the categorisation of apraxia into a few “classical” syndromes is neither practicable nor con- sistent with Liepmann’s original description. Alternatively, contemporary research is reviving the older view that individuals with apraxia need to be characterised according to the specific behavioural conditions in which the movement disorder is elicited. Empirical studies are producing a variety of methods and means to measure apraxia that are uncovering dissociations within the disorder(s) but currently these are not mirrored in improved clinical batteries. In terms of clinical practice better evaluation of apraxia would be greatly enhanced by both an improved consensus regarding teminology within the research literature, as well as the development of better, more detailed clinical assessment tools with reliable and explicit scoring criteria. This would not only advance clinical application but also expedite meaningful clinical research into this vexed area.
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