The amygdala-hippocampus axis may turn out to be of far greater significance in determining who we are than we have previously thought. This axis with its emphasis on memory and emotion reinforces the notion that having a self which remembers appears to be fundamental to our sense of who we are and our survival as an individual in society. The emotional sense of being oneself is closely allied to how we remember who we are. If there was much emotion in our upbringing and we were fussed over we retain memories of a self that is highly appreciated and important and we identify with that. We also believe that in society we should be remembered for who we are or were. Presumably our ultimate survival in human society depends on societal acceptance and recognition. If a person is recognised as being an individual of worth to society, that society is prepared to extend resources to help protect and aid that person’s survival. It is why the successful in society are always preferenced above those lower down the food-chain. It may be frustratingly unfair, but from an social-evolutionary perspective it is understandable.
It is generally believed that we begin to get some idea of us as having a self-element of increasing constancy at around two years old. This builds with time so that by the time we are eight to ten years old we have a pretty good idea of who we think we are. Our self-concepts are of course much influenced by the next big stage in our lives namely puberty but we are pretty much who we are by the end of adolescence. This does not mean we do not change as we go through life. It just means we have more stable and specific notions of who we think we might be.
We change throughout life but the brain has sensitive periods in its development. If that sensitive period is prematurely ended then further changes that could have occurred in the brain do not happen as readily. Once we become our selves our concept of self may stay relatively stable due to the early closure of a sensitive periods of development in our childhood and adolescence.
It seems likely that our essential sense of self would have been created in the first ten years of our lives. Our sense of self is therefore likely to have been created at a time when our ability to regulate emotions due to the immaturity of our brain was compromised. Hence adverse events in childhood loom very large in importance if we identify with them and consider them important reflections of who we are. Trauma is probably the most common cause of premature closure of the development of our sense of self. Clearly this could then have severe ramifications for our ideas of self throughout our lives.
By affecting sensitive periods adversely trauma results in us becoming far less flexible in our development. There still is some brain flexibility but far less than would normally be the case during sensitive periods of brain development. In addition we would have to deal with the psychological trauma that caused the shutting down and our brain immaturity might make this a very difficult problem to resolve.
It is speculated that exposure to harsh uncompromising adult reality commonly subsumed under the heading of trauma often results in compromised neurological development. If a child is exposed to significant aggression or extreme poverty then it is likely that there may be neuro-developmental abnormality. Learning may become prematurely fixed and personality underdevelopment may be similarly fixed. This may explain the fact that certain psychiatric disorders are excessively associated with childhood trauma. Such exposure to traumatic realities may well lead to lasting damage to the developing brain. One could speculate that in general premature closure of the development process might lead to the conviction that we cannot change further. Many psychotherapists see this as the most significant obstacle to future progress.
One important question is whether these changes can be reversed. Can this process of brain shutting down on normal development be reversed in any way to enhance a resumption of a more normal pattern? It appears under certain circumstances that these blocks can be reversed and the brain can experience a resurgence in neuroplasticity. The shutting down of brain plasticity seems to be related to the balance of excitability versus the inhibition of neuronal networks. It is well known that in this sense that children have a lot more excitatory neuronal or synaptic activity and this is slowly reduced or pruned as childhood development proceeds. This pruning essentially stops the brain plasticity that makes learning and developing so effortless for children. One could speculate therefore that anything that increases excitability of neuronal networks could reinstate plasticity. The excitement of curiosity certainly seems to promote new learning. Acetyl choline is a neuro-transmitter which is known to be involved in curiosity and enhances neuroplasticity. Drugs that can affect the actions of acetyl-choline in the brain may well be of use in increasing brain plasticity. The excitation of the brain using electrical stimulation of the brain may speculatively in some people promote increased plasticity.
Neuronal development also seems susceptible to certain drugs commonly used in psychiatry which potentially return them to a state of being more plastic. One of those drugs is prozac which is used a lot in young people and children. When prozac first hit the market as an anti-depressant in the USA it was reputed that a lot of people used it for the purposes of increasing their intelligence and not for depression at all. It may well be that in terms of increased neuro-plasticity those people were actually on the right track after all.
It is generally believed that we begin to get some idea of us as having a self-element of increasing constancy at around two years old. This builds with time so that by the time we are eight to ten years old we have a pretty good idea of who we think we are. Our self-concepts are of course much influenced by the next big stage in our lives namely puberty but we are pretty much who we are by the end of adolescence. This does not mean we do not change as we go through life. It just means we have more stable and specific notions of who we think we might be.
We change throughout life but the brain has sensitive periods in its development. If that sensitive period is prematurely ended then further changes that could have occurred in the brain do not happen as readily. Once we become our selves our concept of self may stay relatively stable due to the early closure of a sensitive periods of development in our childhood and adolescence.
It seems likely that our essential sense of self would have been created in the first ten years of our lives. Our sense of self is therefore likely to have been created at a time when our ability to regulate emotions due to the immaturity of our brain was compromised. Hence adverse events in childhood loom very large in importance if we identify with them and consider them important reflections of who we are. Trauma is probably the most common cause of premature closure of the development of our sense of self. Clearly this could then have severe ramifications for our ideas of self throughout our lives.
By affecting sensitive periods adversely trauma results in us becoming far less flexible in our development. There still is some brain flexibility but far less than would normally be the case during sensitive periods of brain development. In addition we would have to deal with the psychological trauma that caused the shutting down and our brain immaturity might make this a very difficult problem to resolve.
It is speculated that exposure to harsh uncompromising adult reality commonly subsumed under the heading of trauma often results in compromised neurological development. If a child is exposed to significant aggression or extreme poverty then it is likely that there may be neuro-developmental abnormality. Learning may become prematurely fixed and personality underdevelopment may be similarly fixed. This may explain the fact that certain psychiatric disorders are excessively associated with childhood trauma. Such exposure to traumatic realities may well lead to lasting damage to the developing brain. One could speculate that in general premature closure of the development process might lead to the conviction that we cannot change further. Many psychotherapists see this as the most significant obstacle to future progress.
One important question is whether these changes can be reversed. Can this process of brain shutting down on normal development be reversed in any way to enhance a resumption of a more normal pattern? It appears under certain circumstances that these blocks can be reversed and the brain can experience a resurgence in neuroplasticity. The shutting down of brain plasticity seems to be related to the balance of excitability versus the inhibition of neuronal networks. It is well known that in this sense that children have a lot more excitatory neuronal or synaptic activity and this is slowly reduced or pruned as childhood development proceeds. This pruning essentially stops the brain plasticity that makes learning and developing so effortless for children. One could speculate therefore that anything that increases excitability of neuronal networks could reinstate plasticity. The excitement of curiosity certainly seems to promote new learning. Acetyl choline is a neuro-transmitter which is known to be involved in curiosity and enhances neuroplasticity. Drugs that can affect the actions of acetyl-choline in the brain may well be of use in increasing brain plasticity. The excitation of the brain using electrical stimulation of the brain may speculatively in some people promote increased plasticity.
Neuronal development also seems susceptible to certain drugs commonly used in psychiatry which potentially return them to a state of being more plastic. One of those drugs is prozac which is used a lot in young people and children. When prozac first hit the market as an anti-depressant in the USA it was reputed that a lot of people used it for the purposes of increasing their intelligence and not for depression at all. It may well be that in terms of increased neuro-plasticity those people were actually on the right track after all.