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!

Ames Room Illusion

Today’s post is about a visual illusion which at first looks like there is some type of CGI or editing – but I promise it’s just how our brains interpret visual information! Have a look at this image below..

Ames room

In this ‘Ames Room illusion’ the girl appears to be much bigger when in the right hand corner of the room, compared to the girl on the left. However, if you were to take these girls out of the room and stand them next to each other, they would be exactly the same height. So what causes them to look so different?

The answer lies in the way the brain views objects in relation to their context. Even if we knew these girls were the same height, our brains would still interpret this image in the same way (therefore this illusion is ‘cognitively impenetrable’). At first glance, it looks like the girls are standing next to each other, although this isn’t strictly true. We assume that they are standing in a square room, because that’s generally the shape rooms are! However the image below shows it’s true shape, and explains why we view the figures in this way.2000px-Ames_room

The design of this room is so clever, because it is decorated to look square, but this illusion will only work if the scene is viewed from a specific point (see viewing peephole above). So the reason the girl on the left looks so small is simply because she’s further away. The two corners have the same visual angle from this viewing point, so they look as though there is a horizontal wall between them. Therefore, the image of this distorted room which is projected onto the retina is exactly the same as if the walls in the room are parallel. This is how we perceive the room, as our perception is influenced by prior knowledge of what rooms generally look like. This illusion is so strong that people seem to grow or shrink in size as they move from one corner to the other!

This illusion actually has some quite useful applications, mostly in film making instead of CGI when they need to create the effect of some characters being smaller. Notably – this was often used in Lord of the Rings to make the Hobbits seem smaller!

Behavioural Activation

This week’s post is about a technique used as part of cognitive behavioural therapy for people with depression. As you probably know already, symptoms of depression include low mood, low self-esteem, feelings of anxiety and helplessness, and having low motivation and interest in activities which they previously enjoyed.

Behavioural activation focuses on the ‘B’ of the CBT model, in this case on the last symptom in particular – the withdrawal from usual activities and friends. For example, they may start to avoid social engagement and ignore invites from friends or make excuses as to why they can’t meet up, whereas before they would have been happy to go. Although in the short term this avoidance causes a temporary relief, such as a lowering of anxiety, it simply reinforces feelings of low mood or low self-esteem. This maintenance of the condition is illustrated by this diagram below:

Screen Shot 2016-07-28 at 19.49.10

Therefore, in order to break this cycle, behavioural activation aims to change the unhelpful behaviours which continue the cycle of low mood. It does this by gradually building up activities that the person can do, which is turn will improve their mood, and lead eventually to them getting back to activities they used to enjoy. This progression is important, as the change in mood is needed before larger behavioural changes can occur.

Key features of Behavioural Activation are as follows (taken from Jacobson et al, 2001):

  • Firstly, the model is presented to patients by their clinician, who explain a bit about it and why it works. This is called a treatment ‘rationale’ and it is important for the patient to feel confident that this will work. A good relationship and trust with the therapist is also important.
  • Developing treatment goals through collaboration between the patient and the therapist – these goals are new behaviours rather than moods or emotions.
  • Analysis of causes and maintenance factors of the depression
  • Graded task assignment – e.g. starting with something small such as walking to the corner shop. This is scheduled in between sessions, and a hierarchy is discussed with the therapist.
  • Establishing a routine, in the hope this results in improved mood.

Ultimately, the aim of Behavioural Activation is to help the patient re-engage and find joy in activities which they have been avoiding. This will raise mood, and therefore help someone recover from depression.

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!


The McCollough Effect

It’s always a good feeling when I find out about a new illusion that I can share on here – this week’s Brainteaser is another about colour after-effects: The Mccullough Effect.

What makes this different to other colour after-effects is that the stimuli used in adaptation is simpler than the final illusion. This effect was discovered by Celeste McCollough in 1965, and involves alternating black and white lines (known as ‘gratings’) which are viewed as coloured after a period of adaptation. Try it for yourselves here:

First, stare at these images for a minute or so then look at the grid below

McCollough Effect 1

McCollough Effect 2

What you should notice is that these gratings now look coloured, when they are in fact black and white! The vertical lines should look red, whilst the horizontal ones look green.

What is so interesting about these after effects is that unlike others (e.g. here), this effect lasts not just for a few minutes but for hours, or even days. Some studies (e.g. Jones & Holding, 1975) have shown that adaptation for 10 minutes can lead to after effects months later!

Scientists are still not certain which part of the visual system is responsible for this effect or why it is so long-lasting. One theory is that it takes place due to neurons in V1 – the first part of the visual cortex which receives information from the optic nerve via the Lateral Geniculate Nucleus. Only neurons in early visual cortex are sensitive enough for this type of adaptation to occur. A possible reason why this effect lasts for so long could be simply that the adaptation stimulus is rare, so is not seen in the environment for us to de-adapt, whilst others believe this shows a form of associative learning. However, the exact mechanisms are still up for debate.




Are we getting smarter?

Hello everyone, sorry for the lack of blogging over the last month or so – I’ve been doing some extra work in my free time which I’m sure I’ll share on here once it’s published! But I’ve got a bit of a break between deadlines, so I’m back with this post about intelligence and IQ tests which will aim to answer the question: are we getting smarter?

Let’s start off with a bit about IQ tests. There are several which are regularly used in scientific research, such as Raven’s matrices, the Weschler Intelligence Scales, and the Stanford-Binet Intelligence Scale. See how you get on with these example questions and scroll to the bottom for answers!

Raven’s Matrices:

This is a progressive IQ test, with questions becoming harder as you progress through the test. Easier questions at the beginning are used to test children – I’ve done used this before for a research project and it’s relatively simple to explain meaning young children can’t be confused by long written instructions. It is a non-verbal test made of 60 multiple choice questions which measures ‘fluid intelligence’ – or reasoning. Participants are shown a geometric design with a missing piece, and have to choose from multiple options which piece fits best. Have a go at these and see how you get on..





Weschler Adult Intelligence Scale

This test measures cognitive abilities, with the most recent edition – the WAIS-IV, including 4 IQ sub scales: Verbal comprehension, Perceptual reasoning, Working memory and Processing speed. Like the Raven’s matrices, this scale has been adapted for use with children and is also used in a clinical setting, for example when testing for developmental disorders or dementia. See an example below:


So how did you get on? Composite scores from answering all of the questions in these intelligence tests are combined to give a score of Intelligence Quotient, or IQ. IQ tests such as the ones above are developed to give a median score of 100 with each standard deviation of 15 IQ points. This is often illustrated in a bell curve, as shown below:


But are we getting smarter? A scientist called James Flynn has documented the fact that as a population, we are performing better at IQ tests over time. This has therefore become known as the Flynn Effect. Using Weschler tests, it has been estimated that IQ increases by about 3 points per decade. IQ tests such as these have undergone several revisions over time (the first Weschler test was developed in 1939), and scores are standardised using testers to give a median of 100. When these new test subjects take the older versions of the test, they usually score significantly higher than 100, implying our intelligence is increasing. Possible explanations for this increase include better schooling, better nutrition and health. However, there is some debate about whether people are really  getting more intelligent, or are just getting better at taking intelligence tests!

Thanks for reading, I hope you enjoyed this post. I should be back to regular uploads soon!

Answers: a) 3, b) 8, c)1,3,6.

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.


Phobias Part 2 – treatments

This week’s post is the second in a 2 part series about phobias, and will focus on different types of treatment, and what works. If you haven’t already, read part 1 (see here) for more information on types of phobias and possible causes.

If you’r a regular reading of my blog, you may remember that a while back I did a post on Cognitive Behavioural Therapy (CBT) and how that can be used to treat people with phobias. The main principle is to reduce the anxiety felt by encountering the phobia stimulus, be it crowds, flying, or needles. By teaching the patient breathing exercises to help them relax and working to change the thoughts (cognitions) about the phobic stimulus, therapists can help the patient to work towards overcoming their fear. The behavioural part of this technique is gradual exposure to the thing the patient is afraid of, whilst the patient works hard to control their breathing and stay calm. This exposure can help towards changing thoughts which contribute to the phobia such as ‘if I’m in a room with a dog it will bite me’, which in turn reduces fear.

For example, take a look at the diagram below which shows how phobias remain if the fears aren’t challenged. If therapy targets the thoughts, and tests the fear, then it is likely the phobia will be treated successfully.


Another form of exposure therapy which has been used to treat phobias is known as ‘flooding’. Unlike in CBT, where the individual is gradually exposed to their fear, in this technique they are put straight in the worst situation they could imagine. This uses more behavioural techniques – as the body cannot sustain a physiological stress response for a long period of time, people begin to notice they feel calmer, even though they are in the presence of their fear. An example would be putting someone who was scared of birds in a room full of them! This also enables the individual to confront their worst fear and learn that nothing bad happens when they are in that situation.

Thanks for reading – there won’t be a post next week as I’ve got 2 interviews but I’ll be back the week after!


Hi everyone, this week’s post will be the first of two – all about phobias. This first post will cover causes and types of phobias, and the next on will talk more about treatments. And, as no post about phobias is complete without a quick phobia quiz – what do you think these phobias are? (scroll down for answers!)

  1. Agrizoophobia
  2. Suriphobia
  3. Enetophobia
  4. Coulrophobia
  5. Phasmophobia


by BromeliaCarnivor


  1. Fear of wild animals
  2. Fear of mice
  3. Fear of pins
  4. Fear of clowns
  5. Fear of ghosts


Although some of these phobias are unusual, some are more common than others – with Arachnophobia (fear of spiders) probably being one of the most well known. However, there is an important distinction between people who simply don’t like spiders, and would prefer not to be in the same room as them, or not want to touch them, and people who are  afraid of spiders i.e. have Arachnophobia. Sufferers of this phobia will experience extreme anxiety and panic if they come into contact with a spider, or even just look at a picture of one. This is a much more severe reaction.

According to the mental health charity Mind, there can be different reasons for a phobia to develop, from learned experiences to genetics. However, although it is true that some people develop phobias after a bad experience e.g. developing a fear of driving after a car crash, this does not occur for everyone with a phobia. Phobias can also be learnt, from observing other people’s reactions, for example if when you were young your older sibling always screamed and ran away from wasps, you might learn to do the same and develop a phobia of them, even if you’ve never been stung.

One famous (and very unethical) experiment on whether a baby could be given a specific phobia was carried out in the 1920’s by Watson & Raynor. The infant – ‘Little Albert’ had no fears or phobias at the start of the experiment, and the researchers wanted to investigate whether he could be given a phobia of white rats. As this picture shows, before the experiment started, he wasn’t frightened.


This study used principles of classical conditioning to give him a phobia – every time he was given a white rat, a loud noise was made by striking a metal bar with a hammer. Understandably, this noise scared him and made him cry. After this happened several times, he began to become upset when he was presented with the rat alone – the rat had become the conditioned stimulus (to read more about classical conditioning, see my blog post here). They also found that his phobia become generalised to other things that were white an furry, such as a white rabbit or when the experimenter wore a big white beard! No one is really sure what happened to Albert after this experiment, and whether his phobia continued into the rest of his life. It’s safe to say however that experiments like this one would not be allowed to take place now.

Thanks for reading and don’t forget to check back next week for Phobias Part 2.