Neuroplasticity, also known as brain plasticity, is an umbrella term that describes lasting change to the brain throughout an individual’s life course. The term gained prominence in the latter half of the 20th century, when new research[1] showed many aspects of the brain remain changeable (or “plastic”) even into adulthood.[2] This notion contrasts with the previous scientific consensus that the brain develops during a critical period in early childhood, then remains relatively unchangeable (or “static”) afterward.[3]
Neuroplastic change can occur at small scales, such as physical changes to individual neurons, or at whole-brain scales, such as cortical remapping in response to injury; however cortical remapping only occurs during a certain time period meaning that if a child were injured and it resulted in brain damage then cortical remapping would most likely occur, however if an adult was injured and it resulted in brain damage, then cortical remapping would not occur since the brain has made the majority of its connections.[4] Behavior, environmental stimuli, thought, and emotions may also cause neuroplastic change through activity-dependent plasticity, which has significant implications for healthy development, learning, memory, and recovery from brain damage.[4][5][6]
Neuroscientists distinguish synaptic plasticity, which refers to changes in how neurons connect to each other, from non-synaptic plasticity, which refers to changes in the neurons themselves.
Chronic pain
Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from periphery then elicit a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.[32] For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.[33] Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus.[34] However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain,[35] chronic low back pain[36] and carpal tunnel syndrome.[37]
Meditation
A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter.[38][39][40] One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000.[41] Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term, or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, the ability of the body to heal itself, and so on. These functional changes may be caused by changes in the physical structure of the brain.[42][43][44][45]
Fitness and exercise
Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), and vascular endothelial growth factor (VEGF).[46][47][48] Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory.[49][50][51][52] Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i.e., the “cognitive control” of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control.[48][49][53][54] The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus;[48][49][50] moderate improvements seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens.[48][49][50] Higher physical fitness scores (measured by VO2 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.[49]
Human echolocation
Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010[55] and 2011[56] using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.[57]
ADHD stimulants
Reviews of magnetic resonance imaging (MRI) studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia.[58][59][60] Based upon rodent models, the authors of one review proposed that “juvenile exposure to methylphenidate may cause abnormal prefrontal function and impaired plasticity in the healthy brain”.[61] The same authors noted in another review that in juvenile rats, methylphenidate reduced levels of NR2B subunit of the NMDA receptor without altering NR2A levels in the prefrontal cortex, thereby affecting long-term plasticity in the prefrontal cortex.[
