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Journal of Neurology, Neurosurgery, and Psychiatry, 1978, 41, 548-555 Study of anosognosia JOHN CUTTING From the Institute of Psychiatry and King's College Hospital, London SUMMARY Anosognosia (denial of weakness) and "anosognosic phenomena" (other abnormal attitudes to a weak limb) were studied in 100 acute hemiplegics. Both conditions were associated with lesions of either hemisphere. Apathy, visual field defect, and impaired picture identifica- tion were particularly prominent in anosognosia. A failure to integrate information from one side of the body was regarded as fundamental to the condition; explanations in terms of "unilateral neglect" and "agnosia" are discussed. Babinski introduced the word "anosognosia" in 1914 as a description of patients who ignored their hemiplegia. In current usage the term embraces a variety of abnormal attitudes. Chief among these is an explicit verbal denial that the limb is weak. Some patients, although admitting to their dis- ability on direct questioning, minimise its extent, often in a jocular fashion (anosodiaphoria, Babinski, 1914). Yet others experience the limb as strange or not belonging to them, or even attribute ownership to another person (somato- paraphrenia, Gerstmann, 1942). Some express hatred of the limb (miEoplegia, Critchley, 1962), some give it a nickname (personification, Juba, 1949), and some overestimate the strength of an unaffected limb (anosognosic overestimation, Anastasopoulos, 1961). A false belief that the limb is moving (kinaesthetic hallucinations, Walden- strom, 1939) or that a separate limb has appeared in another part of the body (phantom super- numerary limb, Ehrenwald, 1930) may occur. Although these phenomena are generally regarded as related in some way, there is no agreement on an overall classification. Frederiks' (1969) division into "explicit denial" and "anosognosic be- havioural disturbances" (incorporating all the other phenomena) is attractive, and will be used in this report. For the sake of convenience, these will be referred to respectively as "anosognosia" and "anosognosic phenomena." The association of anosognosia with a left hemi- plegia has been found so often that some authors Address for reprint requests: Dr J. Cutting, Institute of Psychiatry, de Crespigny Park, Denmark Hill, London SE5 8AF. Accepted 30 January 1978 have attributed to right hemisphere damage a pre- eminent role in its development (Bogen, 1969; Galin, 1974). It is true that anosognosia for a right hemiplegia has only rarely been recorded. Exclud- ing left handed patients and those with bilateral lesions, only four case reports remain (Von Hagen and Ives, 1937; Nathanson et al., 1952; Weinstein and Kahn, 1955; Welman, 1969). However, the presence of aphasia in patients with left hemis- phere lesions complicates the issue. Gtoss and Kaltenbiick (1955) found that 91% of right hemi- plegics with a field defect and sensory loss, features which had predicted anosognosia in their counterparts with a left hemiplegia, were totally aphasic in the first week after onset. They con- cluded, therefore, that right hemiplegics at risk for developing anosognosia were the very patients in whom aphasia precluded its determination. In the light of these difficulties, the association between anosognosia and right hemisphere damage may be more apparent than real. The independence of anosognosia from a general cognitive impairment is suggested by individual reports of patients with intact orientation (Walden- strom, 1939; Gilliatt and Pratt, 1952). However, three of the only four series of patients (Nathanson et al., 1952; Weinstein and Kahn, 1955; Ullman, 1962) recorded disorientation in every instance of anosognosia, and the authors of the fourth series (Gross and Kaltenback, 1955) maintained that al- though 18% were correctly oriented, they suffered from a milder degree of "confusion," which they termed "lack of critical awareness of surroundings." Resolution of these central issues might lead in part to a clearer appreciation of the nature of 548 Protected by copyright. on May 16, 2020 by guest. http://jnnp.bmj.com/ J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.41.6.548 on 1 June 1978. Downloaded from

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Journal ofNeurology, Neurosurgery, and Psychiatry, 1978, 41, 548-555

Study of anosognosiaJOHN CUTTING

From the Institute of Psychiatry and King's College Hospital, London

SUMMARY Anosognosia (denial of weakness) and "anosognosic phenomena" (other abnormalattitudes to a weak limb) were studied in 100 acute hemiplegics. Both conditions were associatedwith lesions of either hemisphere. Apathy, visual field defect, and impaired picture identifica-tion were particularly prominent in anosognosia. A failure to integrate information from one

side of the body was regarded as fundamental to the condition; explanations in terms of"unilateral neglect" and "agnosia" are discussed.

Babinski introduced the word "anosognosia" in1914 as a description of patients who ignored theirhemiplegia. In current usage the term embracesa variety of abnormal attitudes. Chief among theseis an explicit verbal denial that the limb is weak.Some patients, although admitting to their dis-ability on direct questioning, minimise its extent,often in a jocular fashion (anosodiaphoria,Babinski, 1914). Yet others experience the limbas strange or not belonging to them, or evenattribute ownership to another person (somato-paraphrenia, Gerstmann, 1942). Some expresshatred of the limb (miEoplegia, Critchley, 1962),some give it a nickname (personification, Juba,1949), and some overestimate the strength of anunaffected limb (anosognosic overestimation,Anastasopoulos, 1961). A false belief that the limbis moving (kinaesthetic hallucinations, Walden-strom, 1939) or that a separate limb has appearedin another part of the body (phantom super-numerary limb, Ehrenwald, 1930) may occur.Although these phenomena are generally regardedas related in some way, there is no agreement onan overall classification. Frederiks' (1969) divisioninto "explicit denial" and "anosognosic be-havioural disturbances" (incorporating all theother phenomena) is attractive, and will be usedin this report. For the sake of convenience, thesewill be referred to respectively as "anosognosia"and "anosognosic phenomena."The association of anosognosia with a left hemi-

plegia has been found so often that some authors

Address for reprint requests: Dr J. Cutting, Institute of Psychiatry,de Crespigny Park, Denmark Hill, London SE5 8AF.

Accepted 30 January 1978

have attributed to right hemisphere damage a pre-eminent role in its development (Bogen, 1969;Galin, 1974). It is true that anosognosia for a righthemiplegia has only rarely been recorded. Exclud-ing left handed patients and those with bilaterallesions, only four case reports remain (Von Hagenand Ives, 1937; Nathanson et al., 1952; Weinsteinand Kahn, 1955; Welman, 1969). However, thepresence of aphasia in patients with left hemis-phere lesions complicates the issue. Gtoss andKaltenbiick (1955) found that 91% of right hemi-plegics with a field defect and sensory loss,features which had predicted anosognosia in theircounterparts with a left hemiplegia, were totallyaphasic in the first week after onset. They con-cluded, therefore, that right hemiplegics at risk fordeveloping anosognosia were the very patients inwhom aphasia precluded its determination. In thelight of these difficulties, the association betweenanosognosia and right hemisphere damage may bemore apparent than real.The independence of anosognosia from a general

cognitive impairment is suggested by individualreports of patients with intact orientation (Walden-strom, 1939; Gilliatt and Pratt, 1952). However,three of the only four series of patients (Nathansonet al., 1952; Weinstein and Kahn, 1955; Ullman,1962) recorded disorientation in every instance ofanosognosia, and the authors of the fourth series(Gross and Kaltenback, 1955) maintained that al-though 18% were correctly oriented, they sufferedfrom a milder degree of "confusion," whichthey termed "lack of critical awareness ofsurroundings."

Resolution of these central issues might lead inpart to a clearer appreciation of the nature of

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anosognosia. At present, theories range frompsychodynamic interpretations of motivation(Weinstein and Kahn, 1955) to detailed neuro-physiological explanations of the role of centralsensory pathways (Frederiks, 1969; Waldenstrom,1939). Other factors, in particular "neglect," havebeen less investigated, and the aim of the presentstudy was to examine the basis for the majortheoretical positions by correlating deficits inhigher mental functions with the emergence ofanosognosia and its phenomena in a consecutiveseries of patients with an acute hemiplegia.

Patients and methods

One hundred patients with an acute hemiplegiawere seen over a period of two years in a generalhospital. Weekly visits were paid to all medicalwards, and the notes of all patients with a pro-visional diagnosis of a cerebrovascular accidentwere inspected. Cases were rejected if the hemi-plegia was more than eight days old, if there wasno recorded limb weakness, if any weakness hadtotally recovered by the time the patient was seenby the author, or if the patient was unconsciouson the day of the visit. About 50 patients wereexcluded in this way, and the remaining 100 wereconsidered to be representative of acute hemi-plegics without prolonged unconsciousness orrapid resolution admitted to a general hospital.No detailed analysis of the localisation within a

hemisphere or of the pathology of the lesion wasplanned, but some comment on this is appropriate.The exclusion of any patient whose weakness hadbeen present for longer than a week ensured thata cerebrovascular accident was likely. Investiga-tions were incomplete at the time of the first visit,but notes were inspected subsequently, and in fourcases there was evidence that a tumour and not avascular lesion had been responsible. No patientwith bilateral weakness was included, but threehad pyramidal tract signs on the side opposite tothat currently affected. This suggested that bi-lateral brain damage was present in 3%o.

GENERAL EXAMINATIONGeneral features (age, sex, handedness, occurrenceof a previous paresis, and duration and side ofpresent hemiplegia) were recorded. A neurologicalexamination with emphasis on degree of weakness,sensory loss and visual field defects was thencarried out. Weakness was rated on a four pointscale (1 =slight, 2=moderate, 3=severe, 4=total).Sensory loss was reCorded as present or absent; theextent and nature was noted and, although a crudescale was drawn up, this was not included in the

analyses because it only mirrored the absoluterates of loss.

HIGHER MENTAL FUNCT[IONSix aspects of higher mental function were sys-tematically studied. Orientation, attention, andmemory were assessed by asking patients to orien-tate themselves in time and place, to repeat digits,and to remember a name and address and detailsof their admission. Mood was observed and re-corded as pathological (euphoric, apathetic, ordepressed) if it appeared inappropriate to the cir-cumstances. Personal neglect was regarded, atCritchley's (1953) suggestion, as a disinclinationof the contralateral hand to cross the midline. Inthe presence of weakness it is difficult to separatepersonal neglect from an abnormal attitude to aparalysis, and in left hemisphere lesions, from dis-turbances of body naming. Some indication ofthis, however, for patients with a left hemiplegia,was achieved by asking them to touch parts of thebody on the left side (little finger, thumb, elbow,ear) with the right hand. Visuospatial neglect wasestimated by inspecting their drawings of a face,a clock, and a map of England with six cities. Thesimple neglect test of Albert (1973), which re-quires patients to score out lines on a piece ofpaper, was also used; those with neglect omit lineson one side. Visual perception was tested by pre-senting 20 pictures of moderately uncommon ob-jects-for example, speedometer, accordion-andasking for a correct identification, name, or func-tional description. The task was entirely visual andperformance was easily contrasted with thepatients' abilities in the other language tests given.The test was given to 30 controls (10 Korsakoffsubjects, 10 alcoholics, and 10 patients with per-ipheral neuropathy), and as the lowest identifica-tion score among these was 14 out of 20, anyscore below this was suggestive of impaired visualperception. The mean scores for any groups werealso calculated.

LANGUAGELanguage was assessed for expressive deficits, re-ceptive deficits (by asking questions of increasingcomplexity requiring nonverbal answers, forexample, point to where the illumination of theroom comes from), and for impairment of theabstract attitude (by asking for interpretations offive proverbs, each scored out of 2). The general,neurological, and higher mental function assess-ment will be referred to as the profile of a patient.An anosognosia questionnaire (Table 1) wasdesigned to cover the range of anosognosicphenomena, and to probe anosognosia itself.

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550 John Cutting

Table 1 A nosognosia questionnaire

Anosognosia Anosognosic phenomena

Procedure ifdenial elicitedGeneral questions on general questions Phenomenon Questions

Why are you here? (Arm picked up) What is this? Anosodiaphoria Is it a nuisance? How much troubledoes it cause you? What caused it?

What is the matter with you? Can you lift it? Nonbelonging Do you ever feel that it doesn't belong?Is there anything wrong with your arm or You clearly have Do you feel that it belongs to someoneleg? some problem else ?Is it weak, paralysed or numb? with this? Strange feelings Do you feel the arm is strange or odd?How does it feel? (Asked to lift arms) Can't you see Misoplegia Do you dislike the arm? Do you hate

that the two arms it?are not at the Do you have strong feelings about it?same level? Personification Do you ever call it names?

Kinaesthetic Do you ever feel it moves withouthallucinations your moving it yourself?Overestimation How's the other arm?Phantom Do you ever feel a strange arm lyingsupernumerary beside you separate from the real arm?limb

Results hemiplegics, testable right hemiplegics, and lefthemiplegics-are compared in Table 2. The main

CHARACTERISTICS OF ENTIRE GROUP findings were that the testable group had lessFifty-two patients had a right hemiplegia. Of sensory disturbance, a lower incidence of fieldthese, 30 were so aphasic that it was impossible to defects, and fewer abnormalities of higher mentalassess anosognosia. The remaining 22 had suffi- function. Language deficits were more commoncient preservation of language for an assessment in right hemiplegics. Mood change was depressiveto be carried out. They were free of receptive in right, but predominantly apathetic or euphoricaphasia but five had expressive difficulties. They in left hemiplegics.will be referred to as the "testable" group. Forty-eight patients had a left hemiplegia; none of these ANOSOGNOSIAhad aphasia. The three groups-aphasic right Twenty-eight patients denied a left sided weakness

Table 2 Profiles of right aphasic, right testable, and left hemiplegic patients

Right aphasic Right testable Left

Number 30 22 48Age 68 64 68Sex (Y% male) 50% 55% 65%Left handers - 14% 10%Previous hemiplegia 8% 14% 8%Duration (days) 3.6 4.2 3.8Degree of weakness 3.8 2.3 2.5Sensory loss - 36% 88%Field defect - 9% 77%Disorientation - 32% 56%Mood-total abnormal - 23% 56%

-apathetic - 0% 36%-depressed - 23% 8%-euphoric - 0% 12%

Personal neglect - 0% 21%Visuospatial neglect - 0% 50%Visuoperceptual defect - 38% 53%

mean score - 14.8 13.0Language-expressive dysfunction - 23% 0%

-abstract score - 2.0 3.9Anosognosia - 14% 58%Anosognosic phenomena

Total (no associated anosognosia) - 41% 29%Anosodiaphoria - 9% 4%Nonbelonging - 14% 23%Strange sensations - 0% 6%Misoplegia - 23% 4%Personification - 0% 2%Kinaesthetic hallucinations - 0% 4%Overestimation - 0% 4%Supernumerary phantom - 0% 0%

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(58% of left hemiplegics); there were three in-stances of denial of a right hemiplegia (14% oftestable, 6% of all right hemiplegics). There wasa spectrum of attitudes, ranging from vehementdenial that anything was wrong at all, to admissionthat a stroke had occurred but denial that this hadresulted. in limb weakness. Most would reluctantlyagree that something was wrong, usually describedas "stiffness" or "heaviness." Some patients, inthe course of the interview, would admit to weak-ness, only to deny it minutes later. Others volun-teered the fact that they had suffered a "stroke,"often attributing the source of this information tothe doctor. When questioned as to the effects ofthis "stroke," they denied weakness, and insteadgave some other consequence, for example a"faint." A sample response is given. "Nothingwrong. Sometimes it's a bit stiff. It needs exercise.Something hurts. Something aches." The be-haviour and statements of patients when cross-examined provided some insight into their thoughtprocesses. The impression gained was that bymanipulating the situation one could achieve anadmission that there was some abnormality, butstill fail to convince them that the explanation forthis was weakness in a limb. When presented withoverwhelming evidence, they resorted to evasion("Doctors know more about it than I do"), or in-consequential remarks ("I thought it was a strokeonce, but not now I've seen chaps in the wardwith them").

ANOSOGNOSIC PHENOMENAFourteen patients with a left hemiplegia (29%)showed anosognosic phenomena in the absence ofanosognosia itself; a further four demonstratedboth. Nine patients with a right hemiplegia (41%of testable, 18% of all) exhibited anosognosicphenomena. None had associated anosognosia.Individual phenomena are described. Two patientswith a right, and two with a left hemiplegiademonstrated anosodiaphoria. The experience ofnonbelonging of a limb was present in 11 lefthemiplegics and three right hemiplegics. Theyoffered motor ("It disobeyed me"), sensory ("I'vegot no feeling"), or visual explanations ("Myfingers shrank to short fat fingers"). Threepatients, all left hemiplegics, attributed ownershipto another person ("I felt it could have been a

nurse's hand, a neighbour's, my wife's, adoctor's"). Strange sensations, not to the extentof nonbelonging, were reported by three lefthemiplegics ("lifeless," "cold and clammy").Misoplegia was expressed by two left and fiveright hemiplegics ("I'll hit it with a two-poundhammer when I get back to work; its a bloody

551

nuisance"). Personification was seen in one lefthemiplegic. She claimed that the nurse had origin-ally called the leg "Fred," and she then called herarm "Little Fred;" she further stated that shecould be called "one-handed Pandy." Kinaesthetichallucinations occurred in two left hemiplegics.One said that he "tried gripping, and if I am notlooking, I feel as if I'm moving it, but when Ilook, I'm not." Neither denied their weakness.Overestimation of the strength of the unaffectedarm occurred in two left hemiplegics. The cir-cumstances were different in each case. One, al-though admitting to weakness in the left arm,insisted that the examiner test the strength of hisright arm, which he said was "very strong."Another, with anosognosia, offered this increasedstrength as one of a series of inconsistent explana-tions when faced with the falling away of his leftarm. A supernumerary phantom limb was notclearly identified in this study. Its presence mighthave been inferred from the behaviour of one lefthemiplegic who fumbled in his axilla on cross-examination.

GENERAL, NEUROLOGICAL, AND HIGHER MENTALFUNCTION PROFILEThe profiles of three groups of patients are pre-sented in Table 3. Tests of significance (x2 or ttest, whichever appropriate) were used to compareanosognosics with those with phenomena only, andthe latter with "normal" subjects.

General featuresSex emerged as a moderately significant factor.Men were more likely to show anosognosia or a"normal" attitude, and women the phenomena. Itshould be remarked that men were over-repre-sented in the left hemiplegic group as a whole, acurious finding as the sex distribution for righthemiplegia was equal. Age distinguished thosewith a "normal" attitude from other groups; theformer were younger. Left handedness occurredin some patients from all three groups, and noconclusions can be drawn concerning the effect oflaterality on the development of anosognosia. Ahistory of a previous hemiplegia was more com-mon in patients with phenomena and the durationof hemiplegia from onset was longer in the samegroup.

Neurological featuresDegree of weakness was compared across thegroups, and cannot be said to affect the develop-ment of an abnormal attitude. Sensory loss didnot emerge as a significant factor in the two com-parisons, but there was a clear trend for its inci-

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Table 3 Profiles of patients with aniosognosia, anosognosic phenomena, and a normal attitude

P PAnosognosia Phenomena Normal (anos/phen) (phenlnorm)

Number 31 23 16Sex (% male) 71% 43% 69% < 0.05 NSAge 70 68 60 NS < 0.01Left handers 6% 13% 19% NS NSPrevious hemiplegia 3 % 26% 6% < 0.05 NSDuration (days) 3.4 4.8 4.0 < 0.05 NSDegree of weakness 2.6 2.4 2.3 NS NSSensory loss 87% 65 % 38 % NS NSField defect 90% 39% 19% < 0.001 NSDisorientation 71 % 43% 6% < 0.05 < 0.01Mood-total abnormal 71 % 39% 6% < 0.05 < 0.05

-apathy 51% 4% 0% < 0.001 NS-depression 10% 22% 6% NS NS-euphoria 10% 13% 0% NS NS

Personal neglect 32% 4% 0% < 0.05 NSVisuospatial neglect 52% 24% 6% NS NSVisuoperceptual defect 86% 42% 6% <0.01 <0.05meanscore 11.1 13.8 18.0Abstract score 4.0 2.2 4.6 < 0.05 < 0.05

dence to diminish across the groups. Visual fielddefect was a potent factor in discriminating be-tween patients with anosognosia and those with itsphenomena.

Higher mental functionsThe presence of disorientation significantly separ-ated the three groups. Further analysis revealedthat in right hemiplegics, all three anosognosicsand four of the nine with phenomena were dis-oriented; four of the remaining five with pheno-mena were impaired on tests of attention ormemory. In the left hemiplegics, a lower rate ofcognitive dysfunction prevailed. Of 28 anosog-nosics, 19 were disoriented and a further four hadmemory impairment; of 14 with phenomena, sixwere disoriented and only a further one patienthad deficient memory. Mood change of any kinddistinguished the groups to a significant extent;apathy was virtually restricted to those withanosognosia, while euphoria and depression werethe forms predominantly seen in those withphenomena. Personal neglect was only seen in onepatient who did not have anosognosia, but onlyappeared in one-third of those with anosognosia.Visuospatial neglect failed to emerge as a signifi-cant discriminator, but there was a trend foranosognosics to show this more than other groups.Visuoperceptual deficit appeared a potent factorin separating anosognosia from those with pheno-mena. However, it was not entirely certain thatfailure to identify simple pictures reflected a puredisturbance of visual perception, independent ofsuch variables as neglect or inattention. Abstractlanguage was considerably worse in those withphenomena, an unexpected finding which suggeststhat impairment of metaphorical abilities is not

crucial to the development of anosognosia itself,but appears to play a part in at least some of thephenomena.

Discussion

INCIDENCEAn abnormal attitude towards a recent hemiplegiawas common with damage to either hemisphere.Anosognosia and anosognosic phenomena wereseen, respectively, in 58% and 29% of left hemi-plegics, and in 14% and 40% of right hemiplegics.The estimation of the incidence of anosognosiafor a left hemiplegia is slightly higher than thatof other authors, who give figures ranging from30% to 50%. Anosognosic patients in the presentstudy were seen after only three to four days hadelapsed from the initial ictus, and this early exam-ination may have been responsible for the highincidence. The other authors mentioned (Nathan-son et al., 1952; Gross and Kaltenback, 1955;Ullman, 1962) recorded a longer mean intervalbetween the onset of the stroke and their assess-ment. As chronic hemiplegics rarely exhibitanosognosia (Gilliatt and Pratt, 1952), factorsunique to the acute stage of a cerebrovascularinsult must be regarded as essential to the develop-ment of anosognosia.

LATERALITYThe apparent difference between the incidence ofan abnormal attitude towards a right (54%) andleft hemiplegia (87%) is complicated by the largegroup of 30 right hemiplegics who were aphasic. Ifall the aphasics are assumed to have held anabnormal attitude, not an unreasonable assump-tion, then the figure for all right hemiplegics

552 John Cutting

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would rise to 81 %. It certainly appears that righthemisphere damage is not essential to the develop-ment of an anosognosic attitude. There remainsthe question of whether it has a quantitatively orqualitatively different role than damage to theleft hemisphere. Only six of 48 left hemiplegicswere regarded as holding a normal attitude, while10 of 22 testable right hemiplegics did so. This isslender support for a quantitative difference be-tween hemispheres. Some of the findings lend atleast meagre support to the idea that differentfactors may be responsible in each hemisphere.For instance, left hemiplegics could developanosognosia or its phenomena in the absence ofdisorientation or even impaired memory; in con-trast, all but one right hemiplegic with an abnor-mal attitude had obvious cognitive impairment.

ANOSOGNOSIC PHENOMENA

Although deficits in higher mental functions weremore common in patients with phenomena than innormals, they were less remarkable than in ano-

sognosics. In the main, it appeared that generalfactors distinguished the two groups. Those withanosognosic phenomena were more likely to bewomen and to have had a previous hemiplegia; a

longer period had elapsed between the ictus andthe author's examination than in the anosognosicgroup. The last finding is in agreement with otherauthors (Gilliatt and Pratt, 1952) that the pheno-mena arise at a later stage in the resolution of a

stroke than anosognosia itself. There appears tobe a sex difference in hemispheric distribution oflanguage and visuospatial skills (McGlone andKertesz, 1973), although it is difficult to relatethe sex difference between anosognosia and itsphenomena to this. The previous hemiplegia mighthave provided an experience which rendered theircurrent state more understandable than to thosefor whom a hemiplegia was a novel occurrence.Of the phenomena, anosodiaphoria and the experi-ence of "nonbelonging" were the most likely toshow deficits of higher mental function, and hadtherefore the best claim to be regarded as "patho-logical attitudes." Misoplegia and some of therarer phenomena might be better regarded as

"normal" adaptation phenomena (Critchley, 1953;Frederiks, 1969).

PATHOGENESIS OF ANOSOGNOSIADeficits in higher mental function and field defectwere the most significant correlates of anosog-nosia. The higher level of significance obtainedwith field defect, apathetic mood, and visuoper-ceptual deficit suggests that these should be re-

garded as particularly important. These considera-

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tions allow a critical appraisal of the main theoriesconcerning the nature of anosognosia.An emphasis on "confusion," accentuating a

general tendency of ill people to repudiate theirdisability (Weinstein and Kahn, 1955; Ullman,1962), does not provide a comprehensive accountof anosognosia. A confusional state was not in-variably associated with anosognosia and was notinfrequent in patients without this state. Anosog-nosia is not adequately defined merely as "denialof illness;" these patients would admit to a "heartattack" and even a "stroke," but fail to appreciateweakness of a limb. Kinaesthetic hallucinations(Waldenstrom, 1939; Frederiks, 1969) cannot beregarded as the fundamental element in the con-dition. In the first place, only two patients re-ported them, and neither had anosognosia itself.Secondly, there was evidence that visual factors(field defect, poor picture identification) weremore relevant than kinaesthetic factors. Further,when hemiparetic patients were asked to raiseboth arms, those with anosognosia would acceptthat they came to rest at different levels but fail toappreciate that this might indicate weakness ofone limb. It appeared that in this situation theycould use some of the information pertaining toone side of the body but failed to integrate it intoa judgment about weakness. Unqualified adher-ence to the idea of anosognosia as a "body imagedisorder" with the implication of a right hemi-sphere "centre" (Bogen, 1969; Galin, 1974) is notconsistent with the present results. The term"body image disorder" is, however, thoroughlyambiguous, and while anosognosia can be accom-modated by such a broad definition, the originalproposal of Head and Holmes (1911) of a "bodyschema," essentially a physiological model whichcould account for certain sensory deficits of cor-tical origin, lacks the robustness necessary to ex-plain the diverse manifestations observed in thepresent series.

Psychodynamic, kinaesthetic, and "body image"theories do not, therefore, provide satisfactoryaccounts of anosognosia. Other suggestions can bedivided into two groups, which emphasise either"neglect" or "agnosia."Gross and Kaltenback (1955) introduced the

term "anosognosic complex" to describe the back-ground of neglect, apathy, and inattention out ofwhich they believed that anosognosia developed.Denny-Brown et al. (1952) saw in anosognosia anillustration of "amorphosynthesis," which theyclaimed was a fundamental characteristic ofparietal lobe disease of either hemisphere, andwhich consists of a tendency to extinguish onemember of a stimulus pair and to lose insight into

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perceptual processes. These are adequate descrip-tions of much of anosognosic behaviour. The de-velopment of unilateral neglect in monkeys(Kennard, 1939; Welch and Stuteville, 1958) andin man (Heilman and Valenstein, 1972) fromcontralateral lesions in the frontal lobe provides arelevant experimental model with which to com-pare anosognosia. The deficit in these reports wastransient, affected stimuli from all sensory modali-ties and produced an apparent, but false, hemi-anopia. There was "an apparent lack of recogni-tion of objects" attributed to "a disturbance ofthe more complex integrative processes of thefrontal lobe" (Welch and Stuteville, 1958). Theresemblance to anosognosia is striking. Each con-dition was transient, both visual and kinaestheticsources of information were affected, and therewas a marked failure to identify pictures of simpleobjects. However, a number of anosognosicpatients acknowledged the presence of morbidchange in the affected limb and cannot be re-garded as demonstrating "neglect" unless onebroadens the concept to mean a failure to balanceinformation entering from the two sides (Denny-Brown et al., 1952; Heilman and Valenstein, 1972).Interpreting "neglect" in this way, one can allo-cate patients to points along a spectrum, with, atone end, severe forms giving rise to completedenial of any change in a limb, and, at the other,minor forms where the experience of morbidchange is preserved but the capacity to make ajudgment about the cause of this is disrupted inthe central analysis.Another approach is to regard the deficit as a

form of agnosia. This idea was discussed bySandifer (1946) and Roth (1949), and much of thediscussion on the nature of anosognosia, par-ticularly the role of "confusion" and lower-ordersensory deficits, can be found in the literature onvisual agnosia. Further, Geschwind (1965) arguedthat visual agnosia could be regarded as a lan-guage disorder and this point has been made foranosognosia by Weinstein et al. (1964). A furthercomparison can be drawn between the nature ofvisual agnosia and anosognosia. In the former, adistinction has been made between "apperceptive"and "associational" forms (Taylor and Warring-ton, 1971), and applying this idea to anosognosiait can be argued from the present results that mostpatients have normal apperception in their appre-ciation of morbid change, but disturbance in theassociational sphere by their faulty choice oflinguistic term to express their experience. Others,comparatively few in this study, had little or noappreciation of change in a limb and might be re-garded as showing "apperceptive anosognosia."

John Cutting

In conclusion, I believe that the present studyhas advanced the understanding of anosognosia bypointing out the distinction between this and ano-sognosic phenomena, and by examining the rela-tionship with laterality of hemispheric damage.In demonstrating the significant association withcertain other neuropsychological deficits, I haveindicated the poverty of some theoretical positionsand the relevance of others. In the present stateof knowledge, I believe that the two most com-prehensive approaches attribute anosognosia toeither "neglect" or agnosia. In favour of "neglect"was the prominence of apathy in the present studyand the relevant animal experiments in theliterature. I am, however, impressed by the associ-ated visuoperceptual deficits and by the numberof patients who appreciated morbid change butfailed, even in the absence of disorientation, toarrive at a judgment of weakness, and favour,therefore, an agnosic basis for the condition.

The material in this article is based on an MDthesis awarded by the University of London. Iwish to thank Dr W. A. Lishman for much helpduring the work, and the physicians and neurol-ogists of the Brook General Hospital, London forallowing me to examine patients under their care.

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