Critical Period

Critical and sensitive periods are times when development of a particular area may be most influenced by environmental factors. The terms may be confusing, particularly when applied to behavior, because they do not have commonly accepted meaning and the research designs required to demonstrate them behaviorally can rarely be conducted. Strictly, critical periods are relatively brief and discrete times when particular experiences have irreversible effects regardless of subsequent experience. Effects may be due to the absence of normal, or presence of abnormal, experience. Originating in embryology, they have been applied to numerous areas of human development, including socialization, personality, language, and cognition. The concept is closely related to claims that early experience, as opposed to merely prior experience, has lasting impact on the organism. Critical/sensitive periods are often viewed as “windows of opportunity.” Only when the windows are open can environmental factors influence development.  However,  as  Bateson  suggested,  such “opened or closed” views of the effects of timing of experience on development are oversimplified when applied to complex behavior.

Historical Overview

The embryological critical/sensitive period concept originated in two classic research programs in the 1920 and 1930s:

1. Working with fish  embryos,  Stockard  (1921) found that physical and chemical agents created “monsters” if presented during rapid cell proliferation and differentiation, but had essentially no effect if presented earlier or later. Permanent damage occurred when an agent interrupted normal development during “sensitive periods” or “critical moments.”

2. Studying differentiation in amphibian embryos, Spemann (1938) transplanted cells at various times from their original donor site to a different host site. Cells transplanted early developed appropriate to the host site, whereas those transplanted later developed appropriate to the donor site. Equipotential development was followed by determined development. Spemann viewed differentiation as a process of “cellular induction” occurring during a “critical period” in normal development.

The critical period concept quickly became applied to behavior. Lorenz apparently first used it in 1937 in his account of imprinting, the process through which newly hatched precocial birds presumably develop filial attachments and species identification (but see Gottlieb for an alternative approach). He suggested that imprinting’s “two chief characteristics,” restriction to a narrow time period and irreversibility, were “in common with Spemann’s inductive determination… .” In 1962, Scott stated, “Critical periods determine the direction of social, intellectual, and emotional development.” For Scott, experience during such periods influenced development in at least two ways: (1) acting at a “turning point” leading toward normal or abnormal development, and (2) producing an irreversible effect that subsequent experience cannot modify. Essentially, experience at a critical time directed the organism down a particular one-way developmental path. Scott’s general principle of organization suggested that as any system becomes organized, from differentiating embryonic cells to developing behavior patterns of young animals, reorganization of the system becomes progressively more difficult. That is, “organization inhibits reorganization.”

Indeed, he claimed that major modification can occur only during organization. Other mid–20th century factors brought critical periods to wide attention. Consider:

1. They fit with Freudian psychodynamic theory’s emphasis on the role of early experience in determining personality, then dominant in many areas of psychology and psychiatry.

2. In his influential 1951 review of maternal deprivation, Bowlby stated that depriving young children of maternal care for a prolonged period may have lifelong adverse consequences: “[I]t is a proposition exactly similar in form to those regarding the evil after-effects of rubella in foetal life. . . .”

3. Hebb’s theory proposed that first learning was necessary for optimal brain development and functioning

4. Lenneberg (1967) proposed a critical period for language acquisition. Its beginning owed to lack of maturation, and its end apparently “related to a loss of adaptability and inability for reorganization in the brain… .”

5. A variety of  experimental  nonhuman  research supported the apparent existence of critical periods. For example, infant rats reared in enriched environments had larger brains and better problem-solving abilities than those raised in restricted environments, female goats needed contact with their newborn kids to develop maternal attachment, Harlow’s infant monkeys deprived of maternal care showed aberrant social behavior, young songbirds needed particular early experience to develop normal song, and early hormone manipulation permanently modified sexual behavior in rodents. The latter is of particular interest because it clearly demonstrated the importance of timing: Testosterone injections in newborn female rats or castration of newborn male rats produced opposite-sex behavior (with appropriate hormone replacement) in adulthood, whereas similar manipulations even in later infancy had no such effect. Some of this research is reprinted in books of readings edited by Denenberg and Scott.

Current Embryological Concept

Critical/sensitive periods are associated with the development of virtually all organ systems. In this section, critical period and sensitive period refer to times when teratogens  may  cause  major  morphological  damage and minor morphological/functional damage, respectively, as suggested by Moore and Persaud, who have an excellent figure of human critical/sensitive periods. The embryonic period in humans is often described as “the critical period” since most organogenesis and severe effects of teratogens occur then. Such a description is oversimplified, however, because critical periods for various organ systems have different onsets and durations. The longest, for the central nervous system (CNS), extends to the 16th week of pregnancy, well into the fetal period. Sensitive periods for four systems— CNS, eyes, teeth, and external genitalia—extend for years after birth, resulting in potential adverse effects of abnormal environmental influences or positive effects of supportive environmental influences well into childhood or adolescence. Examples of adverse effects include effects of tetracycline in infancy/early childhood on mottling of permanent teeth and of heavy metals and infections on CNS development. Examples of positive effects include early surgical removal of congenital cataracts on visual acuity and depth/pattern perception and a low phenylalanine diet in infancy on CNS development of those with phenylketonuria.

Critical periods for components of organ systems are more circumscribed. Perhaps most dramatically, thalidomide’s teratogenic effects were limited to 34 to 50 days past the last menstrual period. Ingestion at 34 to 38 days was associated with absence of external ears, whereas ingestion at 38 to 48 days was associated with a complex of malformations, including absence or severe shortening of arms and legs (phocomelia), malformed ears, and hip dislocation. Differing critical periods can make diagnosis of teratogenic syndromes difficult. For example, fetal alcohol syndrome (FAS) is classically diagnosed through a triad of characteristics: facial abnormalities, growth retardation, and CNS dysfunction. Since the critical period for facial features is far shorter than that for the CNS, children whose mothers drank heavily after the end of the critical period for facial features may show serious cognitive and behavioral deficiencies but normal facies. Such children may not meet FAS diagnostic criteria.

Current Behavioral Concept

Many researchers question the value of applying a strict critical period concept to behavioral development. Some supposed critical periods are neither as circumscribed nor as irreversible as originally claimed. Lorenz, Scott, and Bowlby and others appear to have overstated the parallels between the effects of timing of experience in embryo-genesis and those on behavioral development. For example, under certain experimental conditions,  imprinting  can  occur  well  beyond  the  normal end of its “critical period” and can be reversed from one object to another. A critical period for development of human attachment has been questioned both by methodological criticism of early research and by recent findings that some children adopted after extensive early deprivation develop appropriate attachment and social behavior. Little evidence supports the claim that the first 3 years of human life are truly critical for later development, although of undoubted importance. Thus, numerous authors, including Bailey, Bruer, Symons, and Lichtman; Bateson; Bornstein; Bruer; Huttenlocher; and Shonkoff and Phillips, have suggested that critical period, implying discrete length and irreversibility, be replaced with the more flexible sensitive period to describe effects of timing on behavior.

Direct and indirect evidence supports important roles of such sensitive periods in human development. Noninvasive methods of studying brain structure and function are revealing a variety of periods of rapid postnatal brain development and synaptic pruning, particularly experience-expectant ones. Behavioral as well as neurological evidence exists for sensitive periods in development of components of sensory systems, first language learning, motor behavior, and other areas associated with early brain plasticity. Furthermore, aberrant early relationships and other experiences can have broad adverse long-term effects on children, although the underlying processes are not well understood. The complex effects of early experience can be seen in ongoing publications of the  NICHD  Study  of  Early  Child  Care  and Youth Development (http://secc.rti.org/home.cfm). As Bateson suggested, no single window of opportunity applies to timing of environmental influence. Critical/sensitive periods are of different types, lengths, rates of onset and offset, and underlying processes. Bornstein thoughtfully reviews and analyzes these issues. They are also subject to individual differences and different environmental conditions.

References:

1. Bailey, B., Bruer, J. T., Symons, F. J., & Lichtman, J. W. (Eds.). (2001). Critical thinking about critical periods. Baltimore: Paul H. Brookes.
2. Bateson, P. P. G. (1978). How do sensitive periods arise and what are they for? Animal Behaviour, 27, 470–486.
3. Bornstein, M. H. (1989). Sensitive periods in development: Structural characteristics and causal Psychological Bulletin, 105, 179–197.
4. Bruer, T. (1999). The myth of the first three years. New York: Free Press.
5. Denenberg, V. (Ed.). (1978). The development of behavior.Stamford, CT: Sinauer.
6. Gottlieb, G. (1971). Development of species identification in birds. Chicago: University of Chicago
7. Hebb, D. O. (1949). Organization of behavior. New York: Wiley. Huttenlocher, P. (2002). Neural plasticity. Cambridge, MA: Harvard University Press.

8. Lenneberg, H. (1967). Biological foundations of language. New York: Wiley.
9. Lorenz, K. Z. (1937). The companion in the bird’s w Auk, 54, 245–273.
10. Moore, L., & Persaud, T. V. N. (2003). The developing human: Clinically oriented embryology (7th ed.). Philadelphia: Saunders.
11. RTI International. (n.d.). NICHD study of early child care and youth development. Retrieved from http://secc.rti.org/cfm
12. Scott, P. (1962). Critical periods in behavioral development.Science, 138, 949–958.
13. Scott, J. P. (Ed.). (1978). Critical periods. Stroudsberg, PA: Dowden, Hutchinson, & Shonkoff, P., & Phillips, D. A. (Eds.). (2000). From neurons to neighborhoods: The science of early childhood development. Washington, DC: Institute of Medicine Press.
14. Spemann, (1938). Embryonic development and induction.New Haven, CT: Yale University Press.
15. Stockard, C. R. (1921). Developmental rate and structural expression: An experimental study of twins, ‘double monsters’ and single deformities, and the interaction among embryonic organs during their origin and dev American Journal of Anatomy, 28, 115–275.