Lifelong cognitive and motor outcomes after being born small for gestational age or with fetal growth restriction

Authors: Gemma Chavarria Ventura, Harrigan Ryan, Hai-Nian Yu, Kirat Kishore Chand, Paul Bernard Colditz, Julie Anne Wixey

Abstract

Children born with fetal growth restriction (FGR) or small for gestational age (SGA) face an increased risk of motor and cognitive impairments, although prevalence and severity vary across studies due to differences in definitions, assessment methods, and population characteristics. In recent years, advances in technology and clinical awareness have led to a growing body of research on the relationship between fetal growth and neurodevelopmental outcomes. This mini-review synthesises recent findings on the impact of SGA and FGR on neurodevelopment in preterm and term infants across the lifespan. Three databases were screened to identify original studies published between 2020 and 2025 with 40 studies meeting the selection criteria. Evidence suggests that children born SGA or with FGR are at higher risk of cognitive impairments, which may persist into later life; however, results from some preterm cohorts do not show significant associations. Findings on sensory and behavioural outcomes are limited and heterogeneous, reflecting the fewer studies that have addressed these domains. Regarding motor outcomes, reports on cerebral palsy remain inconsistent, with some studies suggesting no increased risk. In contrast, broader evaluations of motor function consistently indicate a higher prevalence, particularly among term-born cohorts. Together, these findings highlight the need for refined definitions, standardised assessment tools, and longitudinal studies to clarify the developmental trajectories of children born with growth complications and to guide early interventions.

Core Tip: Infants born small for gestation age or with fetal growth restriction are at higher risk of cognitive and motor impairments across the life span. While cerebral palsy prevalence remains inconsistently reported, several studies show a higher prevalence, particularly among term-born cohorts.

INTRODUCTION

Being born small for gestational age (SGA) or with fetal growth restriction (FGR) are closely related obstetric conditions that reflect suboptimal fetal growth. Birth weight is largely influenced by the duration of the gestation and the rate of fetal growth[1]. SGA is generally defined as a birth weight below the 10% for a specific gestational age. The World Health Organization provides reference charts for estimated fetal weight by gestational age, and infants falling below the 10% on these charts are classified as SGA[2]. The use of these global charts leads to a higher detection in low-income and middle-income countries due to higher rates of poverty and maternal undernutrition[3]. FGR refers to a pathological inhibition of fetal growth in which the fetus fails to achieve its full genetic growth potential in utero, condition that may result in low birth weight or SGA[4]. The incidence of FGR ranges from 10% to 15% worldwide, depending on country or income level, with additional fetal and maternal variables modulating this proportion[5]. The severity of FGR is influenced by multiple factors, with timing of onset particularly shaping developmental outcomes. FGR can be categorized into early-onset-FGR (EO-FGR), occurring < 32 weeks of gestation and characterized by global, symmetrical growth restriction throughout pregnancy. Late onset-FGR (LO-FGR), which accounts for around 80% of cases, usually arises in the third trimester of pregnancy and is marked by asymmetric growth of body and brain and adaptive circulatory changes[6,7].

Both SGA and FGR are associated with increased neonatal morbidity and long-term neurodevelopmental challenges[8,9]. The fetal growth insults that result in neurocognitive and motor sequelae may occur through mechanisms such as placental insufficiency, hypoxia-ischemia, resulting in altered brain connectivity. SGA and FGR frequently co-occur with prematurity, contributing to their impact on neurodevelopment. While the association between cognitive impairment and preterm SGA and FGR births is well-established, findings among term-born individuals are more variable[10]. Some studies indicate that term SGA and FGR infants are at higher risk for attentional deficits, whereas others report broader cognitive impairments regardless of gestational age, with more pronounced effects observed in term FGR cases[10,11]. Furthermore, both SGA and FGR are consistently linked to long-term motor difficulties, even among term-born individuals. These impairments may include poor coordination, reduced fine and gross motor skills, and lower scores on standardized motor assessments during childhood and adolescence[12,13]. Affected individuals may present with subtle motor dysfunctions and, in the more severe cases, may develop cerebral palsy, which can substantially impact daily functioning and quality of life[9,14].

This mini-review aims to synthesise and critically evaluate the emerging literature on the links between SGA, FGR and gestational age at birth, while also exploring additional factors that may contribute to these associations. To discern the independent effects of these conditions, the present review classifies the neurobehavioral outcomes of SGA and FGR based on preterm and term delivery. Our findings indicate that children born SGA or with FGR exhibit significantly higher rates of neurodevelopmental impairment compared to their appropriate for gestational age (AGA) counterparts across both preterm and term cohorts. Importantly, this review covers a broad age spectrum, providing a comprehensive perspective on long-term outcomes. Moreover, among the studies included, thematic groupings emerged, revealing additional patterns of disease and potential areas for future investigation.

METHODOLOGY

For this narrative review a literature search was conducted using PubMed, EMBASE, and Web of Science to identify original studies published between 2020 and 2025. The search terms included small for gestational age, fetal growth restriction, cognition, motor outcomes, and cerebral palsy. Additionally, reference lists of relevant articles screened to capture further eligible studies. Studies were included if (1) Examined cognitive and/or motor neurodevelopmental outcomes in individuals born SGA and/or FGR at term or preterm; (2) Involved singleton or multiple births from any nationality; and (3) Were human studies published in English. Excluded studies included reviews, non-English, and animal studies. A total of 40 studies met these criteria, an important proportion of which evaluated neurodevelopmental outcomes alongside other perinatal complications. The age at assessment ranged from birth up to 47 years, and a diverse array of both standardized and non-standardized test batteries was employed to evaluate neurodevelopmental outcomes (Table 1)[15-55].

IMPACT OF SGA AND FGR ON COGNITIVE DEVELOPMENT

Effects of SGA on cognitive development in preterm infants

Neurocognitive outcomes in children born preterm and SGA show considerable variability, reflecting the complexity of the contributing factors (Table 2)[15-46]. Several studies assessing infants between 1 year and 2 years old have reported mixed findings. Two studies found that SGA infants had lower developmental scores in cognitive domains compared to AGA[15,16]. However, these findings were not replicated by Lach et al[17], who failed to identify statistically significant differences in neurocognitive outcomes in a similar-aged cohort. Regarding additional factors that may influence cognitive outcomes, Lim et al[18] could not find a clear link between birth weight and cognitive or sensory development in preterm twins born with twin-to-twin transfusion syndrome, while another study by Bae et al[19] identified SGA as a significant factor influencing cognitive outcomes in children with severe retinopathy and bronchopulmonary dysplasia. Besides, early-life hypoglycaemia, a potential contributor to adverse outcomes, showed no significant influence on cognitive performance between hypoglycaemic and normoglycemic SGA infants. However, both groups displayed signs of cognitive impairment, suggesting hypoglycaemia may not be an independent risk factor for cognitive outcome[20]. By age 3, SGA status was associated with cognitive and sensory impairments in two different studies[21,22], although social and behavioural deficits were not detected in the latter[22]. Similarly, in a cohort of preterm children from pregnancies complicated by preeclampsia and maternal renal dysfunction, SGA status showed only a trend toward poorer cognitive performance[23]. At 5 years, Athalye-Jape et al[24] reported higher rates of moderate-severe disability among children born with extreme low birth weight (< 500 g), although SGA itself did not reach statistical significance; notably, hearing issues were prevalent. The inconsistencies in findings likely reflect variations in study design, population characteristics, and the presence of pregnancy-related complications. However, long-term studies reveal more consistent negative impacts associated with SGA. At 8 years, SGA strongly correlated with lower IQ and poorer academic performance[25]. In adulthood, individuals born preterm with very low birth weight scored the lowest across neurocognitive domains compared to their SGA or AGA term-born counterparts, with spatial working memory deficits linked to a higher prevalence of psychiatric disorders (Tables 1 and 2)[26]. Despite discrepancies in individual findings, a consistent observation is that SGA children are more likely to be underweight and exhibit growth stunting, which are considered risk factors for impaired neurocognitive outcomes[15,24,27].

Growing evidence highlights the link between suboptimal growth patterns and cognitive vulnerability, prompting increased efforts to investigate how these factors affect neurodevelopment[56-58]. Cho et al[16] demonstrated a strong association between head growth failure from birth to 35 weeks postmenstrual age and poor neurodevelopment in SGA infants. Another study examining catch-up growth in children with extreme low birth weight found no significant neurodevelopmental differences between SGA and AGA groups, but SGA children exhibited greater early postnatal weight gain and body fat, possibly conferring neuroprotective effects[17]. This indicates that growth patterns are critical in shaping neurodevelopmental outcomes, underscoring the potential for early identification to enable timely therapeutic interventions.

Two studies also explored how different growth reference curves influence the classification of SGA and the results of cognitive assessments. Both reported associations between SGA and major neurodevelopmental disabilities, lower IQ and poor academic achievement[25,28]. However, the diagnostic accuracy of the different growth curves was low, highlighting the need to reassess the effectiveness of current reference standards to identify individuals at risk[25].

Effects of FGR on cognitive development in preterm infants

Another significant contributor to adverse cognitive outcomes in preterm infants is the presence of FGR[59]. An important body of research has focused on outcomes by the age of 2 years. One study of very preterm FGR infants reported poorer cognitive performance and higher risk of developing autism spectrum disorders compared to very preterm AGA infants, along with notable structural brain differences underlying this behavioural phenotype[29]. Similarly, children born with very low birth weight and evidence of fetal vascular malperfusion had a substantially increased risk of neurodevelopmental impairment across multiple domains, with the likelihood of normal cognitive development reduced by more than 70%, even without brain abnormalities at neonatal intensive care unit discharge[30]. Another study confirmed significant cognitive and sensory deficits in preterm FGR infants[31], reinforcing the association between FGR and early developmental challenges. Further insights come from Della Gatta et al[32], who investigated cognitive outcomes in preterm children who experienced EO-FGR with persistent abnormal end diastolic flow, finding that these infants were at higher risk of cognitive impairment. Those with transient abnormal end diastolic flow were also affected, but to a lesser extent. However, Delorme et al[33] failed to identify statistically significant differences in cognitive outcomes between infants with absent or reversed diastolic flow and those with normal or reduced flow. Nonetheless, a notable proportion of FGR infants had cognitive scores below the expected threshold and presented signs of deafness or blindness, highlighting the broader vulnerability within this population[33]. Neither study identified social or behavioural difficulties during early assessments[32,33]. However, by age 4, behavioural problems began to emerge in FGR children born SGA, even when cognitive and sensory impairments were only mild and not statistically significant[34]. Overall, the heterogeneity in findings likely reflects the complex nature of FGR and demonstrate that neurodevelopmental outcomes are influenced not only by FGR itself but also the timing of onset, progression and fetal adaptive responses are critical modifiers of risk. Further, methodological moderators such as assessment tools, age at testing, or confounding comorbidities must be interpreted. This underscores the need for deeper understanding of FGR and better techniques to more accurately assess and quantify the risk faced by affected individuals.

Effects of SGA on cognitive development in term infants

Considering early neurocognitive outcomes in term infants and additional factors that may shape them, Chen et al[35] conducted a study in China exploring the potential role of gut microbiota on neurodevelopment. They found that term SGA infants had lower microbial diversity in the first week of life compared to AGA infants. By 6 months, term-SGA infants with poorer communication scores had increased microbial diversity on day 3 than those with better scores[35]. These findings support the hypothesis that gut microbiome influences neurodevelopment and represent a potential target for future interventions. In contrast, a study in a Pakistani cohort failed to identify statistically significant differences in cognitive and behavioural outcomes between of term SGA and AGA infants at 2 years of age[27]. In addition, maternal factors such as gestational weight gain have been contemplated. Inadequate weight changes during pregnancy have been associated with poorer neurological outcomes at 4 years, including lower scores in problem-solving (odds ratio = 2.08, 95%CI: 1.16-3.56) as well as in emotional domains[36].

Another growing area of investigation focuses on alternative methods for classifying and stratifying birth weight. In this scenario, Tamai et al[37] investigated the association between birth weight and neurodevelopment at 30 months and 66 months. Their findings indicate that the risk of adverse health and developmental delays increased with the severity of SGA in term infants[37]. Similarly, a prospective study in Norway categorized body weights in 0.5 kg intervals, ranging from 1.5 kg to 5.4 kg, and tracked individuals up to the age of 47 years. Children born with less than 3.5 kg at birth were at higher risk of intellectual and sensorial disabilities and showed elevated rates of mental health disorders such as schizophrenia and autism spectrum disorder[38]. This long-term follow-up underscores the importance of birth weight as a determinant of cognitive and mental health outcomes later in life. This is further supported by the study mentioned above which followed affected individuals up to 26 years of age. The study found evidence of impaired cognitive and sensory development, as well as a higher incidence of neuropsychiatric conditions in term SGA individuals compared to those born term AGA, although term SGA individuals performed better than preterm infants[26]. Similarly, another study extending into adulthood reported that SGA status was associated with lower IQ, but these differences became more subtle with increasing age[28]. Together, these findings highlight the heightened risk of impaired cognitive development in SGA infants even born at term and the need of refining birth weight classification methods for better assessment of neurodevelopmental risks. In this context, a study from the Netherlands looked at methods of classifying birth weight by examining fetal growth trajectories and their ability to predict neurodevelopmental outcomes. Participants were categorized as ‘consistently small’ from mid-pregnancy, or as having ‘moderate decrease in weight’ or ‘large decrease in weight’ in later pregnancy. At 6 years of age, children in the ‘consistently small’ group had lowest IQ scores and exhibited more attention deficits than their AGA peers. In contrast, those in the ‘moderate decrease’ or ‘large decrease’ growth trajectories demonstrated neurodevelopmental outcomes comparable to AGA children. These associations remained consistent even after excluding preterm infants from the analysis[39]. Therefore, the research indicates that SGA status might not be the best predictor of cognitive outcomes in term-born individuals, highlighting the importance of considering fetal growth patterns rather than relying solely on birth weight.

Regarding educational performance of SGA infants born at term, Reichman et al[40] conducted a study assessing term SGA children at 9 years of age. The results consistently showed lower vocabulary and academic achievement scores across multiple tests. Notably, this study was conducted in a largely disadvantaged United States population, emphasizing the need to provide support to socioeconomically disadvantaged SGA children[40]. Likewise, a recent study conducted in Vietnam found lower cognitive scores and poorer academic performance, including language and mathematics among term-born SGA individuals at school age. Interestingly, being born preterm but AGA, had no influence on these parameters[41]. Supporting these findings, a Dutch study following children to age 12 found a positive correlation between birth-weight percentiles and school performance and a greater likelihood of attending higher secondary education, with 81%-85% group performing best[42].

The studies cited in this section further highlight the complex relationship between birth weight, fetal growth patterns and additional factors that may have an impact on long-term neurodevelopment, emphasizing the need of multifaceted approach when assessing the risk of adverse cognitive outcomes in SGA infants.

FGR in term born infants has also been associated with neurodevelopmental abnormalities although not all studies have been able to identify this association. An Italian prospective cohort study that investigated neurological development in term individuals with LO-FGR aged 2 years old found subgroup differences, although all remained within normal ranges[43]. Richter et al[44] explored the role of Doppler ultrasound in identifying ‘fetal brain sparing’, a compensatory mechanism in FGR where blood flow is preferentially directed to the brain and other critical organs. They found that this adaptative mechanism and postnatal cerebral oxygen saturation were associated with better overall behavioural outcomes and executive function at 4 years of age. However, postnatal cerebral hyperoxia was negatively associated with brain IQ scores[44], suggesting that responses to FGR critically shape long-term outcomes. Between the age of 5-6 years old, a study in a Taiwanese cohort found that FGR impaired neurodevelopmental outcomes in children born from mothers with hypertensive disorders[45]. Between 5 years and 7 years, Olga et al[46] conducted a study that categorized term individuals into four (1) FGR; (2) AGA with placental dysfunction; (3) Healthy AGA; and (4) Healthy SGA. Individuals in the FGR group showed poorer educational attainment in mid-childhood compared to those with normal fetal growth and no markers of placental dysfunction. Notably, those born healthy SGA showed no cognitive differences with healthy AGA peers[46]. In addition to placental dysfunction, other mechanistic hypotheses that should be considered are inflammation, altered myelination, and epigenetic programming. The contrast in results highlights the need to further investigate the mechanisms and impact of FGR on term-born individuals, and the influence of timing of FGR onset.

IMPACT OF SGA AND FGR ON MOTOR OUTCOMES

Obstetric complications and incidence of cerebral palsy

There is strong evidence that perinatal insults such as FGR, being born SGA or preterm are associated with a higher incidence of cerebral palsy. Among the studies reviewed that analyse this association, Jöud et al[47] found that SGA was a significant risk factor for cerebral palsy in both univariate and multivariate models adjusting for antenatal factors; however, this association disappeared when perinatal factors were included. In relation to preterm birth, a study of ichorionic and monochorionic twins, including cases with twin-to-twin transfusion syndrome, found that cerebral palsy was most frequent in monochorionic twins with transfusion syndrome at 2 years. After excluding these cases, smaller birth weight and greater birth weight discordance were major risk factors for neurodevelopmental impairment[18]. In contrast, in a cohort of very low birth weight infants with no severe brain injury, Bae et al[19] reported only one case of cerebral palsy. At age 3, two Japanese studies reported significant associations between preterm SGA and cerebral palsy[21,48]. Kono et al[48] identified a higher risk among SGA children born to hypertensive mothers, specifically at 24-25 weeks of gestation. Yet, this pattern was inconsistent across gestational ages[48]. A similar heterogeneity was found by Suenaga et al[21] who found an association only among infants born at 26-27 weeks of gestation. These results contrast with those of Hubert et al[22] and Athalye-Jape et al[24], who found no significant associations between being born preterm SGA and an increased incidence of cerebral palsy at 4 years and 5 years of age, respectively.

Regarding the incidence of cerebral palsy in SGA infants born term, a large Norwegian cohort study concluded against this association. Instead, gestational age was a stronger predictor of cerebral palsy risk[49]. Conversely, another extensive longitudinal study accounting for ages between birth and 47 years found a negative correlation between birth weight percentiles and cerebral palsy. The authors suggested that prenatal insults, such as genetic syndromes, intrauterine infections, hypertensive disorders of pregnancy, placental dysfunction and unrecognised placental abnormalities, may underlie the increased cerebral palsy risk, rather than birth weight per se[38]. These contrasting findings may be explained by the latter study’s approach of analysing birth weight as a continuous variable rather than a single percentile cutoff, thereby increasing sensitivity to risk variations. In agreement, Esih et al[50] reported an inverse proportional relationship between birth weight and cerebral palsy risk in children born between 32 weeks and 36 weeks of gestation.

Several studies that account for SGA as a covariate have shown that in preterm infants, SGA status further increased the risk of cerebral palsy (Table 3)[15,17-19,21,22,24-27,30-38,45,47-55]. For instance, Ahmed et al[51] identified SGA, preterm birth, and male sex as significant risk factors. In contrast, Aubert et al[52] found that SGA was linked to higher rates of movement difficulties but not specifically to cerebral palsy. Studies from both Moldova and the UK also identified SGA in term individuals as a significant risk factor for cerebral palsy[53,54]. In addition, Chen et al[45] found that the co-occurrence of FGR and in utero exposure to chronic hypertension or preeclampsia significantly heightened the rate of cerebral palsy.

The prevalence of cerebral palsy in infants exposed to a fetal growth restricted environment has been studied primarily in the context of preterm birth, with studies generally reporting a weak association. In this regard, a study comparing EO-FGR and non-FGR infants found no significant difference in cerebral palsy prevalence between the two groups at 2 years of age[31]. Similarly, a study involving very preterm infants observed a trend toward an association, without reaching statistical significance[33]. Furthermore, in a cohort of SGA-FGR infants, Uberos et al[34] found no association with cerebral palsy at a mean age of 50 months, and concluded that postnatal energy restriction, rather than FGR itself, may be more strongly linked to motor disorders.

Many of the aforementioned studies involved infants exposed to a heterogeneous range of developmental insults. These co-occurring factors may act as potential mediators in the relationship between SGA, FGR and motor neurodevelopmental impairments, and thus represent important avenues for further investigation (Figure 1).

Effects of SGA on motor development in preterm infants

Infants exposed to fetal and perinatal insults may present with mild neuromotor impairments that do not meet the diagnostic criteria for cerebral palsy. Evidence from studies examining early postnatal development, particularly between 1 year and 2 years of age, remain inconsistent. For instance, in a neurodevelopmental assessment of 1 year old infants, Lach et al[17] not only failed to detect impaired cognitive development, but also neuromotor impairments in a cohort of SGA children compared to AGA. In contrast, a study from India reported that preterm SGA infants aged between 12 months and 18 months exhibited poorer motor development than their preterm AGA counterparts[15]. As previously noted, Bae et al[19] observed an elevated risk of neurodevelopmental impairment in infants born with retinopathy of prematurity and bronchopulmonary dysplasia at 24 months; however, this risk was not attributed to deficits in the motor domain. Conversely, Lim et al[18] found that motor impairments significantly contributed to neurodevelopmental delays in a cohort of twins, some of whom had experienced twin-to-twin transfusion syndrome[18].

During school age, particularly between the ages of 5 years and 8 years, several studies have reported neuromotor impairments in children born SGA. In a cohort extremely preterm children, Aubert et al[52] identified SGA as a significant risk factor for movement difficulties, alongside variables such as primiparity and severe brain lesions. Another study found that SGA children exhibited poor motor coordination, with significantly lower scores in the subscale ‘control during movement’ (mean -0.96, 95%CI: -1.78 to -0.13, P = 0.02)[55]. These findings are further supported by Doyle et al[25], who confirmed an association between SGA status and impaired motor performance in preterm infants. Long-term consequences of perinatal morbidities were also evident in a follow-up study extending to 26 years of age, where individuals born preterm with very low birth weight showed significantly poorer outcomes in psychomotor and fine motor speed compared to controls[26].

Findings on neuromotor outcomes in preterm SGA infants during early developmental stages appear to be inconsistent. However, from school age onward, there is an increasing consensus that these children are at heightened risk for motor difficulties. These discrepancies may reflect inherent variability in early motor development, where some infants progress more slowly despite the absence of underlying pathology, potentially masking subtle motor impairments.

Effects of SGA on motor development in term infants

In term-born infants, certain early-life factors have been linked to motor developmental delays. The study by Chen et al[35] found that specific gut microbial compositions negatively correlated with fine motor scores on day 1 and gross motor scores on day 7. The study on maternal weight reported an increased risk of motor delays at the age of 4 years caused by inadequate weight gain during pregnancy[36]. Similarly, Tamai et al[37] found that children with the lowest birth weights had the poorest neurobehavioral outcomes at 2.5 years, including difficulties with tasks such as running. They identified a significant association between lower birth weight for gestational age and heightened risk of neurodevelopmental delay[37]. Another study observed that SGA children scored significantly lower in fine motor domains, but not in gross motor domains at 2-4 years of age. The authors noted key limitations, including the use of a single time-point for assessment and the failure to account for the heterogeneous causes of SGA within the cohort[27]. By adulthood, as previously mentioned, individuals born preterm with very low birth weight continued to show deficits in psychomotor and fine motor speed. However, these impairments were no longer evident in term-born SGA individuals, suggesting a possible catch-up in motor function over time[26]. In general terms, these studies indicate that while term SGA infants may experience motor delays in early childhood, they seem to resolve by adulthood.

Effects of FGR on motor development

The impact of FGR on motor development has been investigated to a lesser extent, with most research focusing on preterm infants around 2 years of age. Delorme et al[33] observed that very preterm neonates with suspected FGR or maternal hypertensive disorders were more likely to be diagnosed with moderate to severe neuromotor disabilities at 2 years. However, two other studies assessing infants at a similar age failed to replicate this association[30,32]. At 50 months, Uberos et al[34] found a slight increase in mild motor impairments among SGA infants, closely associated with postnatal energy restriction, rather than FGR, as mentioned above. As seen in studies in SGA populations, the natural variability in motor development among healthy children may obscure the detection of differences caused by pathological factors, making it challenging to clearly discern the effects of FGR on motor outcomes.

LIMITATIONS

This mini-review has several limitations that constrain the conclusions regarding the impact of SGA and FGR on neurodevelopment in both preterm and term individuals. A major challenge is the considerable heterogeneity in outcome measurements across studies. In term cohorts, the Griffiths Mental Development Scale was the most used tool, whereas in preterm cohorts there was minimal overlap of testing methods. Follow-up ages also varied widely, particularly in preterm studies. Further, differences were seen in study definitions. While preterm births were commonly defined as < 37 weeks, other definitions were used. SGA was often classified as birth weight < 10%, but heterogeneity was introduced by the use of different growth charts and standards depending on where the study was conducted. Some studies even used novel approaches, such as standard deviations or further subdivisions of SGA. Similarly, FGR definitions varied, and distinctions between EO-FGR and LO-FGR were often omitted, despite potentially different outcomes. The lack of standardization of neurodevelopmental tests and potential regional bias toward high-income populations make it difficult to ascertain true statistics. These divergences underscore the need for standardized definitions and assessments protocols to improve comparability and deepen our understanding of the neurodevelopmental outcomes of SGA and FGR born at any gestational age.

CONCLUSION

Overall, this review shows that infants born either SGA or FGR are at higher risk of developing cognitive impairment, with delays often persisting throughout life. However, in preterm cohorts, some studies failed to find significant associations. In addition, sensorial and behavioural outcomes were assessed less frequently and showed mixed results, with some studies reporting increased risks and other findings no differences.

For neuromotor outcomes, evidence for cerebral palsy among preterm SGA and FGR infants was inconsistent, and not all studies observed increased risks of other motor impairments. In term cohorts, few studies investigated cerebral palsy specifically, with conflicting findings across developmental stages. In contrast, studies assessing broader motor impairments in term-born infants showed more consistent evidence of higher risk.

The heterogeneity in both cognitive and motor outcomes likely reflects differences in study design, definitions and underlying biological or environmental factors. Identifying these mediators is key to developing targeted interventions that can reduce long-term neurodevelopmental challenges. Early developmental surveillance and rehabilitation strategies would be extremely beneficial in this vulnerable population. Despite advances in research and clinical practice, further work is needed to fully understand and address the complex impacts of SGA and FGR on neurodevelopment. Finally, it would be advantageous for harmonised protocols and international registries to track longitudinal cognitive-motor trajectories in SGA/FGR cohorts.