486

OBSERVATIONS ONSPEECH DISORDERS IN CHILDREN

By C. WORSTER-DROUGHT, M.A., M.D., F.R.C.P.Consulting Physician to the West End Hospital for Neurology, and formerly in charge of the Department of SpeechDisorders; Consulting Physician-Neurologist, Metropolitan Hospital, London; Hon. Medical Director, Moor House

School for Children Suffering from Speech Disorders, Oxted, Snrrey

Speech is one of the two principal methods bymeans of which we communicate with our fellow-men, the second method being the use of writtenor printed symbols. To ' speak' is not merely toutter words, the faculty of ' speaking' beingessentially a mental process, involving the con-struction of propositions. Each country has itsown particular code or language which is learnedin childhood by its inhabitants, in the first instanceby sound. The, normal child, at first, does notrecognize words as such, but distinguishes theirimplication from the intonation, pitch and rhythmof the speaker's voice in the same way as the moreintelligent animals, such as the dog and horse.Later, the child learns to attach meaning toindividual words and, still later, by the laboriousprocess of education, a knowledge of the con-ventional symbols of written or printed words isacquired; thus spoken words can be permanentlyrecorded. Words, by association, eventuallystand for the objects or actions to which theyrefer. When the child reacts in the same way to aword as he would to the situation for which theword stands, he is said to know the 'meaning'of the word.By a 'speech disorder' we mean some defect

in the faculty of speaking. It is necessary to dis-tinguish between (i) the primary factor of speech,which is a function of the brain, and (2) articula-tion, which depends on the integrity of the nervousand muscular structures concerned with theutterance of words. These structures include thevarious nerve cells and fibres in the brain and inthe medulla or bulb, the peripheral nerves towhich the latter give rise, and the muscularstructures of the lips, tongue, soft palate, larynxand pharynx which these nerves supply. Adisturbance of the cortical or higher speech areas,or of their connections in the brain, results in thedisorder of speech known as ' aphasia'. Whenthe speech defect is due to imperfect articulation,the term 'dysarthria' is employed. Thus, werecognise two main classes of speech disorder:

(I) Aphasia and (2) Dysarthria.In patients suffering from aphasia, the higher

intellectual processes continue to function,although in some cases imperfectly, but thecortical areas which control either the perceptiveprocess of recognizing spoken language or themotor act of speaking are disordered orundeveloped, yet the patient has no paralysis ofthe muscles concerned with speech nor is he deafor blind. In other words, ' aphasia' involves adisorder in the comprehension and/or the for-mulation of words and sentences which probablydepends on a deficiency of memory for thosesymbols, whether spoken or written, by means ofwhich we exchange ideas with other individuals.An aphasic patient, unless his mental faculties areimpaired, can usually communicate quite well bymeans of gesture and pantomime.

For a perfect interchange of ideas two mainprocesses may be postulated: (i) Reception and(2) Execution or Expression. The receptive processincludes the hearing and comprehension of spokenlanguage; also the seeing and understanding ofwritten or printed words and figures. The memo-ries of words heard and seen appear to depend onthe integrity of certain specialized areas of theauditory and visual portions of the cerebral cortex,termed respectively the 'auditory word area'and the' visual word area '. The former is situatedin the superior temporal convolution of the brainand the visual word area in the region of theangular gyrus. Either of these areas may berelatively undeveloped, injured or diseased. Con-sequently, we can distinguish two varieties ofdisordered reception or 'receptive aphasia':(i) Auditory aphasia-the inability to understandspoken language although hearing itself is intact,also known as 'word-deafness', and (2) Visualaphasia-the inability to appreciate written orprinted language although sight is normal, alsotermed 'word blindness', alexia or dyslexia.The expressive or executive element in speech

consists of the motor act of self-expression in

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

October 1957 WORSTER-DROUGHT: Observations on Speech Disorders in Children 487

words, either vocally by talking or by means ofwriting. Every voluntary motor act learned byan individual is accompanied by a conscioussensation of activity, and by repetition such sen-sations become implanted, as it were, in thecerebral cortex as ' kinaesthetic memories '. Thesekinaesthetic memories of the motor acts of speechare co-ordinated by a special area situated at theposterior end of the third or inferior frontalconvolution of the brain and in the adjacent islandof Reil. If this area, known as Broca's area, isdestroyed or diseased, expressive, executive ormotor aphasia results owing to the loss of kinaes-thetic memories for the utterance of words. Simi-larly, if the development of this area is imperfect ordelayed, executive speech is only slowly orimperfectly acquired.The age at which normal children begin to talk

varies considerably. Some children are able to saytwo or three words at or shortly after the age oftwelve months. Many children as a result ofimitation will say a few words quite early in theirsecond year, and most normal children can produceshort sentences by the age of two years. Admit-tedly, there are some exceptions when otherwisenormal children are later in acquiring adequatespeech, even up to the end of their third year.Sometimes such a late development of speech is afamily characteristic. In general, however, if achild does not speak by the age of three years, somedefect in the mechanism of speech is usuallypresent. It is seldom that a really satisfactoryinvestigation can be carried out at such an earlyage and the mistake is often made of regarding thechild as mentally deficient when, in fact, the speechdefect is later shown to be due to an entirelydifferent cause. Usually, therefore, a full investi-gation has to be postponed until a later age. Inpractice, one finds that most speech defectivechildren are brought up for examination as theyapproach school age, that is between four and fiveyears. The first step then is to ascertain whetheran absence of intelligible speech or the presenceof faulty speech exhibited by a particular child isdue to dysarthria, that is, inability properly toarticulate, or to a lack of normal function of eitherthe brain as a whole or of one or more of thecortical speech areas. Accurate investigation asto the cause of a child's speech defect is essential,as on the establishment of an exact diagnosisdepends not only the prognosis regarding thechild's ability to acquire normal or approximatelynormal speech but also decisions as to the neces-sary type of treatment and appropriate form ofeducation.

For the complete investigation of speech-defective children at or approaching school age,a co-ordinated team of workers is essential. At

Moor House School for Children suffering fromSpeech Defects, the team consists of neurologist,psychiatrist, otologist, plastic surgeon, dentalsurgeon, educational psychologist and speechtherapists. In addition, one speech therapistis specially trained in audiometry, including theuse of the peep-show audiometer, and facilitiesexist for consultations with a neuro-surgeon,orthopaedic surgeon and paediatrician, as wellas for reference to radiological and electro-ence-phalographic departments. In many instances,however, it is necessary to admit the child to thein-patient diagnostic section of the School forabout a week; out-patient investigation is lesssatisfactory as affording little or no opportunity forobservation and, if the child lives at a distance,several visits to the clinic at short intervals areexhausting for the child and often impracticablefor the parents.Varieties of Speech Disorder in ChildrenWe find that the children approaching school

age referred for investigation fall into one orother of the following seven categories:

(I) Mental deficiency (amentia).(2) Various forms of congenital or acquired

deafness, usually not complete but partial. If achild hears only imperfectly, his reception ofspoken language is faulty and he cannot be expec-ted to attain normal speech without accuratediagnosis and appropriate treatment.

(3) Organic disorders of the central nervoussystem due either to developmental defects,trauma, or to the results of disease. These casesinclude birth injuries to the brain, perinatal anoxia,kernicterus, and inadequate or faulty developmentof certain parts of the brain or intracranial nervousstructures, that is, various forms of cerebral' agenesis ' (or more strictly' hypogenesis ' whichimplies under-development) and the effects ofbulbar poliomyelitis.

(4) Various forms of congenital, infantile, andjuvenile aphasia, both receptive and expressive orexecutive.

(5) Mechanical defects such as cleft palate,hare-lip, tongue-tie and dental defects.

(6) So-called 'functional' disorders of speechin which there exists no evidence of organic defector disease. Examples include stammering orstuttering, the dyslalias, various tics and faultyhabits of speech, and ' apraxias' of the peripheralorgans of speech.

(7) Psychoneurotic, maladjusted and pre-psychotic children.

I will now consider each of these categories inmore detail, especially from the standpoint ofdiagnosis.

(i) Mental deficiency. The reference to a depart-

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

488 POSTGRADUATE MEDICAL JOURNAL October 1957

ment for speech disorders of children in whomabsence or delay in the development of speech isdue to mental defect is very frequent, and in theinvestigation of a speech defect, this condition isusually the first that it is necessary to exclude. Thediagnosis is made by the application of suitableintelligence tests carried out by an educationalpsychologist, preferably one with experience indealing with children suffering from speech dis-orders. When the child is unable to speak or tounderstand instructions, the assessment has to bemade mainly on performance tests, such as non-verbal items from the Wechsler Intelligence Scalefor Children and with appropriate tests from theStanford-Binet and Collins-Drever scales, inconjunction with observations on the child'sgeneral behaviour.

(2) Variousforms of deafness. Speech deficiencyin children is frequently due to some form ofdeafness, usually congenital but sometimesacquired in infancy as the result of bilateral otitismedia or of meningococcal meningitis, which insome cases involves the auditory nerves, or morerarely, juvenile otosclerosis. If a congenitaldeafness is complete, the child remains dumb(deaf-mutism) unless taught to lip-read at anearly age.

In most children whose speech defect is due todeafness, as seen in a department of speechdisorders, the deafness is only partial. These casesare of two varieties, (a) Generalized reduction inauditory acuity, that is, the hearing defect involvesthe entire range of frequencies, and (b) High-frequency or high-tone deafness in which thechild is deaf only for the higher frequencies;consequently, he cannot hear such sounds ass ' and ' sh '. Low-frequency of' bass ' deafness

also occurs but is comparatively rare. The loss ofhearing in these forms of partial deafness is of theperceptive, inner-ear, or nerve type, and is almostinvariably congenital. It is difficult to locate theexact anatomical site of the lesion in these casesbut there is some evidence favouring a defect in theauditory area of the cerebral cortex, and in high-frequency deafness, a deficient 'representation'of the higher tones.1 Some observers, however,consider that the lesion lies in the cochlea.The diagnosis of hearing defects in children-

especially of partial deafness in young children-is often difficult to establish with certainty, andcareful observation and investigation, often over aconsiderable period, is necessary. A history ofrubella in the mother during the earlier months ofpregnancy is very significant, for this diseasefrequently gives rise to various developmentaldefects in the offspring. The final diagnosis restson accurate audiometry, repeated at intervals forconfirmation. With very young children, however,

the use of an ordinary pure-tone audiometer isusually impracticable. The ' peep-show' audio-meter, devised by Dr. Hallpike and his co-workers,is then most useful to obtain a binaural audiogram.At Moor House School we have found that withpatience and careful training in the application ofan ordinary pure-tone audiometer, it is usuallypossible to obtain reliable audiograms even inchildren of five years of age.When a diagnosis of one of the above types of

deafness is established, the case is referred to anappropriate school for the partially deaf for suit-able education and training, especially in lip-reading.

(3) Organic disorders of the nervous system. Thiscategory comprises a heterogeneous group ofcases which include the various forms of cerebralagenesis or hypogenesis, that is, incomplete orfaulty development, as well as destructive lesionscaused by head-injury at birth, perinatal anoxiaand by natal and post-natal disease. Among thevarious forms of cerebral agenesis, we have :

(a) Congenital cerebral diplegia, also known as'spastic diplegia' and ' Little's disease', inwhich the muscles, especially those of the lowerlimbs, are spastic and partially paralysed. A fewcases may result from birth injury but mostappear to be due to incomplete development ofthe motor cells of the Rolandic area and con-sequently of the pyramidal tracts. Owing to thedeficiency of nerve supply, the muscles of articu-lation may also be affected, the result of which isnot only delay in the appearance of executivespeech but even when some speech is acquired,the utterance is jerky, staccato and somewhatexplosive. Further, many cases show varyingdegrees of mental defect, which is then theprimary factor in the delayed appearance of speech.

(b) Congenital suprabulbar paresis (which hasalso been termed 'congenital pseudo-bulbarparalysis'). In this interesting condition theimpaired development is confined to the supra-bulbar neurones, that is, the tract of nerve-fibresproceeding from the motor cortex of the brain tothe cranial nerve nuclei of the medulla or bulb(cortico-bulbar tract) and which supplies themuscles of articulation. The result is varyingdegrees of spasticity and paralysis of the lips,tongue, soft palate, laryngeal and pharyngealmuscles, either separately or combined. Speech isdysarthric, being slurred and indistinct withdeficient lingual and labial sounds.The extent of the paresis or paralysis varies in

different cases. In what I have termed thecomplete syndrome,2 the child shows weakness orparalysis of the tongue, even protrusion beingabsent; paresis of the orbicularis oris muscle of thelips with consequent inability to' round ' the lips;

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

October X' 57 WORSTER-DROUGHT: Observations on Speech Disorders in Children 4

also, of the soft palate, together with impairmentof swallowing. The mildest manifestation ofcongenital suprabulbar paresis I believe to be anisolated paralysis or weakness of the soft palate,in association with an increased jaw-jerk. Thepalatal palsy causes speech to be nasal in character,known as ' rhinolalia'. Similarly, one may meetwith an almost isolated paresis of the orbicularisoris or of the tongue. Quite frequently the tongueis protruded fairly well but lateral and upwardmovement is entirely lacking. Those cases withinability to protrude the tongue are not infre-quently mistaken for examples of ' tied tongue',and we have met with several examples in whichthe frenum linguae has been unnecessarilydivided and with no beneficial result.

In severe cases, owing to the weakness of thelips and difficulty in swallowing, the accumulationof saliva is uncontrolled and dribbling is prac-tically continuous. This causes the child con-siderable anxiety and discomfort, rendering himself-conscious and impairing his social relation-ships. In the endeavour to relieve this dribbling,in several cases at Moor House School, we havecarried out a series of therapeutic experiments, thelater ones in conjunction with my colleaguesMr. F. T. Moore and Mr. D. Wynn-Williams ofthe Plastic Surgical Unit, Queen Victoria Hospital,East Grinstead. Various drugs of the solanaceousseries-belladonna and stramonium-which in-hibit the secretion of saliva, failed to produce asatisfactory result. Deep X-ray applications tothe parotid glands were tried in the hope ofreducing glandular activity, but the effect provedonly temporary. Next, the duct of each parotidgland (Stensen's duct) was ligatured and in someof the milder cases with satisfactory results. Inmore severe cases, however, dribbling persistedalthough in somewhat reduced degree. Theearlier of these latter cases seen were relieved byremoving one or both submaxillary glands, a pro-cedure which still allows adequate saliva for prac-tical purposes.

In order to improve the rhinolalia (nasal speech)in these cases of suprabulbar paresis, a palato-plasty (Dorrance retro-displacement or so-called'push back ' of the soft palate) or a pharyngoplasty(a palatoplasty combined with a Rosenthal typeof pharyngeal flap) has been carried out eitherby Mr. F. T. Moore or by Mr. D. Wynn-Williams,to assist oro-nasal closure. We found in thosecases in which these operations were performed asa' primary' measure, that is without any excisionof salivary glands, both oro-nasal closure andrhinolalia, as well as the power of swallowing,improved, thus increasing the control and dis-posal of saliva with abolition or reduction in thedribbling. Consequently, either a palatoplasty or

a palato-pharyngoplasty is now performedas- apreliminary measure in all cases of suprabulbarparesis with paralysis or extreme weakness of thepalate. If this operation fails to improve salivarycontrol, excision of one or of both submaxillaryglands is then carried out.

In children, the diagnosis of congenital supra-bulbar paresis has to be made from Parkinsonismresulting from an earlier 'attack of encephalitis.In these latter cases, however, in addition to ahistory suggesting encephalitis, the condition doesnot date from birth and there is usually somemuscular hypertonia of the limbs. Also, thespasticity or paresis is not confined to the lips,tongue and palate, but also affects the facialmuscles as a whole, with rigidity and poverty ofmovement. In addition, there is frequently someform of conduct disorder.

(c) Double hemiplegia. In this disorder there isspastic paralysis on both sides of the body includ-ing legs, arms, face and tongue. The muscles ofarticulation, therefore, are affected in the samemanner as in congenital suprabulbar paresis butwith the addition of spastic weakness or paralysisof all four limbs. In most cases there is a con-siderable degree of mental deficiency.

(d) Congenital hemiplegia is almost invariablyassociated with faulty or delayed development ofthe cortical speech areas resulting in failure ofspeech to appear at the usual age. The affectedcerebral hemisphere, that is, the hemisphere ofthe brain on the opposite side to the hemiplegia,is under-developed or atrophied, constituting a'hemicerebral agenesis'. This reduction in sizeof the affected hemisphere can be well demon-strated by air-encephalography. The exact causeof the hemicerebral deficiency is obscure. Injuryto the affected side of the brain at birth mayaccount for a few of the cases but not for themajority, as I have met with the condition incases of breech-presentation birth, when a head-injury is unusual, and even in children born byCaesarian section. The probable explanation isthat of a developmental defect-a hypogenesis-the affected hemisphere failing fully to develop.

If the left hemisphere is affected, the corticalcells subserving motor function as well as those ofthe potential speech areas fail to develop ade-quately; consequently the child has a right-sidedhemiparesis, is left-handed and the potentialspeech areas in the right cerebral hemispherebecome functional although their development isalmost invariably delayed. Nevertheless, evenwhen the hemiplegia is left-sided and the childof normal intelligence, the appearance of executivespeech is often retarded.

(e) Bilateral athetosis, also termed 'congenitalathetosis' and ' Vogts' syndrome'. Many of the

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

490 POSTGRADUATE MEDICAL JOURNAL October I957

children suffering from this condition are ofnormal intelligence but dysarthria is usuallysevere. In addition to the involuntary athetoidmovements of the limbs and often of the face andtongue, speech is jerky, explosive and indistinct.Many cases can be improved by speech therapy,their speech being rendered at least intelligible.

(f) Ataxias of articulation. In some disorders ofthe nervous system, articulation is indistinct notfrom paralysis but from ataxia or inco-ordinationof the muscles of articulation. In affections of thecerebellum in children, from injury, relativeagenesis of the cerebellum, so-called ' cerebellarencephalitis' and Friedreich's hereditary ataxia,the articulation is slow, laboured and monotonoustogether with a jerky irregularity. Phonation issometimes even more affected than articulationand the utterance may be curiously explosive withpronounced separation of the syllables. Occa-sionally, especially in Friedreich's ataxia, thepatient talks as if he has a foreign body in hismouth; this type of speech has been aptly termed'hot-potato ' speech.

In Sydenham's chorea, articulation may beincoordinate owing to sudden jerky movements ofthe respiratory muscles, tongue and face. Speech,therefore, is hesitant and jerky.

(g) Nuclear and infranuclear affections. Theselesions cause dysarthria and include disorders ofthe bulbar nuclei or of the structures below thislevel, that is, the peripheral nerves supplying themuscles of articulation and also the musclesthemselves.

Facial paralysis occurs in childhood from injuryto the facial nerve or from involvement of thenerve by meningitis at the base of the brain, orfrom spreading suppuration from acute otitismedia. Also, the nucleus of the facial nerve maybe affected in poliomyelitis. In a special form ofmyopathy-the facio-scapulo-humeral or Lan-douzy-Dejerine type-the muscles of the face areatrophied in addition to those of the upper portionof the arm and shoulder girdle. This affection isusually bilateral and the patient's lower lip mayprotrude in a characteristic manner which hasbeen termed' tapir-lip '. In severe facial paralysis,especially if bilateral, the articulation of labialconsonants is impaired.

Paralysis of the soft palate, especially fromdiphtheritic neuropathy and bulbar poliomyelitis,causes difficulty in articulation in the same manneras in congenital cleft-palate, as the naso-pharynxand consequently the nasal cavities cannot be shutoff from the mouth. As a result, the voice is nasal,known as ' rhinolalia ', and certain consonants arealtered (B becomes M, D becomes N, and Kbecomes Ng), rendering utterance as a wholevery indistinct.

The soft palate may also be paresed as a resultof congenital deficiency of its musculature, adiagnosis that can be confirmed only by biopsy.Paralysis of the palate in congenital suprabulbarparesis and double hemiplegia has already beenmentioned.

Affections of the hypoglossal nerve-the motornerve to the tongue-cause paralysis and wastingof the tongue and result from congenital defectsof the hypoglossal nucleus (nuclear agenesis),bulbar poliomyelitis and injury to the nerve. Ifbilateral, the patient will have difficulty in pro-nouncing linguals.

Lesions of the recurrent laryngeal nerve,usually unilateral, cause abductor paralysis ofone vocal cord and render the voice hoarse, andalso impair the pronunciation of vowels but do notinterfere with the articulation of consonants.

Bulbar poliomyelitis can involve any of thebulbar nuclei, that is of the ninth, tenth, eleventhand twelfth cranial nerves, and cause corre-sponding paralysis either of the tongue, lips, softpalate, larynx and pharynx, as well as of thetrapezius and sternomastoid muscles, either ascombined or isolated lesions.

(4) Various forms of aphasia. For practicalpurposes, cases of aphasia in children can bedivided into two main groups:-

(a) Executive or expressive aphasia, in which thechild is unable to express himself in spokenlanguage although understanding all that is saidto him. He is usually able to indicate his needsby gesture and mime.

(b) Receptive aphasia, in which spoken languageis not understood. It follows that in receptiveaphasia of congenital origin, the child, beingunable to understand what is said to him al-though he may be otherwise normal, cannotacquire normal speech.A rare form of congenital receptive aphasia is

that of so-called 'word or language deafness ',which is probably better termed 'congenitalauditory imperception'. Diagnosis is usuallydifficult but the condition is distinguishable fromdeafness or partial deafness by the obtaining of anormal audiogram, if and when audiometry ispossible. Owing to the disorganization of thespeech mechanism which inevitably results fromthis receptive aphasia, the child often develops amethod of vocal expression which is termed'idioglossia', that is, an individual languageconsisting of an extreme form of mispronouncedand ill-expressed conventional language. Whenthe patient has acquired some speech as a resultof treatment, he pronounces his words as he seesthem formed by the speaker's lips and as he hearsthem uttered but he remains unable to distinguishbetween many word-sounds and his speech is

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

October 1957 WORSTER-DROUGHT: Observations on Speech Disorders in Children 491

somewhat different from that of the normal child,being monotonous and often lacking the usualdivision into syllables.

In cases we have investigated, it was found thatalthough the outstanding defect was failure tounderstand the meaning of spoken words, therewas, in some examples, an additional inability toappreciate the significance of less specializedsounds such as to distinguish between differenttypes of bell or between different animal noises.In some cases, also, there was a mild but definitedegree of actual deafness although quite insuffi-cient to account for the failure to learn the under-standing of spoken language. It appeared, there-fore, that the designation 'word-deafness' is toolimited in scope to apply to this condition; alsodeafness as such plays no part in most of the casesand very little, if any, in other cases, spokenlanguage being heard but not understood. Con-sequently, I. M. Allen and I suggested the term'congenital auditory imperception' as probablydescribing more completely the fundamentaldefect.3 The pathological basis probably consistsin a bilateral agenesis or hypogenesis, that is,incomplete development, of the auditory word-areas in the cortex of the temporal lobes.

Inability to appreciate the significance of sym-bols such as letters and figures-so-called ' word-blindness ', also termed ' alexia' and' dyslexia '-is another form of receptive aphasia due to adevelopmental defect. As compared with thecorresponding condition in the auditory field-congenital auditory imperception-dyslexia isrelatively frequent. Again ' word-blindness' isan unsatisfactory designation in that there is noblindness; the child sees words perfectly but doesnot understand their meaning. In most cases, thechild readily learns to recognize and name singleletters and single figures and often words of twoletters, but is unable to appreciate the significanceof three or more letters and similar groups offigures. With regular and continued individualtuition, many cases gradually improve and even-tually acquire some reading ability.

In other examples of aphasia of developmentalorigin, the aphasia is purely executive or expressiveand although the child may be normal in all otherrespects understanding everything said to him,the appearance of adequate vocal speech is con-siderably delayed. Such a condition is besttermed ' developmental expressive aphasia'. Atits first appearance speech is confined to singlewords, usually reinforced by gesture, but pro-nunciation is almost invariably faulty, constitutinga developmental dysarthria. Provided intelligenceis at least average, these cases gradually improveand respond very well to speech therapy.The failure of speech development in some

cases' of congenital hemiplegia has already beenmentioned. This deficiency, also, is of the natureof an executive or expressive aphasia.Acquired expressive or executive aphasia is also

met with in children of school age as a result of alesion of the inferior left frontal convolution inright-handed children and vice-versa' in left-handed children. Such a lesion can follow headinjury, brain-abscess and cerebral tumour, andoccasionally encephalitis complicating one orother of the exanthemata. In cases of traumaticexecutive aphasia, the response to speech therapyis usually very good, but when the aphasia followscerebral abscess the results are not so satisfactoryand in addition to other factors, the child fre-quently suffers from epilepsy. Tumours involvingthe speech area that are amenable to total removalare very rare, but in the few examples met with-meningioma and oligodendroglioma-the resultsof speech therapy have been very good.

Total aphasia, that is a combination of bothreceptive and expressive aphasia, may followbilateral head injuries and some forms of ence-phalitis, especially measles encephalitis. In thesecases, the child loses both the understanding ofspoken language and the faculty of executivespeech. Treatment is usually a slow and laboriousprocess, but in several cases, the ultimate resultshave been well worth the trouble and timeexpended.

(5) Mechanical defects. These include suchconditions as congenital cleft-palate, with or with-out hare-lip ; a congenitally short soft palate; arelatively immobile tongue owing to a shortfrenum; and, in older children, various dentaldefects. The child with a cleft palate exhibits acharacteristic nasal speech known as ' rhinolalia'.Provided closure of the naso-pharynx by a mobilesoft palate has been secured by suitable surgicalmeasures, the response to speech therapy in mostcases is excellent.

Tongue-tie is relieved by incision of theshortened frenum. As I have previously said,several of our cases of congenital suprabulbarparesis, elsewhere and at an earlier age had beenmistaken for tongue-tied children owing to therelative immobility of the tongue and were sub-jected to an unnecessary operation.

(6) Functional disturbances. These comprisedisorders of speech with no recognizable organicor structural defect either in the nervous systemor of the peripheral organs of articulation, andinclude cases of stammering or stuttering and thevarious forms.of dyslalia.

Stammering and stuttering are terms usedsynonymously to denote a spasmodic type ofspeech disorder with which we are all veryfamiliar. Strictly speaking 'stammer' represents

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

492 POSTGRADUATE MEDICAL JOURNAL October 1957

the hesitant utterance and '-stutter' the elementof repetition in the defect but the distinction is ofno practical importance. In Great Britain, theterm 'stammering' is more widely used todescribe this type of speech disorder, while' stuttering' seems to be preferred in America.

Physiological stammering, sometimes termed'primary stuttering' consists in hesitation, repe-titions and prolongations in speech which oftenoccur during the normal development of languagebetween the ages of two and four years as purelytransient phenomena. Such disturbances ofspeech are unaccompanied by awareness oranxiety.

Pathological stammering or ' secondary stutter-ing' are terms applied to the more persistentstammer which usually appears between four andseven years of age, and in some cases occurs as aprolongation of a stage of physiological or primarystammer.There has for long been considerable contro-

versy concerning the causation of stammering andseveral theories have been propounded in theattempt to explain the phenomenon. The subjecthas been complicated by the fact that many obser-vers who have studied the condition have done soonly in adolescents and adults. By this time,possible causattve factors have become obscuredby many secondary manifestations, mainly psy-chological, such as self-consciousness, fear ofridicule, and feelings of inferiority. The observerof these effects has had the inevitable tendency tofind psychopathological explanations for theprimary speech defect, as well as for the secondarymanifestations.

In the majority of cases, the child starts to talkquite normally, but begins to stammer betweenthe ages of four and seven years. Stammer ismuch more common in boys than in girls-fully80 to go per cent. of the cases are boys. Left-handed tendencies have been present in 60 percent. of cases and can nearly always be traced inparents or near relatives. By the time the stammeris established, the boy is right-handed, at least forthe purpose of writing. When seen at the onsetof stammer, the children are usually quite normalin all other respects, and there are seldom anygrounds for describing them as more ' nervous',that is psychologically disturbed or maladjusted,than other children.Among the hypotheses that have been advanced

in explanation of the causation and mechanism ofstammering are:-

(a) The theory of 'handedness', that is, theattempt to convert an inherently left-handed childinto a right-handed one. Such outside interferencewith the development of a dominant cerebralhemisphere in integrating the mechanism neces-

sary for normal speech may lead to a stammer.From the age of two the child begins to establishhis handedness, and also his habits of speech. Inmost individuals the left cerebral hemispherebecomes dominant, and consequently the higherspeech areas are located on the left side of the brainin association with right-handedness. Some delayin the onset of speech and in the preferential useof either hand is not uncommon in the history ofchildren who begin to stammer at the early age ofthree years. A second critical period is when thechild is just beginning to learn to read and write,that is, to acquire graphic language, and is attempt-ing to correlate these two new unilateral cerebralfunctions with speech, which itself is still in asomewhat developmental stage. Thus, if aninherently left-handed child is thwarted in thedominant use of his left hand at the time hiseducation begins, he is liable to develop a stammer.The reverse also applies, that is, the attempt toconvert an innate right-handed child to thedominant use of the left hand. H. Gordon4describes an endeavour to train children in aspecial school to use the left hand, the result beinga wholesale development of stammer.

(b) The theory of deficient auditory imagery ofwords as the primary defect, that is, defectiveword-memory in the sense of an inability to retainmental pictures of words and sentences.

(c) The theory of asymmetry in function-alack of harmony between the three sets of musclesystems necessary for speech, viz., respiratory,vocal and articulatory, in association with emo-tional disturbances such as anxiety, apprehensionand embarrassment. These two factors-physicaland psychological-thus constitute a vicious circle.

(d) The theory that stammering is purely psy-chological in origin and dependent on emotionaldisturbance and maladjustment. The psycho-analytical view, based on the observations ofFreud, postulates that stammering results fromthe attempt to repress from consciousness, intothe unconscious, various painful memories anddisturbing thoughts in order that they may not bebetrayed by speech.

Although 'handedness' undoubtedly playssome part in the aetiology of stammering, it isprobable that the disorder has a multiple originwhich time and space do not allow of discussionin this communication. Also, it must be admittedthat the treatment of stammering is, as yet, by nomeans satisfactory.Many stammerers acquire various tricks, chiefly

as a result of their efforts to overcome or maskthe stammer. Thus, extra noises may be thrownin, for example, sudden inspiratory gruntings orwhooping noises, or the patient may make facialgrimaces and even contortions of his limbs.

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from

October 1957 WORSTER-DROUGHT: Observations on Speech Disorders in Children 493

Various articulative tics or' habit-spasms aremet with in nervous and psychopathic children,sometimes in conjunction with some degree ofstammer. The child's speech may be interruptedby a weird pharyngeal barking or grunting noises.Articulation may be monosyllabic, an extra breathbeing taken for each syllable. Again, speech maybe jumbled up in the most extraordinary manner,although the ' tiqueur' usually interpolates, nowand again, a clearly articulated sentence amongother unintelligible phrases.A purely hysterical stammer is uncommon in

children. When present, it is more frequent ingirls than in boys and usually appears at about thetime of puberty or later. Some cases of hystericalstammer result from mimesis, that is, attemptedimitation of a true stammerer; as a rule thechildren are somewhat maladjusted. Appropriatetreatment usually yields satisfactory results.Similarly 'hysterical mutism', so common as amanifestation of a war psychoneurosis, is rare inyoung children but it is occasionally met with inolder girls as a result of emotional disturbance andauto-suggestion.The condition known as 'lalling' is a normal

phase in the development of speech in childhood.The form of words is changed by substituting onesound for another, or by the omission and ellisionof some of the syllables. Also, there may be a lackof precision in the pronunciation of certain con-sonants, for example, the substitution of theuvular R for the ordinary laryngo-palatal R, orV for Th, W for R, so that' broken reed ' becomes' bwoken weed'. When lalling persists beyondthe usual age for adjustment, the condition istermed ' dyslalia'. Several varieties of dyslaliaare recognised, the most important of which areas follows :-' Simple dyslalia' consists in thedefective articulation of one consonant or one pairof consonants, e.g. 'edephant' or 'evephant'for elephant and 'ting' for king. When severalsounds are mispronounced, the term 'multiple

dyslalia ' is used, while 'general dyslalia ' impliesthe defective articulation of numerous soundsand the mutilation of many words, together withdeficiencies of vocabulary and syntax. ' Lisping',also termed' sigmatism', consists in the substitu-tion of Th for S.

In exceptional cases of general dyslalia, althoughmost of the vowels are pronounced correctly, theconsonants are so mutilated, mispronounced andsubstituted that the child appears to be speaking alanguage entirely of his own, constituting a formof' idioglossia'. Although unintelligible to thosenot acquainted with the child, his language isusually well understood by parents and otherscontinually in contact with him.With the gradual acquisition of speech in cases

of developmental expressive aphasia, such speechis frequently dyslalic until corrected by appro-priate therapy.

In some cases, a dysarthria is due to an apparent'apraxia ' of the lips, tongue or soft palate, eitherseparately or in combination, that is, faulty orinefficient use of these peripheral organs of speechin the absence of any physical signs of disorder oforganic origin. Usually, the condition graduallyimproves, especially with speech therapy.

(7) Psychoneurotic and pre-psychotic children. Inthese cases, there is considerable maladjustment toordinary surroundings and the speech defect isusually one of retarded and inadequate speechdevelopment due to purely psychological causes.Speech, when it appears, almost invariably assumesthe form of a severe dyslalia.

REFERENCES1. WOOLSEY, C. N., and WALZ, E. M. (1942), Bull. Johns Hopk.Hosp., 121, 135.2. WORSTER-DROUGHT, C. (I956), J. Laryng., 70, 453.3. WORSTER-DROUGHT, C., and ALLEN, I. M. (1929),J. Neurol. Psychopath., 9, 193 and (1930), o0, 193; alsoWORSTER DROUGHT, C. (I943), Med. Press, 210, 411.

4. HOBHOUSE, N. (quoted by) (1932), 'Nervous Disorders inInfancy and Childhood', London, p. 140.

RUTHIN CASTLE, NORTH WALESA Clinic for the diagnosis and treatment of Internal Diseases (except Mental or Infectious Diseases). The

Clinic is provided with a staff of doctors, technicians and nurses.The surroundings are beautiful. The climate is mild. There is central heating throughout. The annual

rainfall is 30.5 inches, that is less than the average for England.The Fees are inclusive and vary according to the room occupied., For particulars apply to THE SECRETARY, Ruthin Castle, North Wales.

Telegrams: Castle, Ruthin Telephone: Ruthin 66

copyright. on January 23, 2020 by guest. P

rotected byhttp://pm

j.bmj.com

/P

ostgrad Med J: first published as 10.1136/pgm

j.33.384.486 on 1 October 1957. D

ownloaded from