What do you think?
Rate this book


124 pages, ebook
First published January 1, 2016
‘—the structural and functional differences between individual brains probably outweigh their similarities. It’s very likely that no two brains are alike and, therefore, that there is no such thing as a “textbook brain.” Your brain is, to a large extent, unique, custom-built from the life experiences you have had since being in your mother’s womb, to meet the demands you place on it today. Neuroplasticity therefore lies at the heart of what makes us human, and of what makes each of us different from everyone else.’
‘Sixty years ago, the idea that nervous tissue can change was anathema to neuroscience. It was widely believed that the mature brain is a fixed structure and, therefore, that “you can’t teach an old dog new tricks.” This dogma has since been overturned by a huge body of research which shows not only that the brain can change, but also that it changes continuously throughout life, in one way or another, in response to everything we do and every experience we have.
Neuroplasticity is a catch-all term referring to the many different ways in which the nervous system can change. It is ill-defined by neuroscientists, who use it to describe a wide variety of phenomena. Among the general public, the concept is generally misunderstood, and misconceptions about what neuroplasticity is, and what it is capable of, are rife.’
‘Neuroimaging data can sometimes seem counterintuitive and are often difficult to interpret. One recent study compared brain activity of professional soccer players and swimmers while they performed identical foot movements, and found that the soccer players exhibited less activity in the motor cortical area corresponding to the foot than did the swimmers. The researchers interpreted this as meaning that years of training enable the soccer players to control their foot movements efficiently while also conserving their neural resources—we are only just beginning to understand the many ways in which it can adapt to the demands placed upon it. Technological advances will allow for increasingly sophisticated ways of imaging the brain, and will surely deepen our knowledge of how different types of training affect brain structure and function.’
‘Other research shows that early prescription of fluoxetine (Prozac) and related antidepressants enhances motor recovery after three months in stroke patients undergoing physiotherapy. It’s still not clear why this is the case, however. This group of drugs is known to have anti-inflammatory effects, which may protect the patient’s brain from further damage; they may also facilitate relearning by promoting LTP in newly formed motor pathways.’
‘Addiction and pain are the best understood examples of conditions involving maladaptive forms of neuroplasticity. Addictive drugs activate and hijack the brain’s reward system, and the resulting changes can remain long after the substance has been cleared from the brain, leading to cravings and to compulsive, drug-seeking behaviour. Prolonged pain can induce reorganisation of the spinal cord circuitry involved in processing and then transmitting painful stimuli up to the brain, and these changes can similarly persist long after the stimuli that initially caused the pain have been removed, resulting in chronic pain states that can persist for months or years.’
‘Plastic changes can occur at the peripheral end of pain-sensing neurons beneath the skin, as well as at the synapses they form with second-order sensory neurons in the spinal cord. Activation of the protein sensors rapidly redistributes them in the nerve terminal and alters their functional properties to lower their activation threshold. This hypersensitizes the damaged tissue, so that otherwise innocuous stimuli are perceived to be painful, which aids repair by minimising contact with the damaged tissue. It also increases the firing rate of the pain-sensing neurons, and increases the probability of neurotransmitter release from their nerve terminals in the spinal cord.
These short-term changes are usually reversible. Under some circumstances, however, there can be longer-lasting modifications to the pain system. During inflammation, growth factors released from damaged cells can trigger the synthesis and trafficking of pain receptors and their related signalling molecules in pain-sensing neurons, sensitising the cells to painful stimuli. Trains of impulses generated by these cells can then induce LTP at synapses in the spinal cord. This amplifies the response of the secondary sensory neurons to incoming pain signals, so that repetitive, low-frequency signals produce a progressively larger output—a process called wind-up.
Chronic or persistent pain is also associated with functional and structural changes in the primary somatosensory cortex, but different kinds of pain and injuries affect these changes in different ways. For example, cortical representation of the painful fingers expands in carpel tunnel syndrome, perhaps exacerbating the pain felt by sufferers, while the representation of affected body parts shrinks in complex regional pain syndrome, possibly through disuse. Cortical reorganisation occurs in several steps: within minutes of the initial injury, previously inhibited connections are “unmasked”; later on, axonal sprouting may occur within the tissue being reorganised.’