J. Neuirol. Neuirosurg. Psychiat., 1964, 27, 507

Cortical dysarthria and dysprosody of speechC. W. M. WHITTY

From1 the Departmlent of Neurology, United Oxford Hospitals

The natuLre and indeed the existence of a syndrome ofcortical dysarthria has been the subject of consider-able argument in the past 50 years: some of it acri-monious, and much of it dissolving into semanticdiscussion. The matter has been concisely reviewedby Critchley (1952) in considering articulatory defectsin aphasia. There is no doubt that whatever thedescriptive term used occasional cases occur in whicha known and limited cortical lesion produces achange in speech which is largely confined to articu-lation and presents as dysarthria with little or nodysphasic element.The case reported here showed just such a speech

defect, and in addition a change in 'accentation' andmelody (dysprosody) of speech, with alteration inthe use of gesture which gave the impression ofsomeone talking a foreign language. The cause ofthese symptoms appeared to be an intracerebralhaemorrhage from a small angioma in the territoryof the left middle cerebral artery. Angiography andoperative treatment of the clot allowed an unusuallyprecise localization of the lesion. The anatomicalinformation and unusual clinical features are thoughtto justify a detailed report.

CASE REPORT

A 27-year-old healthy married woman noticed the suddenonset of numbness in the right hand while out walkingabout 4 p.m. one afternoon. An hour or so later she alsonoticed that her right face seemed weak and she dribbledfrom that corner of her mouth. Others said that her speechwas slurred, though it was intelligible and she used correctwords. By 7 p.m., when she was admitted to hospital,she found herself unable to utter any words, even attemptsat phonation producing no sounds. The numbness of thehand had decreased but voluntary movement was im-paired. The facial weakness was also better and she nolonger dribbled.

Subsequent enquiry revealed a past history of migrainefrom the age of 12 to about 23 years. Attacks were usheredin with flashing lights and stars in either field of vision,followed by headache, normally bifrontal and throbbing.Occasionally it was lateralized and had then occurred onboth right and left sides. She also had frequent hay-feverand associated with this would get occasional transientheadaches alwavs localized to the left parietal region. Shehad had no other illness apart from the usual childhoodailments.

She was an only child. There was no family history of

migraine, but her father had had severe hay-fever. Hehad died at the age of 35 of peritonitis. Her mother wasalive and well. The patient had been married for six yearsand had no children. She had been educated entirely inEngland as had her parents and husband. She had learntelementary French at school and had worked as a secre-tary until her marriage. She spoke no foreign language.She was right-handed and there was no family history ofleft-handedness.On examination about four hours after the onset of her

symptoms she was alert and fully cooperative but veryfrightened. She would make no attempt to speak orphonate but indicated answers to questions by headmovements. There was no facial weakness but voluntarymovements were impaired on the right. She could notprotrude her tongue not elevate the palate to order.There was some reduction of sensory appreciation bothto light touch and pin-prick in the right arm. Althoughthere was no apparent weakness in this limb in sponta-neous movements, she was unable to carry out movementson request nor could she imitate them. When seen threehours later she could speak and used words correctly butspeech was slow, hesitant, and slurred. She could nowmove the palate and swallow to order, but lip and tonguemovements were incorrectly executed and she could notprotrude the tongue or make named sounds on request.Some 36 hours later she had no objective sensory

abnormality at all. Spontaneous movements of arms, face,and tongue were normal, but there was still slight dys-praxia to requested or imitated movements of lips andtongue. Her rate of spontaneous speech was also nownormal. However, she spoke with a foreign accent whichseveral independent witnesses regarded as German. Herspeech was also emphasized by gesture of the hands whichwas unusual for her. There was some dysarthric slurringof words, 'rs' being especially liable to mispronunciation,occasional misuse of syllables, and very occasional hesi-tation and apparent searching for the right word.Attempts at such standard phrases as 'West RegistrarStreet' and 'ancient and honourable institution' weredefinitely dysarthric. Nevertheless speech was free, ap-propriate, and completely intelligible. Its most strikingcharacteristic was its apparently foreign accentation, animpression which was strengthened by the dysarthria.In naming a series of objects she made mistakes in aboutone in ten. They were usually approximations to the cor-rect word, e.g., spring for string, bungle for buckle,watch-trap for watch-strap, etc., and mistakes wererealized and attempts at correction made. There was noevidence of any receptive dysphasia as shown by repliesto questions and the execution of simple and complexverbal commands. Reading aloud was correctly done and

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she repeated the sense of the passage accurately. Writingto dictation and copying of printed sentences showed oc-casional mistakes-omission of words or syllables. Thiswas much less so in spontaneous writing. Simple mentalarithmetic was unimpaired. In written calculations, addi-tion and subtraction, she made occasional mistakes,but these were considered dysgraphic rather than dys-calculic. Spontaneous drawings ofa clock-face and a houseand copying of designs were correctly done. In summary,she had a minimal motor dysphasia with slight tongue-lip dyspraxia; but more marked abnormalities were adysarthria and a most striking change in accentation andmelody of speech. This condition remained substantiallyunchanged until exploratory craniotomy 10 days later.

Investigations included normal findings in cerebro-spinal fluid, skull radiographs, full blood count and sede-mentation rate, and serology in blood and cerebrospinalfluid. An electroencephalogram showed a slow waveabnormality in the left fronto-temporal region. A left

FIG. 1. Left carotid angiogram (postero-anterior view).

FIG. 2. Left carotid angiograni (lateral view).

carotid angiogram demonstrated a small angiomatousmalformation arising from an anterior branch of themiddle cerebral artery in the pre-Rolandic area and justabove the Sylvian fissure. It appeared to be superficial,and local vessel displacement suggested an intracerebralclot (Figs. 1 and 2). These findings were confirmed atoperation, when Mr. J. M. Potter noted 'a little increasedvascularity in the immediate vicinity of the Rolandicfissure, 1 cm. above the Sylvian fissure.... The small areaof cortex bearing the vascular malformation was com-pletely excised. This measured approximately 1 cm. by1 cm. by 0 75 cm. Beneath was a clot cavity 8 cm. antero-posteriorly by 4 cm. by 4 cm. which was evacuated.'Her post-operative course was uneventful. She went homeeight days after the operation and at that time had nonominal dysphasia and no dyspraxia. She still spoke witha foreign intonation and slight dysarthria. Her use ofgesture was still considered excessive for her. Whenexamined one month later, seven weeks after the onset,her speech was normal in all respects. Her 'foreign'accent had disappeared. Writing spontaneously and todictation was also normal. She regarded herself as com-pletely normal as did her relatives.

DISCUSSION

The study of aphasia is a fertile field for theoreticaland interpretive argument, in which the contendersdo not always define their terms. The resulting con-fusion is nevertheless more apparent than real. Theevidence is still convincing for two broad types ofspeech defect associated with cortical lesions: one inwhich the trouble is predominantly motor or ex-pressive, the other where comprehension of wordsand their meaning is chiefly impaired. Each tends tobe associated also with a particular site of lesion:the first a limited area at the base of the Rolandicsulcus and the posterior end of the third and secondfrontal convolutions; the second involving a ratherless defined area of the temporo-parieto-occipitalcortex. There is little to contradict and much to con-firm the earlier views postulating Broca's andWernicke's types of dysphasia (Hdcaen and Ange-lergues, 1964). Further more detailed analysis cer-tainly reveals a number of varieties of both types, andinstances in which both expressive and receptive lossare combined. It is to be expected also that ifcompre-hension of words is faulty some aspects of motor ex-pression will be secondarily affected, just as it will beif that part of the body scheme concerned with lipsand tongue is diseased. When, however, full anatomi-cal information of the site of a lesion is available, andthis is unhappily infrequent, such mixed and varie-gated cases still support the broad division, and inthe last resort it is the evidence of relatively puretypes of dysphasia and their anatomical correlationwhich is crucial.A consideration of the cases of localized brain

wounds causing speech defects reported by Marie and

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Foix (1917) and Russell and Espir (1961) lendsample support to this basic classification, even thoughthe anatomical evidence in many of such cases is notas full as we would like. Within the group of mainlymotor defects there are a number of cases in whichthroughout their disability or at some stage of it, thespeech difficulty is best described as dysarthric.Marie and Foix used the term 'anarthric syndromes'for these: and in most severe examples there wasinitially a complete inability to utter words. Later,however, mispronunciation of words and the in-ability to master the French equivalent of our owntest phrases for dysarthria made 'dysarthric' themore appropriate adjective. Marie (1906) originallyinsisted on a pure anarthria whose anatomicalsubstrate lay in a 'lenticular zone' of frontal cortexand sub-cortex between the head of the caudate andthe posterior end of the lenticular nucleus. Thisspeech defect he considered had no necessary con-nexion with aphasia. The latter was for him always acomprehension difficulty and he regarded Broca's'aphemia' as a mixture of anarthria and aphasia.The distinction is one of definition. Despite hisprevious view, in his joint paper with Foix in 1917entitled 'Aphasias of war', anarthric syndromes areincluded. Henschen's (1922) violent objection toMarie's terminology seems to be largely semantic.If dysarthria is defined as due to a fault of bulbarinnervation, then dysarthria from a purely corticallesion must be a contradiction. But dysarthria isprimarily a description of a mode of speech. In thissense some of Marie's cases are excellent examplesof dysarthria. The same can be said of some of thecases recorded by Russell and Espir (1961) and Bay(1962): and in all three series the anatomical locationof lesions is strikingly consistent. All are groupedtowards the lower end of the Rolandic fissure, andmost are rather more anterior than posterior to it.The term 'cortical dysarthria' for these cases seemsdescriptively accurate and appropriate. When it isused, it is common to segregate it from dysphasiaproper (Bay, 1964). Such a usage implies, as it didfor Marie, that dysphasia must by definition entailsome lack of comprehension of the meaning ofwords. This is logical but obscurity may result if theterm 'motor dysphasia' is also retained. Henschen(1922) suggested that Marie's use of anarthria was asource of confusion and should be abandoned. Infact it might add more to clarity if the term motordysphasia were given up in favour of cortical dysar-thria or dyspraxic dysarthria. It is the retention ofthis anomalous use of dysphasia that is confusing.

In the segregation of these two forms of corticalspeech defect the recognition by the subject of mis-takes in words and their attempted correction shouldbe regarded as a crucial distinction. Anatomically

speaking, if the cortical motor apparatus of speech isat fault, wrong words as well as mispronouncedwords may be expected, but as long as their fault isrecognized no comprehension difficulty need bepostulated. Thus what appears at first glance to bean amnesic or receptive dysphasia may in fact be apurely motor one. It is the inability to recognize theerror that makes it a true defect of comprehension.

In earlier accounts of the motor types of dysphasiaan association with dyspraxia of the lips, tongue,and sometimes pharynx and larynx, has been noted.Nathan (1947) reviewed six such cases in great detailand used the term 'apraxic dysarthria' to describethem. He emphasized that 'praxia' was the corticalmotor function par excellence and suggested thatapraxia was in fact the basic lesion in many cases ofmotor dysphasia. Critchley (1960) also discussed thisaspect of aphasia, but concluded that articulatorydyspraxia was an independent entity, though it mightcoexist with dysphasia. The detailed protocols ofmany cases of motor aphasia contain records oflabio-lingual dyspraxia even when this is not specific-ally mentioned. In dyspraxia voluntary and mimeticmovement cannot be carried out, while similarmovements may be perfectly executed as part of aninvoluntary motor sequence. Dysarthria due todyspraxia might therefore be expected to show itselfmost readily in mimetic and requested speech: andthis is in fact its most usual setting, When flow ofspeech is established, the dysarthria becomes lessapparent and during the course of fluent speech it iswhen a word has to be voluntarily sought for thatmispronunciation again occurs.Another occasional association with motor aphasia

is a disordered melody, rhythm, and accentation ofspeech. Monrad-Krohn (1947) has termed this'dysprosody'. It was noted and recorded in dys-phasias before it was named. These cases may givethe impression of someone speaking a foreignlanguage. In Monrad-Krohn's much quoted examplea Norwegian lady born and bred, who had neverbeen out of her native land, was taken by her com-patriots to be a German, because of the dysprosodyfollowing a stroke. Critchley (1962) gave furtherexample of a similar change in English people, inwhom the accent resembled that of a native Welsh-speaking person. Bay (1964) emphasized its constantassociation with dysarthric defects and implied thatit was not uncommon in such a setting, though heappears at times to be describing something lesssubtle than a foreign accent. In its florid form itappears to be rare.The patient reported here had some initial lip and

tongue dyspraxia and for a short while a completeanarthria. As this recovered she had a dysarthria ofspeech which seemed to outlast any formally elicited

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dyspraxia of lips or tongue. She also had for a time adifficulty in using the correct word both in namingobjects and more occasionally in spontaneous speech.There was also evidence of slight dysgraphia, andthis also had been preceded by a more extensivedyspraxia of hand movements. It is noteworthy thatin each case she was at once aware of her mistakesand made some attempt to correct them. It seemsreasonable to formulate her motor disability ofspeech and writing as basically a dyspraxic lesion.The other striking change was the dysprosody that

gave her speech a German accent. This was so markedthat other patients in the ward regarded her as aforeigner. It was present when dysarthria was markedand the two tended to clear together, though theforeign accent was still obvious when dysarthria wasminimal. This phenomenon is doubtless capable offurther and more detailed phonetic analysis whichmay show it to be part of a spectrum of basicallyexecutive alterations in speech. For the present itmust be noted as an unusual and bizarre aspect ofmotor dysphasia. It stands a little aside from thedyspraxias since it is a constant phenomenon whileit lasts; and there is no equivalent here of a deficiencyof voluntary movement which can be performednormally in other contexts, as is seen in dyspraxia.The site of the lesion in the present case was well

established. The angioma from which bleedingoccurred was situated at the base of the Rolandicarea more anterior than posterior. Haemorrhageappears to have been largely intracerebral and initialcerebrospinal fluid showed no blood staining or risein protein. The clot cavity was subcortical andextended frontally for some 8 cm., thus underminingpart of the third and probably second frontal con-volutions. It certainly impinged on Marie's 'zonelenticulaire' and its position is similar to casesdescribed by Nathan (1947), by Bay (1962), and byRussell and Espir (1961). It was confined to thefrontal lobe and there was no evidence of any moreposterior extension, This is worth emphasizingbecause of the suggestion that dyspraxia may beassociated with lesions of the supramarginal gyrus(Pussep and Levin, 1923). The final cortical defectmust have been at least the area 1 cm. by 1 cm. by075 cm. excised at operation. However, since thiswas the seat of an angiomatous malformation beforeany speech symptoms occurred, and its function wastherefore in part defective, it cannot be regarded asnecessarily subserving motor speech in her case. Thespeech defect seems to have been produced by thesubcortical haemorrhage and consequent interrup-tion of function of overlying cortex. Recovery offunction was finally complete. Rate of recovery wasrapid and is more likely to have been by resumptionof function in temporarily disturbed cortex than by a

take-over of function by corresponding cortex of theopposing hemisphere. One can only say 'morelikely' until we know more of the time scales ofimprovement by local recovery and contralateraltake-over. On present evidence this case lends somesupport to Marie's view of cortical dysarthria,dependent on a lesion ofthe 'zone lenticulaire' and toNathan's view that such dysarthria is essentiallydyspraxic in nature. It illustrates once more the needfor segregating the motor speech abnormalities incortical lesions from those involving comprehension.Such a segregation should be maintained in theterminology of the subject and cortical dysarthriaor dyspraxic dysarthria would be suitable terms todescribe many such motor changes. The term motordysphasia is best avoided as its past usage renders itsmeaning equivocal.

It is of incidental interest to note that this womansuffered from migraine, but that its aura bore noanatomical relation to her one established vascularlesion. The presence of other lesions in the vertebro-basilar circulation is not excluded by her carotidangiogram.

SUMMARY

A case is reported of intracerebral haemorrhagefrom an angioma at the base ofthe fissure ofRolandocausing transient cortical dysarthria and dysprosody.The case is taken as evidence in support of the occur-rence of a cortical dysarthria, basically dyspraxic innature and due to a strictly localized frontal lesion.

My thanks are due to Mr. J. M. Potter for supplying mewith the operation findings.

REFERENCES

Bay, E. (1962). Aphasia and non-verbal disorders of language. Brain,85, 411-426.

-(1964). Principles of classification and their influence on ourconcepts of aphasia. In Ciba Foundation Symposium: Disordersof Language, edited by A. V. S. de Reuck and M. O'Connor,p. 122-142. Churchill, London.

Critchley, M.(1952). Articulatorydefects in aphasia.J.Laryng., 66, 1-17.- (1960). Jacksonian ideas and the future, with special reference

to aphasia. Brit. med. J., 2, 6-12.- (1962). Livre Jubilaire de Ludo van Bogaert, p. 182. Antwerp.Hecaen, H., and Angelergues, R. (1964). Localization of symptoms in

aphasia. In Ciba Foundation Symposium: Disorders ofLanguage,edited by A. V. S. de Reuck and M. O'Connor, p. 223-256.Churchill, London.

Henschen, S. E. (1922). Klinische und anatomnische Beitrage zurPathologie des Gehirns, Teil 7: Uber motorische Aphasie undAgraphie. Stockholm.

Marie, P. (1906). Revision de la question de l'aphasie. Sem. nmed.(Paris), 26, 565-571.

-, and Foix, C. (1917). Les aphasies de guerre. Rev. neuirol., 24 (i),53-87.

Monrad-Krohn, G. H. (1947). Dysprosody or altered 'melody oflanguage'. Brain, 70, 405415.

Nathan, P. W. (1947). Facial apraxia and apraxic dysarthria. Ibid.,70, 449478.

Pussep, L., and Levin, L. (1923). Zur Frage der Storungen desSchluckens von apraktischem Charakter (Aphagopraxie).Z. ges. Neurol. Psychiat., 87, 441450.

Russell, W. R., and Espir, M. L. E. (1961). Traumatic Aphasia.Oxford University Press, London.

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