This is sooooo not the last scientific paper I'm ever going to have to write
But it's sure as fuck to be the last one I'm writing this semester! This is my last paper for 'Mind & Brain in Developmental Context' and I feel the need to post it for some reason. I guess out of a sense of "I did this? What? Well...huh."
You don't actually want to read it. Trust me.
The Dynamically Developing Brain
For centuries, the human brain has been considered to be a static system with immutable properties and functions. This ‘set-in-stone’ view has largely propagated due to consistent evidence of the debilitating effects of regional ablation and other physical injury to the brain, in combination with persistent technical limitations of observing the brain in vivo. But in recent decades, technological breakthroughs have allowed the functions of the living brain to be observed over time and in response to stimuli-and the findings have been nothing short of revolutionary. In direct opposition to old beliefs about an unchanging brain, new evidence instead suggests that it is far more dynamic than previously thought, capable of re-wiring itself to compensate for loss, injury, and other insults. This capability, termed neuroplasticity, has completely changed the way researchers consider the mind and brain in their studies.
Norman Doidge’s The Brain That Changes Itself (2007) explores numerous case studies of adults whose brains have managed to adapt to atypical states, including those following brain injury, stroke, and infection. In one particularly striking case, a woman successfully underwent sensory re-training to recover her sense of vestibular perception after an infection decimated the part of her brain responsible for processing information about the position of her body in three-dimensional space (Doidge, 2007). But if the fully formed brain can re-wire itself in adulthood, what are its re-wiring capabilities during sensitive periods of childhood and adolescent development? How does the developing brain organize itself in response to atypical conditions brought about by congenital abnormalities or childhood trauma?
Doidge also describes the story of a woman named Michelle, who was born without a left hemisphere; despite missing half of her brain, Michelle is able to walk, talk, take care of herself, and even hold down a part-time job, all with only minor difficulties. Where her remaining right hemisphere has been unable to compensate-for example, Michelle is still blind in her right visual field-other parts of her brain have made up the difference: “Her brothers used to steal her french fries from her right side, but she’d catch them because what she lacks in vision, she has made up for with supercharged hearing. This hyperdevelopment of hearing, so common in the totally blind, is another sign of the brain’s ability to adjust to a changed situation” (Doidge, 2007).
This “hyperdevelopment of hearing” in the blind is a phenomenon that had been anecdotally reported for many years, but was only recently studied by neuroscientists. Neville & Bavelier (2002) conducted an extensive review of the evidence for neuroplasticity in the context of sensory deprivation in early development. Their analysis of the results of a large number of studies sheds light on the mechanisms by which the brain adapts to atypical sensory experience during sensitive periods of growth and organization that are universal to typically developing children.
In the study of sensory perception, three areas of the cortex are said to be involved in the processing of information from each sensory modality (vision, audition, gustation, olfaction, etc.) First, the primary cortices receive basic input directly from receptor cells associated with a given modality and respond accordingly; for example, certain cells in the primary visual cortex respond only to the sight of vertical lines, while others respond only to horizontal lines. This primary information is then routed to the secondary cortex assigned to the modality, where it is processed on a more complex level (e.g. integrating horizontal and vertical lines to construct the visual impression of an object as a whole). Lastly, the sensory input is processed in the association cortex, in which it is integrated with information from other modalities as well as with cognitive and emotional information; for example, the experience of ‘stopping to smell the roses’ involves the integration of olfactory, visual, and tactile inputs in the association cortices of these modalities. (Foley & Matlin, 2010)
Neuroplasticity of primary cortices between sensory modalities has been previously observed in animal experiments. When connections from one type of sensory input are rerouted to the primary cortex of a different modality (e.g., retinal cells rewired to connect to the primary auditory cortex in ferrets), the cells of the primary cortex begin to respond to the ‘new’ form of input, in addition to the ‘old’ (Neville & Bavelier, 2002). However, because this research involves the surgical re-wiring of neural connections, it tells us little about the plasticity of human sensory cortices in the more ‘natural’ and unpredictable contexts of loss of sensory input due to congenital abnormality, disease, or trauma. As such, the authors question whether the plasticity of primary sensory cortices could be reliably observed in humans, and whether the developmental timing of the loss of a sensory modality may play a role in this plasticity.
While Neville & Bavelier do concede that “[t]here is only scarce evidence to date that compensatory plasticity, in the absence of surgically induced rewiring, can occur in primary cortices in humans or animals”, they discuss at length the “converging evidence that secondary and association cortices can compensate for the loss of one modality” (2002). A plethora of evidence is cited in support of the plasticity of sensory cortices in general, in addition to highlighting the important role played by developmental timing in this process. However, the question of whether or not primary sensory cortices can be recruited for other functions-e.g. whether the basic, preliminary connections between the eyes and the brain show properties of plasticity-remains a point of uncertainty in the literature.
With regard to vision, research suggests that individuals who are blind from an early age have striking differences in the functioning of the association cortex of the occipital lobe compared to sighted subjects. “[S]tudies reported that metabolic activity within the occipital cortex of early blind individuals is higher than that found in blindfolded sighted subjects and equivalent to that of sighted subjects with their eyes open” (Neville & Bavelier, 2002). These results suggest that when visual cortices are deprived of input early in life, they may be recruited for other functions, while blindness later in life (as modeled by the blindfolded sighted subjects in these studies) may result in a decline in activity in the already-organized visual cortex.
The plasticity of sensory cortices has also been found in the context other modalities. Numerous studies have found that deaf adults show “a specific enhancement of behavior performance and neural activity in response to visuo-spatial information presented in the peripheral visual fields” (Neville & Bavelier, 2002). Not only are deaf adults faster at detecting the presence and direction of motion of visual stimuli in the periphery, but the motion-sensitive area MT of the visual cortex is observed to be recruited more often, with greater intensity, and with greater speed in deaf adults than in participants with normal audition (Neville & Bavelier, 2002). However, the mechanisms by which this divergence occurs are still unclear; while these promising results are certainly notable, they highlight the need for more research on the developmental processes that lead to the observed differences in visuo-spatial task performance between deaf and hearing individuals.
Preliminary studies on neuroplasticity in developmental contexts have been limited by the constraints of technology, but the improvement of imaging techniques and research methodology will continually increase the validity of this ongoing research. As with any field of study, more in-depth investigation typically reveals new and more complex uncertainties; however, the accumulation of scientific knowledge on the subject of developmental neuroplasticity will be sure to help illuminate new ways of improving the lives of individuals afflicted with sensory disabilities.
References
Doidge, N. (2007). The brain that changes itself: Stories of personal triumph from the frontiers of brain science. New York, NY: Penguin Books.
Foley, H., & Matlin, M. (2010). Sensation & perception. (5th ed., p. 69). Boston, MA: Allyn & Bacon.
Neville, H., & Bavelier, D. (2002). Human brain plasticity: Evidence from sensory deprivation and altered language experience. Department of Psychology, University of Oregon, Eugene, OR; Department of Brain & Cognitive Sciences, University of Rochester, Rochester, NY.
You don't actually want to read it. Trust me.
The Dynamically Developing Brain
For centuries, the human brain has been considered to be a static system with immutable properties and functions. This ‘set-in-stone’ view has largely propagated due to consistent evidence of the debilitating effects of regional ablation and other physical injury to the brain, in combination with persistent technical limitations of observing the brain in vivo. But in recent decades, technological breakthroughs have allowed the functions of the living brain to be observed over time and in response to stimuli-and the findings have been nothing short of revolutionary. In direct opposition to old beliefs about an unchanging brain, new evidence instead suggests that it is far more dynamic than previously thought, capable of re-wiring itself to compensate for loss, injury, and other insults. This capability, termed neuroplasticity, has completely changed the way researchers consider the mind and brain in their studies.
Norman Doidge’s The Brain That Changes Itself (2007) explores numerous case studies of adults whose brains have managed to adapt to atypical states, including those following brain injury, stroke, and infection. In one particularly striking case, a woman successfully underwent sensory re-training to recover her sense of vestibular perception after an infection decimated the part of her brain responsible for processing information about the position of her body in three-dimensional space (Doidge, 2007). But if the fully formed brain can re-wire itself in adulthood, what are its re-wiring capabilities during sensitive periods of childhood and adolescent development? How does the developing brain organize itself in response to atypical conditions brought about by congenital abnormalities or childhood trauma?
Doidge also describes the story of a woman named Michelle, who was born without a left hemisphere; despite missing half of her brain, Michelle is able to walk, talk, take care of herself, and even hold down a part-time job, all with only minor difficulties. Where her remaining right hemisphere has been unable to compensate-for example, Michelle is still blind in her right visual field-other parts of her brain have made up the difference: “Her brothers used to steal her french fries from her right side, but she’d catch them because what she lacks in vision, she has made up for with supercharged hearing. This hyperdevelopment of hearing, so common in the totally blind, is another sign of the brain’s ability to adjust to a changed situation” (Doidge, 2007).
This “hyperdevelopment of hearing” in the blind is a phenomenon that had been anecdotally reported for many years, but was only recently studied by neuroscientists. Neville & Bavelier (2002) conducted an extensive review of the evidence for neuroplasticity in the context of sensory deprivation in early development. Their analysis of the results of a large number of studies sheds light on the mechanisms by which the brain adapts to atypical sensory experience during sensitive periods of growth and organization that are universal to typically developing children.
In the study of sensory perception, three areas of the cortex are said to be involved in the processing of information from each sensory modality (vision, audition, gustation, olfaction, etc.) First, the primary cortices receive basic input directly from receptor cells associated with a given modality and respond accordingly; for example, certain cells in the primary visual cortex respond only to the sight of vertical lines, while others respond only to horizontal lines. This primary information is then routed to the secondary cortex assigned to the modality, where it is processed on a more complex level (e.g. integrating horizontal and vertical lines to construct the visual impression of an object as a whole). Lastly, the sensory input is processed in the association cortex, in which it is integrated with information from other modalities as well as with cognitive and emotional information; for example, the experience of ‘stopping to smell the roses’ involves the integration of olfactory, visual, and tactile inputs in the association cortices of these modalities. (Foley & Matlin, 2010)
Neuroplasticity of primary cortices between sensory modalities has been previously observed in animal experiments. When connections from one type of sensory input are rerouted to the primary cortex of a different modality (e.g., retinal cells rewired to connect to the primary auditory cortex in ferrets), the cells of the primary cortex begin to respond to the ‘new’ form of input, in addition to the ‘old’ (Neville & Bavelier, 2002). However, because this research involves the surgical re-wiring of neural connections, it tells us little about the plasticity of human sensory cortices in the more ‘natural’ and unpredictable contexts of loss of sensory input due to congenital abnormality, disease, or trauma. As such, the authors question whether the plasticity of primary sensory cortices could be reliably observed in humans, and whether the developmental timing of the loss of a sensory modality may play a role in this plasticity.
While Neville & Bavelier do concede that “[t]here is only scarce evidence to date that compensatory plasticity, in the absence of surgically induced rewiring, can occur in primary cortices in humans or animals”, they discuss at length the “converging evidence that secondary and association cortices can compensate for the loss of one modality” (2002). A plethora of evidence is cited in support of the plasticity of sensory cortices in general, in addition to highlighting the important role played by developmental timing in this process. However, the question of whether or not primary sensory cortices can be recruited for other functions-e.g. whether the basic, preliminary connections between the eyes and the brain show properties of plasticity-remains a point of uncertainty in the literature.
With regard to vision, research suggests that individuals who are blind from an early age have striking differences in the functioning of the association cortex of the occipital lobe compared to sighted subjects. “[S]tudies reported that metabolic activity within the occipital cortex of early blind individuals is higher than that found in blindfolded sighted subjects and equivalent to that of sighted subjects with their eyes open” (Neville & Bavelier, 2002). These results suggest that when visual cortices are deprived of input early in life, they may be recruited for other functions, while blindness later in life (as modeled by the blindfolded sighted subjects in these studies) may result in a decline in activity in the already-organized visual cortex.
The plasticity of sensory cortices has also been found in the context other modalities. Numerous studies have found that deaf adults show “a specific enhancement of behavior performance and neural activity in response to visuo-spatial information presented in the peripheral visual fields” (Neville & Bavelier, 2002). Not only are deaf adults faster at detecting the presence and direction of motion of visual stimuli in the periphery, but the motion-sensitive area MT of the visual cortex is observed to be recruited more often, with greater intensity, and with greater speed in deaf adults than in participants with normal audition (Neville & Bavelier, 2002). However, the mechanisms by which this divergence occurs are still unclear; while these promising results are certainly notable, they highlight the need for more research on the developmental processes that lead to the observed differences in visuo-spatial task performance between deaf and hearing individuals.
Preliminary studies on neuroplasticity in developmental contexts have been limited by the constraints of technology, but the improvement of imaging techniques and research methodology will continually increase the validity of this ongoing research. As with any field of study, more in-depth investigation typically reveals new and more complex uncertainties; however, the accumulation of scientific knowledge on the subject of developmental neuroplasticity will be sure to help illuminate new ways of improving the lives of individuals afflicted with sensory disabilities.
References
Doidge, N. (2007). The brain that changes itself: Stories of personal triumph from the frontiers of brain science. New York, NY: Penguin Books.
Foley, H., & Matlin, M. (2010). Sensation & perception. (5th ed., p. 69). Boston, MA: Allyn & Bacon.
Neville, H., & Bavelier, D. (2002). Human brain plasticity: Evidence from sensory deprivation and altered language experience. Department of Psychology, University of Oregon, Eugene, OR; Department of Brain & Cognitive Sciences, University of Rochester, Rochester, NY.