DOI: 10.1542/peds.2006-3364 2007;120;1012Pediatrics

Fumagalli and Fabio MoscaMaria Lorella Giannì, Odoardo Picciolini, Chiara Vegni, Laura Gardon, Monica

Months of Age in Extremely Low Birth Weight InfantsTwelve-Month Neurofunctional Assessment and Cognitive Performance at 36

  

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of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2007 by the American Academy published, and trademarked by the American Academy of Pediatrics, 141 Northwest Pointpublication, it has been published continuously since 1948. PEDIATRICS is owned, PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly

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ARTICLE

Twelve-Month Neurofunctional Assessment andCognitive Performance at 36 Months of Age inExtremely Low Birth Weight InfantsMaria Lorella Giannı, MD, Odoardo Picciolini, MD, Chiara Vegni, MD, Laura Gardon, PT, Monica Fumagalli, MD, Fabio Mosca, MD

Neonatal Intensive Care Unit, Institute of Pediatrics and Neonatology, Fondazione IRCCS “Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena” University MedicalSchool, Milan, Italy

The authors have indicated they have no financial relationships relevant to this article to disclose.

ABSTRACT

OBJECTIVE. The objective of this study was to investigate whether an early neuro-functional assessment (at 12 months’ corrected age) is predictive of cognitiveoutcome at 36 months of age in extremely low birth weight infants.

METHODS.We conducted an observational longitudinal study. Neurodevelopmentaloutcome by means of a neurofunctional assessment was evaluated at 12 months’corrected age and 36 months’ chronological age in 141 extremely low birth weightchildren. Cognitive outcome was assessed with use of the Griffiths Mental Devel-opmental Scale.

RESULTS.A significant association was found between the 12-month neurofunctionalstatus and cognitive performance at 36 months. A higher general quotient on theGriffiths Mental Developmental Scale at 36 months was observed in infants whoexhibited normal (score: �1) neurodevelopment compared with children whoexhibited minor (score: 2) and major (score: �3) dysfunctions at the 12-monthneurofunctional evaluation (99 � 6.8 vs 85.3 � 16.3 vs 57.3 � 22.0). A score of�2 at the 12-month neurofunctional assessment, abnormal brain MRI results atterm, and chronic lung disease remained predictive of cognitive delay at 36months of age and also after adjustment for confounders.

CONCLUSIONS. The 12-month neurofunctional evaluation may be an additional usefulclinical tool in predicting later cognitive outcome in extremely low birth weightchildren.

www.pediatrics.org/cgi/doi/10.1542/peds.2006-3364

doi:10.1542/peds.2006-3364

KeyWordsneurofunctional assessment, cognitiveoutcome, extremely low birth weightinfants

AbbreviationsVLBW—very low birth weightELBW—extremely low birth weightSGA—small for gestational ageNEC—necrotizing enterocolitisROP—retinopathy of prematurityCLD—chronic lung diseaseHC—head circumferenceGQ—general quotient

Accepted for publication May 29, 2007

Address correspondence to Maria LorellaGiannı, MD, Neonatal Intensive Care Unit,Clinica Mangiagalli, IRCS, University MedicalSchool, Via Commenda 12, 20122 Milano, Italy.E-mail: maria.gianni@unimi.it

PEDIATRICS (ISSN Numbers: Print, 0031-4005;Online, 1098-4275). Copyright © 2007 by theAmerican Academy of Pediatrics

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SURVIVAL OF VERY low birth weight (VLBW; �1500 g)infants has recently improved as a result of advances

in perinatal care.1 Major disabilities occur in 15% to 20%of the VLBW population, with a higher prevalence ininfants with the youngest gestational age and the lowestbirth weight.2 A high rate of learning difficulties, behav-ioral problems, and lower IQ scores, compared with thepopulation mean, is reported in survivors without majordysfunctions, especially extremely low birth weight(ELBW; �1000 g) infants.3 Early detection of infants whoare at high risk for poor neurodevelopmental outcomeremains a challenge for clinicians to make referral for in-tervention and optimize potential outcome. Several au-thors4,5 have investigated the relationship between motorability, mainly investigated by a developmental assessmentof movement, and cognitive performance in ELBW, sug-gesting that early movement problems may be predictiveof later cognitive adverse outcome even in the absence ofdefined neurologic problems.

We previously reported that an early neurofunctionalevaluation in VLBW infants may be an additional usefultool in reassuring parents on the integrity of centralnervous system function.6 Few data are available in theliterature on any hypothetical relationship between cog-nitive outcome of ELBW infants and early neurofunc-tional assessment.7,8 The aim of this study was to exam-ine whether a neurofunctional evaluation at 12 monthsis predictive of cognitive outcome at 36 months of age inELBW infants.

METHODSAmong all consecutive newborn infants who were ad-mitted at the same Institution from 1996 to 2001, 159infants entered the study. Inclusion criterion was birth

weight �1000 g. Exclusion criteria were presence ofcongenital diseases and/or chromosomal abnormalitiesor infant death during postpartum hospital stay. Infantswere scheduled to be prospectively followed up to 36months of age. The Consolidated Standards of ReportingTrials (CONSORT) flowchart of the study is shown in Fig1. Written informed consent was obtained from thenewborns’ parents, and the departmental ethics commit-tee approved the study design.

Presence of gestational hypertension and/or pre-eclampsia, steroids received before delivery, and educa-tional level were investigated as maternal variables. Ges-tational hypertension and preeclampsia were defined,respectively, as de novo hypertension (systolic bloodpressure � 140 mm Hg or diastolic BP � 90 mm Hg)arising after midpregnancy and gestational hypertensionassociated with new-onset proteinuria (�300 mg/24hours). The educational level of mothers was evaluatedand categorized as low (�13 years) or high (�13 years).

Neonatal characteristics (gestational age, being appro-priate or small for gestational age [SGA], birth weight,length, and head circumference); need for mechanicalventilation; and the occurrence of sepsis, necrotizingenterocolitis (NEC; classified as stage 3 according to theclassification of Bell et al9), bronchopulmonary dyspla-sia, and retinopathy of prematurity (ROP) of stage 3 orhigher were recorded prospectively. Gestational age wasbased on the last menstrual period and first-trimesterultrasonogram. Infants with birth weights of �10th or�10th percentile for gestational age, according to theNorth-Italian growth charts, were classified as appropri-ate for gestational age or SGA, respectively.10 Sepsis wasdefined by the presence of a positive blood culture.Patients with NEC were pooled together with those who

FIGURE 1Consolidated Standards of Reporting Trials (CONSORT) flowchart.

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had sepsis because of the strong association of NEC withinfection. Chronic lung disease (CLD) was defined byuse of supplemental oxygen at 36 weeks’ postconcep-tional age. Corrected age was calculated, up to 24months of life, from the chronologic age adjusting forgestational age. Brain MRI was performed at a mean of40 � 2 weeks’ postconceptional age in all newborns. Anabnormal MRI result was defined by the presence ofmajor brain lesions (eg, ventriculomegaly, cystic andnoncystic periventricular leukomalacia, focal parenchy-mal brain lesions).

Infants entered a follow-up program that consisted ofperiodic pediatric visits at 3, 6, 12, and 24 months’corrected age and 36 months’ chronological age and ofevaluation of neurodevelopmental outcome by means ofthe neurofunctional evaluation at 12 months’ correctedage and 36 months’ chronological age. Cognitive out-come was assessed with use of the Griffiths Mental De-velopmental Scale at 36 months’ chronological age.

Weight, length, and head circumference (HC) weremeasured using standardized procedures.11 Growth zscores were then calculated by EuroGrowth 2000 soft-ware (EuroGrowth Study Group, Vienna, Austria).Catch-up growth was defined by a growth z score ofmore than �2 SD.

The neurofunctional evaluation6 was based on thestudy of evoked and spontaneous motility, posturaladaptability, variability of motor patterns, and neuromo-tor and behavioral skills. A detailed description of theneurofunctional assessment is reported in the Appendix.Infants were categorized into 3 groups, according to theneurofunctional status, as normal (score: 0–1), exhibit-ing minor dysfunctions (score: 2), or exhibiting majordysfunctions (score: 3–4). The Griffiths Mental Develop-ment Scale12 and related subscales (locomotor, personalsocial, hearing and speech, hand and eye coordination,performance, and practical reasoning) were adminis-tered by the same expert trained examiner, who wasblind to the neurofunctional evaluation. A general quo-tient (GQ) was then calculated. The mean value of GQwas 100 with an SD of 12. A GQ of �70 was classified assevere developmental delay.

Statistical AnalysisDescriptive data are shown as means � SD or number ofobservations (percentage). Comparison among groupswas performed by the �2 test for discrete variables or byanalysis of variance for continuous variables. Signifi-cance of multiple comparisons was adjusted by the leastsignificant difference test correction. Differences withinpatients in repeated measurements of growth parame-ters were assessed by analysis of variance. Logistic re-gression analysis was used to identify determinants ofdevelopmental delay (GQ � 88) at 36 months of age.Maternal and neonatal characteristics that are known tobe associated with adverse cognitive outcome were en-

tered in the model. Factors examined included maternaleducation, prenatal steroids, maternal hypertension,multiple birth, gender, birth weight, gestational age, be-ing SGA, sepsis, ROP of stage 3 or higher, HC catch-upgrowth at 12 months, neurofunctional status at 12months’ corrected age, CLD, and cranial MRI status atterm.

All statistical analyses were conducted at the � � .05level and were 2-tailed. Statistical analysis was per-formed by using SPSS 12 (SPSS Inc, Chicago, IL).

RESULTSFollow-up data at 36 months’ chronological age wereavailable for 141 (70 girls; 71 boys) infants. One infantdied through the follow-up. No differences in the char-acteristics at birth and in the developmental measures,when last assessed, were observed between infants whowere lost at follow-up and those who were evaluated.The characteristics of the studied population at birth areshown in Table 1.

Maternal hypertension occurred in 35.1% and 39.4%of mothers with infants who exhibited a GQ of �88 and�88, respectively, at 36 months’ chronological age (P �.39). Antenatal steroids were administrated to 50% and59.5% of mothers with infants who exhibited a GQ of�88 and �88, respectively, at 36 months’ chronologicalage (P � .2). Maternal educational level was low in73.1% and 83.8% of mothers with infants who exhib-ited a GQ of �88 and �88, respectively, at 36 months’chronological age (P � .2). The characteristics of thestudied population according to cognitive outcome at 36months’ age are shown in Table 2.

Younger gestational age, being male, ROP of stage 3or higher, and CLD were associated with a GQ of �88 at36 months of age. A GQ of �70 was found in 14.2% (n� 20) of children. Abnormal MRI status was found in72.4% and in 27.6% of infants who exhibited a GQ of�88 and �88, respectively, at 36 months’ chronologicalage (P � .0001).

Mean (SD) weight, length, and HC z scores rangedthrough the first 36 months of life from �2.62 (1.7) at 3months to �1.77 (1.3) at 36 months (P � .0001), from�2.67 (1.5) to �1.01 (1.07; P � .0001), and from �1.57(1.38) to �1.57 (1.03; P � 0.9), respectively. At 36months, 38%, 17%, and 34% of infants had weight,

TABLE 1 Characteristics of the Studied Population at Birth

Infant Characteristics at Birth (N � 141) Value

Birth weight, mean (SD), g 839.5 (122.8)Birth length, mean (SD), cm 33.9 (2.4)Birth HC, mean (SD), cm 24.6 (1.6)Gestational age, mean (SD), wk 28 (1.9)Boys, n (%) 71 (50.4)SGA, n (%) 56 (39.7)Infants ventilated, n (%) 117 (83.0)Multiple birth, n (%) 39 (27.7)

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length, and HC z score less than �2 SD, respectively.Absence of HC catch-up growth at 36 months was asso-ciated with a GQ of �88 at 36 months (P � .05).

Neurofunctional Assessment at 12 Months’ Corrected Age andat 36 Months’ Chronological AgeAt 12 months’ corrected age, the neurofunctional scorewas �1 in 82 (58.2%) infants, 2 in 41 (29%), and �3 in18 (12,8%). The corresponding values at 36 months’chronological age were 67 (47.5%), 52 (36.9%), and 22(15.6%) infants. At the age of 36 months, the neuro-functional status improved, unchanged, or deterioratedin 7 (5%), 108 (76.6%), and 26 (18.4%) infants, respec-tively; 73% and 100% of infants with a score of �1 or�3, respectively, at 12 months’ corrected age had un-changed functional status at 36 months of age. Theclinical disabilities of infants who had a neurofunctionalscore of 2 at 36 months of age were learning disabilitiesand dyspraxia (23%), clumsiness (23%), behavioralproblems (30%), language impairment (10%), psy-chomotor retardation (12%), and hypoacusia (2%). Theclinical features of the infants who had a neurofunc-tional score of �3 at 36 months of age were cerebralpalsy (63%), mental retardation (22%), visual impair-ment (5%), deafness (5%), and autism spectrum (5%).

Neurofunctional Status at 12 Months’ Corrected Age andGriffiths Mental Development Scale at 36 Months’Chronological AgeA significant statistical association between the 12-month neurofunctional status and the GQ assessed at 36months (P � .0001) was found. On posthoc analysis, allcomparisons were significant.

Predicting GQ at 36 Months’ Chronological Age From the 12-Month Neurofunctional AssessmentA logistic regression analysis was performed to identifydeterminants of developmental delay at 36 months (Ta-ble 3). For statistical analysis, patients who had a score of�2 at the 12-month neurofunctional evaluation were

pooled. Abnormal cranial MRI results at term, CLD, anda score of �1 at the neurofunctional evaluation at 12months were found to be independently associated withcognitive delay at 36 months.

DISCUSSIONIn this study, the 12-month neurofunctional assessment,MRI status at term, and CLD remained predictive ofcognitive development at 36 months in ELBW infants,also after adjusting for confounders. In addition, wefound that children who were assessed as normal (score� 1) at the 12-month neurofunctional assessmentshowed significantly higher GQ at 36 months of agecompared with infants who exhibited dysfunctions(score � 2). This finding could be explained by the factthat the detection of dysfunctions at 12 months of agemay reflect the difficulty that the infant experiences inthe learning process and in the development of newtasks, as a result of impairment of the emerging func-tions at that age, evaluated by the neurofunctional ap-proach. As a consequence, the normal process of cogni-tion may be impaired.

Several authors have found an association betweenmotor function assessed at 12 months and cognitiveoutcome at school age. Burns et al4 reported that groupclassification of motor development at age 1 year, inves-tigated using the neurosensory motor developmentalassessment, is predictive of cognitive outcome in ELBWinfants at age 4 years. Jeyaseelan et al5 reported thatmotor difficulties, assessed by use of neurosensory motordevelopmental assessment, in ELBW infants at 2 yearsare strongly associated with later clinical measures ofattention. Roth et al13 and Stewart et al14 found a closerelationship between neuromotor impairment, investi-gated by standardized neurologic examination, and cog-nitive defects at age 4 years. The results of these studiesare consistent with Piaget’s theory15 and the mirror neu-ron system.16,17 According to Piaget, there is a strict in-terrelation between motor and cognitive development:action is considered the foundation of knowledge as it is,

TABLE 2 Characteristics of the Studied Population According to Cognitive Outcome at 36 Months of Age

Characteristic Cognitive Assessment at 36 mo

GQ � 88 (n � 37) GQ � 88 (n � 104) Pa

Birth weight, mean (SD), g 827.8 (143.0) 843.6 (115.0) NSBirth length, mean (SD), cm 33.6 (2.6) 34.1 (2.3) NSBirth HC, mean (SD), cm 24.1 (1.9) 24.7 (1.5) NSGestational age, mean (SD), wk 27.2 (1.8) 28.2 (1.9) �.05Males, n (%) 24.0 (64.9) 47 (45.2) �.05SGA, n (%) 10 (27.0) 46 (44.2) .05Multiple birth, n (%) 12 (32.4) 27 (26.0) NSSepsis, n (%) 8 (22.9) 30 (29.1) NSROP stage 3 or higher, n (%) 10 (27.8) 9 (8.7) �.05CLD, n (%) 25 (67.6) 17 (16.3) �.001

NS indicates not significant.a t or �2 test.

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at first, physical and then it is transformed into mentalaction and representation. Also, the mirror neuron sys-tem, which activates when an individual performs anaction, as well as when he or she observes a similaraction done by another individual, seems to play animportant role in the social cognition process: it seemsnot only to provide an action recognition mechanismbut also to constitute a neural system for coding theintentions of others and allowing imitation learning.18 Inaddition, according to Hadders-Algra,19 both primary(the phase in which the variation in motor behavior isnot geared to external conditions) and secondary (thephase in which the motor performance can be adaptedto specific situations) variability and, consequently, themotor repertoire can be reduced in preterm infants as aresult of perinatal lesions or abnormal cerebral corticaldevelopment. Consistent with these findings, the asso-ciation of the 12-month neurofunctional evaluationwith cognitive performance at 36 months of age may beto some extent explained by the fact that a neurofunc-tional approach includes the evaluation of evoked andspontaneous motility, postural adaptability, and variabil-ity of motor patterns, according to the emerging func-tions of each age.6 The finding of lower GQ at 36 monthsin infants who exhibited minor dysfunctions at the 12-month neurofunctional assessment highlights the im-portance of additional implementation of individualizedcare plans both during hospital stay and in the postdis-charge period because a limited motor repertoire, evenin the absence of brain lesions, may result in deficit ofprocessing information and solving problems throughthe selection of the most appropriate strategies andadaptive solutions. In addition, promoting the infant’sneurobehavioral together with motor organization hasbeen reported to be associated with both medical and

developmental advantages20; therefore, detection of dys-functions at the 12-month neurofunctional evaluationmay represent an additional clinical tool in identifyinginfants who are at risk for poor later cognitive outcomeand could benefit from early intervention.

Although efforts have been made to eliminate theartificial division between the neurologic and the behav-ioral approach to the neurodevelopmental assessment ofpreterm infants, few studies have investigated the rela-tionship between the cognitive outcome of ELBW in-fants and the neurofunctional evaluation. Wallace et al8

reported that preterm neonates who had poor neurobe-havioral performance, assessed as visual-following andauditory-orienting, had significantly lower cognitive testscores at age 1 and 6 years. Costantinou et al7 found thatthe Neurobehavioral Assessment of the Preterm Infants,evaluated before hospital discharge, correlates with cog-nitive outcome at 30 months of age.

There is increasing evidence that cognitive domain inpreterm infants is one of the most common areas of poorfunctioning.21 The prevalence of severe developmentaldelay found in our study is 14.2%. Several multicentertrials2,22–25 reported different rates of developmental dis-abilities in very preterm infants, ranging from 15% to20% up to 35% to 40%. In a meta-analysis, Bhutta etal26 reported that mean cognitive scores of preterm in-fants at school age were 10.9 lower compared with thoseof control subjects, showing a linear correlation withbirth weight and gestational age. In this study, a youngergestational age, being male, absence of HC catch-upgrowth at 36 months, and severe ROP were associatedwith developmental delay at 36 months at univariateanalysis. No association with birth weight was found,probably because in our study, infants with birth weight�600 g were unrepresented. Being male, having poorpostnatal growth, especially of the head, and havingsevere ROP have been reported as risk factors for devel-opmental delay by other authors.2,27,28

In this study, at logistic regression analysis, also ab-normal MRI status at term and the presence of CLDremained predictive of cognitive outcome at 36 months.Abnormal MRI status at term has been reported as astrong predictor of adverse neurodevelopmental out-come by other authors,29 suggesting a role for MRI atterm in risk stratification for preterm infants. There isagreement on the unfavorable effect of CLD, even in theabsence of severe brain lesions, on cognitive outcome inchildren who are born very preterm, which seems topersist into school age.30

In our study, maternal education and being SGA werenot predictive of later cognitive outcome. The effect ofmaternal education on cognitive outcome in ELBW in-fants remains in question. Although several authorshave reported lack of maternal education as a risk factorfor poor cognitive development,2 others did not observeany effect.4,5 Current literature is inconclusive also about

TABLE 3 Variables AssociatedWith a GQ of <88 at 36 Months ofAge: Logistic Regression Analysis

Parameter Adjusted OR(95% CI)

Gestational age (�28 vs �28 wk) 1.70 (0.30–8.40)Birth weight (�800 vs �800 g) 2.70 (0.50–14.00)Gender (male vs female) 1.40 (0.40–5.40)Being SGA (yes vs no) 0.70 (0.10–4.70)Multiple birth (yes vs no) 0.90 (0.20–4.60)Sepsis (yes vs no) 0.50 (0.10–2.40)ROP stage 3 or higher (yes vs no) 0.60 (0.08–3.90)CLD (yes vs no) 8.80 (1.80–42.90)a

HC z score at 12 mo (absence vs presence of catch-upgrowth)

2.30 (0.60–9.70)

Neurofunctional status at 12 mo (normal vs impaired) 0.15 (0.03–0.70)a

MRI status at term (abnormal vs normal) 16.70 (3.30–84.30)b

Maternal hypertension (yes vs no) 0.80 (0.20–3.70)Prenatal steroids (yes vs no) 0.70 (0.20–2.90)Maternal education (low vs high) 1.60 (0.30–8.40)

OR indicates odds ratio; CI, confidence interval.a P � .05.b P � .005.

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the role of being SGA in determining neurodevelopmentoutcome. Some studies31 reported no effect of SGA statuson cognitive outcome, whereas others found a modestassociation between SGA and IQ.32

We did not find any association between sepsis anddevelopmental delay. This finding is in agreement withVohr et al,2 who did not identify sepsis as predictive ofcognitive impairment, whereas Stoll et al33 found a rateof cognitive developmental disability of 33% to 42% ininfants with infection versus 22% in infants withoutinfection.

A potential limitation of the findings of this study isthe loss to follow-up, which was �10%; however, be-cause the patients who were lost to follow-up had sim-ilar characteristics at birth and in the developmentalmeasures, when last assessed, to those reported, this lossis unlikely to bias substantially the associations reported.An additional limitation of this study was that, despite arelatively large sample size, the low rate of severe cog-nitive impairment precluded a separate analysis to iden-tify the variables that were predictive of a GQ of �70.

Because disability, defined as impairment of function,has been recognized to be multidimensional,34,35 thechoice of outcome classifications and assessments re-mains difficult. Additional investigations are warrantedto identify additional, simple methods of neurodevelop-mental assessment in clinical practice that may betterreflect the emerging concept of disability and focus theattention on the consequences of disease rather than ondisease itself. A functional approach to the neurodevel-opmental evaluation that actually investigates not onlyan infant’s motor but also neuromotor and behavioralskills may well relate to later outcomes and focus on theoutcome potential of the infant.

CONCLUSIONSAccording to our findings, the presence of a score of �2at the 12-month neurofunctional assessment representsan early clinical marker of adverse later cognitive out-come. This study suggests that an early neurofunctionalevaluation could be an additional useful tool in alertingclinicians to follow up neurodevelopment strictly to ini-tiate early intervention programs. Additional, largerstudies are desirable to clarify better the role of theneurofunctional assessment in the early identification ofchildren who are at risk for poor later cognitive perfor-mance.

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APPENDIX: NEUROFUNCTIONAL ASSESSMENT OF PREMATURE INFANT AT 12MONTHS

Review Copy

Classification at 12 months

0.typical result: complete patterns

of movement and interaction

1.

slight anomalies which normalize

with facilitation during the exam

2. evident abnormal result:

the anomalies remain during

examination: the function (motor,

postural, adaptive) is moderately

troubled, but possible (not

prevented)

3. the function is difficult:

the anomalies significantly disturb

the function

4.

severe anomalies that upset or

prevent the function, till fixed pathological patterns of

movement

Time: 20 minutes

Date of examination ……………………………Date of

Birth…………………….………….. POSTURAL ANOMALIES

Slight Marked None

Name………………………………..………………. Surname……………………………….……..… Skull

Address……………………………………………….………………………………………………………… NecK

Telephone n°……………………………………………………………………………………………….. Spine

Cronological age…………………………………..Corrected age

…………..……………..…. Chest

Gestational age………………………………….. Birth weight

…………………………………. Upper limbs

Head circumference ……………...Length…………….…..

Weight……………………… Lowers limbs

ITEMS DESCRIPTION SCORE

0 1 2 3 4

ADAPTEDNESS > AUTONOMY

Attention-interaction stability

Feeding function

Gastrrointestinal function

Sleep-wake rhythms

NEUROSENSORY FUNCTION

Visual function

Hearing and language

BEHAVIOURAL FUNCTION

Social interaction

Emotional stability (or hyperactivity)

Personal social behaviour

SPONTANEOUS MOTOR ACTIVITY

Motor skills

POSTURAL PATTERNS

Supine

Prone

Sitting

Standing

TEMPORAL PATTERNS

Balancing (sitting)

Squatting

Equilibration (kneeling, standing)

Lateral abduction reaction of hip

SEQUENCES

Axial rotation

Antigravity rotation

Rolling

Creeping

Rightings

FACILITATION

Lower limb abduction

Hand opening

PRAXIES (FINE- GRAPHO- MOTOR)

Tower building

Shapes matching

“Action patterns”

Quality of play

ANGULAR MEASURES

Adductors

Ischiotibials

Sural triceps

Upper limb extension

PRIMITIVES>PATHOLOGICAL

REFLEXES

Asymetrical tonic neck reflex

Plantar grasp

Babinski (evoked or spontaneous)

PEDIATRICS Volume 120, Number 5, November 2007 1019 by guest on June 13, 2013pediatrics.aappublications.orgDownloaded from

DOI: 10.1542/peds.2006-3364 2007;120;1012Pediatrics

Fumagalli and Fabio MoscaMaria Lorella Giannì, Odoardo Picciolini, Chiara Vegni, Laura Gardon, Monica

Months of Age in Extremely Low Birth Weight InfantsTwelve-Month Neurofunctional Assessment and Cognitive Performance at 36

  

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