Introduction
Infants generally have a large head compared to the rest of their habitus, and the cervical group of paraspinal muscles is relatively weak at birth. Hence the reason for the notable head lag, especially during the first few weeks of life. During this stage, caregivers routinely support the infant's head until neck control is achieved. The gross motor skill development in infants typically follows a cephalocaudal sequence, and the gain of postural control heralds it. Postural control is an infant's ability to stabilize the center of their body mass/trunk with a dynamic or static base. This innate maturational process of the neck and trunk muscles is expected to evolve rapidly during the infancy stage. When an infant is pulled by the hand from a lying to sitting position, the expected response is to activate the head righting reflex and maintain the head position in line with his/her shoulders. Conversely, infant head lag is observed when the head seems to flop around or lags posteriorly behind the trunk during the pull-to-sit maneuver.
Several articles have maintained that head lag should be absent by age 3 to 4 months when infants typically experience an increased ability to control their neck muscles.[1] Once neck control is attained, infants participate actively in a normal pick-up routine by stiffening their neck muscles while tensing up their trunk to decrease the lag between the chin and chest.[2] Persistent head lag beyond age 4 months has been associated with poor neurodevelopmental outcomes.[3]
There is a higher incidence of head lag amongst preterm neonates and infants with cerebral palsy, and it is a likely predictor of developmental outcome. It may, however, not be accurate in predicting neurobehavioral effects when used as an isolated metric. A possible explanation could be that assessing one isolated response is not enough to predict neurodevelopmental outcomes accurately. Many studies have suggested that a combination of neonatal responses, like reflex responses, postural reactions, and tone, may hold the potential to predict alteration in brain development correctly.[4][5]
Studies have also shown that head lag combined with other early childhood developmental alterations may be intricately linked with a higher risk of autism in specific populations. Head lag was more commonly observed in siblings of children with autism spectrum disorder (ASD) than low-risk infants.[3] Similarly, developmental problems relating to postural instability and axial hypotonicity have been described in infants with ASD.[6][7]
Etiology
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Etiology
Essentially, infant head lag can be physiological or pathological. Physiological head lag is attributed to the expected delay in the development of the neuromuscular pathway. In contrast, pathological infant head lag can be caused by myogenic and/or neurogenic deviations and several underlying problems, resulting in postural instability and axial hypotonicity.
Head lag could result from abnormal sensory functioning. Failure to detect a change in head position (attributable to abnormal feedback from the vestibular-ocular righting and proprioception systems) could lead to an inability to make the necessary motor adjustments in anticipation of a change in positioning.[3] This explanation is reasonable, considering previous research suggesting problems with anticipatory motor and postural control, and in the addition of sensory input.[8][9][8]
According to several studies, head and neck control is affected by various medical conditions such as prematurity, cerebral injury, low birth weight, and environmental factors, including extensive mechanical ventilation in the neonatal period.[10][11][12] Head lag also provides useful clinical information regarding the muscle tone of a preterm infant. The delay in head righting during infancy may be attributed to poorly developed muscle tone in preemies. Healthy preterm infants without any identifiable neurological pathology may have poor motor development, contrasted with term infants, and prolonged head lag in preterm infants has been documented even at term-equivalent age.[13][14]
Epidemiology
Head lag is more prevalent in preterm infants up to term-equivalent age; contrarily, most full-term infants can maintain their head position during the pull-to-sit test.[1][13] An article published by the American Journal of Occupational Therapy investigated changes in head lag across postmenstrual age (PMA) in infants born before 30 weeks gestation. It revealed that 90% of infants exhibited head lag at 30 weeks PMA, about 60.5% at 34 weeks PMA, and 57.8% at term-equivalent age. More head lag was also witnessed in infants who had perinatal complications.[1]
One prospective study at Hadassah Medical Centre in Jerusalem, Israel, found that only 4% of full-term newborn infants had head lag on routine clinical examination. However, 20% of these infants with head lag had other risk factors, including vacuum delivery, probable sepsis, and congenital malformations. In the remaining 80% (i.e., the group without risk factors), 62.5% had mild head lag, and 37.5% had moderate to severe head lag.[15]
History and Physical
The routine newborn/infant examination involves a neurological assessment of muscle tone. Head and neck control is a critical component of that examination. Mild head lag is a common finding in newborns and usually resolves by itself; however, the presence of severe persistent head lag beyond 3 to 4 months of age typically points to disorders related to hypotonia and muscle weakness in infancy.[15] Thus, obtaining a comprehensive history is crucial in narrowing the long list of differential diagnoses for hypotonia.
Specific attention must be given to pregnancy, birth history, post-natal period, developmental milestones, and family history. Perinatal risk factors include low gestational age, polyhydramnios, breech presentation, parental age, drug or teratogen exposure, consanguinity, maternal diseases (epilepsy/diabetes), congenital infections (TORCHES), or post-natal insults (sepsis and prolonged NICU stay).
A complete physical examination is necessary to assess for potential syndromes and other associated causes of infantile hypotonia. Dysmorphic features increase the chances of CNS dysfunction as an explanation for hypotonia, and a finding of ptosis is suggestive of neuromuscular junction disorders.[16]
When assessing tone, it helps to keep the child relaxed, not crying, and alert. Truncal and nuchal tone examination is done using vertical and horizontal suspension tests. On horizontal suspension, the infant should maintain a straight back with the head upright and limbs flexed. On vertical suspension, a vigorous infant should keep the head upright while sitting. The degree of head lag is measured by how far the head falls posteriorly behind the shoulders during the pull-to-sit test.[13]
Head lag can be divided into three categories based on severity. Mild head lag is when the infant tries to maintain his/her head when pulled forward to a sitting position. Moderate head lag occurred when no effort was made to keep the head in an upright position while being pulled forward, but he/she could maintain the head position while sitting. Severe head lag is when an infant cannot raise his head during the pull-to-sit maneuver and failed to hold his/her head upright while sitting.[15]
Evaluation
A detailed and schematic approach is required in the evaluation of a newborn with head lag. This approach starts with a comprehensive clinical examination and history. Isolated infant head lag before 3 to 4 months, in the absence of other features of hypotonia or syndromic face, can be observed with little concern for further investigations. However, persistent head lag or severe head lag with or without other generalized hypotonia features needs to be worked extensively.
A study in Israel found that a simple clinical test, a "feeding test,” could differentiate physiological from pathological infant head lag. In that study, healthy newborns were fed with a follow-up post-prandial reassessment of their head lag. Fifteen minutes after feeding, about 92% showed improvement or complete disappearance of head lag with a rise in serum glucose, and the remaining infants with persistent head lag were later diagnosed with pathological causes (Soto syndrome, hypothyroidism, and cerebral palsy).[15]
Investigations to consider based on the suspected differential diagnosis for pathological head lag include TSH, free T4, electrolytes (including calcium), septic screen, and more specific tests like CT/MRI head/neck, EEG, karyotype, urine and serum amino acids, urine organic acids, blood gas, serum ammonia, liver function tests, aldolase, creatine kinase and appropriate referral to a neurologist.[17]
Treatment / Management
Physiological infant head lag has a benign presentation, and watchful waiting is most times sufficient, as most of the cases will resolve before the age of four months (and four months corrected gestational age in preterm infants) without any intervention. However, an interdisciplinary approach is required to assess and manage pathological head lag (i.e., persistent head lag after four months or severe head lag before four months of age) while addressing the underlying etiology. A pediatrician, child neurologist, medical geneticist, a physical and occupational therapist can work together to accomplish optimal results.
Systematic reviews have demonstrated that early intervention, through specific motor training routines and global developmental programs where parents are taught how to promote infant development, maybe the most reliable approach to promoting infant motor and cognitive development for groups at risk of developmental motor disorder.[18] Occupational therapists and physical therapists play an essential role in addressing sensorimotor skills to improve infants' participation. Some motor training routines include home exercises like reverse cradling, tummy time, toys, and strengthening the neck muscles.(A1)
Differential Diagnosis
Most pathologic causes of infant head lag are linked to conditions causing neonatal/infantile hypotonia. These conditions make up a list of differential diagnoses to consider when assessing an infant with persistent or severe head lag. This includes chromosome disorders (i.e., Prader Willi), Hypoxic-ischemic injuries, cerebral dysgenesis, spinal cord injuries, spinal muscular atrophies, congenital hypomyelination neuropathy, familial dysautonomia, infantile neuronal degeneration, CNS infections (i.e., meningitis and encephalitis), infantile botulism, congenital and transient myasthenia gravis, muscular dystrophies, metabolic myopathies (i.e., hypothyroidism), central core disease/fiber myopathies and other congenital myopathies.[17]
Prognosis
Otherwise, healthy infants with physiological head lag have a good prognosis; typically, symptoms resolve without intervention. On the other hand, pathological head lag is dependent on early effective physical therapy and treatment of the underlying etiology.
Complications
Infants with head lag can have trouble breastfeeding due to poor latching. Other problems are specific to the associated secondary cause, e.g., respiratory distress in infantile myasthenia gravis.
Deterrence and Patient Education
Assessment of head lag should be a routine part of well child care in the first six months of life. It is essential to properly educate the parents about the timeline of motor developmental milestones. This information helps prevent unnecessary anxiety and intervention by the parents while also keeping them abreast of what to expect and when to see a physician for further evaluation of a pathological head lag. Head lag beyond four months typically requires investigation, and early intervention through home physical therapy, with the parents, actively involved, has been shown to improve outcomes.[18]
Enhancing Healthcare Team Outcomes
Like many disease conditions, early detection is critical in the management of infant head lag. During well-visits, pediatricians and family physicians must watch for red flags like significant hypotonia or concern for developmental delay, based on the perinatal risk factors and family history. In infants with a higher risk of developing autism (positive family history of ASD in siblings), findings suggest the need for developmental surveillance, promoting earlier access to intervention. [Level 3]
Pediatric neurologists and medical geneticists should also be consulted early to evaluate suspected CNS pathologies, syndromes, and genetic diseases associated with infant head lag.[19][20] This interprofessional team approach can spur earlier intervention, promptly addressing issues contributing to head lag and improving patient outcomes. Occupational therapists and physical therapists also play a crucial role in early identification and intervention to address sensorimotor and social skills to enhance participation in infants with red flags for ASD.[3] [Level 5]
References
Pineda RG, Reynolds LC, Seefeldt K, Hilton CL, Rogers CL, Inder TE. Head Lag in Infancy: What Is It Telling Us? The American journal of occupational therapy : official publication of the American Occupational Therapy Association. 2016 Jan-Feb:70(1):7001220010p1-8. doi: 10.5014/ajot.2016.017558. Epub [PubMed PMID: 26709421]
Fantasia V, Markova G, Fasulo A, Costall A, Reddy V. Not Just Being Lifted: Infants are Sensitive to Delay During a Pick-Up Routine. Frontiers in psychology. 2015:6():2065. doi: 10.3389/fpsyg.2015.02065. Epub 2016 Jan 20 [PubMed PMID: 26834674]
Flanagan JE, Landa R, Bhat A, Bauman M. Head lag in infants at risk for autism: a preliminary study. The American journal of occupational therapy : official publication of the American Occupational Therapy Association. 2012 Sep-Oct:66(5):577-85. doi: 10.5014/ajot.2012.004192. Epub [PubMed PMID: 22917124]
Level 2 (mid-level) evidenceFutagi Y,Suzuki Y,Goto M, Clinical significance of plantar grasp response in infants. Pediatric neurology. 1999 Feb; [PubMed PMID: 10082338]
Level 2 (mid-level) evidenceFutagi Y,Tagawa T,Otani K, Primitive reflex profiles in infants: differences based on categories of neurological abnormality. Brain [PubMed PMID: 1456382]
Bryson SE, Zwaigenbaum L, Brian J, Roberts W, Szatmari P, Rombough V, McDermott C. A prospective case series of high-risk infants who developed autism. Journal of autism and developmental disorders. 2007 Jan:37(1):12-24 [PubMed PMID: 17211728]
Level 3 (low-level) evidenceAdrien JL, Lenoir P, Martineau J, Perrot A, Hameury L, Larmande C, Sauvage D. Blind ratings of early symptoms of autism based upon family home movies. Journal of the American Academy of Child and Adolescent Psychiatry. 1993 May:32(3):617-26 [PubMed PMID: 7684363]
Minshew NJ, Sung K, Jones BL, Furman JM. Underdevelopment of the postural control system in autism. Neurology. 2004 Dec 14:63(11):2056-61 [PubMed PMID: 15596750]
Martineau J, Schmitz C, Assaiante C, Blanc R, Barthélémy C. Impairment of a cortical event-related desynchronisation during a bimanual load-lifting task in children with autistic disorder. Neuroscience letters. 2004 Sep 9:367(3):298-303 [PubMed PMID: 15337253]
Level 3 (low-level) evidenceJeng SF, Yau KI, Liao HF, Chen LC, Chen PS. Prognostic factors for walking attainment in very low-birthweight preterm infants. Early human development. 2000 Sep:59(3):159-73 [PubMed PMID: 10996272]
Samsom JF, de Groot L, Bezemer PD, Lafeber HN, Fetter WP. Muscle power development during the first year of life predicts neuromotor behaviour at 7 years in preterm born high-risk infants. Early human development. 2002 Jul:68(2):103-18 [PubMed PMID: 12113996]
Tsai WH, Hwang YS, Hung TY, Weng SF, Lin SJ, Chang WT. Association between mechanical ventilation and neurodevelopmental disorders in a nationwide cohort of extremely low birth weight infants. Research in developmental disabilities. 2014 Jul:35(7):1544-50. doi: 10.1016/j.ridd.2014.03.048. Epub 2014 Apr 23 [PubMed PMID: 24769371]
Level 2 (mid-level) evidenceAllen MC, Capute AJ. Tone and reflex development before term. Pediatrics. 1990 Mar:85(3 Pt 2):393-9 [PubMed PMID: 2304800]
Pineda RG, Tjoeng TH, Vavasseur C, Kidokoro H, Neil JJ, Inder T. Patterns of altered neurobehavior in preterm infants within the neonatal intensive care unit. The Journal of pediatrics. 2013 Mar:162(3):470-476.e1. doi: 10.1016/j.jpeds.2012.08.011. Epub 2012 Oct 1 [PubMed PMID: 23036482]
Level 2 (mid-level) evidenceLinder N, Tsur M, Kuint J, German B, Birenbaum E, Mazkereth R, Lubin D, Reichman B, Barzilai A. A simple clinical test for differentiating physiological from pathological head lag in full-term newborn infants. European journal of pediatrics. 1998 Jun:157(6):502-4 [PubMed PMID: 9667409]
Crawford TO. Clinical evaluation of the floppy infant. Pediatric annals. 1992 Jun:21(6):348-54 [PubMed PMID: 1620559]
Leyenaar J, Camfield P, Camfield C. A schematic approach to hypotonia in infancy. Paediatrics & child health. 2005 Sep:10(7):397-400 [PubMed PMID: 19668647]
Blauw-Hospers CH, Dirks T, Hulshof LJ, Bos AF, Hadders-Algra M. Pediatric physical therapy in infancy: from nightmare to dream? A two-arm randomized trial. Physical therapy. 2011 Sep:91(9):1323-38. doi: 10.2522/ptj.20100205. Epub 2011 Jun 30 [PubMed PMID: 21719636]
Level 1 (high-level) evidenceLanda R, Garrett-Mayer E. Development in infants with autism spectrum disorders: a prospective study. Journal of child psychology and psychiatry, and allied disciplines. 2006 Jun:47(6):629-38 [PubMed PMID: 16712640]
Level 2 (mid-level) evidenceJohnson CP, Myers SM, American Academy of Pediatrics Council on Children With Disabilities. Identification and evaluation of children with autism spectrum disorders. Pediatrics. 2007 Nov:120(5):1183-215 [PubMed PMID: 17967920]