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).
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.
It has been argued that faces are a special type of stimuli, which we are able to process easier than other items in the environment. For example, young infants prefer to look at features forming a face, rather than scrambled features (e.g., Johnson & Morton, 1991), which suggests that we have this enhanced ability to process faces from birth. Thomas (1980) argued that faces are processed more holistically than other objects. But how are faces processed in the brain?
One hypothesis is that there is a special area in the brain for processing faces – the Fusiform Face Area located in the fusiform gyrus (shown below). This was named by Kanwisher (1997) in a fMRI study which found that this area was more active in participants when they viewed faces, rather than other stimuli. It also showed more activity for whole faces, rather than scrambled ones. They therefore concluded that this cortical area is specialised for processing faces.
Further evidence for this area being specialised for face perception is shown by patients with prosopagnosia – an inability to recognise faces. One of the causes of this disorder is damage to the FFA and surrounding cortical areas, which suggests this area is important for normal face perception.
However, although this area might be important for face perception, there is evidence from patients with damage to the FFA who have no trouble detecting faces (e.g. Tranel et al, 1998). Therefore, the FFA might not be necessary for face perception. Some studies have also suggested that the FFA alone isn’t sufficient for normal face perception. Behrmann (2003) found that patients who had prosopagnosia from birth (not from neurological damage) had intact FFA and normal activity there. This evidence suggests that things might be a bit more complicated than simply having one area which is responsible for face perception.
One alternative explanation is that there is a network of cortical areas, which all interact to process faces (Haxby, 2000). This study used a pattern analysis method and found that several other areas in the brain were active when participants were shown pictures of faces e.g. the superior temporal sulcus and lateral occipital gyri, suggesting the theory of a single area such as the FFA is over-simplified.
I hope you enjoyed this post, and thank you for reading.