Brain plasticity; Rewiring the brain

Once upon a time, researchers and scientist theorised that the brain stops developing within the first few years of life. The connections the brain makes during the ‘critical period’ are fixed for life. However, there is mounting evidence, from human and animal studies, that this view underestimates the brain. The brain has a remarkable ability to continually make new connections throughout our life, it has an extraordinary ability to compensate for injury and disease by ‘rewiring’ itself. Neuroplasticity, or brain plasticity, refers to this ability to form new connections, reorganise already established neural networks and compensate for injury and disease.

Brain plasticity
Brain plasticity

There are many different definitions and explanations of brain plasticity. It is referred to as the brain’s ability to reorganise itself and form new connections throughout life. Brain plasticity allows the brain to adapt to disease or injury, by allowing neurons to adjust their activity in response to new situations or changes to the environment. Learning new things or processing/memorising information cause lasting functional changes to the brain. These changes in neural connections is essentially brian plasticity. Changes in neural pathways is a result of changes in environment, behaviour, thinking, emotions and neural processes. The brain;s ability to reorganise itself and form neural connections is what makes the brain resilient.  Brain plasticity enables the brain to overcome stroke, injury, birth abnormalities, learning disabilities, depression, addiction, obsessive thought patterns and other brain defects.

There are many types of brain plasticity. Positive brain plasticity, which enhances healthy functioning of the brain. Negative brain plasticity, which promotes unhealthy functioning of the brain. Synaptic plasticity occurs between neurons, whereas non-synaptic plasticity occurs within the neuron. Developmental plasticity occurs during early life, and is important for developing our ability to function. Injury induced plasticity is the brain’s way of adapting to trauma.

Positive Neuroplasticity

Positive brain plasticity involves changes to structures and functions of the brain, which results in beneficial outcomes. For example, improving the efficiency of neural networks responsible for higher cognitive functions such as attention, memory, mood.

There are many ways in which we can promote neuroplastic change. Positive brain plasticity is when the brain becomes more efficient and organised. For example, if we repeatedly practise our times tables, eventually, the connections between different parts of the brain become stronger. We make less errors and can recite them faster. CBT, meditation and mindfulness can all promote brain plasticity. These practices improve neural function, strengthen connections between neurons.

neuroplasticitybrain plasticity
Positive Brain Plasticity- Mindfulness

Negative Brain Plasticity

Negative brain plasticity causes changes to the neural connections in the brain, which can be harmful to us. For example, negative thoughts can promote neural changes and connections associated with conditions such as depression, and anxiety (how to overcome panic and anxiety attacks. Also overuse of drugs and alcohol enhances negative plasticity by rewiring our our reward system and memories.

Synaptic plasticity

Synaptic plasticity is the basis for learning and memory. Furthermore, it also alters the number of receptors on each synapse (synapses are the connections between neurons that transmit chemical messages). When we learn new information and skills, these ‘connections’ get stronger. There are two types of synaptic plasticity, short term and long term. Both types can go in two different directions, enhancement/excitation and depression. Enhancement strengthens the connection, whereas depression weakens it. Short term synaptic plasticity usually lasts tens of milliseconds. Short term excitation is a result of increased level of certain types of neurotransmitters available at the synapse. Whereas short term depression is a result of a decreased level of neurotransmitters, long term synaptic plasticity lasts for hours. Long term excitation strengthens synaptic connections, whereas long term depression weakens these connections.

As synaptic plasticity is responsible for our learning ability, information retention, forming and maintaining neural connections, when this process goes wrong, it can have negative consequences. For example, synaptic plasticity plays a key role in addiction. Drugs hi-jack the synaptic plasticity mechanisms by creating long lasting memories of the drug experience.

Non-synaptic plasticity

This type of plasticity occurs away from the synapse. Non-synaptic plasticity, makes changes to the way in which the structures in the axon and cell body carry out their functions. The mechanisms of this types of plasticity are not yet well understood.

Developmental plasticity

In the first few years of life, our brains change rapidly. This is also known as developmental plasticity. Although it is most prominent during our formative years, it occurs throughout our lives. Developmental plasticity means our neural connections are constantly undergoing change in response to our childhood experiences and our environment. Our processing of sensory information, informs the neural changes. Synaptogenesis, synaptic pruning, neural migration and myelination, are the main processes through which development plasticity occurs.

Synaptogenesis – rapid expansion in formation of synapses so that the brain can successfully process the high volume of incoming sensory stimuli. This process is controlled by our genetics.

Synaptic pruning – Reduction of synaptic connections to enable the brain to function more efficiently. Essentially, connections that aren’t used or aren’t efficient are ‘pruned’ or ‘disconnected’.

Neural migration – this process occurs whilst we are still in the womb. Between 8 and 29 weeks of gestation, neurons ‘migrate’ to different parts of the brain.

Myelination – This process starts during fetal development and continues until adolescence. Myelination is when neurons are protected and insulated a myelin sheath. Myelination improves the transmission of messages down the neuron’s axon.

Injury induced plasticity

Following injury, the brain has demonstrated the extraordinary ability to take over a given function that the damaged part of the brain was responsible for. This ability has been noted in many case studies of brain injury and brain abnormalities. Some stroke sufferers have displayed remarkable feats of recovering functions lost due to brain damage.

There are two distinct mechanisms through which the brain attempts to restore its functionality. Recovery and Compensation. Recovery involves restoring the neural tissue, the behaviour it controlled, as well as recovering the level of activity of the behaviour. So for instance, if an individual suffers a stroke, which affects a small area of the motor cortex responsible for controlling arm movement, in recovery, the tissue which sustains damage is restored. The action of moving the arm and the range of motion the individual has, of the arm, prior to the stroke, is also restored. Compensation is the brains way of compensating for the injury. Compensation for the injury involves recruiting new neural networks to take over functions the damaged areas were responsible for.

Two stages of recovery for injury induced plasticity

Researcher Heidi Reyst, proposes that recovery can occur in two stages. Stage 1 is spontaneous recovery. The brain recovers from injury and change, on its own and without help from training and rehabilitation. The researcher proposes three different processes for this stage:

  1. Diaschisis reversal – reversing the changes in blood flow, metabolic function and neuron excitability. Essentially, the areas of the brain that are disrupted by injury, are restored to their pre-injury functioning.
  2. Kinematic changes – changes in movement patterns. They way in which an individual’s movement post injury is different prior to injury as a result of compensatory mechanisms.
  3. Cortical reorganisation – rewiring and restructuring of the brain. Using neurogenesis, axonal sprouting (intact axons sprouts new nerve endings to reconnect with neurons) and blood vessel formation.

Stage 2 is training induced recovery. This stage involves compensation, recruiting new neural networks or brain areas to carry out functions, the damaged area used to be responsible for.  For example, if the left frontal lobe (which controls language function) is damaged, the right frontal lobe will be recruited to improve language function. As well as compensation, retraining is an essential part of injury induced brain plasticity. This involves training the nearby brain tissue to reorganise and control the lost functions.

There are products available to help patients improve brain plasticity and train the brain tissue to help recover after brain injury. CogniFit is an online program that uses fun brain games and assessments to track and improve the cognitive skills affected by the brain injury.

In a nut shell, brain plasticity on the whole is a wonderful thing! Our brains possess the fascinating ability to adapt to pretty much any situation that is thrown at it! Whether it be in utero, childhood, while we learning, overcoming depression or post injury. The brain is the pretty good at bouncing back. Pretty amazing stuff! Am I right?!

Any questions or suggestions? Please leave a comment below 🙂

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