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INTRACRANIAL IRRITATION IN THE NEWBORN:IMMEDIATE AND LONG TERM PROGNOSIS

BY

W. S. CRAIGFrom the Department of Paediatrics and Child Health, University of Leeds

(RECEIVED FOR PUBLICATION DECEMBER 19, 1949)

Neonatal morbidity no less than neonatalmortality remains an outstanding paediatricproblem. Numerous investigations have studiedthe frequency with which stillbirths and neonataldeaths are due to intracranial trauma. Much lessthat is reliable is known concerning the subsequentprogress of infants who survive intracranial birthinjury. A number of published studies deal withthe clinical diagnosis of intracranial birth trauma,but only a small number deal with prognosis andan even more limited number with permanentsequelae. This paper summarizes clinical observa-tions made in the course of a follow-up survey of593 infants who were diagnosed as suffering fromintracranial irritation following birth and who weresubsequently kept under observation for periodsvarying from six months to five years or more.

The LiteratureDiagosis. Huenekens (1923) draws attention to

the way in which the study of diagnosis of cerebralhaemorrhage in the newborn has been neglected,and comments upon the frequency with which infatal cases doubtful diagnoses are entered on deathcertificates when in reality the cause of death hasbeen cerebral haemorrhage. He allows thatsymptoms arising from birth trauma are oftenelusive and recommends that indefinite symptomslacking explanation should always lead to suspicionof cerebral haemorrhage. Capon (1922) holds theview that symptoms of intracranial trauma arereadily recognizable except in the 'slightest case.'Fleming (1931) on the other hand is of the opinionthat diagnosis of intracranial haemorrhage in thenewborn during life is extremely difficult.

Basing his opinion on a retrospective study ofcases verified at necropsy as having suffered fromthe late effects of cerebral birth injury, Benda (1945)considers that cerebral damage can be recognizedin most cases immediately after birth, and in allcases within a few weeks, or at most, months afterbirth. The view is expressed by Ehrenfest (1922)

that although*small haemorrhages may not give riseto any symptoms, signs may develop which arestrongly suggestive of intracranial trauma but whichbecause of their indefinite character or rapid dis-appearance, may be attributable to 'concussion ofthe brain' or 'fleeting oedema' rather than tohaemorrhage. He considers that immediate prog-nosis is especially grave where convulsions recur atshort intervals, and that it is hopeless when aparalytic state follows a convulsive phase.There is a considerable measure of agreement in

the descriptions given of symptomatology. Munro(1928) lists as important a poor cry, hypertonicity,cyanosis, disinclination to nurse, a tense fontanelle,apathy, abnormal respirations, 'irritable c.n.s.', andnystagmus. Tyson and Crawford (1931) attachimportance to fretfulness and cyanosis aggravated bymanipulation. The intermittent nature of cyanoticattacks is stressed by Clein (1929). Particular impor-tance is attached by Capon (1922) to disinclination tosuck. Fleming (1931) considers that a bulgingfontanelle is an unusual finding. Sharpe andMaclaire (1924) found changes of the fontanellevariable and inconstant. Whereas Fleming (1931)considers muscular rigidity as having diagnosticvalue, Capon (1922) states that paralysis is not usuallya prominent feature. Sharpe and Maclaire (1924) areof the opinion that while some infants with intra-cranial birth trauma present severe symptoms, theclinical picture in others is slight and in some maybe normal.Many writers favour lumbar puncture as a routine

method of diagnosis. Capon (1922) urges that thereshould be no delay in carrying out the procedure insuspected cases. Fleming (1931) considers thatcerebrospinal fluid which is pigmented or uniformlystained with crenated red cells is probably the mostreliable finding in diagnosis. His view is shared bySharpe and Maclaire (1924) who found blood-stainedfluid in 130% of 100 babies who represented con-secutive deliveries and were lumbar-puncturedwithin 24 to 48 hours after birth. Tyson and

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Crawford (1931) and Munro (1928) attachimportance to evidences of increased intracranialpressure, but the former states that he, obtaineda blood-stained fluid in one of every fiveapparently normal newborn babies who werelumbar-punctured. On the other hand Benda(1945) declares categorically that a blood-stainedspinal fluid is encountered so often after birth thatno significance is to be attached to the finding if itis the only one in an otherwise normal child. Theopinion concurs with that of Smith (1934). As aresult of clinicopathological investigations Craig(1935 and 1938) concluded that success in securingearly, reliable diagnosis is dependent not on a studyof individual signs alone, but on tecognition ofsigns (or their absence) in conjunction with physio-gnomical observations and observations on thebehaviour pattern of the infant.Immediate Prognosis. In the opinion of Ehrenfest

(1922) the immediate effect of intracranial birthtrauma is dependent upon the.extent and locationof the resulting haemorrhage. According to Capon(1922) the immediate prognosis is favourable if theinfant survives the fifth day of life, but caution iscalled for where convulsions and twitching move-ments are present and where there is bulging of theanterior fontanelle. Fleming and Morton (1930)emphasize that the outlook in the case of a pre-mature infant is especially poor. Ford (1944)describes how in cases which recover early symptomsmay disappear either slowly or rapidly and how, incontrast, some infants remain in a precarious statefor a number of weeks. The same writer commentson the way in which apparent paralysis of one ormore extremities associated with rigidity, twitchingmovements, or flaccidity may disappear. In somecases disappearance is final and complete while inothers evidence of true paralysis may appear manymonths later. Munro (1930) is of the opinion thata ' hypertonic baby has more than an even chance 'while a ' cyanotic baby has less than an even chance 'to live. He considers that prognosis is worst wherecyanosis is associated with apathy and abnormalrespirations.

In the experience of Ford (1944) relapses are mostlikely to occur about the sixth or seventh day of life.Sustained improvement is most slow in the case ofpremature infants. Craig (1938) draws attention tothe occasional recurrence of haemorrhage from ahealing tentorial tear with fatal results in the secondweek following delivery. He considers that signsarising from intracerebral haemorrhage are liableto violent aggravation after the tenth day of life.

Ultimate Prognosis. Ford (.1944) refers to thelack of agreement concerning the nature of sequelaewhich may result from cerebral birth trauma in the

newborn, and Munro (1928) comments on the lackof evidence concerning the end results of thedifferent forms of treatment of infants who survive.Accepting that severe cerebral injury can give riseto delayed sequelae Ehrenfest (1922) expresses theview that it has not been established that similarresults may follow intracranial birth trauma oflimited degree. At the same time he points out thatdoubts on this last point are in some measure dueto the frequency with which the early signs ofcerebral birth injury are missed. Various attemptshave been made to correlate the effects of birthinjury with subsequent physical or mental dis-abilities. Some few writers have conductedfollow-up surveys of infants diagnosed as havingsurvived cerebral birth injury. Other writers haveadopted the reverse procedure and conductedretrospective studies of the birth histories ofchildren examined on account of various forms ofhandicap.Munro (1928) records a series of 117 infants

suffering at birth from cranial or intracranialdamage. Fifty-eight of the infants were dischargedfrom hospital 'relieved or improved.' Trace waslost of ten of these. Of the remaining 48, four wereestablished as dying from causes related to theircerebral condition, two developed hydrocephalus,and one epilepsy. One of the cases of hydro-cephalus suffered from fits. Twenty-four childrenwere normal in all respects at the age of 2- years.Munro concludes that residual phenomena canusually be recognized before the first birthday, andalways before the end of the second year, and thatthe most common late result of cerebral damage inthe newborn is hydrocephalus associated with eitherepilepsy or idiocy. Benda (1945) considers that latesequelae are invariably recognizable by the age of9 months.

In a series of 103 cases of cerebral birth injuryreported by Fleming and Mortor (1930) 53 survivedthe early weeks of life. Of the survivors, fivedeveloped mental or physical defects. One of thesefive patients was considered to be a true case ofcerebral diplegia. Fleming (1931) gives asymmetricalparalysis, hydrocephalus and mental deficiency asthe most common sequelae. According to Anderson(1945) cerebral palsies are the commonest finding.In Capon's (1922) opinion paralysis is not usuallynoticed until after the age of 6 months. Roberts(1939) considers that of children surviving cerebralhaemorrhage at birth 75% develop normally andthat only a relatively small number develop spasticpareses.Ford (1944) gives clinical details of 33 cases

showing evidence of disabilities which he considersto have resulted from cerebral birth trauma. His

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INTRACRANIAL IRRITATION IN NEWBORNS

findings have led him to conclude that hemiplegiais the commonest disability; that monoplegia iscommon, and that in general any impairmnt ofmental function is slight and not associated withmarked personality changes. Ford refers to theoccurrence in some cases of athetoid movements,of unilateral cerebellar ataxia, and of rapid growthof the head in the early weeks or months of life.In his experience convulsions are common, and mildpalsies sometimes lessen in degree. He describesfour cases of double hemiplegia. Striking obesitywas a feature of a few of his cases.Ford considers that ultimate prognosis is not good

where the presence of a residual disability has beenestablished. There is always the possibility that adisability may become more obvious with age.Epileptiform convulsions are given by Benda (1945)as one of the commonest results of birth injury inhis series of mentally deficient children. He con-siders that convulsions are of special value indiagnosis because of their relatively early time ofonset, and that neurological disorders of a motorand sensory type rank second in signii.Ford emphasizes that the appearance of convulsionsmay be delayed until 10 or more years after birth.Epilepsy, regardless of the age of appearance, maybe associated with mental deterioration and Fordis satisfied makes for a poor prognosis.

Within recent years increasng interest has beenfocused on the possibility of certain disabilitiesformerly attributed to birth injury being in factevidences of developmental errors. This aspect isdealt with by Ehrenfest (1922), Ford (1926 and 1944),Benda (1945), and McGovern and Yannet (1947).There is an increasing tendency to attribute cerebraldiplegia to errors of cerebral development. Com-paring cerebral palsies with palsies of differentaetiology McGovern and Yannet comment upon thehigh proportion of first born and the smalleraverage size of head among the former, and uponthe advanced maternal age and the increasedincidence of prematurity in the latter group.According to Ford (1926) the heads of the diplegiccases are usually either definitely microcephalic orslightly below normal size, whereas meningealhaemorrhage causes rapid enlargement of the head.

Different conclusions were arrived at by Benda(1945) as a result of post-mortem studies on 130mentally deficient children. His series included11 cases of children with spastic paraplegia. Ofthese cases, three conformed to the clinical picturedescribed by Little, and at necropsy the cerebrallesions were only detectable microscopically.

In the opinion of Fleming and Morton (1930)neonatal symptoms of intracranial irritation offerno clue as to the likelihood or otherwise of the

development of sequelae. Permanent and completerecovery can follow the most violent neonatalclinical course, and eventual disability may developin infants who show only slight evidence of stressfollowing birth. Fleming suggests that the occur-rence and character of sequelae are determined bythe site rather than by the extent of intracranialhaemorrhage. Ford (1944) arrived independentlyat similar conclusions concerning difficulties in theway of accurate long-term prognosis. He drawsattention to the scarcity of reliable publishedinformation on the subject. Rydberg (1932) foundthat of 41 children surviving cerebral birth injuryonly 10 developed normally. Ford does not acceptRydberg's finding as typical and estimates thatless than 15% of infants surviving cerebral birthinjury subsequently show evidence of disability.

The Present InvestwtnThe General Plan and Scope. The objects of the

investigation were twofold. The primary object wasclinical study of the subsequent development ofinfants diagnosed as having survived intracranialirritation at birth. As a secondary objective theinvestigation aimed at correlating sequelae (wherethey occurred) with symptoms recorded during theneonatal period, and at applying the findings of thatcorrelation to a study of prognosis in relation tointranial irritation in the newborn.DURATON. The clinical investigations forming

the basis of this paper were begun in March, 1931,and completed in October, 1948. During the period1938-41 no new cases were added to the series anddelay occurred in following up a proportion of thechildren included in the investigation before 1939.

SOURCES OF MATERIAL. Children included in theseries have been drawn from a variety of sourcesdetermined by the place and nature of the writer'swork at different times. In the total series of 593children, 405 were seen in Edinburgh, and theremainder in the Home Counties and Yorkshire.The series includes 529 childern born in maternityhospitals or maternity homes, and 64 born at home.Of those born at home, 37 were removed to hospitalshortly after delivery. A proportion of the babiesstudied in the Home Counties were born in wartimeemgnc maternity homes intended for normaldeliveries only.CLUICAL APPRAISAL. This was concerned with

diagnosis during the neonatal period of intracranialirritation and intracranial birth injury, and withrecognition at the time of follow-up examination ofdepartures from normal physical and mentaldevelopment.Apart from a few exceptions children included in

the series were examined by me personally within

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two days of birth. The great majority were first seenwithin 24 hours of birth and thereafter at shortintervals throughout the neonatal period. Particularattention was paid to advising midwives and housesurgeons on the clinical signs to be looked for inthe early recognition of intracranial irritation. Asa result, I was enabled to see many more infants atan earlier stage after delivery than would otherwisehave been possible. The suspicions of the residentstaff were not always confirmed. Cases included inthe present series consist only of those in which adiagnosis of clinical irritation was based on mypersonal observations.

It was originally intended that children includedin the series should be re-examined at the age of6 months and subsequently at ages approximatingto their first, third, and fifth birthdays. This provedimpracticable and it became necessary to re-examinechildren as and when other circumstances permittedrather than according to preconceived age intervals.Large numbers of children were seen at follow-upclinics associated with maternity hospitals. Manyothers were visited in their own homes. Some werere-examined by arrangement at infant welfareclinics. Follow-up examinations were directedtowards a clinical assessment of the child's physical,emotional and mental state. The opportunity ofre-examination was taken to review the history ofthe patient and his family with the object of ensuringthat no factor likely to cast doubt on an apparentassociation of abnormalities with the natal historyhad been missed. The writer carried out all follow-up examinations.

REcoRDS.-Clinical findings were recorded at thetime of all examinations during the neonatal periodand on all subsequent occasions. Negative andpositive observations were recorded. In every casedetailed information was obtained concerning thepregnancy, the labour, maternal health, and familyhistory.

Cliical Criteria

Intracranial Irritation after Birth Flagrantevidences of intracranial haemorrhage in themature newborn child of normal size are notdifficult to recognize. Nevertheless the clinicalpicture presented by the newborn infant withintracranial trauma can readily be masked by thepresence of other factors. Where asphyxia ofsevere degree exists, signs directly attributable tohaemorrhage are more difficult to recognize. Inthe premature infant intracranial damage of severedegree may give rise to surprisingly slight, evenfleeting clinical signs. Atelectasis is a frequent,if not almost constant accompaniment of intra-cranial trauma. The extent to which the clinical

features arising from intracranial damage aremodified by complicating atelectasis varies.Haemorrhage in certain forms and under certaincircumstances may be accompanied by oedemawhich may involve the meninges or the meningesand brain substance, and which may be more severein character than the haemorrhage itself.

Invaluable as clinical signs are in contributingto a diagnosis of intracranial birth trauma, finaldecision as to diagnosis requires to take account ofthe antenatal history of the mother and the detailedcharacter of the labour considered in relation to thematurity and size of the infant. Inevitably reliabilityin diagnosis is most difficult to achieve in thosecases in which recognizable clinical features areminimal either because they are of themselves slightor because they are masked by the operation of othervariable factors, whether related to mother or infant.It was realized at the outset of the investigation thatcases presenting minimal clinical signs were ofparticular importance, and that failure either torecognize them or correctly to interpret theirsignificnce might invalidate any general con-clusions. It was decided, therefore, to conduct aparallel investigation intended to correlate clinicalfindings during life with pathological findings afterdeath in newborn infants showing evidence ofintracranial haemorrhage at necropsy. The resultsof this other investigation have already beenpublished (Craig, 1935 and 1938) and provide thebasis for clinical diagnosis adopted in the inquirywhich is the subject of this paper. The two investi-gations are to be considered as complementary.As a further measure intended to favour greater

reliability in diagnosis the ante-natal and obstetricalhistories of all children provisionally listed forinclusion in this investigation were subjected to afinal review. In the few instances where retro-spective study of the history and records pointed tothe possibility of haemolytic disease of the newborn,to gross atelectasis persistent for reasons not whollyattributable to coincident intracranial irritation, orto haemorrhage no matter how slight from the skin,the mucous membrane or any of the orifices, the casewas excluded from the final series. A similar coursewas adopted in the case ofa small number of childrenborn of mothers whose pregnancies had beencharacterized by abnormal events or experiences,which, no matter how remotely, might have inter-fered with normal foetal development in utero.Account was taken of known exposure of themother to infection, maternal illness, and x-raytherapy during pregnancy, and of threatenedabortion or miscarriage. Any child showingevidence of a developmental anomaly was auto-matically excluded from the series. Nineteen

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children were eliminated for one or other of thesereasons. It is realized that an excessively rigidprocess of exclusion may have been adopted.Nevertheless it was felt that the main purpose ofthe investigation could only be achieved if primeimportance were attached to the elimination so faras practicable of possible sources of error.

Examination of a specimenof the cerebrospinal fluid hasnot been considered eithernecessary or desirable inarriving at a diagnosis. Aclear fluid does not exclude thepossibility of cerebral haemor-rhage any more than a blood-stained fluid is confirmation ofthe presence of cerebralhaemorrhage. Also it is myfirm conviction that lumbarpuncture is not in the interestsof the patient where the signspoint to intracranial irritation,provided always that there isno possibility of meningitis.

Late Sequelae of IntracranialIrriation at Birth An outlineof the follow-up procedureadopted has already beengiven. Any child who at thetime of re-examination showedevidence of impaired physicalor mental development or con-cerning whom a history ofepilepsy or of abnormal be-haviour was obtained, wassubmitted to a completephysical examination. At thesame time, fturher particularswere sought concerning the FK;. 1.-Infant agefamily history and thehealth of previous children, especially of anyfamilial tendency to epilepsy or psychopathic historyin connexion with any member of the family.Inquiries were also made concerning any hereditaryor familial conditions which might not have beenpreviously disclosed. In the case of those childrenin whom palsies were found, particular note wasmade as to whether the paralysis was symmetricalor asymmetrical in distribution; the degree ofspasticity associated with the paralysis; and theseverity of any mental impairmnt accompanyingthe physical handicap. Account was taken ofincidental errors of development not previouslynoted. Cases of microcephaly were excluded. Inthe final assessment especial importance wasattached to evaluation of essentially natal factors.

As in the case of criteria applied in diagnosisduring the neonatal period, a policy of rigid exclu-sion was adopted in the case of any child with whosehandicap there appeared to be a possibility of acontributory factor arising from a hereditary back-ground, a familial tendency, a developmental erroror disease in the interval between birth and

d five days with signs of severe intracranial irritation.

re-examination. Twelve children included in theoriginal survey were excluded from the final serieson these grounds.

Tbe C1hical Series and Clnical ObservationsIntraanial Irritation after Delivery. The present

series consists of 593 infants who showed evidenceof intracranial irritation at some time during thefirst ten days of life and all of whom lived for notless than six months and were first re-examinedabout that age. Of the 593 infants, 444 were first-born infants. Delivery was spontaneous in 261(including 55 breech presentations), instrumental in316, and by Caesarean section in 16 infants. The316 instrumental deliveries included 36 cases inwhich there was a breech presentation, and 102 cases

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in which either manual or instrumental rotation ofthe presting head had been carried out beforedelivery. There were 189 premature infants(Le., infants weighing 54 lb. or kss); 338 infantsborn at term; and 66 infants considered to bepost-mature.The cases included in the series are summarized

in Table 1.Cloical Pictue in the Early Days aad Weeks of

Life. Early in the course of the investigation,attpts were made to group cases according to theprobable nature and distribution of the underlyingpathological process. It soon became evident thatany such grouping might ultimately prove mislead-ing. As a prefeable basis for study of prognosisit was decided to consider cases in groups determinedby the severity or otherwise of the clinical picturepresent in the early days. Cases composing theseries under investigation have, therefore, beengrouped as follows:

(A) GRoss oR VIOLET CLiNCAL Swm. Casesin this group include infants showing evidence of

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DAY OF LI FEEXCESSIVE ALERTNESSFROWNING FACIESANXIOUS EXPRESSIONNECK RIGIDITYFULLNESS OF FONTANELLEVIOLENT EYE MOVEMENTSVOMITINGEXAGGERATED REFLEXESCONVULSIONSCYANOSISREADINESS FOR FLUIDS

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gross asphyxia followed by the development ofconvulsions; unquestionable neck rigidity or actualneck retraction; bulging of the fontanelle and ocularsigns; and intense physical and mental restlenessfollowing a phase of inactivity. Constant findingswere a strangely anxious expression and a whollyunnatural concentration of ga giving place attimes to a frowning or scowling expression. Thefrown if not present could often be easily elicitedby gently flexing the neck. The awareness, and attimes actual aletness, of these infants were more inkeeping with an age of several weeks rather than ofseveral days (Fig. 1). Vomiting over a period of afew days was a frequent finding. So also were signsof great exhaustion. In some cases fine tremors andathetoid movements were recognizable. In all casesthere was markedly exaggerated resonse to externalstimuli. A slight rise in temperature was common.Pulse and respirations showed variations of alltypes and of all degrs of severity. It is sometimesstated that a reluctance to take fluids is a featuof severe intracranial damage in the newborn.

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Fk;. 2.-Diagram of a case showing gross physical sign of intranial irritation.Prolonged labour; elderly motnr; foetal distress; asphyxia at birth. Spastic paralysis noted at 2 months and

confirmed at 3 years. Poor intelligence at 5 yers. (Appendix: Case No. 590.)

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INTRACRANIAL IRRITATION IN NEWBORNSWhile this is the case during such time as severe _asphyxia persists, the statement is not in accor-dance with my own experience, in so far as infants _who survive are concerned. These infants are often -incapable of indicating their need for fluids, but inthe hands of a nurse experienced in handling the _ill newborn infant, can, except during periods ofconvulsive movements, be given the fluid require- -ments by mouth and without difficulty. As is tobe expected, weight progress is interfered with, but Dnot to a serious extent (Fig. 2). _

Fifty-three infants in the total series showed Agross clinical evidence of intracranial irritation. AOf these eight were premature, 36 born at term, RIand nine post-mature. Delivery was spontaneousin nine, instrumental in 43, and by Caesarean Isection in one infant. Rotation of the head wascarried out before instrumental delivery in 22instances. a

(B) SEVERE CLiNICAL SIGNS. These infants(Fig. 3) resembled those in the previous group intheir exaggerated response to external stimuli, andin their alert rather anxious facies. On the otherhand they showed no evidence of neck retraction,and while in many instances there was a fullness,there was no taut distension of the fontanelle.There were instances of nystagmus and otherabnormal ocular movements but these had noneof the violent characteristics of the grossly severeclinical picture. Exaggeration of the tendon reflexeswas constant and many cases showed transient

FIG. 3.-Diagram of a case showing severe clinical signs ofintracranial irritation.

Instrumental rotation of head and instrumental extraction.Considerable bruising at birth. Right spastic hemiplegia

confirmed at 5 years. (Appendix: Case No. 181.)

-1G. 4.-Diagram of a case showing pronounced but notsevere clinical signs.

itaneous delivery: breech presentation. First attemptspeech at 3 years: gross mental disability at 5 years.

(Appendix: Case No. 191.)

witching of the face and extremities. Physicalieakness was not at first a feature. There was,owever, an element of physical lethargy whichontrasted with the alert facial expression. Theethargy gradually gave place to a noticeable rest--ssness. At no time did these infants show anyisinclination for fluids. Initially their colour was[ightly cyanosed, but rapidly improved althoughi some cases there was a tendency for mild attacks,f cyanosis to recur over a period of several days.lulse and respiration, but not the temperature,sometimes showed slight departures from normal.There was little interference with weight progress.

Infants in this group numbered 104 of whom27 were premature, 56 were born at term, and 21were post-mature. Thirty-two infants weredelivered spontaneously, 69 instrumentally, andthree by Caesarean section. Instrumental deliveryfollowed rotation of the head in 38 cases.

(C) PRONOUNCED CLINICAL SIGNS. Diagnosisin the case of these infants (Fig. 4) depended onappreciation of the baby's unnatural alertness,precocious expression, apparent concentration onhis surroundings, disinclination to sleep and slight'jumpiness' when approached-all considered inrelation to the history of birth. In no otherrespect did these infants give cause for concern.Their general physical condition was satisfyingand improved progressively. There were noabnormal movements of face, limbs, or eyes.Temperature, pulse, and respiration were normal.Usually all clinical signs disappeared in the courseof three to four days.Of the 238 infants in this group, 91 were

premature, 113 were born at term, and 34 werepost-mature. Seventy infants were delivered

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ARCHIVES OF DISEASE IN CHILDHOODspontaneously, 164 instrumentally, and four byCaesarean section. Rotation of the head wascarried out before instrumental delivery in 42 cases.

(D) 'MiNoR AND TRANSITORY CLINICAL SIGNS.These infants (Fig. 5) provided a striking clinicalcontrast to those already described. Their con-dition was invariably unsatisfactory at birth. In away difficult to describe, fragility dominated theclinical picture. In much the same way the generalcondition gave cause for more concern than thelocal trauma. There was a pronounced andpersistent disinclination to take fluids. A cry when

FIG. 5.-Diagram showing transitory or ' minorSpontaneous delivery: frail at birth. Spasticity of both adeficient development of left leg noted at age of 5 month!

No. 63.)

heard was characteristically weak and whining.Flickering nystagmoid movements of the eyes tookplace but at irregular intervals so that detection ofthem at the time of any one examination was tosome extent a matter of chance. The same waslargely true concerning twitching movements of theextremities and to a lesser extent twitching of theface. No assistance was to be gained from examina-tion of the fontanelle. The weight progress wascharacteristic. With remarkable consistence therewas a slow gradual decline for some 10 to 14 daysfollowed by a prolonged and anxious period duringwhich little if any of the loss was recovered.Subsequent improvement of the weight was signi-ficantly slow and could be measured only over longperiods. Of particular importance from the pointof view of diagnosis was the absence of any of thosecharacteristics of the facies which were so out-standing a feature in infants included in the otherclinical groups.The group includes 187 infants, of whom 63 were

born prematurely, 122 were born at term, and two

were post-mature. Delivery was spontaneous in141, instrumental in 40, and by Caesarean sectionin 6.

(E) DELAYED CLWICAL SIGNS OF CONSIDERABLESEVERrrY. This was a small but clearly definedgroup (Fig. 6). The clinical picture was so character-istic that sisters and house physicians having seenonly one case were quick to recognize the resem-blance to it on the occurrence of the second. All11 babies in this group were large, full term infantsand delivery of nine was spontaneous. A remarkablefeature of these nine deliveries was that they were

all associated either withvioienE pains resuiing in pre-cipitate delivery, or withlabours which had been pro-longed despite persistentlystrong pains. The remainingtwo of the total 11 cases weredelivered by Caesarean sectionafter unsuccessful trial oflabour.

Exhaustion rather thanshock dominated the pictureat birth. Excessive quiet andabnormal activity persisted.The eyes remained constantlyopen; the expression of theface was sullen and frowning;

clinical signs. the body temperature was low,Lrms and left leg and and the pulse and respirations. (Appendix: Case were slow. Without exception,

tendon reflexes were absentor difficult to elicit. There was

no neck rigidity, no bulging of the fontanelle,and no cry. Fluids, when offered, were takenlazily. The clinical picture remained static for aperiod varying from 10 to 13 days except thatcharacteristically the weight fell with pronouncedrapidity. At the end of that period the eyes showedevidence of becoming progressively sunken and aphase of slow decline set in. An even more dramaticchange followed. Abnormal inactivity gave way tointense and continuous restlessness. Previouslyunnaturally quiet, the infant began to cry in apiercing fashion. The sullen frowning facialexpression was transformed overnight into one ofunmistakable and intense fear. In the case of fourinfants this transformation was accompanied by adegree of frenzied activity which must be seen to beappreciated. Freed from the restraint of cot clothesthese infants almost flung themselves from side tosidein a way suggestive of agonizing pain and difficult tocredit as being possible in babies of such tender age.Therewereno convulsions. Intensive sedative therapywas effective in controlling these developments.

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FI1G. 6. Diagram showing delaved clinical signs of considerable severitySpontaneous deliven-: prolonged labour: foetal distress. Nystagmus, ataxia. and doubtful deafness at 2-3 years.

(Appendix: Case No. 689.)

Infants and Children Included in the Follow-upSurvey. All 593 infants included in Table 1 w-ereseen and examined about the age of 6 months. Ofthese 593 infants, 306 were followed up to an ageof not less than 5 vears, 55 to the age of 3 years,and 111 to the age of 1 year. Several factorscontributed to the failure to follow up for morethan three years 4000 of children included in theoriginal series. In the great majority of cases, lossof contact resulted from families changing theirplace of residence, a factor which was appreciablyaggravated during the war years. Thirty-six childrenare known to have died in the course of the surney.Reliable information was not obtained concerningthe causes of death.

Residual Phenomena in Children Included in theFollow-up Survey. The presence of physical ormental disability, separately or coincidentally wasconfirmed in the case of 52 children, and a reliablehistorv of conv-ulsions in the absence of evidenceof either physical or mental disability was obtainedin four cases. Clinical details concerning the 56children involved are summarized in the Appendix.Physical disability alone was present in 19 children.Physical and mental disability were both present in18 children. The mental condition was doubtfulin four other children with physical disability.

Mental disability was evident in nine childrenshowing no signs of physical handicap and wassuspected in one other child wvithout physicaldisability.

Hemiplegia w-as the commonest form of physicalhandicap, and as in other paralyses was severe insome cases and slight in others. Instances wereencountered of flaccid pareses which showed pro-gressive or retrogressive. but gradual. changes inseverity over limited periods of time. The seriesincludes two cases of spastic diplegia w\hich were notassociated with microcephaly and which wereconsidered to be the result of birth trauma and notevidence of errors in foetal development. Alldegrees of mental disability were encountered.Pronounced personality changes w-ere an associatedfeature in a small number of cases.The findings are summarized in Tables 2. 3. 4.

and 5. From Table 5 it will be seen that whilephysical disabilities were first recognized aftervarving intervals of time following birth the greatmajority were suspected in the first year of life, butthat instances occurred of physical handicap firste'idencing itself between the ages of 1 and 6 years.In contrast mental disability was not seriouslysuspected in any child under the age of 9 months.and in most cases was first suspected around the

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334 ARCHIVES OF DISEASE IN CHILDHOODTABLE 1

593 INFANTs wIrH INTRAcRANAL IRTATION FOLLOWING DELIVERY

Maturity

Premature Full-term Post-MatureNature of Delivery

Other than Other than Other thanFirst First First First First First

Pregnancy Pregnancy Pregnancy Pregnancy Pregnancy Pregnancy

SpontaneousVertex 89 18 66 18 10 5

Breech . . .. 23 7 14 7 4

InstrumentalVertex .. .. 31 13 89 26 17 2

Vertex preceded bymanual or instrumentalrotation ofthe head 63 24 13 2

Breech .. .. 5 3 7 11 9 1

Caesarean Section 6 7 2 1

189 338 66

TABLE 2

CHiDREN wrnm PHYSCAL DsAnxrmsn

Number of Cases with

Disability Associated Mental DisabilityNo Associated TotalMental Disability Doubtful Moderate Severe Number

A B C D E F

Hemiplegia 11 1 4 1 17

Monoplegia .. .. 4 1 3 8

Bilateral asymmerical paralysis .. 3 1 1 5

Spastic diplegiac* .. .. 1 1 2

Hydrocephalus .. .. 1 1 1 1 4

Ataxia and/or athetosis .. .. 2 3 5

Totals.. .. .. .. 19 4 12 6 41

Nitt case showed evidc of miiocpbaIy.



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INTRACRANIAL IRRITATION IN NEWBORNSTABLE 3

CHnDREN wrrH MEwrAL DsABrr

Number of Cases with

Associated Physical DisabilityNo

Associated BilateralDegree of Mental Physical Hemi- Mono- Asym- Spastic Hydro- Ataxia Total

Disability Disability plegia plegia metrical Diplegia cephalus and or NumberParalysis Athetosis of Cases

A B C D E F G H I

Severe emotionalinstability . (1) (1)

Mental DisabilityDoubtful .. I 1 1 1 1 5

Moderate .. 6 4 3 1 1 1 2 18

Severe.. .. 3 1 1 1 3 9

Totals .. .. 10 6 4 2 2 3 5 32

age of 3 years. Convulsions first occurred in themajority of cases involved at some time during thefirst six months of life, but in some few cases theirfirst appearance was delayed until about the secondor third birthday.

TABLE 4CHIDREN WrrH CONVULsiONS OCCuRRING AFER THE

AGE oF THREE WEEKS

No. ofConvulsions Cases

Not associated with physical or mental dis-ability wt p i d i ol .. 4

Associated with physical disability only 6Associated with mental disabilityonly 3

Associated with probable mental disabilityonly........I

Associated with physical and mental dis-ability .........4

Total .. . . . . 18

Limitations of the InvesigationL It is importantthat limitations attached to the investigation shouldreceive full recognition in any assessment of theresults. The following are among these limitations:

(i) The collection of new clinical material wassubject to interruption during the period 1938-1941,

thus temporarily interfering with the continuity ofthe investigation.

(ii) The clinical material included in the investiga-tion was drawn from a number of widely separatedgeographical areas in Scotland and England. Theresults, therefore, have no local, geographical, orregional sigificance.

(iii) Of cases included in the series under dis-cussion, over 92% were born in maternity hospitalsand maternity homes with the result that the findingsof the inquiry inevitably reflect the influence ofthe high incidence of first and abnormal preanciescharacteristic of institutional midwifery.

(iv) Maternity hospitals or hospital departmentsand maternity homes in which children included inthe investigation were born totalled 12. Obstetricalprocedures and nursing methods varied frominstitution to institution. General deductionsconcerning aetiological factors are as a result notjustifiable. On the other hand, the variations inobstetrical and nursing procedure in no wayinvalidate deductions which are based on a correla-tion of clinical findings with the obstetrical historyand relate to an individual infant.

(v) The follow-up survey does not include acontrol series of children with an uneventfulneonatal history.Sunmar it may be said that the investigation

under consideration consists of a clinical studybased upon material unavoidably obtained in a waywhich precludes any statistical analysis.Diansis The clinical observations on which a

diagnosis of intracranial irritation was based have

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TABE 5

APPROXMATE AGE OF FIRST RECOGNiTN OF REsiDUAL PHENOMENA OR LATE SEQUELAE

No. of Children

Age Disability Convulsions

Physical Mental Associated Alonewith Disability

A B C D E

Birth-i month .. 21

1,12-2/12 .. 1 3 2

2,,12-3/12 .. 2 1

3/12-4,12 .. 8 2

4/12-5/12 .. 2 1 1

5/12-6/12 .. 1

6/12-7/12 7 1

7/12-8,,/12 .. I. 1 1

8/12-9/12

9/12-10/12 .. .. 1 1

10/12-11/12 ..

11/12-l year .. 2

I year-2 years 5 3 1

2 years-3 years .. 4 3 1

3 years 4years .. 3 7 1

4 years-5 years

5 years-6 years .. 1 2

6 years-7 years

7 years-8 years

8 years-9 years 1

already been described. In an earlier publication(1938) the writer emphasized the importance of aphysiognomical diagnosis which takes account of theobstetrical history, of the maturity of the child, andof the condition of the fontanelle. Subsequentstudies (unpublished) concerned with the correlationof observations during life and post-mortem findingsin fatal cases have confirmed these conclusions.

Clinical signs were of all degrees of severity.They were present within 48 or 72 hours of birthin the great majority of cases. Very exceptionally

their appearance was delayed until the second weekof life. Violent signs were rarely met with inpremature infants, whose frail condition tended toexercise a 'damping' effect on outward evidencesof intracranial irritation. Moderately pronouncedevidences of intracranial irritation were not, how-ever, confined to premature infants, but occurredin babies of all degrees of maturity and size.

Tbe Undelying Patology. The term 'intra-cranial irritation' has been used throughout inpreference to cerebral haemorrhage as being more

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INTRACRANIAL IRRITATION IN NEWBORNSin keeping with the clinical purpose of this study,and because it embraces both cerebral and meningealoedema which so often figure largely in necropsyfindings on fatal cases.

It is possible to hazard a guess as to the patho-logical nature of the underlying intracranial con-dition in a proportion of those cases presentingsevere signs and symptoms. To attempt to do soin all cases would have introduced a problematicalelement contrary to the interests of the investigation.Allowing this, there is one group of six cases whichjustifies special attention.The group consists of the following cases in the

Appendix, nos. 119, 203, 311, 481, 689, and 698.These six children (of whom five were first childrenand one a second child), had in common that theysuffered from severe mental disability and showedevidence of an ataxic gait and/or intention tremorand/or athetosis. Three of the six children hadnystagmus. Delivery of five was spontaneous and ofone by high forceps. Presentation in one of thespontaneous deliveries was a breech. Foetal distreswas recorded in two instances. Labour was pro-longed in four cases, and there were violent pains ina fifth. All six children were large at birth rangingfrom 8 lb. to 12j lb., and showed signs of extremeexhaustion over a period of several days. In allsix cases there was delay in the appearance of signspointing to cerebral irritation, and after theirappearance these signs assumed a violent form.The day after birth on which signs of intracranialirritation appeared varied from the fifth to thethirteenth. In many respects the obstetricalhistories and the clinical course in the neonatalperiod of these children resemble those previouslydescribed in connexion with fatal cases showingsigns of gross intracerebral haemorrhage at necropsy(Craig, 1938). It appears possible, at least, thatsome if not all of the six cases in the present seriessurvived intracerebral birth haemorrhage, and thatthe haemorrhage, as judged by the clinical mani-festations, had involved the cerebellum and/ormid-brain.A further point of significnce is that of cases

included in the present series, not one presentedclinical features simulating those described inconnexion with intraventricular haemorrhage(Craig, 1938).

Prognosis. immediate prognosis is especially gravewhere in the hours immediately following deliverytheinfant remains in a state of complete collapse andersistently pale. Breathing is gasping, shallow, and

irregular. The pulse is almost imperceptible. Thestate of the fontanelle, the reactions to externalstimuli, and the temperature afford no informationof value. In the presence of such a clinical picture,

more especially when associated with periods ofdeep cyanosis, death is likely to occur within48 hours of birth.The occurrence of violent signs and symptoms of

necessity makes for increased gravity of theprognosis but is not incompatible with survival.A small number of the infants in the present seriespresented clinical pictures which were among thestormiest I had seen at any time. The severity ofclinical manifestations must be judged in con-junction with their frequency, persistence, andduration. Pronounced convulsive as distinct frommild twitching movements in a premature infantmore often than not presage death. Violentirritability, a bulging fontanelle, intense restlessnessand convulsions when they appear for the first timein the second week of life point to the recurrenceof haemorrhage or of an unusual pathology, andare to be considered of grave prognostic significnce.Vomiting which begins on the first day or two of lifeand persists in the absence of a primary alimentaryor urinary cause is of serious sigifince duringsuch time as it lasts. Head retraction of any degree,more especially if associated with recognizable neckrigidity is strongly suggestive of massive sub-tentorial bleeding with its attendant risks of pressuresymptoms. A full, as distinct from a taut fontanelleis, of itself, not of great signif in prognosis.Its significance is dependent upon the character andseverity of other detectable signs. Importanceattaches to an infant's readiness to take fluids. Inthe small infant with minor or transitory signs ofcerebral irritation readiness to take fluids isfrequently the first evidence of improvement.Among infants showing the grosser signs of intra-cranial irritation, it is characteristic of those whoeventually survive that they show a consistentreadiness to take fluids from the early hours of life.In contrast, disinclination for fluids is a frequentfinding in those newly born infants who ultimatelydie in the first week of life as a result of cerebralinjury.Even in those cases in which presenting signs are

moderate or only slight, it is a wise rule to postponegiving an unreservedly confident immediate prog-nosis until the end of the first week. Relapses areliable to occur on the third day, but more especiallyon the fifth or sixth day. On the other hand it is acommon experience, particularly where the patientis a full-term infant, to find improvement whichpreviously has been vague, assuming definite formon or around the seventh day of life.As a case of intermediate severity responds to

treatment, twitching and convulsive movementsdisappear; responses to external stimuli lose someof their violence; movements of the eyes become

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ARCHIVES OF DISEASE IN CHILDHOODless and less agitated in character; in succession thefrown disappears from the brow, the apprehensionfrom the expression, and the concentration fromthe gaze; and eventually the eyes from beingcontinuously open remain closed. Changes in thefontanelle tend to lag behind the disappearance ofother signs. Depending upon its condition shortlyafter the delivery, the fontanelle becomes less tenseand bulging so that it conveys an impression of' boggy fullness ' to the examining fingr. Eventu-ally, although it may not be until the third or fourthweek of life, the fontanelle conforms with the usualnormal findings.As improvement in the general condition becomes

more evident, various minor changes occur whichcollectively justify confidence in prognosis. Theinfant sleeps unbrokenly between feeds. His crywhen hungry assumes a normal character wherebefore it was either petulant or infrequent. Move-ments of the tongue which were restless and lackingapparent purpose become rhythmic. To hear theinfant 'smacking his lips ' as he fixes on the breastor teat with obvious satisfaction is a reliablyreassuring sign. So also is the way in which astheir condition improves these infants can be seenlazily stretching their limbs. The picture is one ofcontentment and replete satisfaction.

Pulse and temperature observations have aprognostic value in a limited number of cases only.An appreciably raised temperature is not oftenencountered.A detailed study of the obstetrical and clinical

histories of the 56 children who developed residualnhennnmna nr late seanlaeP affnrds nn cuie ac tnultimate prognosis. Disability of one kind oranother developed alike in premature, full-term,andpost-mature infants surviving signs ofneonatalintranial irritation, and the preponderance ofchildren with birth weights of between 54 and104 lb. (Table 5) was no more than was accountedfor by the preponderance of such children in thecomplete series (Table 1).

Physical debility, alone or in association withmental disability was recorded in infants born be-fore, at and after term. No instance wasencountered of mental disabiity withoutassociated physical handicap among infants bornprematurely. A feature of the obstetric historiesO1 11IIIAlL UQVIIJjJiJ WCA4MLUM Was LU4L WlUl` Fin 12 premature births there was only one *instanc of rapid delivery and one caseof foetal distress, in the births of 44 .infantseach weighing over 54 lb., foetal distress wasrecorded in seven, prolonged labour in 11, violentpains in two, and precipitate delivery in one. Therewas no evidence of asphyxia at birth in any of the

12 premature infants. Of the other 44 infants, ninewere recorded as being asphyxiated at birth(Table 6).

Correlation of the clinical picture during theneonatal period with the clinical findings noted inthe course of the follow-up survey does not suggestthat the severity of the early post-natal signs bearsany direct relation to the likelihood of residualphenomena developing, or to the nature of thephenomena in those cases in which they do develop(Table 7). Of the premature infants who ultimatelydeveloped physical or physical and mental disability,not one had presented violent or gross signs duringthe early days or weeks of life (Table 7 andAppendix). On the other hand, among infantsweighing more than 54 lb. at birth, there were manyinstances of violent neonatal clinical courses beingfollowed by uneventful physical and mental develop-ment, and a number of examples of severe disability(physical and/or mental) occurrng as sequelaedespite the fact that signs of intracranial irritationfollowing birth had been minimal (e.g., Appendix,Case Nos. 191, 396, 580, 611). The one exceptionto this generalization is that prognosis with regardto physical and mental development is especialypoor in cases of the type which suggests survivalfrom intracerebral haemorrhage. One baby in thislast group was noted as being markedly obese whenre-examined at the age of 5 years (Appendix: CaseNo. 481).Symptoms may be measured by their severity.

They may be measured also by their duration

wa. 7.-Diagram showing duration of neonatal symptoms.Limited to infants whose records were sufficiently

detailed for inclusion in this figure.

regardless of their severity. Fig. 7 shows theduration of neonatal symptoms of intrranialiritation in infants of the present series accordingas they did or did not subsequently develop residual

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TABU 6

ANALYSLS OF DATA OF 56 CHILDREN SHOWING RESIDUAL PHENOMENA OR LATE SEQUELAE IN RELATION TONATAL FACToRS

Number of Children

Late SequelaePlace in and/or ResidualFamily Labour Delivery Phenomena

Birth I Spontaneous Instrumental Asphyxia DisabilityWeight _ at(lb.) Caes. Birth

5+~~~~~~~~~- and IUnder .. 5 7t. I 1 10 7 3 23I~ ~ 0Sjand 711 0~~~~~~ ~~~C5 3 1 7 3 28

104 andOVer 28 12 7 102 116 2 12 8 1 1 6 15 715 3

Overl10 2 2 1 2 1 1 3 1 |1 2

' Manual or instrumetal rotatit One may have becn first child.

u After fa7ledforep2

TABLE 7

CORRELATnON OF NEONATAL CLINCAL PICTURE AND NATURE OF REsiDUAL PHENOMENA IN 56 CmIDREN

Number of Children

Neonatal Clinical Picture: Symptoms Sequelae and Clinical Phenomena

Birth [ DisabilityBirth ! ~~~~~~~~~~~~~~~~Convul-Weight Gross,- Pro- M~e Mild or Physical sions

(lb.) Violent nounced M Transitory Delayed Physical Mental and Mental onlyA B C D E F G H I J

54 andunder 3 9 8 3 110 andover 5j 10 8 15 3 4 15 7 15 3Over 1I 1 2 1 1 1 2

I , i l , 1 ! I~~~~~~~~~~~~~~~~~~~~~I.______________________________________________________

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phenomena. The number of children showingpermanent effects is too small to allow of firmconclusions. Nevertheless the figures in the diagramdo suggest, at least, that a persistence of neonatalsymptoms of intracranial irritation may be morecharacteristic of the histories ofchildren who developsequelae than those of children who survive intra-cranial irritation without subsequent disability.The possibility merits careful investigation in viewof its obvious bearing on treatment.A point of some importance in relation to

prognosis is the delay which may take place in thefirst appearance of residual phenomena (Table 5).Study of the 56 children in whom such phenomenadeveloped affords no clue as to which cases areliable to develop late sequelae, or as to which casesknown to have some form of disability are likely tobe further complicated by disability of another kindor by convulsions.

Treatment in the Neontal Period. The keystonesto treatment are prevention, anticipation, andsimplicity. Prevention is primarily an obstetricalresponsibility. Anticipation is the concern of bothobstetrician and paediatrician. Responsibility forinstituting simple therapeutic measures and forreducing disturbance to a minimum rests with thepaediatrician and the midwife or maternity nurse.From the paediatric point of view, anticipation

should begin with appreciation derived from a studyof the obstetrical history of the possibility, at least,of intracranial trauma, and with recognition at theearliest possible moment of signs at all suggestive ofintracranial irritation. Even a tentative diagnosiscalls for immediate transfer of the infant to a roomwhere he can be assured of complete quiet. For thenecessary degree of quiet there must be no bangingor constant opening and shutting of doors, and nounnecessary bustling to and fro of nursing staff.Visitors must be excluded. Draughts must beeliminated. The baby must be shielded from directlight whether natural or artificial. Body temperaturemust be maintained. The nurses in attendanceshould be selected for their experience in handlingthe ailing newly born child, and because of theirproved ability to feed and attend to the toilet ofinfants with the minimum of disturbance.Lumbar puncture is contraindicated even where

the diagnosis remains in doubt. The operation isnot a difficult one, but the extent to which the infantmay be disturbed is too dependent upon the skill inhandling by physician and nurse. Symptoms canreadily be aggravated by inexpert handling andwhile imuediate prognosis may not be materiallyaffected, too little is known of the effects on ultimateprognosis to warrant lumbar puncture beingundertaken other than in exceptional circumstances.

Nor has lumbar puncture a place in therapy. I haveseen several cases in which lumbar puncture hasprecipitated a change for the worse in the generalcondition, but have not encountered any case inwhich there has been completely convincing proofof clinical improvement following lumbar puncture.The position of the child is important. If there

is a tendency for secretion to collect in the airpassages the infant should be kept flat. Otherwisethe head of the cot should be raised, and the child'shead further elevated by propping him up slightlyon firm pillows. Oxygen should be administered toall severe and moderately severe cases, to all infantswho are premature, and to any case showingevidence of cyanosis whether transitory or per-sistent, and whether severe or slight. An oxygenchamber is always desirable. The value of a facemask is open to question and may contribute torestlessness, and the use of a nasal catheter isinadvisable on account of the risks of trauma to thenasal mucosa.

Medicinal therapy is of first importance. In myexperience, there is rarely, if ever, occasion for useof any preparation other than chloral hydrate. Theadvantages of the drug are that it can be employedin relatively large doses at short intervals, and thatits influence can be easily and rapidly adjusted tomeet changing requirements by alteration of thedosage or the interval between doses or both.Failure of chloral hydrate to prove effective is almostinvariably, if not always, due to inadequate dosage.In cases of extreme severity, one grain can be givenhalf-hourly until violent symptoms are controlled.Subsequent dosage should be determined in thelight of the persistence and severity of signs, of thedegree of somnolence if present, and of the infant'sreadiness or otherwise to take fluids. Chloralhydrate does not give rise to gastric irritation in thenewborn. It should never be withdrawn suddenly.Dosage should be reduced very gradually, reductionlagging behind successive evidences of improvementin the clinical condition. The drug should continueto be administered in half grain doses three or fourtimes daily for several days after the completedisappearance of all symptoms.An infant with signs, no matter how slight,

suggestive of intracranial irritation, should not belifted from his cot. Oesophageal feeding may benecessary in the case of small infants, but in generalbabies with intracranial irritation take fluidssatisfactorily from a spoon if feeding is in the handsof an experienced nurse. There is no call forrestriction of fluids or for any special modificationof feeds on account of the infant's intracranialcondition. It goes without saying that breast milkshould be given wherever possible. The decision

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as to when a child who has been under observationor treatment for intracranial irritation should beput to the breast must rest with the paediatricianwho should be present on the first occasion. Wheresymptoms of intracranial irritation have been slight,two days should be allowed to elapse between theirdisappearance and the beginning of feeding at thebreast. In severe cases a much longer interval mustbe insisted upon, account being taken of the child'sgeneral condition.

I have not been convinced of the claims made forrectal hypertonic salines. Injections of this sort areby no means always retained and they are liableto cause unwarranted disturbance of the patient.The same can be said of vitamin K preparationsadministered hypodermically. Clinical experiencehas not suggested that vitamin K given afterdelivery influences the course of intracranialhaemorrhage resulting from trauma, and the practicehas been adopted of limiting its use to prematureinfants, in whom there is a greater likelihood ofthere being an associated hypoprothrombinaemia.Penicillin should be given orally when there is anysuggestion of excessive secretion in the respiratorypassages, when there is reason to suspect thepresence of extensive ateectasis, or when there is ahistory of foetal distress.A further point which requires emphasis is the

frequency with which the prospects of an infant whohas been born at home and who shows signs ofintracranial irritation are prejudiced by precipitateand sometimes panic-like removal to hospital.Transfer under these circumstances should not belightly undertaken, no matter how unsatisfactorythe home conditions. Every effort should be madeto secure the services of a district nurse or maternitynurse if one is not already in attendance, andintensive sedative therapy should be given trial, itmay be over a period of two or three days beforethe infant is subjected to the risks entailed inremoval. Premature transfer and ill-consideredhandling in the course of transfer undoubtedlycontribute to avoidable deaths in infants withcerebral birth trauma.

Treatment is not complete which does not haveregard to the emotional distress undergone by theparents. Mere mention of intracranial injury orsuspected intracranial injury inevitably gives rise tounderstandable fears in the minds of the parents ofa newly born infant. Their cooperation and confi-dence can best be won by a simple, sympathetic butstrictly honest explanation of the probable courseof events.

Prognosis is more likely to be reliable if it attachesas much importance to the obstetrical history as tothe clinical symptoms presented by the child. The

fact that a delivery has been instrumental is of lessimportance than the related circumstances of thedelivery. A history of foetal dists or of severeasphyxia, whether the infant be premature ormature, is of greater signifi than the fact thatinstruments were applied. Rotation of the head,whether manually or instrumentally, before forcepsextraction tends to favour the occurrence of intra-cranial irritation. So also do prolonged labour,violent pains, and precipitate delivery-irrespectiveof the size of the infant.Asked as to the prospects of immediate survival a

guarded prognosis is called for until the end of thefirst week, but greater encouragement can be givenwith survival of each day after the fourth or fifth.Concerning ultimate prognosis, and subject to therenot being already presumptive evidence ofpermanentdisability, the clinician is entitled to emphasize therelative rarity with which sequelae occur in childrenwho survive the neonatal period. He is under anobligation to reassure the mother on the groundsthat severe symptoms at birth bear no constantrelation to the likelihood of subsequent disability.

Clinical observations made over a period of 17years in the course of a follow-up survey of 593children diagnosed as having survived symptoms ofintracranial irritation following birth are sum-marized. The investigation is a continuation ofearlier published clinicopathological studies ofintracranial haemorrhage in the newborn.The histories and clinical findings of all children

were carefully considered in relation to the possibleoperation of any familial, hereditary, or develop-mental factor. Children in connexion with whomany such factor was established or suspected wereexcluded from the series.

Children included in the series were examinedpersonally within two days of birth, on severaloccasions during the neonatal period, and subse-quently at varying intervals over a period rangingfrom one to five years.Of the 593 children included in the series, 472

were followed up to the age of 1 year, 361 to theage of 3 years, and 306 to an age of not less than5 years.

Neonatal symptoms of intracranial irritation aregrouped according as they were violent (53 cases),severe (104 cases), pronounced (238 cases),mild or transitory (187 cases), or delayed (11cases).The presence of physical or mental disability,

separately or in association was confirmed in the

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ARCHIVES OF DISEASE IN CHILDHOODcase of 52 children in the course of the follow-upsurvey. A reliable history of convulsions wasobtained in the cas of four other children withoutother handicap.

Physical disability was found alone in 19 children,and in association with severe mental disability insix, with moderate mental disability in 12, and withdoubtful mental disability in four children. Hemi-plegia was the most common physical handicap(Table 2).Mental disability without associated physical

handicap was present in nine children. Of these,mental handicap was of severe degree in three andof moderate degree in six (Table 3).

Physical handicap in the case of the 41 children inwhom it was present was detected under the ageof 6 months in 16, between the age of 6 months andI year in 12, and over the age of I year in 13. Ofthe 27 childrenin whom it was confirmed, mentaldisability was first suspected under the age of 12months in one, between the ages of 1 year and4 years in 13, and after the age of 5 years in two.Information on this point concerning 11 childrenin the group was unreliable.

Convulsions occurring after the first three weeksof life were a feature of 18 cases. They wereassociated with the presence of physical and/ormental disability in 14 cases. The time of theirfirst occurrence varied. In 13 infants epileptiformattacks began within the first seven months oflife; in four children between the ages of Iand 4 years; and in one child after the age of8 years.

It is emphasized that the investigation consists ofa clinical study based upon clinical materialunavoidably selected in such a way as to precludeany statistical analysis.The importance of physiognomical diagnosis and

of study of the behaviour pattem of the infant inarriving at a diagnosis of intacranial irritation inthe newborn is emphasized. The clinical pictureas it is found in the premature infant is contrastedwith that encountered in the child born at term orafter term. It is suggested that infants in whomsymptoms of severe cerebral irritation arise fromgross intracerebral haemorrhage present a character-istic clinical picture.

Immediate prognosis is discussed. It is con-sidered that severe asphyxia and/or early violentsigns while adding to the gravity of immediateprognosis are not incompatible with survival. Thepossibility of relapses occurring towards the end ofthe first week of life is stressed, and the especialdangers of violent signs delayed in their firstappearance until the second week of life areemphasized. Importance is attached to study of the

facies and behaviour pattern of the infant as ofgreater aid in determining prognosis than observa-tions concerning changes in the state of thefontanelle and the character of the cry. Specialvalue attaches to readiness to take fluids as justifyinga certain measure of sober optimism.

Ultimate prognosis is considered in relation tothe nature and severity of symptoms presenting inthe early days of life. Symptoms of intracranialirritation in the neonatal period are considered tooffer no reliable indication as to the likelihood ofpermanent sequelae developing, or as to the natureor time of development of residua should theysubsequently appear. Infants in whom severeintracerebral haemorrhage is suspected constitute apossible exception.

It is suggested that the fact that a delivery has beeninstrumental is of less importance than relatedcircumstances of the delivery, and that irrespectiveof the size or maturity of the child, and of theprecise method of delivery, significance attaches toa history of foetal distress, severe asphyxia, pro-longed labour, violent pains or precipitate deliverywhere a newborn infant shows any signs evenslightly suggestive of intracranial irritation.

Simplicity in treatment is urged. Expert nursingcare is essential. Handling should be reduced to aminimum. Absolute quiet and protection fromexternal stimuli are important. Body temperatureand adequate fluid intake must be maintained.Position is important. Lumbar puncture is contra-indicated. Chloral hydrate is the drug of choice,given early, in large doses and frequently.The view is held that the standards of nursing and

medical care and the methods of treatment employedcertainly have a direct bearing on immediateprognosis, and may have a bearing on ultimateprognosis by limiting the time during whichsymptoms of intracranial irritation persist.Importance is attached to responsibility for the

nursing care of newly-born infants with signs ofintracranial irritation being given to nurses withspecial experience and training in the nursing ofailing newly-born and premature infants.

Precipitate transfer to hospital of a newborninfant born at home and showing signs of intra-cranial irritation is condemned as contributing toavoidable deaths. Greater use of facilities fordomiciliary nursing care and careful selection oftime for transfer to hospital (if eventually necessary)are advocated.

It is the rare exception and not the rule for aninfant who survives signs of post-natal intracranialirritation and in whom there are no signs of residualdisability during the neonatal period, to developpermanent sequelae.

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INTRACRANIAL IRRITATION IN NEWBORNS 343This investigation has only been made possible by the

unstinted help received from colleagues in different partsof the country. To name a few would be to show lack ofappreciation of the many. I can only express my deepindebtedness to the obstetricians, family doctors, medicalofficers of health, maternity and child welfare medicalofficers, midwives, health visitors and distict nurses whoconstitute 'the many.'

RESERENcEsAnderson, N. A. (1945). In Mitchell-Nelson: 'Text-

book of Pediatrics,' ed. Nelson, W. E. 4th ed.Philadelphia.

Benda, C. E. (1945). Medicine, Baltimore, 24, 71.Capon, N. B. (1922). J. Obstet. Gynaec. Brit. Emp.,

29, 572.Clein, N. W. (1929). Amer. J. Dis. Child., 37, 750.Craig, W. S. (1935). Edinb. med. J., 42, 599.

(1938). Archives of Disease in Childhood, 13, 89.Ehrenfest, H. (1922). 'Birth Injuries of the Child.'

New York.

Fleming, G. B. (1931). Brit. med. J., 2, 481.and Morton, E. D. (1930). Archives of Diseasein Childhood, 5, 361.

Ford, F. R. (1926). Medicine, Bakimore, 5, 121.(1944). 'Diseases of the Nervous System inInfancy, Childhood and Adolescence.' llinois.

Huenekens, E. J. (1923). J. Amer. med. Ass., 81, 624.McGovern, J., and Yannet, H. (1947). Amer. I. Dis.

Child., 74, 121.Munro, D. (1928). Surg. Gynec. Obstet., 47, 622.

(1930). New Engl. J. Med., 203, 502.Roberts, M. H. (1939). J. Amer. med. Ass., 113, 280.Rydberg, E. (1932). Acta. path. microbiol. scand.

Suppl. 10.Sharpe, W., and Maclaire, A. S. (1924). Surg. Gynec.

Obstet., 38, 200.Smith, L. H. (1934). Amer. J. Obstet. Gynec., 28, 89.Tyson, R. M., and Crawford, W. H. (1931). Ibid.,

21, 694.



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344 ARCHIVES OF DISEASE IN CHILDHOOD

APPENDIXDETAiLS RELATING TO CHILDREN SHOWING REsiDUAL PHENOMENA OR LATE SEQUELAE

ApproximateAge(s) atwhich Ante-natal and Natal Evidences of

Series Examined History: OtherNumber (yrs.) Salient Features Physical Disability Disability of Mind Observations

A B C D E F

18 X:1:3:5 B.W. 94 lb. C.l. R. lower limb spastic Moderatementaldefect: Convulsions at age 3High forceps. Severe and appreciably smaller emotionally unstable. months and 2 years.asphyxia and bruising than L. leg (9 months).at birth. Convulsionsduring first 48 hours.

23 4:14:3 B.W. 64 lb. C.1. Spastic R. arm and Moderately severe dis- Emotionally extremelyProlonged labour. For- L. leg (6 months). ability (2 yrs.). restless.ceps delivery. Frail Mild hydrocephalus.condition. Twitchingof extremities.

24 4:1:34 B.W. 7 lb. C.2. Pronounced delay in Speech and behaviour Convulsions at age ofFoetal distress. Vertex sitting up and walk- babyish at 34 yrs. 6 months and 14presentation. Forceps ing. months. Head grewdelivery after manual abnormally rapidly dur-rotation. Severe con- ing first 4 weeks.vulsions.

42 4:1 B.W. 84 lb. C.2. Hydrocephalus sus- Doubtful. Clinical picture of ex-S.D. following pitres- pected at age 6 wks. treme irritation per-sin. Violent terminal and confirmed at age sisted for 2 weeks afterpains. Restless. Con- 3 months. birth. Condition criticalvulsion 2nd day. Full for 4 weeks.fontanelle.

63 4:14:3:5 B.W. 4 lb. C.1. Spasticity of both arms Doubtful. General physical con-S.D. Exhaustion and and L. leg (5 months): dition poor.frailty: nystagnus: deficient developmenttwitching of extremi- L. leg.ties.

77 4:1 B.W. 8 lb. C.l. L. hemiplegia (6 Died at time of recur-Forceps. Severe as- months). rence of convulsions atphyxia. Convulsions age 2 years.during first 48 hours.

119 1:1:3:5 B.W. 84 lb. C.l. Coarse ataxia involv- Severe. Intense rest- Slow improvement dur-S.D. Unnaturally ing limbs and trunk, lessness of mind and ing age period 3 weeks-quiet at birth. Twitch- and divergent strabis- body apparently pro- 3 months.ing of extremities, mus (44 months). gressive from early days.cerebral cry, and grossphysical weakness de-veloped about 13thday.

131 4:1:3 B.W. 64 lb. C.I. Poorly developed L. General behaviour in Died as a result ofForceps. Asphyxia. leg-noticed at 11 keeping with moderate ? laryngitis aged 4 years.Convulsions age 7 months. disability.days.

140 4:14:34 B.W. 64 lb. C.I. Not walking at 34 Not talking andProlonged labour. For- years. almost certainly im-ceps. Frail. Mild con- paired mentality at 34vulsions during first years.24 hours.

C.l =First child, C.2 =Second child, etc.: B.W. =Birth weight.



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ApproxiateAge(s) atwhich Ant-natal and Natal Evidences of


A B C D E F

154 i:1 :4 B.W. 74 lb. C.1. Severe. Vicios tem- Poor general physicalS.D. Anxious expres- perament. Extreme development.sion: too alert: slight restessness Littletransient bogginess of power of concentra-fontanelle. tion.

163 4:4:5 B.W. 5 lb. ? place Spastcity of legs noted Present-degree diffi- Attending special schoolin family. S.D. Frai. at 3 months, and some cult to assess at age 84 years.Disiclination for stiffness of arms atfluids. Nystagmus. 6 months. PictureWeak convulsive typical of spasticmowvements. Slight diplegia at time offullness of fontanelle. examinaton at 5

years.

165 I+:1:5 B.W. 114 lb. C.1. Slight paralyss R. arm Behaviour rather child- Condition of R. legInstrumental rotation and R. leg first noticed ish but not of degree showed improvement atand extraction. As- at 7 months. to suggst disability of age 5 years.phyxia: facial paresis: mind.convulsions: vomiting.

181 i:3:5 B.W. 10 lb. C2. General physical de- Nil. Stated to be aboveInstrumental rotation velopment slow. Wt. average at school atand extraction. Gross at 6 months 134 lb. age 11 years.cephalo-haematoma and at 1 yr. 17 lb.and facial bruising. Noted at 34 yrs, to beVery alert Slight con- chlmsy with R. handvulsions. and dragging R. foot

at 4 years. R. spastichemiplegia confirmedat 5 years.

191 4:1:3:54 B.W. 84 lb. C.l. Weight progress satis- Foolish expression Considered ineducableS.D. Breeh presenta- factory at 6 months noted at 1 year: no at 74 years.tion. Alert expression: but not holding head concentration. Firstfrowning: too awake: up. No paralysis at attempts at speech 3slight fullness of 3 years or 5 years. years Gross mentalfontanelle for 4-5 days. disability at 5 years.

203 1:3 B.W. 9 lb. C.I. Athetoid movements Scvere-of imbecilic Expressioness facies:Prolonged labour. Ex- and tremor of head degree (9 months). constant drooling.treme exhaustion. In- (11 months). Ataxictense restlessness with gait (24 years).cerebral cry commenc-ing 10th day. Expres-sion of fear. Grossloss of weight., Re-covery gradual overweeks.

230 4:4:14:4 B.W. 6 lb. C.l. No localized impair- Moderately severe dis-Foetal distess Instru- ment on physical ability. Furtive ex-mental rotation and examination at 3 and presson. Restless. De-extion. Intense 6 months and at 1I sucive Little con-restlessness: painful and 4 years but slow centration. Shuns othercry, twitching for seven to sit up and walk. children and is shunnedhours. by them. AU dcvel-

opedgraduallyafter 3rdbirthday.

233 I:4:1:5 B.W. 51 lb. C.6. R. emiare gradu- Subnormal mentality Not attending school atPrecipitate defivery fol- ally spastic at 5 years Parents 7 yearslowing prolonged form during first 10 first anxious at age ofperiod of poor pains. weeks of life. R. leg 3 yeasLimp. Diinclination poorly deveoped atfor fluids. Nystagmus. 12 months.Facial twitching. Flac-cid paresis R limbs.

S.D. =Spontaneous delivery. CS. =Caesarean sctdon.25

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Series History: OtherNumber (yrs.) Salient Features Physical Disability Disability of Mind Observations

A B C D E F

243 4:1:1:4:5 B.W. 7 lb. C.l. Salaam convulsions inForceps. Excessive infancy. Grand malakltness, nystagmus, superimposed at age 24apprehensive facies years.several days.

260 4:1 B.W. 5 lb. C.3. Large head noticed atS.D. Breech presenta- 6 months. Hydro-tion. Nystagmus and cephalus confirmed atslight fullness of time of examination atfontanelle. Frail. I year. Circumference

then 224 in.269 1:1:3 B.W. 74 lb. C.3. Delay in walking. Dis- Some disability sug-

Manual rotation of inclination to use R. gested by delay in firsthead forceps delivery. arm noted at 4 months: attempts at speech untilConvulsions on first flaccid paresis of R. age of 3 years, and byday. Excessively alert arm and R. leg abnormal degee ofVomiting. suspected at I year constant rslssness.

and confirmed at 3years.

300 4:14:6 B.W. 34 lb. C.2. L. hemiplegia noted at No recognizable Convulsions at 6 weeksForceps. FraiL whin- 15 months; said to disability although and 11 weeks.ing, disclination for have been noticed at ' scholastcally ' childfluids, slight twitch of 7 months. Poor gen- said to be behind hisface and extremities. eral condition at 5 classfellows.

years.

309 4:14:44 B.W. 74 lb. C.l. Slight stiffness of legs Some disability. Began attendance atS.D. after pains of suspected at 3 months. Moderate in degree. special school at age25 hours' duration. Definite adductor 64 years.Distress at birth. spasm of legs presentAgitated expression at 15 months, alsoand movements ofeyes. doubtful athetoidConvulsions 2nd day. movements of arms.

At 44 years typicalpicture of cerebraldiplegia.

311 4:14:4 B.W. 8 lb. C.l. Slow in sitting up. Gross. Aggressivetem- Constant restlessness ofS.D. Short labour Unsteady gait at 2 perament. Destructive. mind and body.te ting in ex- years. Coarse tror No affection fortremly violent pains. on purposive use of parents. Dirty inExtreme exhaustion of hands or arms. habits. Foolish speech.mother and child.Infant limp one weekthen violently ressfor several days. Sub-sequent progress veryslow.

348 4:14:3:5 B.W. 8 lb. C.l. Suggestion of impaired Convulsions at 4Instrumental rotation mentality at 5 years. months. Recurrence ofand delivery. Bulging epileptiform convul-fontanelle. Head re- sions at 3 years andtraction. Great rest- subsequently.kzsness.

349 4:4:54 B.W. 84 lb. C.1. Spastic paresis of L. Head noted as growingForceps-delayed 2nd arm noted at 6 months. rapidly during periodstage-rotation ofhead 5-7 months.manually. Severe headmoulding. Highpitched cry: facialparesis: twitching:nystagmus: dartingtongue.

C. 1= First child, C. 2 Second chikl, etc.: B. W. = Birth weight

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INTRACRANIAL IRRITATION IN NEWBORNS 347



A B C D E F

359 1:4 B.W. 7 lb. C.2. Flaccid paralysis of R.Low forceps. Shrill arm suspected at 1 year.cry. Facial paresis. Confirmed at 4 years.Restless, agitated ex-pression. Some full-ness of fontanelle.

360 1:2 B.W. 7 lb. C.l. Hydrocephalus present Severe disability, evi-High forceps. Bruising at 6 months-said to dent at 2 years.of scalp and face. have been suspectedSevere shock. Bulging at 4 months. R.fontanelle: convulsions hemiplegia.on first day. R. armpesistently spastic.

369 1:34:5 B.W. 74 lb. C.I. At 3 months spasticity Definite but probably AttendingspecialschoolProlonged labour, ma- of both legs, R. more less than appearances at 7N years.ternal exhaustion, than L. Paralysis of suggested.foetal distress, forceps R. arm noted byapplied. Slight fullness parents at 11 months.of fontanelie. Violent On examination atnystagmus. Weakness 34 years spasticityof legs suspected. marked in R. arm,

moderate in R. legand slight in L. leg.

377 1:14:5 B.W. 8 lb. C.I. Spastic paralysis of Delay in speech and Child attending aInstrnental rotation slight degree of L. arm walking. Definite but special school at ageand extraction. Critical and L. leg suspected limited mental dis- 9 years.condition 9 days. One at 1 year by parents ability recorded at 5violent convulsion. and confirmed by years.

examination at 18months.

391 3:5 B.W. 8 lb. C.l. Flaccid paralysis of R. Circumference of headCS. following failed arm readily recogniz- at 3 years 21 in.forceps. Foetal dis- able at examination attress: knotted cord. 3 years. Said to haveVery quiet but easily been nrst noticed atdisturbed. Reflexes 2 years.exaggerated. Precoci-ous expression.

396 1:1:3:5 B.W. 71 lb. C.4. Nil found on examina- Nil.Low forceps. Abnor- tion at 6 months, Imally quiet and still: year, and 3 years.nystagmus: boggy R. hemipklgia presentfontanelle. at 5 years-noted

by parents at 4years.

434 1:1:2 B.W. 9 lb. C.3. Nil on examination at Head held up at 1 year. Collapse and blueS.D. Labour 3 hours. 3 months, apart from Not sitting up or attack at 3 weeks.Contrasting general gross asymmetry of talking, grasping things Salaam convulsionsquietness with alert head. or stretching out for began at 4 months ardfrowning expression. objects at 2 years. Dis- persisted, occurring atSlight fullness of ability certain but ? intervals until age offontanelle. degree. 18 months.

440 4:11:5 B.W. 10 lb. C.l. Spasticity of R. leg Circumference of hezdProlonged labour. slight adductor spasm at 18 months 204 in.Manual rotation of and flecion at kneehead: forceps. Slight noted at 3 months:twitching face, Capel's still present 18 monthssign -, and severe and R. leg smallerclutching of hands 2nd than L.day. Frowning ecpres-sion.

S. D. =Spontaneous delivery. C. S. = Caesarean section.



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348 ARCHIVES OF DISEASE IN CHlLDHOOD


Series Examined History: OtherNumber (yrs.) Salient Features Physical Disability Disability of Mind Observ

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