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The Development of the Brain During Early Childhood

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The early development of the brain begins soon after conception. Firstly, developing tissues begin to fold, the central cavity filled with fluid thickens. The forebrain begins to develop around 3 months and the spinal cord at 7 weeks. The first step in brain development is proliferation and migration, the brain begins to produce new cells and neurons, in-fact many more neurons that are present through till adulthood are produced, cells split into two, stem cells remain in place and continue to divide, the newly formed neurons and glia move to their new location in the nervous system. Secondly, differentiation occurs, this is the forming of axons and dendrites which give neurons their distinct shape from other cells, the axon usually grows first and once it has reached target length, dendrites form. Third is myelination, glia cells produce a fatty sheath which covers axons known as myelin, this speeds up transmission between neurons, fatty sheath is continuously developed over decades as connections are strengthened through learning and experience, myelin first covers axons in the spinal cord and later in the hindbrain. Lastly, synaptogenesis occurs, this is the formation of synapses, a process which occurs continuously throughout life as we learn additional information, synapses which are not useful prune. No new neurons are produced after birth.

Axon pathfinding refers to the process of the axon knowing where its place is in the brain, a study into how this occurs came from Weiss, 1924, who attached an extra leg to a salamander, after a while, the extra leg began to move in synchrony with the others. This is evidence that axons can find their own way in the nervous system. Speary, 1943, conducted experiments with newts whereby he cut the optic nerve to see if it would reconnect to the same areas, and this was the case. However, when the eye turned 180 degrees the axons grew again to connect to the exact same location, causing the newt to see the world upside down, Speary concluded that axons follow a chemical gradient to find where to go.

During development as a child, neurons engage in neural competition, whereby some neurons survive whilst others are eliminated. Useful axons are provided with neurtrophin, a growth factor released by muscles which promotes revival and growth of axons. Axons which are not useful, and therefore not exposed to NGF undergo aptosis, a pre-programmed ‘suicide’ for neurons, whereby the neuron destroys itself. After maturity, apoptotic mechanism of neurons becomes dormant. Evidence for apoptosis comes from Jiang et al, 2009. Jiang and colleagues reported that the visual cortex is thicker in people who are blind at birth than people who become blind later, this is because synapses cannot use visual experience to classify which are useful and which are not, hence pruning does not take place and the same number of synapses remain throughout development. People who become blind in adulthood have a less thick visual cortex, their early sight experience allowed pruning to occur and irrelevant synapses were destroyed.

The brain is the fastest developing organ in human beings. At birth, it weighs around 350 grams but will weigh around 1000 grams by the first year, the adult brain weighs between 1200-1400 grams, highlighting the importance of the first year of life for synaptic development. Yet, the brain will continue develop throughout an individual’s life time, through a process known as fine tuning. Axons and dendrites continue to modify their structure throughout lifetime, they gain new spines as we learn new information and strengthen connections through processing information, they also lose spines if they are no longer relevant, meaning the brain can continually reorganise itself to become more efficient. Enriched environments in the brain will often result in thicker cortex, this is due to more dendritic branches being formed. Maguire et al, 2000, found that taxi drivers have increased GM in their hippocampus due to their expert knowledge on the roads. People who learn to play string instruments such as the guitar have a different organisation in M1 motor neurons to cater for the skill.

The learning of language also produces increase GM volume; however, this reorganisation of the brain differs depending on the age language is acquired. Children who have been raised in bilingual households show different brain activation during sentence production than people who learn new languages in adulthood, (Kim et al, 1997). The later the second language is acquired, the less effect it has on GM density (Mechelli et al, 2004). However, there is a critical learning period for language, (Lenneberg 1967) a lack of early exposure to language can lead to permanent impairment. This is also the case for deaf children, if not taught sign language at an early age it is much harder for them to pick it up in adulthood, also, cochlear implants are shown to be most effective if installed within the first two years of life, suggesting a critical period for the brain in reorganising both auditory and language cortices. Thea brain also can reorganise its structures to make up for impairments, Sadato et al, 1996, found that blind subjects show activation of primary and secondary visual cortices during tactile discrimination tasks (braille).

Brain reorganisation and plasticity also means that in some cases of damage to areas of the brain, survivors can show subtle to significant behavioural recovery. Diaschisis refers to the process where following brain damage, surviving areas increase or reorganise their activity to avoid decreased activity brought on by damage to other parts of the brain. Neuron super sensitivity also occurs, this is where postsynaptic regions deprived of input develop increased sensitivity to the neurotransmitter they do receive to make up for the lack of chemical release. Denervation sensitivity involves axons showing a heightened sensitivity to NT after the destruction of incoming axons, or disuse supersensitivty, whereby nerves become more sensitive to NT after inactivity of an incoming axon.

Destroyed cell bodies cannot be replaced, but damaged axons will grow back under certain circumstances, in the peripheral NS axons can follow myelin sheath back to target and gradually grow back, although sometimes they can reattach incorrectly after damage, this is known as axon sprouting, non-damaged axons will attach to vacant receptors.

Lateralisation of the brain, the process by which different structures become specialised for certain functions, can also be reorganised after damage. An example of lateralisation is the speciality of both the left and right hemispheres for different functions, each hemisphere is connected to the contralateral side of the body and communicates through the corpus callosum via electrical impulses. The right hemisphere is known as being dominant for recognising emotions and comprehending complex visual patterns, whereas the left hemisphere is specialised for language. This contralateral speciality is portrayed in split brain patients. When a shape is shown to the left hemisphere, patients report seeing a circle, however if projected to the right hemisphere they report seeing nothing, this is because the right hemisphere can no longer communicate with the left to draw on language abilities – we can’t verbalise what we see. Patients who are shown the word keyring will only see the word ring, this is because it’s processed by the left hemisphere, and will only write the word ring as the right hand is commanded by the motor cortex in the left hemisphere. However, if the reach for an object with their left hand, either the key or the ring, they will reach for a key, this is because the left hand is controlled by the right hemisphere which sees the word key. The corpus callosum grows during adolescence, so evidence for limited connections between the two hemispheres comes from young children who can sometimes behave as split brain patients. Gallin et al, 1979, asked three and five year olds to judge if fabrics were different or the same, and they could only do so if they touched each fabric with the same hand, suggesting a lack of communication between hemispheres. This can be implemented in treatments to help people recover after a stroke, Nelles et al, 2001, used a PET scanner to study plasticity after a hemiparetic stroke, and found that patients who did not have the treatment only activated the IPC, after the treatment patients showed activation in the IPC, pre-motor cortex and contralateral sensory motor cortex, this shows that rehabilitation and physiotherapy training can induce reorganisation of brain function for motor systems. Sensory neurons can also reorganise themselves, if a hand in amputated the face will begin to produce more sensory neurons to make up for it, patients with no hands sometimes feel a ‘phantom limb’ when the face receives sensory stimuli, the motor cortex will think it’s working the hand, when it is the face, (Pons et al, 1991).

However, the problem with these studies of split-brain patients is that it is not a common occurrence. Normally, split-brain patients have other faults in their brain, such as uncontrolled seizures or have a kind of developmental impairment. Instead, the WADA test was developed to study lateralisation in normal individuals. Before brain surgery, a barbiturate is injected into one of the internal carotid arteries, a drug is then injected into one hemisphere at a time to shut down the function of that hemisphere, this makes it possible to evaluate the efficiency of the opposite hemisphere, in a way it induces ‘split-brain’ syndrome in healthy subjects.

There can also be an effect on behaviour and cognition because of hemisphere damage. Damage to the left hemisphere will increase the ability to accurately judge emotion, this is because the right hemisphere is no longer receiving interference from the left. Etcoff et al, 2012, had normal participants and participants with left hemisphere damage watch a video and asked to predict if they were lying. Healthy participants only did this at chance, whereas patients with hemisphere damage got this right 60% of the time, the lack of activity in the left hemisphere causes enhanced ability in the right hemisphere to process gestures and facial expressions – without receiving interference from auditory input. Participants with left hemisphere damage also better identified the emotional meaning of sounds such as crying and laughter when presented to the left ear – again indicating right hemisphere dominance for perceiving emotional content.

However, the way in which we study lateralisation and plasticity can be confounded. It is well known that skill learning and repition can lead to a decrease in response time and increase in performance accuracy. Thus, comparisons between imaging data acquired may be confounded with differences in performance. Neural activation differs as a function of task pacing, and changes in activation between pre-and post training may reflect changes in performance (transfer from explicit to implicit) rather than reorganisation in underpinning neural architecture. Plasticity is also confounded with time; first subjects will exhibit anxiety when taking part in Fmri studies and this will gradually be reduced with experience. Initial high anxiety levels may express themselves in different ways can cause confounds, e.g. increasing head motion which will cause spurious increases in activation, or on the other hand, increased vigilance will initially increase activation in brain regions and result as anxiety subsides. Thus, activation may not be due to higher levels of effort in training but rather due to anxiety.

Lastly, cannot establish causal relationships with neuroimaging techniques, TMS and stimulation is needed to identify the exact processes which cause lateralisation.

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