Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:152-158

Motor neglectD LAPLANE,* JD DEGOSt

From the H6pital de la Salp&riere, * Paris and the H6pital Henri Mondor, t Creteil, France

SUMMARY Motor neglect is characterised by an underutilisation of one side, without defects ofstrength, reflexes or sensibility. Twenty cases of frontal, parietal and thalamic lesions causingmotor neglect, but all without sensory neglect, are reported. It is proposed that the cerebralstructures involved in motor neglect are the same as those for sensory neglect and for thepreparation of movement. As in sensory neglect, the multiplicity of the structures concernedsuggests that this interconnection is necessary to maintain a sufficient level of activity. Predomi-nance of left sided neglect by right sided lesions suggests that the left hemisphere is dominant fordeliberate activity; hemispheric dominance could be applied to sensory neglect where consciousawareness would play the role of deliberate activity.

The terms unilateral motor neglect or unilateralhemi-inattention are used nearly interchangeably inthe classic as well as in contemporary literature andreviews. Neglect may either be global' or partial(dissociated), as is the case with a visual and spatialneglect, a sensory neglect, a hemicorporeal neglectand even a olfactory neglect.2 Unilateral underutil-isation of the limbs is frequently reported as aphenomenon associated with the "Neglect Syn-drome". Its isolated appearance was mentioned inthe older literature2-4 under various names. With PCastaigne,56 we have drawn attention to a distur-bance of spontaneous movement involving one halfof the body and having the appearance of hemi-plegia, yet with normal strength and dexterity, whichcan be proven by prompting an extraordinary efforton the part of the patient during the examination.We have called this disorder Motor Neglect.The purpose of this communication is to present

20 cases of motor neglect in which localisation of thelesion is sufficiently well defined to allow a discus-sion of the topography of the lesion and the possiblepathophysiological mechanisms involved.

Patients

Motor neglect was unilateral in each of the cases andincluded, on the affected side, the following charac-teristics: underutilisation of the upper extremity for

Address for reprint requests: Prof D Laplane, H6pital de la Salpet-rire, 47 Boulevard de l'Hopital, 75651 Paris Cedex 13, France.

Received 26 June 1982 and in revised form 13 September 1982.Accepted 30 September 1982

tasks that could be performed with the "healthyside" even when this was inconvenient (for examplewhen they required a change in position of thebody); non participation or feeble participation inbimanual tasks (such as clapping, opening a bottle,buttoning or unbuttoning a garment); under- ornon-participation of the hand in gesturing whenspeaking; lack of arm swing when walking. Thisspontaneous underutilisation contrasted with nearnormal movement and strength, when the examineractively encouraged the patient to use the arm. Insome cases, the patient described the disturbance bysaying that the hand was lazy or unreliable, althoughthe required task finally was performed correctly.The patient had to "command" the hand to per-form, he had to think of using it. In other cases,when the right hand was affected, the patient wouldsay that he had become a left hander whereas he hadbeen right handed. The disturbance rarely affectedthe upper limb alone; it usually involved bothextremities but predominantly the upper. In thelower extremity the disorder was manifested by a lagin movement and a reduced range of motion, andautomatic movements were specially disturbed: theaffected leg lagged behind the good one when walk-ing, or the leg stayed on the bed when the patientattempted to get up, causing falls. Here, as in thecase of the arm, deliberate effort would compensatefor the disturbance.

In order to avoid confusing motor neglect withclassical hemiplegia we have reported in this seriesonly cases that did not have a marked reduction ofmuscle strength or other motor or reflex distur-bance. We have included cases with hypotonia andother disorders of movement that increased or

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tended to make motor neglect more obvious, butwhich were not constant; these were: (1) Lack ofspontaneous "placing reaction". This was almostconstant. When the patient was sitting, he let hishand rest along his body or between his legs ratherthan putting it " normally" on his thigh or on the armof a chair. The leg could also be left in an uncom-fortable position such as behind the body, or besidethe chair, sometimes "lying on the back of the toes".In some cases, it tended to upset the equilibrium.When the subject moved from one place to another,no attempt was made by the hand to avoid hittingobjects (for instance, the back of a chair); and suchincidents did not produce change in the patient'sposture. At times, the hand could be left to dragpassively on the surface of a bed or table. As thepatient got into bed, the arm or leg would be lefthanging out of bed. In other instances, the armmight be caught up under the body or the leg becrossed under the healthy leg in an uncomfortableposition which the patient did not seem to notice.However, in all cases, a comment from the examineror a mere exhortation to assume a better positionwithout specification, caused the patient to rectifyhis posture. (2) The insufficient or delayed reactionto assume correct posture could be so severe as to beabsent; in this case the patient, losing his balance,fell to the affected side. There was no attempt toavoid the fall, or to minimise the shock. (3) Therewas a lack of automatic withdrawal reaction to pain-ful stimulation, which could be striking: the patient,who appreciated pain normally, did not move thelimb away although he protested and attempted touse the healthy limb to retrieve the affected one orfence away the painful stimulus. This sign, at times,was difficult to interpret as some patients believedthat they must stoically sustain painful stimulation.(4) In some cases voluntary gesture was faulty and itappeared as if there was an error in the appreciationof the necessary energy to reach a point in the cor-poreal or extracorporeal space; the movementalways fell short of the target (hypometria). Forinstance, when the patient is asked to put his fingerto his nose, he bent his head forward to compensatefor the inadequate movement of the arm while, inother circumstances, he was able to raise the elbowmuch higher, as, for instance, when pointing at theceiling.To prevent confusion with the syndrome of sen-

sory neglect, we have excluded from our study, allpatients presenting sensory disturbances includingthose with asomato-agnosia or denial. Some of ourpatients presented some degree of visual neglectfrom the beginning; in two cases this neglect-appeared to be secondary to extension of the origi-nal lesion.

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In all of the cases in this report, the preciseanatomical localisation of the lesion has been asses-sed by the associated findings on neurologicalexamination, surgical intervention and/oranatomopathological verification. (Cases of motorneglect associated with subdural hematoma havebeen eliminated from the study as they do not leadto anatomical conclusions.)

Results

Twenty cases of pure motor neglect have beenobserved; 15 had frontal lesions, four parietallesions and one a thalamic lesion. All the patientsconsidered themselves to be right handed. The lownumber of cases of motor neglect or parietal origin isdue to the fact that we excluded patients presentingsensory neglect syndromes or other sensory distur-bances that may represent elements of sensory neg-lect. The findings of the motor neglect syndromewere always on the opposite side to the lesion, andare summarised in table 1 for 12 patients withlesions in the right hemisphere and in table 2 foreight patients with left hemispheric lesions.The retro-Rolandic lesions were all large glioblas-

tomas that did not easily lend themselves toanatomo-clinical correlations. Two were essentiallyparietal, one parietotemporal, and one temporal butwith "laminating" of the parietal area which showedmultiple neuronal changes and gliosis.The frontal lesions were in three groups:

(A) Six small lesions (five metastases-cases 2, 3, 6,13 and 14-and one glioblastoma-case 5) locatedin the white substance of the posterior part of Floverlapping F2 in front of the pre-Rolandic sulcus.(B) Lesions larger in size and/or involving less welldefined anatomical landmarks and comprising threecases of corticectomy of the medial aspect of thefrontal lobe including the supplementary motor areaand the adjacent cingulate area7 performed forintractable epilepsy (cases 7, 8 and 16); a case ofischaemia localised only by gamma scintilography inthe pre-Rolantic area (case 1); a parasagittal menin-gioma under coronal suture (case 4); and a left fron-tal glioblastoma (case 15).(C) Flat lesions ("en plaque") involving the externalcortex of the frontal lobe (meningioma "en plaque"case 10, and frontal lobectomy indenting and cuttingthrough the back of the posterior part of F1-F2, case9).The thalamic lesion consisted of a nucleus of

confluent lacunae in the ventro-lateral region of thethalamus, but overlapping the internal capsule andthe subthalamic region.

In all of our patients, motor neglect lasted a fewdays to a few weeks. After that, it evolved either to

Table 1 Motor neglect lesions of the right cerebral hemisphere

Case no Location of Type of Abnormal Lack of withdrawal Hypometria Visual neglectlesion lesion placement to pain

1* Frontal Ischaemic Yes Yes Yes Yes2t Frontal Metastasis Yes Yes Yes Yes3t Frontal Metastasis Yes ? ? No4 Frontal Meningioma Yes No No No5 Frontal Glioblastoma Yes Yes Yes No6 Frontal Metastasis Yes Yes No No/Yes (-)7t Frontal Corticectomy ? Yes No ?8t Frontal Corticectomy ? Yes No ?9 Frontal Lobectomy Yes No Yes No

10 Frontal Meningioma Yes Yes Yes No11§ Parietal Glioblastoma Yes Yes Yes No/Yes (-)1 2 11 Thalamus Ischaemic Yes Yes No ?

* Castaigne P. et al.5t Castaigne P. et al.5t Laplane D. et al.7§ Vitrey et al."

Laplane D.9(-) The visual neglect has appeared in a 2d time.

Table 2 Motor neglect lesions ofthe left cerebral hemisphere

Case nio Location of Type of Abnormal Lack of withdrawal Hypometria Visual neglectlesion lesion placement to pain

13t Frontal Metastasis Yes Yes Yes Yes14 Frontal Metastasis Yes No No No15 Frontal Glioblastoma Yes I? Yes Yes16t Frontal Corticectomy No Yes No No17 Frontal Ischaemic Yes No No No18 Temporoparietal Glioblastoma No No No19* Temporal Glioblastoma Yes Yes Yes Yes20* Parietal Glioblastoma Yes Yes Yes No

* Castaigne P. et al.'t Castaigne P. et al.'t Laplane D. et al.7

hemiplegia (due to spreading of the lesion) orrecovery (removal of the lesion or spontaneousrecovery following ischaemic injury or surgical cor-ticectomy).

Discussion

Unilateral pure or isolated motor neglect, defined bythe existence of spontaneous non-utilisation orunderutilisation of the limbs on one side, with nearnormal strength and utilisation as a result of deliber-ate effort has been found in 20 patients without sen-sory deficit. The lesion responsible for this syndromewas either in the frontal lobe where, in six out of 15of our cases, it was limited to the white matter in thedepth of the posterior part of Fl and of overlappingF2, or was large and retro-rolandic, involving theparietal lobe. In one case, the lesion was in the ven-trolateral nucleus of the thalamus. The clinical syn-drome of motor neglect was identical regardless ofthe site of the lesion. The site of lesion could only be

suspected from disturbances sometimes associatedwith the syndrome of motor neglect (for example,clinical frontal lobe findings, disorder of language,hemianopsia or visuo-spatial disorders and cerebel-lar sydrome) and not from the motor neglect itself.Isolated unilateral motor neglect involving disorderof "automatic" placement of the limbs is in ourexperience, due to a contralateral lesion of the reg-ion of the foot of Fl. In some cases, this findingallowed us to direct surgical investigations andintervention to the appropriate region.

Unilateral reduction in the range of motion, dis-proportionate to the motor deficit, is observed inpatients affected with various disorders, including aleft hemiparesis, hemiparkinsonism, hemichorea,'°thalamic syndrome," and unilateral neglect.'2 13 Thereduction in the range of motion is often cited onlyin passing; when this phenomenon is analysed it isoften done in a psychological manner, the prefer-ence for utilising the healthy hand being consideredas "quite natural". Some authors have, however,offered an interpretation which takes into account

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the organisation of movement, disorder of the sen-sory afferents,'2 1' hemi-inattention.'

Isolated unilateral underutilisation has alreadybeen described in a more or less explicit manner andunder various names. Hartmann3 described anakinesia of the left limbs secondary to an ischaemiclesion of the right frontal white matter at the level ofF2. Liepmann in 19084 took the psychoparalysis on"Bruns" paralysis out of the category of apraxia:"This disturbance is not linked to loss of memory forthe movement but rather to the fact that the limb isunderutilised; this is why, when the movement isachieved, it is normal. This abnormality is thereforehalf-way between paralysis and apraxia. The seat ofthe disorder is probably the central cerebral cortex,and includes perhaps, the adjacent anterior andposterior cortex". Wilson in 1908'5 reported anobservation of "absence of initiative". The patientwas a wounded man observed after the extraction ofa bullet lodged into the right parietal lobe. For a fewdays, he displayed astereognosis with disorders ofdeep sensation which appeared mild, and a non-utilisation of the left hand in spite of normalstrength. Thomas and Ajuriaguerra'6 described simi-lar patients in which they gave a detailed descriptionof the deficit which is very much like our own; in theabsence of any sensory or motor abnormality, thepatients underutilised the limb. They interpretedthis as a sign of hemispheric lesion, without giving amore precise localisation. Zoll'7 reported five casesof motor neglect which, strangely, he called anosog-nosia following thalamic coagulation; he incrimi-nated lesions of the ventral intermediate nucleus ofthe thalamus as responsible for the syndrome.We have explored the existence of motor neglect

due to parietal lesions and upper frontal lesions5 6 inthe absence of motor and sensory deficits and in theabsence of other elements of the syndrome of neg-lect. Recently, Valenstein and Heilman,"8 observedunilateral hypokinesia and motor extinction of theleft side after haemorrhage affecting the right caud-ate nucleus. Although the technique of examinationwas very different from the one we used, the caseswere probably similar. However, the lesions werefar from being limited to the caudate nucleus, butaffected the entire anterior limb of the internal cap-sule and thus resembled the frontal lesion present insome of our patients.

It is only recently that motor neglect has beenstudied in animals. However, in the past severalstudies dealt indirectly with the subject. The unilat-eral or asymmetric destruction of the posterior col-umns'9 or of the pyramidal tract20 causes an under-utilisation of the corresponding limbs which can bepartially ameliorated by creating or aggravating con-tralateral lesions. Unilateral hypokinesia was

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described after contralateral lesion of the tegmen-tum of the upper pons and of the mesencephalon,2'by a lesion located at any point of the rubro-olivocerebellar loop22 and by an ipsilateral hemicerebel-lectomy.23 Humphrey24 published a review of disor-ders of motility observed in man and animalsaffected by parietal lobe lesions. He reported amarked decrease in the frequency of spontaneous,purposeful movements and of visual tactile placingresponses of the arm and hand contralateral to thesite of the lesion. He stated that "it may be prema-ture to extract from the numerous and sometimesvarying descriptions of the parietal lobe syndrome, aparticular set of disturbances that appears to beprimarily attentive or motor in nature". However,Watson et a125 showed, thanks to cross-conditioningstimulation, that the motor neglect, observed in themonkey after a lesion of the arcuate fasciculus or ofthe mesencephalic reticular formation, is "inducedby the loss of the intention to make the correctmotor response for a perceived stimulus and not bysensory or sensory attentional defect". One wonderswhether the motor behaviour of unilateral neglectsyndromes following either frontal lesions26 parietallobe,27 anterior cingulate gyrus28 or mesencephalicreticular formatoin2930 are all dependent upon thesame mechanism. The topographic analogy thatexists between the structures which when injuredresult in unilateral negiect in animals and the struc-tures whose lesions result in motor neglect in man isstriking. It is all the more so because in addition tothe cases presented here, we have also found casesof motor neglect associated with other neurologicsigns that indicated that the lesion responsible wasprobably, though not certainly (which made usexclude them from this study) located in themesencephalic area.3'The motor neglect mechanism cannot be attri-

buted either to a sensory disorder or to a sensoryneglect syndrome (patients with these findings wereexcluded from this study). The hypothesis of ahemispheric hypo-arousal initially put forward byHeilman' does not allow for the explanation ofunimodal neglect. Yingling et at32 partially removedthis difficulty by showing that the stimulation ofspecific parts of the nucleus reticularis thalamiabolished the corresponding evoked corticalresponses (visual/auditory or tactile). However, weare not sure that these findings apply to unimodal orpredominantly unimodal neglect due to frontal orparietal cortical lesions. It is even less clear that theyapply to motor neglect.

It seems more logical to regard motor neglect asthe result of a defect of movement preprogrammingand organisation. It is striking that the structures, inwhich lesions are liable to result in motor neglect are

Laplane, Degos

concerned with the preparation or planning ofmovement: the parietal association areas,33 34 secon-dary motor area,35 the premotor cortex,24 thethalamus, and notably the ventrolateral nucleus.36-40These structures and the motor areas are, physio-logically and anatomically, largely interconnected.24Therefore, one can hypothesise that motor neglect isa disorder related to a defect in the "triggering" ofthese structures which prepare and programmemovement and that the interconnections betweenthese different structures are necessary to maintaineach one at a sufficient functional level. It is possiblethat the underutilisation observed in the partial andasymmetrical lesions of the sensitive afferents'9 or ofthe pyramidal tract20 or in Parkinsonism may be dueto the same mechanism of the lowering of the func-tional level of all the structures of a hemisphere par-ticipating in the organisation of motricity. Asregards the motor neglect itself, the reversibility ofthis disorder in situations of emergency, when itbecomes urgently necessary to act, proves that otherpossibilities for a "preparatory" motor system doexist. The transitory character of the motor neglectin the presence of non-progressive lesions (surgicalcorticectomy) shows also the existence of alternativesystems.Valenstein and Heilman'8 offer two possible

explanations for the hypokinesia and motor extinc-tion they observed. First they compared the distur-bance to the unilateral hypokinesia induced in ani-mals by lesions of the dopaminergic system. How-ever, as already pointed out, the lesions of thepatients are far from being limited to the caudatenucleus but also affect the anterior limb of the inter-nal capsule and tend to resemble the frontal lesionsof our patients. The second possible explanation wasthat the activation system of the healthy hemispherehelps the diseased hemisphere (in their cases theright hemisphere) in planning motor actions exceptwhen it is occupied with its own tasks. This interpre-tation is compatible with the one we now propose.

In the present series of cases of motor neglect, themethod of patient selection was responsible for theweak preponderance of patients with right hemis-pheric lesion and left motor neglect. Cases in whichsome form of sensory neglect was present wereexcluded with the purpose of demonstrating theindependence of pure motor neglect. However, if wehad included all cases of motor neglect observed,regardless of the type of associated neurologicalfindings, we would have found a higher incidence ofright hemispheric lesions as all other authors have inunilateral neglect. In order to explain this preval-ence, Heilman and Watson' suggested that the cor-ticoreticular loop, which they thought to be theanatomical support of the unilateral hemispheric

arousal, is more discretely organised in the righthemisphere, a statement they do not support withfacts. Recently, Heilman and Vanden Abell4 haveoffered another hypothesis according to which theright hemisphere has a dominant role in attention. Itremains to be demonstrated whether this hypothesisis well founded, and if it is, whether it offers a realexplanation.

In the circumstances in which our patients wereexamined it was verbal exhortation which madeapparent the dissociation between motor ability andautomatic utilisation of the affected limbs. Thus,rather than speaking of a voluntary effort, as isusual, it would probably be more accurate to suggestthat the reason for improvement is a motivation setup from language. The role of language appears toplay an important role during examination; evenwhen the patient is not given explicit instructions, hefeels motivated by the presence of the examiner andattempts to guess what it is that the observer wantsfrom him. Therefore, he has a tendency to repro-duce or repeat behaviour that has been requiredfrom him previously. Even outside of the examiningsituation, the role of language in voluntary effort isnaively, but strongly, shown by the patients whoexplain that they must order the lazy hand to per-form.There are several other reasons for believing that

in all deliberate motor acts of man, the dominanthemisphere plays a preponderant role. The evidenceis drawn from observations made in patients withhemisphere disconnection: following a division ofthe cerebral commisures, not only "all patientsshowed some degree of left-sided apraxia to verbalcommands" for an extremely variable period of time(one day to more than 5 years)42 but also "there wasa tendency to use the left hand less than usual underordinary circumstances. Special effort and stimula-tion were often necessary to bring the left hand intoaction".4 In a case of Marchiafava-Bignami diseasewith hemisphere disconnection syndrome, Barbizetet al4 have observed the same paucity of gesturingwith the left limbs. In addition a specific study of thepatient's behaviour while performing everydayroutine movements could lead to the assumptionthat the left hand was not, or was imperfectly awareof what the patient wanted to do deliberately, evenunder the influence of a primary drive, as in drinkingor smoking. Similar observations seem to have beenmade by Schott et al.45 They write: "during theexamination, the patient denies being left-handedand wants to use his right hand, and in everydaygestures the left hand acts, but every so often itopposes and resists the right hand, which is alwaysmore efficient." Akelaitis46 described similarbehaviour, although he curiously interpreted it as

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being of epileptic or psychiatric origin. This role oflanguage dominance in motor intention of deliber-ate actions agrees with the existing correlation be-tween the preferred utilisation of the right limbs andthe speech dominance of the left cerebral hemi-sphere, in right-handed individuals. Inhibition ofmotor performances of the right hand, but not of theleft, by interference of verbal tasks has beenreported in right-handed individuals.47-50 Thisstrongly suggests that motor organisation of theright arm is language dependent.We propose another possible explanation of left

lateralisation of motor neglect: different lesions ofthe systems that programme and organise move-ment24 might cause a defect in the initiation andfollow through of motion; if the lesion is located inthe right hemisphere, verbal incitation and/or thedeliberate will of the subject elaborated by the lefthemisphere may compensate, at least partially, forthe motor disturbance, as long as the corpus cal-losum is intact. On the other hand, in the left hemis-phere language and movement are so intricatelyorganised that it makes the occurrence of thecharacteristic dissociation of motor neglect lesslikely. The predominance of left sided motor neglectcould not be verified in lesions located at a subcorti-cal level, for example in the thalamus.'7 One canassume that at this level, the same alternative pro-cesses through verbal exhortation and deliberatevoluntary effort may be at play in the left as well as

the right hemisphere. On this hypothesis, it isassumed that the left hemisphere, responsible forlanguage, plays a dominant role in the programmingand organisation of movement, through deliberateconscious effort; and that movement of the rightlimbs and language are intimately related becausetheir organisation has developed simultaneously;this may be either genetic, educational or both.One must stress that the language in question is

not necessarily a very elaborate one. Encourage-ments at a very simple linguistic level improve theperformance of the "neglected" hand. There are infact reasons to believe that the left hemisphereplays, from birth, a predominant role in the dis-crimination of sounds in the mother's language;51 52the role of maternal language in inciting movementis quite evident. Several sorts of evidence supportthe idea that the mechanism of motor and sensoryneglect are closely related: frequency of association,topographic proximity of lesions causing both ofthem; secondary appearance of visual neglect in twoof our patients due to the growth of the tumourresponsible for the initial motor neglect. Thus thehypothesis that we propose to explain motor neglectcould also be applied to sensory neglect. Awareness,that is conscious awareness, would play the role of

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deliberate and purposeful effort in motor neglect,assuming that it has the same relationships with theleft hemisphere and language.

The authors wish to acknowledge their gratitude to JMassiou for help in translation and to Dr MRamirez-Lassepas for revision of the manuscript,criticism and helpful suggestions.

Since acceptance of our manuscript, a study on"None sensory neglect from parieto-temporallesions in monkeys" by Valenstein E, Heilman KM,Watson RT and Van Den Abell T has beenreported. It confirms our suggestion that the motorbehaviour of neglect observed in parietal lesionsshould be interpreted as "non sensory".

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