Why do we forget?

I realised earlier today that whilst I’ve written several posts about memory, for example this one, about the different types of memory, the link between smell and memory, whether our memory is trustworthy, and about those with perfect memory syndrome, I’ve never actually written a post about the opposite – forgetting. Why is it that we often can’t remember something so simple as what we had to eat yesterday, or a piece of information we need to know for an exam? Read on to find out more..


One theory is the Trace Decay Theory of forgetting. This assumes that memories leave a trace in the brain, and if we don’t activate this trace (by thinking about the memory) then it fades, or decays. This theory involves our short term memory, which has a limited duration and can only hold onto information for around 30 seconds. However, it is actually pretty hard to test, meaning there isn’t much evidence to support it. It also doesn’t explain why people can remember things even though they haven’t thought about them for years, which is at odds with trace decay theory.

An alternative theory involving the short term memory is Displacement Theory. This theory is based on evidence which has shown the capacity of the short term memory to be between 5 and 9 items (Miller, 1956). Once new information enters our short term memory, other items in there are displaced. This has been illustrated by asking participants to remember a list of words. Results of experiments using this method have found that people are more likely to remember the words at the beginning and at the end, the ones in the middle have been ‘displaced’.


Interference Theory explains forgetting in terms of our long term memory. Have you ever typed in your old password and wondered why it wasn’t working? That’s an example of proactive interference – old knowledge interfering with what we know now. Or how about if you’ve broken your new phone and have to go back to using your old one, but keep pressing the wrong buttons? That’s retroactive interference – new knowledge interfering with what you used to know. Anderson (2003) explains interference as a failure of inhibition in the brain, whilst it might be useful to forget some things over time (e.g. what you had for dinner 3 weeks ago), there are other things which we need to remember, despite new learning. A single retrieval cue (such as sitting at your computer) can link to more than one memory (your old and new password), meaning the correct memory needs to be selected. However a problem with this mechanism means that as well as forgetting potentially distracting memories, problems with inhibiting other memories triggered by the same cue means that useful things are forgotten too.

The above theories assume that the memory has been forgotten because it no longer exists. But what if the problem isn’t with the memory itself, but the process of remembering known as retrieval? Retrieval failure happens when the memory is still contained in our long term memory, but we are unable to access it because certain cues are not there. These cues can be anything such as context about where you were when you learnt the information (external), or how you were feeling (internal). Goddon & Baddeley (1975) asked a group of divers to take part in a memory experiment. Half learnt a word list on land, and half underwater. Half of the group who learnt the list on land then had to recall the list on land, whilst the other half had to do this task underwater. The same happened to the participants in the underwater learning group. They found that participants who had to recall the words in the same setting as they learnt them in performed significantly better than those whose context had changed.

What about when forgetting is more serious? Amnesia is more severe than the types of forgetting we experience in day to day life, as it can involve forgetting large proportions of previous life events or information and is often caused by trauma to the brain. Perhaps the most famous case of amnesia was in Patient H.M., who had most of his hippocampus (structure in the centre of the brain which is thought to be responsible for long term memory) removed to cure his severe epilepsy. Whilst successful in reducing his seizures, he was left unable to retain any new information for more than a few minutes. If you’d like to read more about what H.M.’s case taught us about human memory, I’ve also written a post about that here.



Anderson, M.C., 2003. Rethinking interference theory: Executive control and the mechanisms of forgetting. Journal of memory and language49(4), pp.415-445.

Godden, D.R. and Baddeley, A.D., 1975. Context‐dependent memory in two natural environments: On land and underwater. British Journal of psychology66(3), pp.325-331.

Miller, G. (1956). The magical number seven, plus or minus two: Some limits on our capacity for processing information. The psychological review, 63, 81-97.

Scoville WB, Milner B. J. 1957. Neurol. Neurosurg. Psychiatry. 20:11–21



The Nocebo Effect

The Placebo Effect: a psychological effect in which a treatment which contains no active medical substance causes an improvement in symptoms. For example, a participant in a trial takes a sugar pill believing it could be real medication and find their back pain goes away.

This effect has been well documented and is relatively well known (for more information read my blog post here). But what about the Nocebo effect? In this instance, the opposite happens. A participant in a trial takes a sugar pill, or receives a fake injection, and start to feel negative side effects of the medication. How is this possible when no active medication was received?

To begin to explain how this effect occurs, I’ll start by telling you a bit about how clinical trials are conducted. Before a participant consents to take part in the study, they have to read a participant information sheet which explains all the details of a trial and what will happen. In a drug trial, such as one testing a new medication to help persistent back pain, participants will also have to read a list of potential side effects, much like those you find on the leaflet that comes in the box with medication. When participants sign up, they are told that they might receive the real medication, or they might receive a sugar pill. Having the control group of those who receive fake medication is important in clinical trials, as it allows you to show that any improvement is due to the medication being tested and not other factors such as symptoms improving over time. The reason control groups are given fake medication instead of having no medication at all allows for researchers to see how much of the improvement of the real medication is due to it’s active ingredients, and to show that participants haven’t just got better because of the placebo effect.

image from http://www.thehealthsite.com/diseases-conditions/mind-blowing-facts-about-the-nocebo-effect-k0517/

Even though participants have received the placebo medication they can still believe it is the real one – a placebo should be administered in exactly the same way as the real medication to be a true control. Therefore, it is this belief that they have taken the real drugs that can lead them to report side effects from it. One review of the evidence shows that around a quarter of participants taking a placebo drug experience adverse side effects from it, and that this can be higher than the participants taking the real medication! (Barksy et al, 2002). Visual cues can also induce nocebo effects: one study tested how participants rated the effectiveness and side effects of either branded or unbranded drugs (both in fact were placebos). Perhaps unsurprisingly, participants rated the branded drugs as more effective, and thought the unbranded drugs caused more side effects (Faasse et al 2013).

Several explanations have been put forward to explain the nocebo effect, including conditioned responses or participant’s expectations. For example, a doctor giving you an injection warns you that it might hurt, so you feel subjectively more pain than if they had been reassuring. Some studies investigating the neural basis of the nocebo effect in pain have hypothesised that the effect is caused by increased activity in certain areas of the brain such as the hippocampal network (which is involved in pain modulation) (Ploghaus et al, 2001). This activity is in turn caused by increased anxiety, brought on by the expectation of pain.

This brings a certain ethical dilemma for healthcare professionals and those running clinical trials. It is important the the patient or participant is given all of the information, in order to give informed consent. However, if giving someone more information would cause them to feel more pain, what would you do?



Barsky, A.J., Saintfort, R., Rogers, M.P. and Borus, J.F., 2002. Nonspecific medication side effects and the nocebo phenomenon. Jama287(5), pp.622-627.

Faasse, K., Cundy, T., Gamble, G. and Petrie, K.J., 2013. The effect of an apparent change to a branded or generic medication on drug effectiveness and side effects. Psychosomatic medicine75(1), pp.90-96.

Ploghaus, A., Narain, C., Beckmann, C.F., Clare, S., Bantick, S., Wise, R., Matthews, P.M., Rawlins, J.N.P. and Tracey, I., 2001. Exacerbation of pain by anxiety is associated with activity in a hippocampal network. Journal of Neuroscience21(24), pp.9896-9903.

Why do we dream?

Have you ever stopped to wonder why we dream at night? From sweet dreams to recurring nightmares, our mind is rarely silent – regardless of whether we can really remember their content in the morning.

Sometimes, we find our dreams are linked to things going on in our lives right now, worries about future events or strong memories from the past. This therefore seems to suggest that dreams are in some way linked to our memory, but exactly how, no one seemed sure.

Recent research has investigated the role of dreams and REM sleep (the phase of deep sleep) in the consolidation of long term memory. Consolidation just means the process whereby our memories move from short term to long term storage. In our long term memory, memories are stored for recall. Rehearsal (thinking about) these long term memories briefly involves short term processing, and this rehearsal strengthens the storage of these memories. Dreams may play a part in this consolidation and rehearsal process.

To find out more about REM sleep and our sleep cycle then why not read my previous post here.


Photo by clownbusiness/Shutterstock, with additional illustration by Lisa Larson-Walker

As I mentioned early, our dreams can have similarities to events which have taken place in our lives. Some research has focused on investigating the content of our dreams and found that the events which tend to be included in our dreams are ones which are rated as more emotional, although not more stressful, than those not incorporated (Malinoski & Horton, 2014). This suggests that REM sleep might help to process emotional memories. Further evidence to support this hypothesis is that levels of REM sleep are lower in people with depression (Cartwright, 1983) and PTSD (Ross et al, 1989).

However, although these dreams can contain elements of real life, they are often distorted: it is rare for the complete memory to be ‘played out’ in our dream. It is been suggested that this is because during sleep we cannot access full episodic memories (memories of events) but instead just traces of them.  This has been hypothesised to be due to reduced hippocampus (the part of our brain involved in memory processing) activity during REM sleep (Buzsàki, 1996). The fact that our dreams can contain strange events or impossibilities is thought to be due to a lack of activity in the prefrontal cortex – the area involved in attention and logic (Stickgold et al, 2001).

In addition to consolidating episodic memories another proposed function of our dreams is to enhance learning of procedural tasks (Smith et al, 1996). Studies in rats have found increased levels of REM sleep after procedural learning, and that less REM sleep resulted in poorer memory (Smith et al, 1985).

Whilst REM sleep and our dreams may be useful for certain types of memory consolidation, it doesn’t mean that this is the only way consolidation takes place, or that it is needed to consolidate every type of memory (Stickgold et al, 2001). The authors of this review hypothesize that dreaming enables the brain “to identify and evaluate novel cortical associations in the light of emotions… during REM”. To put it simply, when we dream our brain is working on processing new memories, learning procedures, and our emotions to events.



Epilepsy is a neurological condition characterised by repeated seizures. Seizures are caused by electrical activity in the brain, although may appear differently from person to person (not all seizures involve convulsions, despite what you might think).

As with many conditions there is not a single cause that can be identified as a precursor to epilepsy. Genetics (a mutation in the KCNC1 gene has recently been identified as a cause of a progressive inherited form of epilepsy – Muona et al 2015), brain tumours, or head injuries, and the cause of many patients’ epilepsy remains unknown. Several studies have shown that you are more likely to develop epilepsy after a head injury e.g. Christensen et al (2009) found that people were 2% more likely to develop epilepsy after a mild head injury. This rose to 7% more likely following a severe head injury, with risk also increasing slightly with age.

The image below is taken from the EFEPA and shows what to do if someone is having a seizure:


As mentioned earlier there are different types of epileptic seizures which depends on which part of the brain they originate in. Seizures can be classified by how much of the brain is affected: partial/focal seizures (when only a small part of the brain is affected) or generalised (if most of the brain, or all of it, it affected).

Focal seizures can also originate in different parts of the brain, with the temporal lobe being the most comment (epilepsy.com). The temporal lobe is the part of the brain above your ear, and is responsible for processing hearing, and our memories (this is simplified – it does a bit more than this!). Therefore, one of the common features of temporal lobe epilepsy is memory disturbances (Ko et al, 2013). The famous patient H.M.’s amnesia was caused by an operation to remove the source of his severe temporal epilepsy – this was carried out in the 50s before brain functions were accurately known and too much of the medial temporal lobe was taken away. This destroyed part of the hippocampus, the structure in the brain responsible for memory processing. Due to the nature of his amnesia, he was probably one of the most studied individuals ever in psychology. See this post for more on H.M. and memory research. Operations are carried out to remove part of the temporal lobe in patients now with much better outcomes!

The second most common is frontal lobe epilepsy, where seizures originate in the front part of the brain. They often occur during sleep, and can affect the motor areas of the brain, leading to problems with motor skills (e.g. Beleza & Pinho, 2011). If patients are not eligible for surgery to remove the specific part of the brain responsible for the seizures, anti-convulsive medication and electrical brain stimulation can be helpful in reducing symptoms (Kellinghaus & Luders, 2004).




Déjà vu

I’m sure you’ve all experienced that feeling where you find yourself thinking that things you are currently experiencing have happened before. Déjà vu (meaning ‘already seen’) can feel kind of creepy, but why does it happen?

Déjà vu has been reported to occur in about 60-80% of the healthy population (e.g. Adachi et al, 2003), but is also thought to be linked to temporal lobe epilepsy (Stevens, 1990). There have been several different theories about why this occurs, including the two sides of the brain not functioning together, a sense of familiarity to one part of an experience being mistakenly applied to it all, a problem with how we perceive the timescale of an event, so that something which is happening at the moment is viewed as happening long ago, or a problem with processing sensory information, so that it is processed and reviewed at the same time (see review by Wild, 2005 for a full list).


There have also been several attempts to use neuroanatomy to explain déjà vu. Brázdil et al (2012) compared the brains of healthy participants who did or did not experience déjà vu using an imaging technique called source-based morphometry to measure the amount of grey matter (neurons) in different cortical areas. They found a correlation in certain subcortical areas of the brain (the hippocampus, STS, insula cortices, basal ganglia, and thalami) between lower amount of grey matter and an increase in déjà vu experienced. Several of these structures are in the mesial temporal lobe, which could therefore explain the link between increased déjà vu in patients with temporal lobe epilepsy.

Work to establish the anatomical basis of déjà vu in patients with temporal lobe epilepsy has also suggested that these mesial areas of the temporal lobe are involved. Bancaud et al (1994) studied the anatomical basis of déjà vu using electrodes in epileptic patients prior to surgery which were placed in the temporal lobe, the hippocampus, and the amygdala (you may remember from previous posts that the hippocampus is a structure important for memory, whilst the amygdala is thought to be involved in emotional processing).  They found that déjà vu could be induced by stimulating all of these areas, but that it was 10 times more likely to occur if stimulation was in the hippocampus or amygdala, suggesting that these areas are key to experiencing déjà vu.

As well as occurring in epilepsy, déjà vu is a feature of other psychiatric disorders including schizophrenia, anxiety disorders (like PTSD), depression, and dissociative disorders. There have also been reported cases of constant déjà vu, with sufferers constantly feeling as though their current experiences have happened before. For example, one case study of a 23 year old male was reported by Wells et al 2014, who concluded that it was caused by his severe anxiety and tendency of depersonalisation. This patient did not show a memory deficit, although other cases of persistent déjà vu have been reported amongst elderly patients with dementia.

One of the things I find interesting about déjà vu is that it is a feature of several psychiatric disorders as well as something which occurs in most of the healthy population. It doesn’t seem that psychiatrists are entirely sure about why is occurs in some people but not others, and like with several other areas of psychology – more research is needed to be sure of it’s true course. Thanks for reading this week’s post, I’ll try to be back soon with more new material!

The Placebo Effect

Hi everyone, I’m back after a bit of a break – will try and get back in the routine of regular posts!

This week’s post is something I’ve been wanted to blog about for ages: the Placebo effect. This is well known, having been the subject of films, TV documentaries, and a televised experiment by Derren Brown. When you think of placebos, I bet the majority of you imagine a sugar pill, which when taken, helps reduce negative symptoms.  However, there is far more to placebos than this, and their existence can cause some problems when developing effective new treatments.

So to start off, what is a placebo? A placebo can be considered any substance, (a sugar pill, water, injection of saline solution) which normally has no medical effect on the body, although when disguised as a plausible treatment, causes a very real response.

Interestingly, the effects of a placebo are increased with the perceived impact of the ‘medicine’. So for example, taking 2 sugar pills will create a larger effect than just taking one, having an injection of saline solution will create a larger effect than taking pills, etc.

This seems to point to an explanation for the placebo effect – our expectations. We think taking a tablet will get rid of our headache, and so it does, whether or not that tablet actually includes any active ingredients. This could be due to classical conditioning: that the act of taking a pill has been linked with the lessening of pain, and so taking a sugar pill results in the conditioned response of pain reducing (Stockhorst et al 2000). Placebos can have a similar affect on the brain as taking the real medication, for example Fuente-Fernández et al (2001) investigated it with patient with Parkinson’s disease, and found that taking a placebo caused a similar amount of dopamine to be released as L-Dopa – the drug used to manage symptoms of PD by increasing the amount of dopamine in the brain.

As I mentioned earlier, the existence of the placebo effect has a large impact on clinical trials investigating the effectiveness of new medicines. For example, say you have invented a new drug which could be used to treat anxiety, and have just begun trialling it on human participants. How do you know that any reported improvements in symptoms are due to the active ingredients in the drug, and not simply that taking the drug has caused an improvement via the placebo effect?

Fortunately, you can get around this problem by carefully designing your study. Most studies have a control group who don’t receive any treatment, whilst those in the intervention group do. However, to rule out the placebo effect, there needs to be an active control group, who receive exactly the same intervention apart from the drug they are actually given is a placebo. That way if there is an improvement in the active control group it can be attributed to the placebo effect. For the drug to be considered effective, participants in the intervention group should have a larger improvement, and this different can be attributed to the active ingredient in the drug.

placebo effect

As well as affecting drug trials, the placebo effect can also affect studies into psychological treatments, and here is it much more difficult to control for. Boot et al (2013) recommend that an active control group isn’t enough, you really need to try to make participants’ expectations the same in both the intervention and the control groups. As you can imagine, this is a lot more difficult for psychological interventions as it is a lot harder to hide what kind of treatment each group are getting.

Although this makes research more complicated, setting up studies with adequate controls are needed for us to be able to take proper conclusions from them.. or we could be spending a lot of time and effort to design something which doesn’t have any special effects at all!


Smell and Memory

I’m sure this has happened to you before – you’re walking down the street and you smell something that takes you back to a holiday, or a time when you were younger. It could be the smell of a sweet shop or someone’s perfume, and you are taken straight back to a moment from years ago. But why are smells so linked to memories?

A simple answer is that this link is due to how the brain is organised. Our sense of smell is triggered by a molecule that enters our nose and binds to the hair-like projections (cilia) on neurons at the top of your nasal passage. These neurons project to a part of the brain called the olfactory bulb, which run along the front of the brain, at the bottom. This structure is thought to be involved in interpreting these signals and processing information about smells.

What’s interesting about the olfactory bulb is that it’s the one part of the brain responsible for our senses that has projections to and from the areas of our brain responsible for memory and emotion – the hippocampus and amygdala. You can see this from the image below:



This explains why smells can trigger memories and emotions. The hippocampus is responsible for our episodic memories in particular – personal memories about our lives, which is why it is this type of memory activated by smell. One theory about why these connections exist between the hippocampus and the olfactory bulb is that they enable us to recognise smells from previous experience.

Studies have shown that using smells to trigger memories can be more effective than cuing them with words. For example, Maylor et al (2002) asked young and old adults to recall autobiographical memories associated with 6 cue words. They were then shown the same words and were asked to recall new memories, and for half of these words the appropriate smell was presented too. The researchers found that for both age groups, the participants recalled twice as many memories when the smell was presented too, showing the large impact of smell and memory recall.


The Mind’s Eye

For the vast majority of you, if I asked you, right now, to imagine a beach – all golden sands and blue sky then I doubt it would be a problem. We ‘see’ the beach with our mind’s eye, even though there is no beach in front of us, and it’s most likely still grey and raining outside. The fact that our mind can generate images this lifelike is extraordinary, and something which I will explore more in this week’s post.

Something also interesting about our ability to generate these mental images, is that we can manipulate them in our minds. We do not see a flat, 2D object, but something we can move, or interact with. This was investigated in one study by Shepard & Metzler (1971) which used novel shapes so that previous experiences could not affect the results. Participants were shown pairs of shapes like the ones in the image below, and were asked to decide whether they were the same shape, or mirror images of each other, as quickly as possible.

As you can see, this requires some concentration! The researchers found that there was a strong linear relationship between the time it took for participants to respond and the angle of rotation. From this, they concluded that people rotate mental images at about 60º per second.

Interestingly, other studies have shown that this rotation speed of mental imagery is affected by the laws of physics – which at first glance seems improbable. I mean if you’re imagining something, why can’t you move it however you’d like? Parsons (1987) found that people find it difficult to rotate a mental image if it is physically difficult for this to happen – they used the example of imagining a foot rotating from someone’s ankle.

This effect is thought to occur as mental imagery, such as the examples above, rely on motor imagery – neuroimaging studies have shown that the motor cortex is active when we perform mental image rotation. As physical movement is constrained by the laws of physics, so are our transformations of mental images.

Mental imagery is also strongly related to visual perception, as shown in this early experiment by Perky (1910). Participants were asked to imagine the image of a given object on the dark screen in front of them, however they didn’t know that a faint picture of that object was also projected onto the screen. They found that although the participants do not notice the projected picture, they report that the image they’re imagining has the same properties as this picture e.g. the same rotation and size. This result suggests there must be some overlap between our mental imagery and our perceptions. More recent studies have also shown our mental imagery has some of the same properties as our visual perception, such as increased sensitively to the lower visual field.

Now, go back to your mental image of the beach, and try to imagine what life would be like if you kept really trying to conjure up that image, but were always unable to. Although most of us take our ability to have mental imagery for granted, a small percentage of people are unable to visualise mental images. This is known as aphantasia, and people with this condition are unable to visualise aspects of a memory, although they will be able to describe it. Scientists who have studied this condition believe that there is a spectrum of the vividness of which people experience mental imagery, with aphantasia being at the bottom.

Thanks for reading, and please subscribe if you don’t want to miss out on a new post every Thursday!

Being left handed

As a left handed person and psychology graduate, this is a post I’ve wanted to write for a while because there’s actually a lot I don’t know about how being left handed affects the brain. Me and my dad are both left handed, but at opposite ends of the spectrum – he writes with his left hand (but that’s about it) whereas for me, even picking up something with my right hand feels weird and requires conscious effort. So if being left handed is genetic, why this difference?

Another reason I wanted to find out more information is that I actually quite like being left handed, despite the obvious irritation of everything from scissors to tin openers to computer keyboards being biased to the right-hander (and don’t even get me started on trying to write in anything other than biro). And there might even be some benefits to being a leftie, with theories that it’s linked to creativity, sports, or being good at playing an instrument. Here’s what we know:

About 10% of the population are left handed, although as you can see from the comparison between me and my dad, the degree of left handedness can vary. Men are also more likely to be left handed than women (e.g. Papadatou-Pastou et al, 2008). Scientists still aren’t sure of the exact cause of being left handed, although they are sure there is some genetic component – studies have shown that you are more likely to be left handed if one of your parents is (e.g. McManus & Brydon, 1991b).

Handedness has also been thought to relate closely to language functions in the brain. As you may remember if you read this post, in most people, language functions are lateralised to the left hemisphere (see below). As each hemisphere controls the opposite side of the body, there is thought to be a relationship between hand dominance and language, with right- handers having right side preference due to language functions located in the dominant left hemisphere.


However, in left-handers this relationship is not so clean cut – only about 30% are thought to have their language dominance in their right hemisphere. I actually participated in an fMRI experiment at uni which tested my handedness and language location in the brain, which found that even though I’m left handed, my language functions are normally lateralised in the left hemisphere. So opposite language lateralisation in the brain can’t be the only reason people are left handed, the process is way more complex, and still not something science fully understands.

Several studies have identified a link between being left handed and creativity. For example, Newland (1981) asked almost 100 right handed, and 100 left handed people to complete a test on creative thinking. The results showed that left handed participants scored more highly on all 4 sub-tests, suggesting they have greater creativity. Another study by Coren (1995) found that left-handers have better divergent thinking skills than right-handers – in other words, they are better at exploratory thinking to find solutions and create ideas. Being better at divergent thinking could explain why left handed people are more creative, and thought to be better at logic.

There is a lot of anecdotal evidence which suggests left-handers are smarter, or better at politics e.g. Mensa reported that 20% of its members are left handed (which is double what you’d expect, at 10% of the population). However, unfortunately, I can’t seem to find any actual experiments comparing IQ that back this up! Studies have shown however that professional orchestras have a higher proportion of left-handers, and that during school, a high proportion of children who excel at maths are left-handed.

Annoyingly, there don’t seem to be answers to all my questions about left handedness, and there is still a way to go to establish the genetic basis and to understand how the brain is organised in left handed individuals. Regardless, I hope you found this post interesting and let me know in the comments if there’s anything else you’d like me to feature on this blog.





Brain Plasticity

Although you might think that the structure of your brain is formed before you are born and does not change, this actually isn’t the case. As we grow and learn, the brain is constantly making new connections and pathways between different areas. It used to be believed that anything which had not been developed by a ‘critical period’ during childhood would be lost, with little change after this time, although we now know this is not true.

For example, our different skills and experiences can help to shape our brain. This has been particularly studied using musicians, as extensive practice and repetition of certain fine-tuned motor actions can result in more of the motor cortex being involved in directing the actions of the hand and fingers.

Pascual-Leone et al (1995) found that novices learning to play a simple exercise on a piano over 5 days showed an increase in size in the cortical areas involved in the movement of the fingers. Schlaugh (2001) carried out fMRI to compare the size of the intrasulcal length (part of the motor cortex) in professional musicians and controls, and found it was much longer for musicians in the right hemisphere (which controls the left hand). This is shown in the image below, taken from this paper.


It is through the process of brain plasticity that new memories are formed. Motor memories such as becoming more accomplished at music are one type of memory which alter the brain structure, but our personal memories also change our brain. This occurs through the process of Long-term Potentiation (LTP), which is the process of connections between cells at synapses strengthened. It mainly occurs in the hippocampus and other cortical areas responsible for our long term memories. This process is illustrated by the image below:


Brain plasticity is also encouraged in treatment and rehabilitation from brain injury. For example, after a stroke it has been found that giving excitatory stimulation to the damaged areas can improve function (e.g. improving language function – Szaflarski et al, 2011). Just by encouraging movement in people who have had a stroke can also help them to regain function of limbs on their impaired side.

Thank you for reading and don’t forget to check back next week for another post!