Chloe Zhang
Neuroplasticity, or brain plasticity, is the ability of the brain to adapt and change through growth and reorganization. This process can be triggered by learning new skills, environmental changes, or adapting to sensory or cognitive deficits. There is ample evidence that the congenital or acquired loss of a sensory input triggers a myriad of brain neuroplastic changes. For example, in the case of vision loss, the visually deprived occipital cortex at rest is metabolically hyperactive, and tactile input and other forms of non-visual input activate the occipital cortex in congenitally blind individuals. Similarly, studies have shown that in the case of hearing loss, early cochlear implantation can allow children to learn the mother language and acquire acoustic communication. These examples demonstrate how plasticity reacts to sensory loss, leading to functional and structural changes in the brain.
| Characteristics | Values |
|---|---|
| Definition | Neuroplasticity is the ability of neural networks in the brain to change through growth and reorganization. |
| Congenital or acquired loss of sensory input | There is evidence that congenital or acquired loss of a sensory input triggers brain neuroplastic changes. |
| Brain imaging techniques | PET, (f)MRI, MEG and diffusion imaging are some modern non-invasive brain imaging techniques that have been used to study brain plasticity following sensory loss. |
| Visual system | The visually-deprived occipital cortex at rest is metabolically hyperactive. |
| Tactile input | Tactile input and other forms of non-visual input activate the occipital cortex in congenitally blind and, to a lesser extent, in late blind subjects. |
| Structural changes | Brain morphometric and diffusion imaging studies have shed light on structural changes associated with sensory loss. |
| Auditory input | Later studies have shown brain plastic changes following loss of auditory input. |
| Other senses | Studies have also shown brain plastic changes following loss of smell, taste, and somatosensory input, though to a lesser extent. |
| Therapeutic progress | Understanding the mechanisms underlying brain plasticity following sensory loss can lead to novel avenues for therapeutic progress. |
| Brain development | Studies of the sensory-deprived brain can help shed light on normal brain development and function. |
| Brain repair | During brain repair following injury, plastic changes aim to maximize function despite the damage. |
| Neuronal pathways | Plasticity is the mechanism for encoding, changing behaviors, and learning. |
| Physiotherapy | Neuroplastic-specific techniques in physiotherapy can include locomotion training and neurostimulation techniques to improve mobility through cortical reorganization. |
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What You'll Learn
Neuroplastic changes following congenital or acquired sensory loss
Neuroplasticity refers to the brain's ability to reorganise and rewire its neural connections, enabling it to adapt and function differently from its prior state. This process can occur in response to learning new skills, environmental changes, recovering from injuries, or adapting to sensory or cognitive deficits.
There is ample evidence that congenital or acquired loss of a sensory input triggers a myriad of brain neuroplastic changes. The first brain imaging studies focused on the visual system and revealed that the occipital cortex is metabolically hyperactive in visually deprived individuals. Ensuing studies showed that tactile input and other forms of non-visual input activate the occipital cortex in congenitally blind and, to a lesser extent, in late blind subjects. Brain morphometric and diffusion imaging studies have further shed light on the associated structural changes.
Later studies also dealt with brain plastic changes following the loss of auditory input, and to a lesser extent, following the loss of smell, taste, and somatosensory input. These studies have helped to shed light on normal brain development and function. For example, in the auditory system, congenital hearing loss has been shown to affect auditory development. However, the implantation of a sensory prosthesis activating the auditory system has prevented deficits and induced functional maturation of the auditory system.
Significant, although typically less extensive, plastic changes may also occur in populations suffering from noncongenital sensory loss. This neuroplasticity is evident in atypical brain activation in the blind compared to the sighted, as well as in behavioural manifestations, such as sensory hyperacuity and specific cognitive skills. For instance, blind individuals need to compensate for the lack of vision, a modality that normally allows one to "know what is where by looking" and facilitates spatial coding.
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Brain plasticity and therapeutic progress
Neuroplasticity, also known as neural plasticity or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. It involves adaptive structural and functional changes to the brain. The brain is born immature and then adapts to sensory inputs after birth. The process of neuroplasticity can occur in response to learning new skills, experiencing environmental changes, recovering from injuries, or adapting to sensory or cognitive deficits.
The study of brain plasticity following sensory loss has gained momentum with the advent of modern non-invasive brain imaging techniques such as PET, (f)MRI, MEG, and diffusion imaging. These techniques have revealed that the occipital cortex is metabolically hyperactive in visually deprived individuals. Furthermore, tactile input and other forms of non-visual input activate the occipital cortex in congenitally blind individuals and, to a lesser extent, in late blind individuals. These findings have shed light on the structural and functional changes that occur in the brain following sensory loss.
Brain plasticity-based therapeutics represent an attempt to address neurological distortions and drive positive neurological corrections. While this field is still in its infancy, initial studies indicate that computerized, neuroplasticity-based training can effectively drive behavioral and physiological changes in the schizophrenic brain. For example, this type of training has been shown to improve symptoms in patients with schizophrenia, a complex neurological disorder.
Additionally, brain plasticity has implications for therapeutic progress in sensory loss. For instance, in the case of congenital hearing loss, implantation of a sensory prosthesis that activates the auditory system can prevent deficits and induce functional maturation of the auditory system. Similarly, in prelingually deaf children, early cochlear implantation enables them to learn the mother language and acquire acoustic communication skills. Understanding the mechanisms of brain plasticity following sensory loss can help develop novel treatments and improve our understanding of normal brain development and function.
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Brain imaging techniques and sensory loss
The study of brain plasticity following sensory loss has gained momentum with the advent of modern non-invasive brain imaging techniques. These techniques have provided evidence that congenital or acquired loss of a sensory input triggers a myriad of brain neuroplastic changes.
The first brain imaging studies primarily focused on the visual system and blindness, revealing that the occipital cortex of visually deprived individuals is metabolically hyperactive. Subsequent studies found that tactile input and other forms of non-visual stimuli activate the occipital cortex in congenitally blind individuals and, to a lesser extent, in late-blind individuals. These findings suggest that the occipital cortex, typically associated with visual processing, undergoes functional reorganization in response to sensory loss.
Brain morphometric and diffusion imaging studies have further elucidated the structural changes associated with sensory loss. While initial research predominantly focused on visual loss, subsequent investigations have explored brain plasticity following auditory deprivation and, to a lesser extent, the loss of smell, taste, and somatosensory input. Diffusion imaging, in particular, has been instrumental in understanding the structural alterations in the brain following sensory loss.
In addition to blindness and visual loss, brain imaging techniques have also been applied to studying cross-modal plasticity in deafness. For example, Mitzetlfelt et al. used visual evoked potentials (VEPs) to investigate stimulus-driven neural activity associated with visual localization in deaf kittens. While some studies have focused on peripheral sensory loss, others have examined central nervous system damage and the subsequent brain plasticity.
Furthermore, brain imaging techniques have contributed to our understanding of neuroplasticity in adult brains. For instance, intrinsic signal optical imaging has demonstrated that cortical functional representations in adult animals are not fixed but dynamic and continuously modified by experiences. This "experience-dependent" plasticity has been observed in various mammalian species and has implications for rehabilitation, recovery from injuries, sensory-motor skill improvements, and learning.
Overall, brain imaging techniques have been instrumental in advancing our understanding of brain plasticity following sensory loss. By visualizing structural and functional changes in the brain, these techniques have provided insights into the dynamic nature of the brain's ability to reorganize and adapt in response to sensory deprivation or damage.
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Sensory substitution and brain plasticity
Neuroplasticity, also known as neural plasticity or just plasticity, is the ability of neural networks in the brain to change through growth and reorganization. It refers to the brain's ability to adapt and function in ways that differ from its prior state. For instance, in the case of congenital hearing loss, the implantation of a sensory prosthesis activating the auditory system has prevented deficits and induced the functional maturation of the auditory system.
The idea of sensory substitution was introduced in the 1980s by Paul Bach-y-Rita. It concerns human perception and the plasticity of the human brain, allowing us to study neuroscience more through neuroimaging. A sensory substitution system consists of three parts: a sensor, a coupling system, and a stimulator. The sensor records stimuli and gives them to a coupling system that interprets these signals and transmits them to a stimulator. In the case of sensory augmentation, the sensor obtains signals of a kind not originally available to the bearer.
The first sensory substitution system was developed by Bach-y-Rita et al. as a means of brain plasticity in congenitally blind individuals. The system was designed to use one sensory modality, mainly tactition, to gain environmental information to be used by another sensory modality, mainly vision. In the 1960s, Paul Bach-y-Rita invented a device that was tested on a small number of people. The device involved a person sitting in a chair embedded with nubs that vibrated to translate images received in a camera, allowing a form of vision via sensory substitution.
Modern sensory substitution devices aim to enable activities of daily living such as object recognition, navigation, and non-text sign identification. These devices exploit multiple afferent streams, including tactile (hand, tongue, back) and auditory channels. This unique attribute can provide information about normal interactions between sensory subsystems and how they can be remodelled in the setting of blindness. In addition, sensory substitution devices can be used to study the cross-modal interactions of the brain in tasks that more accurately represent daily activities.
Sensory substitution devices have been used in combination with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) to investigate the mechanisms of cross-modal neuroplasticity in the blind. Brain imaging studies have shown that upon visual impairments and blindness, the visual cortices undergo a huge functional reorganization such that they are activated by other sensory modalities. This cross-modal plasticity was also found through functional imaging of congenitally blind patients, which showed a cross-modal recruitment of the occipital cortex during perceptual tasks such as Braille reading, tactile perception, tactual object recognition, sound localization, and sound discrimination.
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Brain plasticity and normal brain development
Brain plasticity, also known as neuroplasticity, is the ability of neural networks in the brain to change through growth and reorganization. It is a fundamental property of neurons that allows them to modify the strength and efficacy of synaptic transmission through a diverse number of activity-dependent mechanisms. The brain is born immature and then adapts to sensory inputs after birth, which is why plasticity is highly experience-dependent, especially in the early stages of life. Learning is the key to neural adaptation, and plasticity is the mechanism for encoding and changing behaviours.
The brain's plasticity allows it to adapt and function differently from its prior state. This process can occur when learning new skills, experiencing environmental changes, recovering from injuries, or adapting to sensory or cognitive deficits. For example, in the case of congenital hearing loss, the implantation of a sensory prosthesis activating the auditory system has prevented deficits and induced the functional maturation of the auditory system. Similarly, blind people may undergo cross-modal plasticity, resulting in enhanced abilities in other senses.
Neuroplasticity can also aid in brain recovery after damage caused by events like strokes or traumatic injuries. This ability to manipulate specific neuronal pathways and synapses has important implications for physiotherapeutic clinical interventions that can improve health. For instance, physical neurorehabilitation can enhance brain and neuromuscular adaptation. Studies on rats have shown that brain cells surrounding a damaged area can change their function and shape to take on the functions of the damaged cells. Similar, though less effective, changes have been observed in human brains following injury.
There is ample evidence that congenital or acquired loss of a sensory input triggers a myriad of brain neuroplastic changes. The advent of modern non-invasive brain imaging techniques such as PET, (f)MRI, MEG, and diffusion imaging has allowed scientists to study the mechanisms mediating brain plasticity following sensory loss. These studies have revealed that the occipital cortex is metabolically hyperactive in visually-deprived individuals. Furthermore, tactile input and other forms of non-visual input activate the occipital cortex in congenitally blind individuals and, to a lesser extent, in those who became blind later in life.
In summary, brain plasticity is a dynamic and ever-evolving process that allows the brain to adapt and recover from various sensory, cognitive, and physical challenges. Studies of the sensory-deprived brain can help us understand normal brain development and function, as well as develop novel therapeutic interventions.
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Frequently asked questions
Plasticity is the ability of any structure, in this case, the brain, to change by an external stimulus. It is also referred to as neuroplasticity or neural plasticity.
There is evidence that congenital or acquired loss of a sensory input triggers brain neuroplastic changes. Brain imaging studies have shown that the occipital cortex is metabolically hyperactive in visually-deprived individuals. Other studies have shown that tactile input and other forms of non-visual input activate the occipital cortex in congenitally blind individuals and, to a lesser extent, in late blind individuals.
Studies of the sensory-deprived brain can help us understand normal brain development and function. This knowledge can be applied to develop novel treatments and therapies, such as sensory substitution, to restore lost functions. Additionally, plasticity can aid in brain recovery after damage caused by events like stroke or traumatic injury.
