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APRAXIAKenneth M. Heilman

ABSTRACT

Humans need to perform skilled movements to successfully interact with their envi-ronment as well as take care of themselves and others. These important skilledpurposeful actions are primarily performed by the forelimb, and the loss of theseskills is called apraxia. This review describes the means of testing, the patho-physiology, and the clinical characteristics that define five different general formsof forelimb apraxia including: (1) ideational apraxia, an inability to correctly se-quence a series of acts leading to a goal; (2) conceptual apraxia, a loss of me-chanical tool knowledge; (3) ideomotor apraxia, a loss of the knowledge of howwhen making transitive and intransitive movements to correctly posture and movethe forelimb in space; (4) dissociation apraxia, a modality-specific deficit in elicit-ing learned skilled acts; and (5) limb-kinetic apraxia, a loss of hand-finger deftness.

Continuum Lifelong Learning Neurol 2010;16(4):8698.

INTRODUCTION

The two major goals of humans brainsare to maintain body homeostasis andto allow us to successfully interact withthe environment. It is the upper limbsor forelimbs that perform most of theinteractions with objects in the environ-ment, as well as a persons own body.The joints and muscles of humans up-per limb, including the arm, forearm,hand, and fingers allow us to performalmost any type of movement. To suc-cessfully interact with the environment,the goal-oriented movements made bythe forelimb have to be guided by in-structions or programs from the brain.

Apraxia is a term first used by Steinthal

to describe impairments of humansability to correctly carry out purpose-ful skilled movements.1 There are twomajor forms of forelimb apraxia: task spe-cific and general. Task-specific apraxiasare disorders that are limited primar-ily to one form of activity (eg, dress-ing apraxia, constructional apraxia, and

apraxic agraphia). Because of space lim-itations these task-specific disorders

will not be discussed in this article. Inthis article, however, we will discussthe forms of forelimb apraxia that aregeneral and can impair almost all pur-

poseful movements made by the fore-limb. Many disorders might impair apersons ability to perform purposefulskilled movements, and the diagnosisof apraxia is in part one of exclusion.If a person cannot make purposefulmovements because of deficits suchas weakness, abnormal movements (eg,tremor, chorea, ballismus, myoclonus),severe sensory-perceptual deficits, orcognitive impairments, such as an im-

paired comprehension or attention, thenthis disorder is not considered a formof apraxia. The forelimb apraxias that

we will discuss can be induced by a va-riety of diseases. We will not be able todiscuss all these diseases in detail; how-ever, any neurologic disease that impairsthe neuronal networks responsible for

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Relationship Disclosure:Dr Heilman has received personal compensation for review activities from Journal Watch.Dr Heilmans compensation and/or research work has been funded entirely or in part by a grant to his universityfrom a governmental organization, a nonprofit tax-exempt organization, Myriad Pharmaceuticals, Inc., NovartisPharmaceuticals Corporation, Esai Pharmaceuticals, and the Alzheimers Association.Unlabeled Use of Products/Investigational Use Disclosure: Dr Heilman has nothing to disclose.

Copyright # 2010, American Academy of Neurology. All rights reserved.

KEY POINT

A Apraxia is

defined as an

inability to

correctly carryout purposeful

skilled

movements

when this

deficit is not

caused by

elemental motor

or sensory deficits,

abnormal

involuntary

movements,

or cognitive

disorders.

Copyright @ American Academy of Neurology. Unauthorized reproduction of this article is prohibited.


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programming these movements can in-duce apraxia. For example, apraxia is of-ten observed with hemispheric strokes,especially those that injure the left he-misphere; degenerative diseases suchas Alzheimer disease; and corticobasaldegeneration. At least five types of gen-eral forelimb apraxia have been iden-tified, and the diagnosis of the specific

type of apraxia is dependent on themeans by which errors are elicited andthe types of errors made by the patient(Figure 6-1). In the next sections theclinical aspects, means of testing, andpathophysiology of each of these fivedisorders will be briefly described.

IDEATIONAL APRAXIA

Clinical Description

Unfortunately, the term ideational

apraxia has been used to label manydifferent disorders, including dissocia-tion apraxia2 and conceptual apraxia.3

DeRenzi and Lucchelli used this termfor patients with ideomotor apraxia

who are impaired when they use ac-tual tools and implements.4 However,Poizner and colleagues demonstratedthat patients with ideomotor apraxiacan often be impaired when using ac-tual tools.5 Liepmann suggested thatthe term ideational apraxia be used for

the disorder in which patients have aninability to correctly sequence a seriesof acts that lead to a goal (Case 6-1).6

Tests

To test for ideational apraxia, all thematerial to complete a goal, such asmaking a ham and cheese sandwich,should be placed before the subject.

The subject should be asked to make aham and cheese sandwich.

Pathophysiology

Most often the patients with ideationalapraxia have some form of degenera-tive dementia. This disorder has, how-ever, not been systematically studiedin the various forms of degenerativedementia. Liepmann thought that thelesion that induced this disorder waslocated in the left occipital parietal re-gion.6 However, the support for his hy-pothesis is not strong, and injury to theprefrontal regions, especially in the lefthemisphere, is frequently associated withsequencing deficits.

CONCEPTUAL APRAXIA


Although making changes in the envi-ronment can be performed by just us-ing ones hands and fingers, many tasks

Continuum Lifelong Learning Neurol 2010;16(4)

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FIGURE 6-1 Cartoon of system mediating purposeful movements. Ovals with letters aredifferent lesion sites.

SMA = supplementary motor area; a = dissociation apraxia, b = conceptual apraxia,c = ideomotor apraxia; d = limb-kinetic apraxia.

KEY POINTS

A The term

ideational

apraxia has

been suggestedfor the disorder

in which

patients have

an inability to

correctly

sequence a

series of acts

that lead to

a goal.

A Conceptual

apraxia is

the loss ofmechanical

knowledge.

Subtypes of

conceptual

apraxia include

problem

unawareness,

tool-selection

deficit,

tool-action

association

deficit, and

impairedknowledge

of mechanical

advantage.



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cannot be accomplished by just theforelimbs in the absence of tools. Toolsprovide the user with mechanical ad-

vantages. Several steps are necessary incorrectly using a tool or implement toalter the environment or ones own self.The first step is the recognition thatsomething needs to be altered. Somepatients cannot identify that an alter-ation action is required.7 This subtypeof conceptual apraxia is called prob-

lem unawareness. Also, some patientscannotrecognize the tool that is neededto perform or complete the requiredaction or the tool that works on specificobjects (eg, hammers are used withnails) (Case 6-2). This impairment iscalled a tool-selection deficit. In addi-tion, some patients might not recall thetype of actions associated with specifictools and implements, a tool-actionassociation deficit (eg, hammers areused to pound).3,8A more complex form

of mechanical knowledge is knowingthe characteristics of a tool that allowit to perform a given action. For ex-ample, when attempting to drive a nailinto a piece of wood and no hammeris available in the tool chest, the pa-tient with impaired mechanical advan-tage knowledge might select a screw-driver rather than a wrench from thischest.9 Mechanical knowledge is alsoimportant for tool development, and

patients with conceptual apraxia are of-ten unable to correctly develop tools.9

Conceptual apraxia is the loss of me-chanical knowledge. There are severalsubtypes of conceptual apraxia: problemunawareness, tool-selection deficit, tool-actionassociation deficit, and impairedmechanical advantage knowledge.

Tests

(1)Problem awareness: Schwartz andcolleagues developed a test in which

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Case 6-2A 76-year-old retired carpenter was working on building a house for Habitat for Humanity. Hehad retired because he was having some memory problems. While hammering a nail into a board,the nail bent. He wanted to take this nail out, but his hammer did not have a claw. In his toolchest he found a knife, and with the knife he tried to cut the wood around the nail so he couldremove it from the board but found this was not working. His friend seeing him do this said, Usethe pliers! This man was later diagnosed as having Alzheimer disease.

Comment. The loss of mechanical knowledge exhibited by this man is called conceptualapraxia.


Case 6-1A 69-year-old woman had been an excellent cook her entire life. In the past few months, herhusband noticed that she appeared to have some problems controlling her temper and was not

keeping the house as clean as she used to keep it, but thought these changes were just part ofaging. One morning, wanting to make a cheese omelet for her husband, she took out the liquideggs, slices of American cheese, and butter. After putting the frying pan on the gas range, sheturned on the range and waited until the pan got hot. She then dropped the cheese onto the hotpan and after a few minutes poured the eggs on top of the cheese. The cheese melted andafter the eggs hardened, she tried to slide the cheese omelet onto the plate but found it wasstuck to the frying pan. By the time she got the eggs and cheese out of the pan she had madescrambled cheese eggs. This action alarmed her husband, who made an appointment for her to beseen in a memory disorder clinic.

Comment. The patients inability to correctly order her acts to make a final product ischaracteristic of the disorder called ideational apraxia.

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patients are shown a series of picturesof items that need work and then areasked to show the action that would

be required to complete this job.

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Forexample, a picture might show a pieceof wood on two carpenter horses thatis only partially sawed in half, and thepatient would need to show a saw-ing motion. (2)Tool selection:Patientsare shown the picture of an incom-plete task, such as a nail that is onlypartially driven into the wood. Theyare shown an array of five differenttools, such as a handsaw, wrench, ham-mer, screwdriver, and knife, and are

asked to select the tool to be usedto complete this task. (3) Mechanicaladvantagealternative tools: Patientsare shown a series of pictures that arethe same as above, but in this testthe tool that usually performs this ac-tion is not present and the patientmust find an alternative tool to com-plete the task. For example, after beingshown a partially driven-in nail, the pa-tient is shown five tools (eg, handsaw,

wrench, screwdriver, knife, and wirecutter and is asked to point to the toolhe or she would use to complete thetask. (4) Mechanical advantagetool

fabrication:Ochipa and colleagues de-veloped a test in which subjects wouldhave to make a tool to solve a mechan-ical problem.9 For example, they had toretrieve a block with an eye hook on topthat was in the bottom of a Plexiglascylinder and were provided with astraight wire. To correctly solve this

problem, they had to bend the wire tomake a hook that they could place inthe eye and use this wire with hook toretrieve the wooden block.

Pathophysiology

In right-handed people these mechan-ical knowledge representations arestored in the left hemisphere. For exam-ple, patients with a callosal disconnec-tion demonstrate conceptual apraxia ofthe nonpreferred (left) hand, which is

controlled by their disconnected righthemisphere.10 In addition, Heilman andcolleagues studied right-handed pa-

tients who had either right or left hemi-sphere cerebral infarctions and foundthat conceptual apraxia was more com-monly associated with left than right he-misphere injury.11 Although Liepmannthought that conceptual mechanicalknowledge is stored in the caudal pa-rietal lobe,6 DeRenzi and Luccelli lo-cated these representations in thetemporoparietal junction.4 Heilman andcolleagues, however, could find no spe-cific anatomic region that appearedto be

critical for inducing conceptual apraxia.This result might have been related tohaving an inadequate number of sub-jects, or that each subtypeof conceptualapraxia might have a different locali-zation, or that in right-handed peoplemechanical knowledge may be widelydistributed in the left hemisphere. Asmentioned, conceptual apraxia can beassociated with diseases that cause fo-cal brain damage, such as stroke, but itis also commonly seen in patients suf-feringwith degenerativedementia, suchas Alzheimer disease.9

IDEOMOTOR APRAXIA


Patients with ideomotor apraxia (IMA)make three types of spatial errors: (1)postural errors or internal configura-tion errors; (2) egocentric movementerrors (use of incorrect joints or in-

correct coordination between joints);and (3) allocentric movement errors inwhich their actions are not correctlytargeted to the real or imaginary ob-ject upon which the tool works.

When pantomiming a transitive act,patients with IMA will often fail to placetheir hand, forearm, and arm in theposition that would enable them tocorrectly hold a tool or implement(Case 6-3). Goodglass and Kaplan no-ticed that when patients are asked to


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KEY POINT

A Patients with

ideomotor

apraxia make

three types ofspatial errors:

(1) postural

errors or internal

configuration

errors; (2)

egocentric

movement errors

(use of incorrect

joints or incorrect

coordination

between

joints); and

(3) allocentric

movement errors

in which their

actions are

not correctly

targeted to the

real or imaginary

object upon

which the

tool works.



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pantomime the use of a tool or imple-ment, they will often use their hand andfingers as the tool, a practice called bodypart as tool errors (BPTEs).12When askedto pantomime the use of a tool, evenhealthy people will often make BPTEs,but when asked to not use the hand andfingers as if they were tools and instead toshow the examiner how they would usethe actual tool, healthy people usuallystop making BPTEs. Many patients withIMA, however, unlike healthy people, willcontinue to make BPTEs even when theyare repeatedly corrected.13 In addition toforming the correct posture to hold thetool or implement, when properly using atool, people have to move the forelimbjoints in the proper fashion in order toallow the tool to perform the desiredfunction. If people either move the in-

correct joint or joints or do not properlycoordinate multiple joint movements,they will move their hand and armincorrectly through space.5,14 To use atool properly they must target the toolto the object upon which the tool

works (Case 6-3). In addition to mak-ing egocentric postural and egocentricmovement errors, patients with IMAalso fail to properly direct their actionat the real or pretended target of theaction, an allocentric error.

Tests

The most sensitive test for assessing IMA is

asking patients to gesture (pantomime)

transitive movement (such as using a tool)

to verbal command. Although patients

with IMA typically improve when imitating

the examiners pantomimes of transitive

acts, theperformance of patients with IMA

often remains impaired.In addition,whenusing actual tools or implements, their

performance might improve even further.

This improvement might occur because

they are provided with visual and tactile

cues. Skilled movements also have char-

acteristic temporal patterns. For example,

when using a hammer, the upswing is

usually slower that the downswing. Pa-

tients with IMA often also move at in-

correct speeds.5 Since some diseases,

such as corticobasal degeneration and

infarctions of the corpus callosum, can

cause apraxia of one forelimb, both

forelimbs should be tested. If one fore-

limb has an elemental sensory or motor

disorder, such as weakness, that would

prevent testing, the opposite ipsilesional

limb can still be tested. In addition to

testing gesture to command, imitation of

both meaningful and meaningless move-

ments and with using actual objects, pa-

tients should be tested to learn if they

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Case 6-3A 55-year-old dentist returned to work after a 3-month world cruise. Hisfirst patient had a cavity that was not deep. His assistant inserted a drill

bit into the drill and handed him the drill so that he could clean out thedecay. He asked the patient to open her mouth and pressed on thepedal that made the drill rotate when he realized that he was not sure howto correctly move the drill in the patients mouth. He told the patienthe could not work on her teeth and apologized. When examined in theclinic and asked to pantomime transitive movements, he made posturaland movement errors, could not imitate transitive movements, and evenhad trouble using actual tools. His deficit was much worse in his rightthan left hand. In subsequent visits, he developed some plastic rigidity inthat arm and myoclonus.

Comment. This mans spatial errors were typical of IMA. The presenceof unilateral IMA, asymmetric rigidity, and myoclonus suggest that this

man had corticobasal degeneration.


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can discriminate between correct and

incorrect pantomimes.

Pathophysiology

IMA is associated with injury to severalstructures, including the inferior pari-etal lobe, the premotor cortex (sup-plementary motor area [SMA] andconvexity premotor cortex), and the cor-pus callosum. Subcortical lesions thatinvolve the basal ganglia, the thalamus,and the white matter connecting theseareas with the cortex can also beassociated with IMA. The means by

which injury in each of these areas

causes IMA will be discussed later.Callosal disconnection.Liepmann

and Maas reported Ochs, a right-handedpatient with a prior right hemiparesisfrom an infarction in the pons, who alsohad a new lesion of his corpus callo-sum.15 When tested, this patient wasunable to correctly pantomime to com-mands with his left arm, which couldhave been attributed to disconnectionbetween a left hemispheremediatedlanguage network and the right hemi-spheres motor areas, a language-motordisconnection. LiepmannandMaas,how-ever, also noted that this patient wasimpaired imitating and using actualobjects with his left forelimb. Since aperson does not need language to imi-tate or use actual objects, this pa-tients errors could not be explainedby a language disconnection. Liepmannand Maas suggested that the left hemi-sphere of right-handed people con-

tains memories of the spatial-temporalpatterns required to make purpose-ful skilled movements, and injury ofthe corpus callosum disconnects thesemovementformulasfromtherighthe-mispheres motor areas.15 Subsequentreports of patients with callosal le-sions16,17 could not replicate the ob-servations of Liepmann and Maas, butlater Watson and Heilman,10 as well asGraff-Radford and colleagues,18 reportedpatients who could not correctly panto-

mime or imitate transitive acts and notcorrectly use tools with their left handbut could correctly do so with their right

hand. These patients pattern of deficitsappears to support Liepmanns postulatethat the left hemisphere of right-handedpeople contains spatial-temporal move-ment representations (movement for-mula), and an injury of the corpuscallosum disconnected these move-ment representations from the righthemispheres motor areas, inducing aunilateral (left) IMA.

Left hemisphere injury. Liepmannstudied a population of right-handed

patients who had damage confined toeither their left or right hemisphere andfound that none of the patients withright hemisphere injury had IMA, but50% of patients with left hemisphereinjury had IMA.15 These injuries oc-curred in several areas.

Parietal lobe.Liepmann noted thatwhen a person with a left hemisphereinjury demonstrated signs of IMA, it

was highly likely that the person hadan injury to the inferior parietal lobe.6

Geschwind posited that inferior parie-tal lesions cause IMA because they in-duce a disconnection by damaging asubcortical white matter pathway.19Ac-cording to Geschwind, when a patientis given a command to perform a ges-ture, the incoming verbal message isdecoded in the Wernicke area, but thismessage must then be transmitted tothe left premotor convexity cortex areafor the command to be implemented

by the left primary motor cortex. Theleft hemispheres premotor cortex con-nects with the primary motor cortex ofthe left hemisphere as well as the pre-motor cortex of the right hemisphere.Thus, when attempting to carry out ver-bal commands, a disconnection of the

Wernicke area from premotor cortexwould prevent the premotor cortex inboth hemispheres from getting instruc-tions about the movement that wasrequested.


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KEY POINT

A Ideomotor

apraxia is

associated with

injury to severalstructures,

including the

inferior parietal

lobe, the

premotor cortex

(supplementary

motor area

and convexity

premotor

cortex), and the

corpus callosum.



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In addition to being impaired at pan-tomiming to verbal commands, patients

who have IMA from left inferior parietal

lesions are also impaired when attempt-ing to imitate. Geschwindthought that aleft hemisphere white matter pathwaythat connects the visual association areain the left hemisphere with the premo-tor area in this hemisphere is importantfor mediating manual imitation. How-ever, to imitate gestures, a person doesnot need speech-language, and thusthere should be no reason why theundamaged right hemisphere couldnot transmit visual information from

the visual association areas to the pre-motor areas. In addition, many patients

with apraxia from left hemisphere injuryare also impaired at correctly using ac-tual tools and implements. Geschwindsdisconnection hypothesis cannot fullyaccount for these patients inability tocorrectly imitate gestures or use ac-tual tools.19

An alternative movement repres-entation hypothesis was advanced byHeilman and colleagues20 and Rothiand colleagues.21 These investigatorssuggested that in right-handed peoplethe movement formula or movementrepresentations (praxicons) that con-tain the spatial and temporal parame-ters of purposeful actions are stored inthe left parietal lobe in the region ofthe supramarginal and angular gyri. Ifthese praxicons become injured, de-graded, or destroyed, thepatient shouldnot only demonstrate deficits of pan-

tomiming to command, imitating, andusing actual objects, but because theserepresentations are degraded, thesepatients should be unable to discrimi-nate between correctly and incorrectlyperformed transitive pantomimes per-formed by the examiner. If these pra-

xicons are intact, but they are unableto access the premotor areas or thepremotor areas are injured, these pa-tients would also be expected to dem-onstrate IMA. However, these patients

who have IMA but have an intact leftinferior parietal lobe, with intact prax-icons, should be able to discriminate

between incorrect and correct panto-mimes performed by the examiner.Heilman and colleagues20 and Rothiand colleagues21 tested patients withanterior and posterior left hemispherecerebral lesions by assessing for thepresence of IMA as well as attemptingto learn if they had a disorder of pan-tomime discrimination. These investi-gators found that some patients withanterior lesions and some with poste-rior lesions had the production deficits

typical of IMA, but only the patients withposterior damage had discriminationdisturbances. These results providedevidence against the parietal discon-nection hypothesis of IMA and sup-port the postulate that injury of theinferior parietal lobe induces IMA be-cause this injury degrades the praxi-cons stored in this area. Halsband andcolleagues22 replicated the results ofHeilman and colleagues20 and Rothiand colleagues.21 Convergent evidencefor the postulate that the left inferiorparietal lobe stores movement repre-sentations also comes from functionalimaging studies performed with normalright-handed subjects.23

In addition to strokes that damagethe inferior parietal lobe, patients with

Alzheimer disease often demonstrate IMA.Since these patients with Alzheimerdisease have trouble recognizing cor-rect from incorrect postures, their IMA

is probably related to degenerationof the inferior parietal lobe, which isknown to be affected by the patho-logic changes associated with Alzheimerdisease.

Supplementary motor area. Themovement representations or praxi-cons that are stored in the left inferiorparietal lobe are probably stored in athree-dimensional supramodal (visuo-kinesthetic-spatial) code. The SMA re-ceives projections from parietal neurons

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and projects directly to the convexitypremotor cortex as well as to theprimarymotor cortex. Physiologic studies have

demonstrated that the neurons in thesupplementary motor cortex dischargebefore neurons in the primary motorcortex. Complex movements, such asthose used in tasks that require transi-tive movements, increase blood flowin the SMA as well as in primary motorcortex. When subjects do not move butplan on making complex learned skilledmovements, the blood flow (indicatingsynaptic activity) to the SMA increases.

Watson and colleagues reported several

patients who sustained left-sided medialfrontal lesions that included the SMA,and these patients demonstrated IMA.24

These patients with SMA lesions weredifferent than patients with left inferiorparietal lesions because the patients

with the SMA lesions could discrimi-nate between correctly and incorrectlyperformed pantomimes. It was thoughtthat they could discriminate becausethe praxicons were intact.

Convexity premotor cortex.Geschwind also thought that the con-

vexity premotor cortex, which connectswith the motor cortex in the same he-misphere and the premotor cortex ofthe opposite hemisphere, was part ofthe pathway by which a person nor-mally performs gestures to command.19

Unfortunately, few studies have at-tempted to learn whether lesions ofthe left convexity premotor cortex in-duce IMA. Faglioni and Basso mention

that they had difficulty finding any well-documented cases in which patientshad IMA as a result of injury to convexitypremotor region.25 However, Kolb andMilner,26 Barrett and colleagues,27 andHaaland and colleagues28 did reportpatients with frontal convexity premo-tor injury who appeared to have anIMA. Freund and Hummelsheim, how-ever, studied a population of patients

with convexity premotor lesions andalso found that these patients had limb-

kinetic apraxia rather than IMA.29 Thisform of apraxia will be discussed later.

Basal ganglia and thalamus. Re-

ports have demonstrated that IMA canbe caused by subcortical lesions.30,31

Portions of the basal ganglia, such asthe putamen, have strong connections

with areas of the cortex, such as thepremotor areas, that when injured in-duce IMA. In addition, portions of thethalamus also connect with areas of thecortex that when injured induce IMA.For example, the pulvinar has strongconnections with the inferior parietallobes. Pramstaller and Marsden per-

formed an analysis of 82 cases of apraxiathat appeared to be caused by subcor-tical lesions and reported that lesionsconfined to the basal ganglia, includ-ing the putamen, caudate nucleus, andglobus pallidus, rarely, if ever, causeIMA.32 Unfortunately, in many of thereports reviewed by Pramstaller andMarsden, the subjects were tested withimitation and not pantomime to com-mand. In addition these patients per-formance was scored as either correct

versus incorrect, and this scoring sys-tem might have been insensitive. Hanna-Pladdy and colleagues studied andcompared patients with cortical andsubcortical strokes.33 Although theparticipants with subcortical strokeshad involvement of the subcortical

white matter, much of this white mat-ter carries fibers from the cortex tobasal ganglia and from the thalamusback to the cortex. These investigators

found that both the cortical and thesubcortical lesion groups made apraxicerrors, but the patients with corticallesions were more impaired. Hanna-Pladdy and colleagues found that thesubcortical group made more posturalerrors than did the cortical group, butthe patients with cortical lesions mademore sequencing and content errors(which are associated with conceptualapraxia).33 In regard to the thalamus,there have been several case reports


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of patients who developed IMA fromlesions of the left thalamus in theregion of the pulvinar nucleus,34 and,

as mentioned, this nucleus is con-nected with the inferior parietal lobes.

DISSOCIATION ANDCONDUCTION APRAXIA

Clinical

Patients who have intact praxicons butare impaired at accessing-activatingthese movement representations fromstimuli in one modality have dissocia-tion apraxia (Case 6-4). This term is

used because their movement repre-sentations have been dissociated fromcertain types of sensory input. Heilman2

first described three patients with verbaldissociation apraxia. DeRenzi and col-leagues35 reported patients who weresimilar to those reported by Heilman36

but in addition reported patients whodid not have a visual agnosia and couldname tools presentedto them, but couldnot perform correctly when seeingtools. Unlike the patients reported byHeilman,36 however, these patients per-formed normally to verbal command.Merians and colleagues37 described apatient who had a left ventral temporal-occipital lesion and was impaired at imi-tating the examiners pantomimes butperformed normally to verbal command.This disorder appears to be anotherform of dissociation apraxia, which has

also been called visuo-imitative apraxiaand conduction apraxia.38

Testing

The methods used to test for the dif-ferent forms of dissociation apraxia arethe same as those used to test for IMA.

Pathophysiology

The patients reported by Heilman2

and DeRenzi and colleagues35who haddissociation apraxia of both hands prob-ably had a left hemisphere injury thateither induced a hemispheric language-movement formula disconnection or

a vision-movement formula disconnec-tion. Thus, depending on thelocation ofthe lesion, stimuli from one of thesemodalities (eg, speech-language) wasnot capable of activating the movementrepresentations, but stimuli in othermodalities (eg, vision) were able to ac-tivate these representations. Unfortu-nately, the anatomic loci of the lesionsthat cause many of these intrahemi-spheric disassociation apraxias remainunknown.

LIMB-KINETIC APRAXIA


Many acts performed by people wheneither using their hand-fingers directly,such as buttoning a shirt, or the use oftools, such as a pair of scissors, requiredeft movements. Patients with a loss

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Case 6-4A 43-year-old school teacher developed an anomic aphasia. When she wastested for IMA, she was asked to show how she would put a key into a doorlock and open the door lock. After hearing the command, she lookedat her open hand with all her fingers fully extended and repeatedlysaid, Unlock the door. Although it appeared that she might have aspeech comprehension disorder, her comprehension remained intact.When, however, the examiner took out a key and she saw the key, sheimmediately performed the pantomime correctly.

Comment. The inability to correctly pantomime when the command ispresented in one modality but is correctly performed in another modality iscalled dissociation apraxia.

KEY POINTS

A The inability

to correctly

pantomine

when thecommand is

presented in

one modality

but is correctly

performed in

another modality

is called

dissociation

apraxia.

A The loss of

deftness,

includingthe ability to

make precise

independent but

coordinated finger

movements, is

called limb-kinetic

apraxia.


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of deftness might be unable to performthese motor acts. This loss of deftness or

dexterity is calledlimb-kinetic apraxia(melokinetic apraxia, innervatory apraxia)by Liepmann (Case 6-5).6

Tests

Many tests of deftness or dexterity areavailable, but the coin-rotation task isone of the simplest and sensitive bed-side tests. In this test, patients are givenan American nickel in their palm and areasked to rotate the nickel between their

thumb, index, and middle fingers asrapidly as possible for 20 revolutions.39

Another test, often used by neuropsy-chologists, is the pegboard test. In thistest, patients repeatedly lift one peg at atime, carry the peg to the hole, and thenplace the peg in the hole. Lifting onepeg at a time and placing the peg ac-curately in the hole requires deftness.Both hands of patients shouldbe tested.Typically,patientswithhemisphericdam-age have a contralesional loss of deft-

ness. Heilman and colleagues40 as wellas Hanna-Pladdy and colleagues39 have,however, found that people with righthand preference are more likely to havean additional ipsilateral loss of deftness(limb-kinetic apraxia) with left than

with right hemispheric dysfunction.

Pathophysiology

Liepmann thought that a lesion of theprimary sensorimotor cortex caused

limb-kinetic apraxia.6 Lawrence andKuypers demonstrated a loss of preci-

sion grasp in monkeys with lesions ofthe pyramid that interrupted the cor-ticospinal tract.41 However, Freund andHummelsheim reported that damageto the premotor cortex is also asso-ciated with limb-kinetic apraxia.29 Con-

verging evidence of the role of pre-motor cortex in programming deftfinger movements comes from the workof Nirkko and colleagues, who, usingfMRI, demonstrated that discrete uni-lateral distal finger movements wereassociated with activation of the con-

vexity premotor cortex.42

In people who are right handed, lefthemisphere injury can induce ipsilateral(as well as contralesional) limb-kineticapraxia.39,40 In contrast, in right-handedpatients with right hemisphere dysfunc-tion who have limb-kinetic apraxia, thisdisorder is usually limited to the con-tralesional left hand. This asymmetrysuggests that right-handed people have

asymmetric control of their hands suchthat their left hemisphere has strongeripsilateral control of spinal motor neu-rons than does the right hemisphere.Physiologic studies in normal subjectsappear to support this hypothesis,43 butit remains unclear whether this ipsilat-eral (left hemisphereleft hand) controlis mediated by an ipsilateral cortico-spinal pathway or by influencing the op-posite hemisphere by way of the corpuscallosum or both.


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Case 6-5A 78-year-old man with a history of hypertension had the sudden onset of a right hemiparesis andtrouble speaking (a nonfluent aphasia with intact comprehension and impaired repetition and

naming). Over a period of several days the weakness in his arm and hand abated, and whenexamined 1 month after this stroke, the strength in his right forelimb, including his fingers wasnormal. He noticed, however, that he had trouble buttoning his shirt and performing otheractivities that required fine precise movements (deftness or dexterity). His brain imaging revealedthat he had a stroke that injured his motor cortex and par triangularis and opercularis (Broca area)of his left hemisphere.

Comment. The loss of deftness, including the ability to make precise independent butcoordinated finger movements, is called limb-kinetic apraxia.



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