In developmental psychology and developmental biology, a critical period is a phase in the life span during which an organism has heightened sensitivity to exogenous stimuli that are compulsory for the development of a particular skill. If the organism does not receive the appropriate stimulus during this "critical period", it may be difficult, ultimately less successful, or even impossible, to develop some functions later in life. The general idea is that failure to learn a particular skill allows the cortical areas normally allocated for that function to fall into disuse; as a result these unused brain areas will eventually adapt to perform a different function and therefore will no longer be available to perform other functions. The concurrence of critical periods for the auditory, visual, and vestibular systems suggests that the time period may be universal for emergent sensory systems.
This is fundamentally different from the sensitive period, which is a more extended period of time during development when an individual is more receptive to specific types of environmental stimuli, usually because nervous system development is especially sensitive to certain sensory stimuli. This makes the individual more predisposed to learning.
For example, the critical period for the development of a human child's binocular vision is thought to be between three and eight months, with sensitivity to damage extending up to at least three years of age. Further critical periods have been identified for the development of hearing and the vestibular system. There are critical periods during early postnatal development in which imprinting can occur, such as when a greylag goose becomes attached to a parent figure within the first 36 hours after hatching. A young chaffinch must hear an adult singing before it sexually matures, or it will never properly learn the highly intricate song. These observations have led some to hypothesise a critical period for certain areas of human learning, particularly language acquisition.
Confirming the existence of a critical period for a particular ability requires evidence that there is a point after which the associated behavior is no longer correlated with age and ability stays at the same level (in text citation). Those who are exposed to the stimuli after the critical period should perform significantly worse than those who were exposed to the same stimuli at the appropriate time. Some experimental research into critical periods has involved depriving animals of stimuli at different stages of development while other studies have looked at children deprived of certain experiences due to illness (such as temporary blindness), or social isolation (such as feral children). Many of the studies investigating a critical period for language acquisition have focused on deaf children of hearing parents.
First language acquisition
The Critical Period Hypothesis states that the first few years of life constitute the time during which language develops readily and after which (sometime between age 5 and puberty) language acquisition is much more difficult and ultimately less successful. The critical period hypothesis was proposed by linguist Eric Lenneberg in 1967.
Penfield and Roberts (1959) and Lenneberg (1967) were the first to propose a critical period for first language acquisition. This hypothesis was based on evidence from (1) feral children and victims of child abuse who were reared without exposure to human language and thus were unable to fully acquire the ability to produce it; (2) deaf children who were unable to develop spoken language after puberty; (3) evidence that children with aphasia have a better chance at recovery than aphasiac adults. The critical hypothesis, Lenneberg (1967) states that the early-to-mid childhood (age 5 to puberty) constitutes the time during which language develops readily and after which language acquisition is much more difficult and ultimately less successful.
The CPH was developed further by Pinker (1994), who proposed that language acquisition is guaranteed during childhood, progressively jeopardized until puberty ends, and is improbable thereafter. According to Pinker, physiological changes in the brain are conceivable causes of the terminus of the critical period for language acquisition.
The most famous cases of children who did not acquire language normally are Genie and Victor of Aveyron. However, it is also possible that these children were retarded from infancy and abandoned because of this, or that inability to develop language came from the bizarre and inhuman treatment they suffered.
Other evidence comes from neuropsychology where it is known that adults, well beyond the critical period, are more likely to suffer permanent language impairment from brain damage than are children, believed to be due to youthful resiliency of neural reorganization. The nature of this phenomenon, however, has been one of the most fiercely debated issues in psycholinguistics and cognitive science in general for decades.
Second language acquisition
The theory has often been extended to a critical period for second language acquisition, although this is much less widely accepted. Certainly, older learners of a second language rarely achieve the native-like fluency that younger learners display, despite often progressing faster than children in the initial stages. This is generally accepted as evidence supporting the CPH. David Singleton (1995) states that in learning a second language, "younger = better in the long run," but points out that there are many exceptions, noting that five percent of adult bilinguals master a second language even though they begin learning it when they are well into adulthood — long after any critical period has presumably come to a close. "The critical period hypothesis holds that first language acquisition must occur before cerebral lateralization is complete, at about the age of puberty. One prediction of this hypothesis is that second language acquisition will be relatively fast, successful, and qualitatively similar to first language only if it occurs before the age of puberty."
In mammals, neurons in the brain which process vision actually develop after birth based on signals from the eyes. A landmark experiment by David H. Hubel and Torsten Wiesel (1963) showed that cats which had one eye sewn shut from birth to three months of age (monocular deprivation) only fully developed vision in the open eye. They showed that columns in the primary visual cortex receiving inputs from the other eye took over the areas that would normally receive input from the deprived eye. In general electrophysiological analyses of axons and neurons in the lateral geniculate nucleus showed that the visual receptive field properties was comparable to adult cats; however, the layers of cortex that were deprived had less activity and fewer responses were able to be isolated. The kittens had abnormally small ocular dominance columns (part of the brain that processes sight) connected to the closed eye, and abnormally large columns connected to the open eye. This did not happen to adult cats even when one eye was sewn shut for a year. Later experiments in monkeys found similar results.
In a follow-up experiment, Hubel and Wiesel (1963) explored the cortical responses present in kittens after binocular deprivation; they found it difficult to find any active cells in the cortex, and the responses they did get were either slow-moving or fast-fatiguing. Furthermore, the cells that did respond selected for edges and bars with distinct orientation preferences. Nevertheless, these kittens developed normal binocularity. Hubel and Wiesel first explained the mechanism, known as orientation selectivity, in the mammalian visual cortex. Orientation tuning, a model that originated with their model, is the concept that receptive fields of neurons in the LGN that excite a cortical simple cell are arranged in rows. This model was important because it was able to describe a critical period for the proper development of normal ocular dominance columns in the lateral geniculate nucleus, and thus able to explain the effects of monocular deprivation during this critical period. The critical period for cats is about three months and for monkeys, about six months.
In a similar experiment, Antonini and Stryker (1993) examined the anatomical changes that can be observed after monocular deprivation. The compared geniculocortical axonal arbors in monocularly deprived animals in the long term (4- weeks) to short term (6–7 days) during the critical period established by Hubel and Wiesel (1993). They found that in the long term, monocular deprivation causes reduced branching at the end of neurons, while the amount of afferents allocated to the nondeprived eye increased. Even in the short term, Antonini and Stryker (1993) found that geniculocortical neurons were similarly affected. This supports the aforementioned concept of a critical period for proper neural development for vision in the cortex.
In humans, some babies are born blind in one or both eyes, for example, due to cataracts. Even when their vision is restored later by treatment, their sight would not function in the normal way as for someone who had binocular vision from birth or had surgery to restore vision shortly after birth. Therefore, it is important to treat babies born blind soon if their condition is treatable.
In psychology, imprinting is any type of rapid learning that occurs in a particular life stage that is occurs independently of the outcome of behavior. Konrad Lorenz is well known for his classic studies of filial imprinting in graylag geese. Lorenz studied a phenomenon in which the geese bonded with the first moving object they encounter. This seemed to be irreversible and only developed during a brief “critical period,” which was about 24 hrs after hatching.
Many studies have supported a correlation between the type of auditory stimuli present in the early postnatal environment and the development on the topographical and structural development of the auditory system.
First reports on critical periods came from deaf children and animals that received a cochlear implant to restore hearing. Approximately at the same time, both an electroencephalographic study by Sharma, Dorman and Spahr  and an in-vivo investigation of the cortical plasticity in deaf cats by Kral and colleagues  demonstrated that the adaptation to the cochlear implant is subject to an early, developmentally-sensitive period. These data demonstrate, both for human children and for animals, that understanding the critical period has consequences for medical therapy of hearing loss. M. Merzenich and colleagues showed two years later that during an early critical period, noise exposure can affect the frequency organization of the auditory cortex.
Recent studies have examined the possibility of a critical period for thalamocortical connectivity in the auditory system. For example, Zhou and Merzenich (2008) studied the effects of noise on development in the primary auditory cortex in rats. In their study, rats were exposed to pulsed noise during the critical period and the effect on cortical processing was measured. Rats that were exposed to pulsed noise during the critical period had cortical neurons that were less able to respond to repeated stimuli; the early auditory environment interrupted normal structural organization during development.
In a related study, Barkat, Polley and Hensch (2011) looked at how exposure to different sound frequencies influences the development of the tonotopic map in the primary auditory cortex and the ventral medical geniculate body. In this experiment, mice were reared either in normal environments or in the presence of 7 kHz tones during early postnatal days. They found that mice that were exposed to an abnormal auditory environment during a critical period P11- P15 had an atypical tonotopic map in the primary auditory cortex. These studies support the notion that exposure to certain sounds within the critical period can influence the development of tonotopic maps and the response properties of neurons. In general, the early auditory environment influences the structural development and response specificity of the primary auditory cortex.
In our vestibular system, neurons are undeveloped at neuronal birth and mature during the critical period of the first 2-3 postnatal weeks. Hence, disruption of maturation during this period can cause changes in normal balance and movement through space. Animals with abnormal vestibular development tend to have irregular motor skills. Studies have consistently shown that animals with genetic vestibular deficiencies during this critical period have altered vestibular phenotypes, most likely as a result of lack insufficient input from the semicircular canals and dopaminergic abnormalities. Moreover, exposure to abnormal vestibular stimuli during the critical period is associated with irregular motor development.
Recent studies also support the possibility of a critical period for the development of neurons that mediate memory processing. Experimental evidence supports that notion that young neurons in the adult dentate gyrus have a critical period (about 1–3 weeks after neuronal birth) during which time they are integral to memory formation. Although the exact reasoning behind this observation is indefinite, studies suggest that the functional properties of neurons at this age make them most appropriate for this purpose; these neurons : (1) Remain hyperactive during the formation of memories; (2) are more excitable; and (3) More easily depolarizable due to GABAergic effects. It is also possible that hyperplasticity makes there neurons more useful in memory formation; if these young neurons had more plasticity than adult neurons in the same context, they would be able to be more influential in smaller numbers. The role of these neurons in the adult dentate gyrus in memory processing is further supported by the fact that behavioral experiments have shown that an intact dentate gyrus is integral to hippocampal memory formation. It is speculated that the dentate gyrus acts a relay station for information relating to memory storage. The likelihood of a critical period could change the way we view memory processing because it would ultimately mean that the collection of neurons present is constantly being replenished as new neurons replace old ones. If a critical period does indeed exist this could possibly mean that: (1) Diverse populations of neurons that represent events occurring soon after one another may connect those event temporally in the memory formation and processing; OR (2) These different populations of neurons may distinguish between similar events, independent of temporal position; OR (3) Separate populations may mediate the formation of new memories when the same events occur frequently.
- Behavioral Cusp
- Child development
- Critical Period Hypothesis
- Developmental Psychology
- Malleable intelligence
- Universal grammar
- Sensitive periods
- Siegler, Robert (2006). How Children Develop, Exploring Child Develop Student Media Tool Kit & Scientific American Reader to Accompany How Children Develop. New York: Worth Publishers. ISBN 0-7167-6113-0.
- Eugéne D, Deforges S, Vibert N, Vidal P-P (2009). "Vestibular Critical Period, Maturation of Central Vestibular Neurons, and Locomotor Control". Basic and Clinical Aspects of Vertigo and Dizziness. doi:10.1111/j.1749-6632.2008.03727.x].
- Pinker, Steven (1994). The Language Instinct. New York: Morrow.
- Snow, C.E.; Hoefnagel-Höhle, M. (December 1978). "The Critical Period for Language Acquisition: Evidence from Second-Language Learning". Child Development 49 (4): 1114–1128. doi:10.1111/j.1467-8624.1978.tb04080.x. JSTOR 1128751.
- Wiesel, TN, Hubel DH (1963). "Effects of visual deprivation on morphology and physiology of cell in the cat's lateral geniculate body". Journal of Neurophysiology 26 (6): 978–993. PMID 14084170.
- Experiment Module: Effects of Visual Deprivation During the Critical Period for Development of Vision. McGill University, The Brain from Top to Bottom
- Antonini A, Stryker MP (June 1993). "Rapid Remodeling of Axonal Arbors in the Visual Cortex". Science 260 (5115): 1819–21. Bibcode:1993Sci...260.1819A. doi:10.1126/science.8511592. JSTOR 2881379.
- Higley, M. J.; Strittmatter, S. M. (2010). "Lynx for Braking Plasticity". Science 330 (6008): 1189–1190. doi:10.1126/science.1198983. PMC 3244692. PMID 21109660.
- Kisilevsky BS, Sylvia MJ, Xing X, Hefeung H, Hai HY, Ke Z, Zengping W (2003). "Effects of experience on fetal voice recognition". Psychological Science 14 (3): 220–4. doi:10.1111/1467-9280.02435. PMID 12741744.
- Kral A (2013). "Auditory critical periods: A review from system's perspective". Neuroscience 247: 117–133. doi:10.1016/j.neuroscience.2013.05.021. PMID 23707979.
- Sharma A, Dorman MF, Spahr AJ (2002). "A sensitive period for the development of the central auditory system in children with cochlear implants: implications for age of implantation.". Ear Hear 23: 532–29. doi:10.1097/00003446-200212000-00004.
- Kral A, Harmann R, Tillein J, Heid S, Klinke R (2002). "Hearing after congenital deafness: central auditory plasticity in deafness". Cerebral Cortex 12 (8): 797–807. doi:10.1093/cercor/12.8.797.
- Kral A, Sharma A (2002). "Developmental neuroplasticity after cochlear implantation.". Trends Neuroscience 35: 111–122. doi:10.1016/j.tins.2011.09.004.
- Nakahara et al. (2004). "Specialization of primary auditory cortex processing by sound exposure in the "critical period"". PNAS 4 (101): 7170–7174.
- Barkat TR, Polley DB, Hensch TK (September 2011). "A critical period for auditory thalamocortical connectivity". Nature Neuroscience 14 (9): 1189–96. doi:10.1038/nn.2882. PMID 21804538.
- Zhou X, Merzenich MM (1993). "Enduring Effects of early structured noise exposure on temporal modulation in the primary auditory cortex". Proceedings of the National Academy of Sciences 105 (11): 4423–8. Bibcode:2008PNAS..105.4423Z. doi:10.1073/pnas.0800009105.
- Aasebø, IEJ; Blankvoort, Stefan; Tashiro, Ayumu (2011). "Critical maturational period of new neuron in adult dentate gyrus for their involvement in memory formation". European Journal of Neuroscience 33 (6): 1094–1100. doi:10.1111/j.1460-9568.2011.07608.x. PMID 21395853.