Journal ofNeurology, Neurosurgery, and Psychiatry, 1978, 41, 556-563

Dissociated disorders of speaking and writing inaphasiaA. BASSO, A. TABORELLI, AND L. A. VIGNOLO

From the Centro di Neuropsicologia, Clinica Neurologica, Milan, Italy

S U M M A R Y Of 500 left brain-damaged patients with educational level above elementaryschool investigated with a standard quantitative battery for dissociation between oral andwritten expression, speech was found to be selectively impaired in seven (three with "pureanarthria," two with anarthria in the context of Broca's aphasia, and two with fluent aphasiawith remarkable sparing of writing), and writing in another seven (two with "pure" agraphia,two with "agraphia with mild alexia," and three with "agraphia with mild fluent aphasia.") Thenature of three conditions (pure anarthria, fluent aphasia with sparing of writing, and pure

agraphia) is discussed, with evidence of a selective association between pure agraphia andlesions of the upper left parietal lobule.

The classic forms of aphasia showing dissociationbetween oral and written expression are still con-troversial in many respects. Anarthria, where oralexpression is selectively impaired, is generally ac-cepted as an independent entity, but its frequencyis a matter of discussion-ranging from 4% of allaphasias, as recently maintained by Tissot et al.(1970), to exceedingly rare as believed by Souques(1928) who declared that he had collected onlynine convincing cases in 20 years. As to pureagraphia, in which writing is altered selectively, itsvery existence as an independent syndrome isquestioned. Chedru and Geschwind (1972b) havedescribed isolated agraphias in studies of con-fusional states and have suggested that many,and perhaps the majority, of cases of isolatedagraphia in the literature are examples of thismechanism.The aim of our study was twofold: in the first

place, we wished to ascertain the presence and theincidence of a conspicuous dissociation betweenoral and written expression in a large sample ofleft brain-damaged patients with language dis-orders; in the second place, we wished to verify towhat extent such dissociated syndromes corre-sponded to the classic forms of anarthria andpure agraphia.

Supported by a CNR grant. Presented at the NeuropsychologicalSymposium, Roc Amadour, France, June 1976.Address for reprint requests: Professor L. A. Vignolo, Clinica Neuro-logica, Padiglione Ponti, Via F. Sforza 35, Milan 20122, Italy.Accepted 5 January 1978

Materials and methods

We have analysed the records of 500 consecutivepatients with left hemisphere damage, referredto our Aphasia Unit from 1962 to 1975 for langu-age evaluation, and examined by means of astandard language battery. Only patients with sixor more years of schooling were considered, sinceat lower educational levels writing may be verypoor even in normal adults and, as a consequence,its disorders cannot be reliably assessed. Patientswith left handedness, bilateral lesions, or incom-plete records were excluded from the study.

This group of 500 patients constituted a fairlyrepresentative sample of left brain-damagedpatients with educational level above elementaryschool, as it included both inpatients and out-patients suffering from lesions of different aetiolo-gies (mainly vascular), examined at different timeintervals from the onset of the cerebral symptoms.The standard aphasia examination included 16

subtests, which afforded a quantitative score forthe main aspects of language behaviour, as well asan accurate recording of the type of errors inspeech and writing (see Tables 1 and 2). The re-sults of the nonverbal scale of the WAIS wereavailable for all patients, as well as those of testsfor the apraxias (oral: imitation of buccofacialgestures; ideomotor: imitation of intransitiveupper limb gestures; constructional: copying geo-metrical drawings; and apraxia of use: showingthe use of actual objects). Acalculia, finger

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agnosia, and right-left discrimination were notassessed systematically.The dissociation between oral and written ex-

pression was defined on the basis of the scoresobtained on the following four subtests: (a) oraldescription of an event; (b) oral naming of 20 pic-tures of objects; (c) writing a letter to a relativeor friend; (d) written naming of 20 pictures, thesame as used for oral naming.

In tests a and c communication was scored 0(none), 1 (poor), 2 (sufficient), 3 (good). In tests band d communication was scored as percentage ofcorrect naming responses (ranging 0 to 100 points).

Oral expression was judged to be selectivelyimpaired (in comparison to written expression)whenever the oral description score was 0, whilethe writing a letter score was 2 or more, the oralnaming score was less than 35 and was exceededby the written naming score by 35 points or more.These criteria were of course reversed for de-

fining a selective impairment of written expression.

Results

A clear dissociation between oral and written ex-pression, as defined in this study, was found in 14of 500 patients. Speech was selectively impairedin seven patients and writing in seven. In theformer group, three patients showed the classicalsyndrome of "pure anarthria," two had a severeanarthria in the context of Broca's aphasia, andtwo were fluent aphasics with remarkably goodwriting. Within the latter group, the writing defectwas quite isolated from other language disordersin two patients (thus realising the picture of so-called "pure agraphia)," while it was associatedwith slight, but definite reading disorders in twoother patients (labelled "agraphia with mildalexia"), and with slight oral language disordersof the nonfluent type in three patients (labelled"agraphia with mild fluent aphasia"). The maincharacteristics of patients in each group, shownin Table 1 and 2, will be described.

PATIENTS WITH SELECTIVE IMPAIRMENT OF ORALEXPRESSION (TABLE 1)The three patients with pure anarthria showed acommon feature, consisting of a combination ofphonemic distortions and articulation defects,which disrupted speech output, no matter howelicited. In addition to oral description and namingwhich were poor by definition, repetition andreading aloud were also severely impaired. Bycontrast, all other aspects of language investigatedby the standard aphasia battery were preserved.In particular, writing to command, to dictation,

and to copy were normal or minimally defective.Writing a letter was perfect in patients 01 and03, while it showed only two errors in patient 02.Contrary to the observation of Alajouanine et al.(1939), writing in our cases was never agrammatic.Transcription from print to script was easy andflawless. Auditory verbal comprehension was ex-cellent, even when examined by such an exactingtool as the Token Test (patients 01 and 03 scored37 out of 39, and patient 02, 31 out of 39). Noneof these patients were clinically demented and,indeed, the IQs obtained on the WAIS nonverbalsubtests ranged higher than expected of patientsof comparable educational level, suffering from aleft hemisphere lesion and aphasia.

Differential features were also observed. In onepatient (01) the disorder was confined strictly tooral expression from the very onset of the illness-a cerebrovascular accident. Anarthria presentedas an abrupt, total suppression of speech; thislasted for about two days, then evolved to rareutterances and, finally, to a "syndrome of phoneticdisintegration" (Alajouanine et al., 1939) thatgradually disappeared within a few days. Themotor defect was limited to a mild right lowerfacial weakness. There was no oral apraxia. Thepatient was perfectly alert throughout and, fromthe very beginning, he tried to overcome his in-ability to communicate through speech by resort-ing spontaneously to paper and pencil. In our ex-perience, this behaviour is never found in Broca'saphasia.The other two patients (02 and 03) were ex-

amined long after the stroke; therefore, the possi-bility that pure anarthria here was the residualsymptom of an ordinary Broca's aphasia cannotbe ruled out. Both patients had severe oralapraxia. Speech in 02 showed a "syndrome ofphonetic disintegration" with paralytic dysarthria.Phonemes were omitted, substituted, or misplaced;articulation was slurred; oral outflow was scarce,but relatively rapid; the patient tended to talkrather fast and occasionally produced short runsresembling phonemic jargon. Self-pacing waspossible and resulted in a slower, more under-standable speech. This aspect of pure anarthriahas been observed before, for example, by Tissotet al. (1970), who have pointed out that theextreme slowing of the rate of speech, which istypical of Broca's aphasia, is not an obligatoryfeature of isolated anarthria.

In patient 03, phonemic distortions and slurredarticulation were overshadowed by a concomitantweakness of phonation: words were uttered in analmost imperceptible whisper, which often pre-vented the accurate recording of errors. Voluntary

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Table 1 Clinical and neuropsychological features of patients with poorer speech than writing

Pure anarthria Broca's aphasia Fluent aphasia

Patient number 01 02 03 04 05 06 07Age (yr) 67 69 52 35 34 69 24Years of schooling 13 17 17 6 7 8 13Lesion

aetiology V V V V V N (Abl) N (Abl)length of illness 3 d 7 mo 24 mo 7 d 14 mo 3 mo 13 mo

Neurological defectsMD + + + + -SD _VFD - _ _ _ _ - +

ApraxiasBFA - + + + + - -IMA - - - - - - -

AU - - - - - - -

CA - - - - - - -

WAIS QIP 99 111 106 63 99 117 97Oral expressionD 0 0 0 0 0 0 0N 20 35 0 10 30 20 35

Auditory comprehensionwords 100 95 100 100 100 100 100sentences 100 95 100 80 100 95 85

Repetitionwords 40 30 0 0 25 95 100sentences 40 40 0 0 30 50 20

Written expressionL 3 3 3 2 2 2 2words 90 100 95 50 90 65 85

Reading comprehensionwords 100 95 100 100 100 100 100sentences 100 100 100 50 100 100 100

Reading aloudwords 30 50 0 0 30 95 95sentences 15 40 0 0 33 100 100

Dictationwords 90 100 100 60 100 90 90sentences 100 100 65 65 70 35 30

Copyingwords 100 100 100 100 100 100 100Bl/sl 100 100 100 100 100 100 100

The language examination scores are expressed in percentages of correct responses, except D (Oral Description) and L (Writing a Letter) scoreswhich range from 0 to 3; V=vascular; N =neoplastic; Abl =ablation. d=days; mo =months; MD =right motor defect; SD =right sensorydefect; VFD =right homonymous visual field defect; BFA=buccofacial (oral) apraxia; IMA=ideomotor apraxia; AU =apraxia of use; CA=constructional apraxia; + =present; -=absent; ? =not tested; * =right lower face only; N =naming; BI/sl =transcription from block lettersto small handwritten letters.

efforts to increase the volume of voice weregenerally ineffective. Examination of the vocalcords failed to show evidence of peripheral in-volvement. This difficulty of phonation isreminiscent of that recorded by Alajouanine et al.(1939) in their case Louise Cha.

Broca's aphasia with severe anarthria andrelatively good writingBoth patients in this category (04 and 05) differedfrom the preceding ones because writing, whilemuch better than speech, was not intact. Thespeech disorder consisted of a typical "syndromeof phonetic disintegration" with reduction of thespeech outflow, syllabic scansions, and laboriousarticulation. In addition to oral description andnaming, repetition'aand reading aloud were severelyi*apaired (score 0). Oral apraxia and right hemi-paresis were present in both cases. The disorder

was recent in one patient (seven days) and long-standing in the other (14 months). The lesion wasvascular in nature; its precise intrahemisphericsite could not be ascertained.

Fluent aphasia with remarkably good writingPatients 06 and 07, who showed this condition,were an unexpected and most interesting finding.Speech in these patients, while perfectly fluentand without the least disorder of articulation, wasseverely altered by anomias, paraphasias, and cir-cumlocutions. By contrast, writing, though notintact, was sufficiently good to fulfil the criteria ofdissociation. The sites of lesions in these patientswere quite comparable, as shown in the Figure:one of them (06) had undergone excision of asmall, well-circumscribed tumour in the middlethird of the second left temporal convolution,while in the other (07) the anterior half of the

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Dissociated disorders of speaking and writing in aphasia

Table 2 Clinical and neuropsychological features of patients with poorer writing than speech

Pure agraphia Agraphia with mild alexia Agraphia with mildfluent aphasia

Patient number WI W2 W3 W4 W5 W6 W7Age (yr) 44 56 83 65 61 66 72Years of schooling 17 6 8 9 13 1 1 8Lesion

aetiology V (Abl) N (AbI) V V V V Vlength of illness 3-i mo 28 d 2 mo 4 mo 5 d 16 d 20 d

Neurological defectsMD - - - - -+SD - - + ? - + -VFD + - + - - _ -

ApraxiasBFA - - - - - - -IMA - - - - ? - -AU - - + - ? - -CA - - - - ?- -

WAIS QIP 68 84 83 78 91 81 83Oral expressionD 2 2 2 2 2 2 2N 85 95 95 75 75 60 80

Auditory comprehensionwords 90 100 100 85 100 100 100sentences 85 100 60 90 90 90 75

Repetitionwords 100 95 100 100 100 85 85sentences 80 60 100 100 80 60 30

Written expressionL 0 0 0 0 0 0 0words 0 35 15 10 10 25 15

Reading comprehensionwords 95 100 100 65 100 100 100sentences 50 75 0 0 75 50 80

Reading aloudwords 100 100 90 45 65 80 0sentences 100 85 50 0 15 82 0

Dictationwords 10 60 0 10 30 0 0sentences 0 0 0 0 15 0 0

Copyingwords 65 65 22 0 66 55 45Bi/sl 72 95 60 0 100 50 16

Abbreviations and footnotes as for Table 1 except * = right lower limb only.

left temporal lobe had been ablated in order toremove an angioma with satellite haematoma.Both cases, then, had lesions bordering theposterior language area from below and in front,but sparing entirely the posterior and superiormarginal zones in the parietal lobe.

PATIENTS WITH SELECTIVE IMPAIRMENT OF WRITTENEXPRESSION (TABLE 2)In all seven patients, the defect in writing to com-mand was, by definition, severe. In addition, writ-ing of words and sentences to dictation was alsogrossly impaired. On the other hand, copyingwords and the transcription of isolated lettersfrom print to script were relatively preserved,except in patients W3 and W4 with mild alexia inaddition to agraphia. The quality of the writingdefect was evaluated by recording presence andseverity of linguistic, motor, and spatial errors, asdefined by Chedru and Geshwind (1972b). It wasfound that all seven patients, including those withpure agraphia, had predominantly linguistic errors.

Moderate motor errors, consisting of an awkwardand "trembling" handwriting (with occasionaladditions of a few loops and curves to letters) oc-curred in two patients, one with "pure agraphia"and the other with "agraphia plus alexia."Minimal spatial disorders, consisting merely of asomewhat irregular alignment of words, occurredin three patients, one in each subgroup. A moredetailed analysis of the linguistic errors in thevarious tasks was then undertaken.Writing to command Writing a letter was impos-sible in patient WI, who confined himself totracing two capital letters (J, A), seemingly unre-lated to each other, in the upper left corner of thesheet; his signature, however, was perfect. Theperformances of the other six patients showed acommon pattern. The general arrangement of theletter-that is, the opening "Dear . . .," followedby a two or three line message, the greetings andthe signature-was correct; the length of the letterwas reasonable, as the total number of words (ex-cluding the signature) ranged from 11 to 29

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560

Figure Site of lesions in fluent aphasia with goodwriting (cases 06 and 07), pure agraphia (WI and W2),and agraphia with mild alexia (W3).

(R= 19). The text consisted mainly of neologisms,among which one occasional comprehensible wordcould be recognised; perseveration of parts of neo-logisms sometimes occurred. In contrast with thetext, the signature was always flawless.On the naming task, one patient (Wl) wrote

isolated letters or perseverating short neologisms,four (W3, W4, W5, W7) wrote predominantlyneologisms plus a few misspelled but recognisablewords, and two (W2, W6) wrote exclusively mis-spelled words. Such misspellings were similar inquality to those encountered in writing to dictation(see below, Table 3). There were no substitutionsof entire words and whenever one occasionalword finding difficulty was recorded, it occurred inspeech earlier than in writing. Thus, errors inwriting to command were always phonemic ratherthan lexical. This seems to confirm the notionthat the link between oral and written language isestablished at the phonological level.Writing to dictation A detailed analysis of errorswas made for writing to dictation of single words.Results, shown in Table 3, indicate that graphemesubstitutions were the most frequent type of error,followed by omissions, while additions were rele-

A. Basso, A. Taborelli, and L. A. Vignolo

vant only in agraphia with mild aphasia; con-sonants and vowels were about equally affected,and graphemes in middle and initial position weremisspelled or omitted more frequently than thosein final position. A word of caution is necessaryin interpreting the figures given in this Table:even in the absence of motor disorders, the indi-vidual differences and the particular characteristicsof each patient's handwriting made it sometimesimpossible to decipher precisely a given letter inthe context of a word, so as to differentiate it fromsimilar ones (for example, a from o, t from 1, andso on). Thus, a certain degree of error wasinevitable.The locus of the lesion was known in the two

patients with pure agraphia and in one patientwith agraphia plus alexia (see Figure). Bothpatients with pure agraphia had parietal (para-sagittal) lesions. Patient WI had sustained a cere-brovascular accident and had undergone surgerywith emptying of intracerebral left parieto-occipital haematoma. In patient W2 a central(Rolandic) meningioma had been excised. PatientW3 with agraphia plus alexia sustained a cerebro-vascular accident; the isotope brain scanning indi-cated that the lesion was in the upper posteriorparietal-occipital area.

Discussion

The present study provides evidence that a clini-cally conspicuous dissociation between oral andwritten expression exists in a small number of leftbrain-damaged patients with language disorders(1.4% in our sample), either speech or writingbeing specifically impaired. Among such dis-sociated cases, three conditions are particularlyinteresting-anarthria, fluent aphasia with sparingof writing, and pure agraphia.

Table 3 Analysis of performances in writing 10 single words to dictation

Errors in misspelled words

Type oferrors Incorrect PositionType grapheme within word

Patient MisspelledSyndrome number Neologisms words 0 Ad S C V I M F

Pure agraphia WI 3 6 5 1 12 14 13 6 5 1W2 - 4 1 - 4 1 4 1 3 1

Agraphia with mild alexia W3 2 8 9 1 5 7 7 3 4 2W4 - 9 8 3 11 4 15 4 7 5

Agraphia with mild fluent aphasia W5 - 7 2 6 7 5 4 5 5 1W6 3 7 5 6 7 6 6 5 6 2W7 5 5 7 3 5 5 7 2 4 2

Total 37 20 51 42 56 26 34 14% 35 18 47 43 57 35 46 19

0 =omissions; Ad =additions; S =substitutions; C=consonant; V=vowel; I =initial; M=middle; F =final.

Dissociated disorders of speaking and writing in aphasia

PURE ANARTHRIA

The analysis of cases with selective impairment oforal expression confirms the generally acceptedview that, after a stroke, anarthria may occur in aremarkably isolated state with respect to otherlanguage defects. This condition is extremely rare

(three cases in 500), as maintained by Souques(1928). As Dejerine (1914) pointed out, pureanarthria may be found both immediately afterthe stroke (as in case 01) and long after it (as incases 02 and 03); in the latter event, it is possiblethat it is a residual symptom of Broca's aphasia.The continuity between pure anarthria and Broca'saphasia is also suggested by the existence of casesof Broca's aphasia with particularly severe anarth-ria, in contrast with relatively good writing (cases04 and 05).The core of pure anarthria, as seen in our

patients, consists of an unique combination oflinguistic errors (phonemic omissions, substitutions,methatheses, assimilations and so on) and articu-latory disorders (particularly depending on weak-ness of the articulatory muscles). The resultingspeech pattern corresponds, in a general way, tothe classic descriptions of this conditions (seeAlajouanine et al. (1939) and Lecours and Lher-mitte (1976) for a summary of the traditionalconcepts). The mechanism of this disorder is stillobscure. It certainly cannot be attributed to oralapraxia, which was absent in one case out ofthree. On the other hand, the associated presenceof rapidly uttered speech (case 02) and aphonia(case 03) stresses the need for further studiesfocusing on the possible subtypes of this syndromeand on its precise boundaries with purely dysar-thric or dysphonic disorders or both.

Little can be said about the intrahemisphericlocus of the lesion responsible for pure anarthriain our cases, except that the neurological andneuropsychological evidence pointed to central-anterior lesions-whether cortical, subcortical, or

both we do not know.

FLUENT APHASIA WITH RELATIVE SPARING OF

WRITING

Sparing of writing in fluent aphasia is a most un-usual phenomenon. Occasional descriptions ofsuch dissociation have been given by Head (1926)and Alajouanine and Lhermitte (1960). In hisreview of the literature on the agraphias up to1969, Leischner did mention this possibility, butdid not discuss its implications in terms of eithermechanism or localisation. To our knowledge, thefirst detailed report of this dissociation is the 1974paper by Lhermitte and Derouesne. They des-cribed two remarkable cases, one with a cerebro-

vascular accident in the left Sylvian region and theother with a closed head injury; both of them hadmainly phonemic paraphasias and neologisms inoral expression, while writing was distinctly betterthan speech. A similar discrepancy has been re-ported recently by Hier and Mohr (1977) in apatient who developed fluent, nonphonemic para-phasic speech with relative sparing of writtennaming, after an episode of necrotising temporallobe encephalitis.The nature of the lesion in Lhermitte and

Derouesne's cases did not permit a more preciseassessment of its intrahemispheric localisation,while in Hier and Mohr's patient a CT scan showedan extensive temporal lobe lesion and someatrophy in the region of the right Sylvian fissure.Our cases may contribute some information tothis point, at least in a negative way. In both ofthem the lesions involved the left temporal lobe,either at the anterior (case 06) or inferior (07)border of Wernicke's area, and they spared theposterior and superior marginal areas in theparietal lobe. Although caution is necessary ininterpreting the localisation of tumour lesions, wefeel that one can safely state that the brain damagein our cases entirely spared the posterior andsuperior marginal areas of the language zone inthe parietal lobe. The point we wish to stress isthe association of relative integrity of writing withintegrity of such parietal areas. We shall comeback to the possible meaning of this associationwhen discussing the localisation of lesions pro-ducing selective impairment of writing.

PURE AGRAPHIAPatients WI and W2 demonstrate that a focallesion of the left (dominant) hemisphere can pro-duce an isolated agraphia without other languagedisorders. The nature of this extremely rare defect(two cases in 500) is open to discussion. Unfor-tunately, the obvious limitations of a large retro-spective survey such as this (for example, lack ofsystematic information about writing with rightand left hand, typing, spelling aloud and so on)prevents us from discussing the disconnectionmechanisms hypothesised by Geschwind and co-workers (Heilman et al., 1973, 1974). Likewise, wecannot say whether or not other components ofthe Gerstmann syndrome were present to a signifi-cant degree. In spite of these drawbacks, a fewsimple points can be made.

In the first place, the absence of other aphasicdisorders must be stressed: the only detectableabnormalities of speech were occasional hesita-tions during oral description in patient WI andone single anomia throughout the entire examina-

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tion in W2. Writing errors, however, were essen-tially linguistic, in the form of neologisms and mis-spellings, while limb and finger apraxia (at least,on imitation) were consistently absent. Thesefindings, in our view, support the notion that pureagraphia does not depend upon impairment ofmovement or gesture, but is a selective disorder oflanguage output.

In the second place, the hypothesis, advancedby Chedru and Geschwind (1972a, b) is worth veri-fying. These authors maintain that often isolatedagraphia may not be attributable to focal lesions,but is, in many cases, rather the result of con-fusional states defined as "reduction and/orready shifting of attention." The following re-corded clinical aspects of our patients have beenconsidered to be indirect clues to a possible diffuseinvolvement of the left hemisphere, entailing anattention disorder. General clues: dementia (asexpressed by poor WAIS score), space-occupyinglesions with evidence of raised intracranial pres-sure, and writing examined shortly after the onsetof brain damage. Specific clues: omissions ofletters at the end of the word and perseverationsin writing to command. These were the mostcommon writing errors that Chedru and Gesch-wind found to be associated with mild confusion.The results were inconclusive. Case WI did showperseveration in writing to command and had aparticularly low nonverbal IQ, but his verbal IQwas as expected (93). Both Wl and W2 had space-occupying lesions; however, these had been re-moved 14 weeks (WI) and four weeks (W2) beforethe language examination, leaving no signs ofraised intracranial pressure. Moreover, the factthat letter substitutions were more frequent thanomissions, and that the middle or initial parts ofthe word were more often altered than the finalpart, points to a specific encoding disorder, ratherthan to an unspecific consequence of defectiveattention. Therefore, while diffuse brain disordermay perhaps have contributed to some aspects ofpure agraphia (such as perseverations in WI), itcertainly cannot be held responsible for the bulkof this disorder. On the contrary, the availableevidence suggests that, in our cases, the isolatedwriting defect was due to a particular localisationof the cerebral lesion-that is, to damage of thesuperior and posterior parietal areas of the lefthemisphere. These areas were damaged in thetwo patients with posterior lesions (WI and W2)whose writing was selectively impaired; conversely,they were intact in the two patients with posteriorlesions (06 and 07) whose writing was selectivelyspared. As the two "groups" were quite compar-able with respect to other clinical variables (see

Table 2 and 3), this double dissociation probablyreflects the different locus of lesion within the lefthemisphere. It is noteworthy that in the one otherpatient whose lesion could be localised (W3),severe agraphia with mild alexia was also associ-ated with a posterior parietal lesion.The notion that damage to the upper posterior

parietal lobe is crucial in producing a selectivedisorder of writing is supported by a number ofpublished findings (for example, Marie et al.,1917), and has been explicitly stated by Russelland Espir (1961). They reported the "surprising"finding of a small group of gunshot wounds caus-ing relatively pure agraphia through deep para-sagittal lesions of the left posterior parietal lobe,and they pointed out that "this area of the brainis very much concerned with those correlationsof body image and spatial orientation which maylead to apraxia and other remarkable parietal lobesyndromes." Indeed, the association betweenagraphia without other language defects andlesions of the upper posterior parietal lobe is oftenfound in the records of cases that have been pub-lished as outstanding examples of other neuro-psychological disorders, such as the patients withautotopagnosia described by De Renzi andFaglioni (1963) and De Renzi and Scotti (1970).At any rate, the hypothesis may be advanced thatthe posterior superior left parietal lobule in manis crucial for the sensorimotor linguistic integra-tion needed for writing. The question deservesfurther study.

We wish to thank Dr Norman Geschwind for hishelpful advice on the manuscript.

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