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1.0 Introduction


Our chosen article is a review of Barbara Arrowsmith-Young’s book, The Woman Who Changed Her Brain. Written by Tanveer Ahmed, it was published to the Sydney Morning Herald on the 9th of June, 2012.

The book explores the concept of neuroplasticity by detailing how one can potentially ‘train’ their brain with specific cognitive exercises in order to overcome learning disabilities. This often involves rewiring parts of the brain that were formerly damaged, as was the case with Arrowsmith-Young.

From a young age, she was unable to conceptualise causality. This meant her comprehension was poor, simple arithmetic was beyond her grasp, and she faced difficulty with conversations. She couldn’t even make sense of the relationship between the hands on a clock. Despite this, she ‘stumbled through school’ by mainly relying on her excellent visual and audio memory.

At 25, she was inspired by the Russian neuropsychologist Aleksandr Luria, who worked with brain-damaged soldiers and helped them overcome their dysfunction. She also read the work of an American researcher who proved that rats' brains physically changed in response to stimulation.

She then created a variety of mental exercises, often involving flash cards, which she persistently practiced until she had rewired the parts of her brain that weren't working. Ahmed writes, ‘Her fog had lifted for good’. This style of mental physiotherapy, which has corrected the mental disabilities of about 30 children and adults across Canada and the US, conceptualizes the brain as a muscle that needs training.

We chose this article because of its potential implications; that we can take our mental abilities into our own hands, sharpen, and enhance them. That, to an extent, the science of neuroplasticity is accessible to everyone. Neuroplasticity is a growing field of research in neuroscience, and new findings can improve the quality of life for thousands.


2.0 Neuroscientific Context


2.1.0: Background


Neuroplasticity is the innate modifications in the brain that may occur through changes in behavioural, environmental and neurological conditions, as well as physical trauma. Young’s method of training her brain was through cognitive exercises that would actively involve parts of her brain that were not functioning properly. Through much practice this method trained her brain to deal with tasks involving reasoning, logic, connection and interpretation; essentially understanding her memories. While this article touches on several issues related to the neuroplasticity of learning, two particular topics discussed here are the cellular mechanisms of learning and an example of behavioural techniques that can induce neuroplastic change.

Learning is an intrinsically plastic activity where information, skill, beliefs or values, is modified or newly acquired. It is how sensory feedback is interpreted, memories are formed, relationships between disparate information are made and how humans cope with the reality that surrounds them. Learning and its involvement in memory is an important topic of research in the field of neuroscience and there have been several attempts to understand the underlying cellular mechanisms. Some of the more widely recognized mechanisms are known as long term potentiation (LTP) and the opposing process, long term depression (LTD). Both these mechanisms have been shown to induce neuroplastic changes in certain areas of the brain, particularly the hippocampus and the cerebellum.

Following cognitive therapy is Constraint induced therapy (CIMT) which is behavioural technique that appears to enhance the neuroplasticity late after the brain damage by involving the brain that does not function properly. Like the Young’s method of cognitive exercises, CIMT improves the function of paretic limb that was paralysed in only after two weeks by rapid and major cortical reorganization.

What follows is a summary on learning and cognitive therapy.

2.2.0: Long Term Potentiation


LTP is widely considered to be one of the primary mechanisms underpinning learning and memory. It is also one of the most well known experimental models for elucidating synaptic plasticity. The best known form of LTP is induced by the activation of N-methyl-D-aspartate (NMDA) receptor, which is a type of glutamate receptor. NMDA receptors exhibit three basic properties which are associativity, cooperativity and input sensitivity (Bliss & Collingridge, 1993),
  • Associatiavity is the potentiation of a weak stimulus if it is activated simultaneously with a strong stimulus from a different source.
  • Cooperativity is characterized by a threshold for induction of LTP. Overcoming this threshold can be due to the induction of a singular strong stimulus or simultaneous weaker stimuli.
  • Input sensitivity refers to the sensitivity of LTP, where once induced an LTP at one synapse does not migrate to other synapses, and potentiation is shared only via the rules of cooperativity and associativity.

NMDA receptor dependent LTP is prevalent in a variety of excitatory systems in the brain including the hippocampus and the cerebellum.

2.2.1: Long Term Depression


LTD is often depicted as the opposite effect of LTP and is thought to be a result of decreases in post-synaptic receptor density via prolonged NDMA receptor activation that is below the threshold necessary for inducing synaptic potentiation (Dudek & Bear, 1992). Like LTP activity, LTD is also exhibited due to NMDA receptor activation and follows the properties described in the previous section. There have been some evidence that LTD has a role in the removal of memory (Malleret, 2010) and it can be extrapolated LTD is a mechanism for unlearning thus leading the way for learning via LTP activity.

NMDA receptor activity dependent LTD has been shown to be involved in many systems of the brain including the cerebellum and the hippocampus.

2.2.2: Brain Regions Involved in Learning


As the diagram below shows there are two main regions of the brain that are involved in learning and memory, namely hippocampus and cerebellum.


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Figure 1: Excitability of hippocampus and cerebellum through NMDA receptor acitivity

The hippocampus is an important part of the brain and belongs to the limbic system, which has a variety of functions affecting behaviour, emotions, motivation, learning and memory (Malleret, 2010). The role of the hippocampus is involved in the consolidation of memory. It is closely associated with the cerebral cortex as through which it interprets sensory and motor information as memories. Damage to the hippocampus has been associated with the inability to form new conscious memories, although have shown to implicit memory.

The cerebellum plays an important role in motor control and may also be closely associated to attention and language
(Daoudal, 2003). While the cerebellum is not involved in the initiation of movement it contributes fine motor control and coordination. Damage to this region of the brain is shown lead to diminished fine motor control, posture and motor learning.


2.3.0: Constraint induced therapy (CIMT)


CIMT has been hailed as a radical new approach to stroke rehabilitation and the guiding theory is that impairment of hand function is exacerbated by the learned non-use and that this in turn leads to a loss of cortical representation of the upper limb. Similar studies have suggested that CIMT can lead to large improvements in function of hand more than a year after stroke.


2.3.1: Affect of CIMT


Constraint induction technique abolishes disinclination to attempt to use the affected limb which has been arisen through a conditioning process. Early after a stroke, it is argued that attempts to use the paretic limb fail and there is therefore selective reinforcement of use of the other hand. The forced used of paretic limb during the CIMT is thought to cause extinction of this “learned non-use” and subsequently, spontaneous attempts to us that hand become more frequent. Also the repeated and sustained practice causes use-dependent cortical reorganization which reverses a loss of cortical representation of the upper limb that had been caused by the non-use.

“The learned non-use model” shows the functional ability of the paretic hand before CIMT


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FIgure 2: The learned non use model


2.3.2: Current observations


A focus of the current excitement about CIMT is that it has provided the first clear evidence of brain changes related to rehabilitation therapy. Liepert et al. (2000) used TMS to study 13 patients who underwent CIMT therapy and it was showed that before CIMT, there was an average of 40% fewer active sites across the damaged hemisphere than the intact hemisphere. This result was stable across two pre-treatment assessments. Immediately after the treatment, the situation was reversed by having 37% more active sites for the paretic hand. Liepert et al. (2000) used these results as evidence of recovery of cortical representation of the paretic limb and stated that reduced excitability of the damaged hemisphere before CIMT was consistent with diminished representation due at least in part to reduced use of the paretic limb. The increased number of active sites after CIMT was seen as a reduction of this abnormality and recovery of a normal balance between the hemispheres.



3.0 Analysis


3.1: Target Audience


The article was published in the Sydney Morning Herald, so we can assume that the intended audience doesn’t require a neuroscientific, or even scientific background. However, as a book review, it was clearly written for adults with an interest in literature and possibly psychology. Technical jargon was almost entirely excluded, and the light tone makes for relaxed reading. The article was located in the entertainment section, so the target audience would be primarily looking for entertainment possibly with scientific reports; not a ‘hard science’, peer-reviewed paper.


3.2: Purpose and Biases


As a book review, the article must summarize Young’s journey through rewiring her brain succinctly and without too many technical details. However, this purpose conflicts with its credibility as a piece of science journalism. For example, Bliss and Collingridge (1993) showed that LTP (one of the primary mechanisms underpinning memory and learning) is best induced by the activation of NMDA receptors. These are most prevalent in the hippocampus and cerebellum where most learning and memory take place. Young’s learning aids bear similarity to a current technique called Constraint Induced Movement Therapy (CIMT), which has been shown to result in cortical reorganisation. The book review fails to mention any of this. Instead it states ‘She spent hours on this and other exercises, persisting until she rewired parts of her brain that had not been working.’ Clearly, what we are given in the article is a gross simplification of neuroplasticity.
The article also suffers from commercial interests. Its main purpose is to sell the book, and this may have influenced the way events in the book are portrayed. Details regarding her journey through the literature in search of answers are glossed over, while other parts such as the inspirational qualities of her transformation have been enhanced.


3.3: Quality of Information and Accordance with Scientific Consensus


As detailed in the neuroscientific context section, Liepert et al. (2000) showed that cortical representations of a damaged limb increased from 40% less active sites to 37% more active sites following CIMT. These findings are backed up by fMRI scans which show higher cortical activity. Thus, although what the article presents is simplified, it is still plausible. It remains only plausible, however, because Liepert et al.’s study applied to brain maps of limbs, rather than a more abstract inability to conceptualise causality. Nonetheless, Ahmed is a certified psychiatrist, lending the article greater credibility.
A more serious problem however, is the way neuroplasticity is depicted in the article. This may be an effort to appeal to the general public. At present, behavioural therapies such as CIMT are very difficult to implement without a qualified psychologist, as these therapies are both specific and complicated. While it may be gratifying to believe that we can undertake such treatments ourselves and succeed, the truth is that Young’s case is an extraordinary example, and neuroscience is still well out of the realm of self-help literature.


3.4: Evaluation


This review, like any other, simplifies where complicated, and exaggerates where it makes for interesting reading. That doesn’t make it a failure; it merely means that newspaper articles aren’t a source of scientific fact. Where the article does succeed is providing an insight into the science of neuroplasticity, provoking interest in the field, and narrating the story of a courageous individual who overcame their circumstances.


4.0 Appendix

Originally we were divided as to which neuroscience topic we should look it. What we did know originally was that we were all interested in how the brain is able to change itself and adapt to new situations or to damage (external and internal). This eventuated in the decision that our topic be ‘Neuroplasticity’. The next step was to see whether or not we would be specific about which part of the brain we would be looking at, but we decided that looking into separate brain regions would overcomplicate the subject, thus the decision to remain in the broader scheme of things.
The article that we found not only addressed the topic clearly it was also very recent, having only been published earlier this year – a review written by well-know Dr. Tanveer Ahmad, a psychiatrist and journalist based in Sydney. After the decision was made, we decided to have at least one relevant article apiece regarding this subject as a form of background/context/reference for botht the subject of Neuroplasticity as well as our main article.
With our search for articles, we used databases such as SIRIUS (courtesy of the USNW Library), PubMed, and other such scientific peer-review article databases.


With regards to the meetings, we were able to successfully communicate and delegate tasks that had deadlines and we are happy to say that so far, nearly all of the deadlines have been met.
Addressing the discussion posts, we were slow to start as our group itself was formed at a date later to everyone else. We were slow off the ball, however we did manage to find and successfully analyse an article that addressed our core topic, that being Neuroplasticity.
We received some comments regarding our information in the wiki; with regards to the comments made about our background sections, we decided to combine the two, making it more understandable and readable. Another issue that was raised was the lack of information on LTP's opposite, LTD. We explained LTD (gave it its own section) and connected it back to the original theme, that being neuroplasticity.
Referencing was added to all the diagrams to ensure no plagiarism, and LTP was no longer referred to as a model but rather a mechanism. This addressed most of the issues that were raised by our reviewers.
There were also concerns about some of the references and information being outdated; The information present in these sources is still quite relevant and many of the modern sources still reference them, hence we made no changes to the source of the information or the referneces used. Another suggestion was adding extra detail to the exact methods in which Young used to treat herself, however we did not see it as overly important to the discussion at hand and it would also require purchasing the book to be able to elaborate on her procedures.

We await more reviews and comments!


5.0 References


- DriemeyerJ, Bojke J, Gaser C, Buchel C., May A (2008) Changes in Gray Matter Induced by Learning- Revisited. PloS ONE 3(7)
- A. May, G. Hajak, S. Ga¨nßbauer, T. Steffens, B. Langguth, T. Kleinjung and P. Eichhammer (2007) Structural Brain Alterations following 5 Days of Intervention: Dynamic Aspects of Neuroplasticity,
- Bliss TV, Collingridge GL (January 1993). "A synaptic model of memory: long-term potentiation in the hippocampus". Nature 361 (6407): 31–39
- Daoudal G, Debanne D (2003) Long-term plasticity of intrinsic excitability: learning rules and mechanisms. Learn Mem 10:456–465.
- Dudek, S. M., & Bear, M. F. (1992). Homosynaptic long-term depression in area CAl of hippocampus and effects of N-methyl-D-aspartate receptor blockade. Neurobiology , 4363-4367.
- Malleret, G. (2010). Bidirectional Regulation of Hippocampal Long-Term Synaptic Plasticity and Its Influence on Opposing Forms of Memory. The Journal of Neuroscience , 3813-3825.


Administration and Group Work:


Division of Labour


Bassel:
- Manage appendix 21/9/2012 (Worth 10%)

Rachel:
- Neuro-scientific Context completed and uploaded by 14/9/2012 (Worth 50%)
- Appendix by 21/9/2012 (Worth 10%)

Satya:
- Neuro-scientific Context completed and uploaded by 14/9/2012 (Worth 50%)
- Appendix by 21/9/2012 (Worth 10%)

Sujay:
- Introduction completed and uploaded by 14/9/2012 (Worth 15%)
- Analysis completed and uploaded by 21/9/2012 (Worth 25%)
- Appendix by 21/9/2012 (Worth 10%)

Deadlines for Meetings


Meeting 1: 24th August. Objectives: Meet with other group members, decided upon what media piece to use. By next meeting, everyone should have read the article.

Meeting 2: Over facebook: Everyone finds one relevant article in the current scientific literature based on neuroplasticity
Meet again to compare our results with what the article says

Meeting 3: 7th September, Objectives: Discuss literature gathered, compose one paragraph for each to add to better understand the neuroscientific context.

Meeting 4: 14th September, Discuss the completed introduction and neuroscientific context. Also, discuss analysis. (Subject to change)

Meeting 5: 21st September, Entire group reviews completed project. (Subject to change)

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Bassel, Sujay, Satya, Rachel