Dissociative symptoms represent effectively the perception of an individual that either a limb doesn’t move or there is sensory disturbance without there being any structural, disease or injury to explain.


Such dissociative symptoms cause a lot of difficulty in the setting of litigation whereby the presence of symptoms is often given as the evidence that there must have been an injury to cause the symptoms. It is my personal thesis that this is not correct and that injury should be proved first and then symptoms considered thereafter as to whether or not they fit what we understand about brain functioning.


As an example, migraine sufferers can spend three days in bed wiped out with vomiting and severe light and sound sensitivity as well as having all kinds of neurological deficit. Investigation either within or outside the attack reveals usually no abnormality, particularly in primary migraine. This doesn’t for one moment suggest that the individual is either making it up or not suffering, it merely confirms how the brain is capable of getting it wrong.

In the case of migraine, we know that it is a pathway within the brain stem, known as the trigemino cervical neurovascular pathway that needs to fire in order for head and facial pain to occur.


This pathway activates six other areas of the brain at least which can be identified with appropriate functional MRI scanning. Not surprisingly, some of the other areas include where memories are formulated, the visual cortex as well as the motor and sensory cortices. The activation of these centres would appear to be the mechanism by which behaviours develop associated with the migraine attack.


Migraine in itself is not considered a dissociative disorder, but frequently migraine sufferers do develop sensory symptoms or altered feelings about their skin, scalp or face. Imaging in this group still usually doesn’t reveal any abnormality. Most neurologists and neuroscientists would regard this as being part of the migraine process.


What has now emerged in a paper published in the Journal known as “Frontiers in Systems Neuroscience” is a demonstration that in spite of the complexity of the human brain, it is likely that human thought can be “whittled down to an algorithm that lies in the theory of connectivity”.


The theory of connectivity first proposed in 2015, suggests that how we acquire and process knowledge can be explained by the way in which different neurons interact and align in separate areas of the brain. On this basis, such connections are capable of producing perceptions, memories, generalised knowledge as well as flexible actions. In a way it actually explains every aspect of human behaviour. The neuroscientist who has proposed this theory from scientific study a Dr Tsien who is a neuroscientist working at The Medical College of Georgia at Augusta University has demonstrated how groups of similar neurons “come together to handle tasks such as recognising food, shelter and threats”.


He calls these groups of neurons cliques which can then cluster together to form “functional connectivity motifs (FCMs)”. When these clusters do work together these are then able to handle any additional ideas that may arise. The theory suggests that the more complex the task the larger the group of FCMs.


This theory has been tested by analysing how the theory or algorithm performed in seven different regions of the brain all of which handled what are known as primal basic responses. Primal basic responses include the desire for food, shelter and fear. The testing was in laboratory small animals. By offering different food combinations and monitoring brain responses the research team documented fifteen unique combinations of neuron clusters.

It would seem according to the research team that these cliques of neurons “appeared pre-wired”. They came to this conclusion as the activation appeared immediately when the food choices were given suggesting that this was intrinsic to the animal.


They also determined that this same mathematical rule remained largely intact when the so called NMDA receptor which is one of the master switches for learning and memory was disabled, but only after the brain had matured.


This is important work in understanding how we lay down memories and then the way in which we extract information and react to it. In terms of the dissociative disorder, it means that whatever the reason an individual will probably have connectivity of different neuronal cliques which the suffering individual then considers are the norm as a learnt pathway or a group of pathways or neuronal clusters.


Like in migraine the challenge is then in turning off the activity of these cliques or clusters in order to return the individual to normal.


This is quite different to the situation where there is structural brain damage. Unless there is sufficient plasticity to allow other areas of the brain to take over the functions of the damaged part then the deficiency although likely to follow a trajectory of recovery, will be permanent.


Where individuals have normal structural brain scans with high resolution MRI then this should be regarded as reassuring and on a balance of probabilities lead to significant recovery.


The problem within the legal process is that such negativity as occurs with the constant asking and reflecting on the negative with what is also known as catastrophization “I will never get better!” means that treatment programmes have to be intense and prolonged in order to get best outcome. Catastrophization has in effect the same effect as described above. This can also be described as a “nocebo” effect. The more negative the thinking, the worse the individual gets. This doesn’t however, mean that they will not recover. It just means that all modalities of treatment must be given as part of a multi-disciplinary treatment programme.