Patient H.M.

Today’s blog post is about one of the most studied individuals in psychology and neuroscience. By studying him, scientists were able to massively expand their knowledge of how to human brain is structured, and how different abilities (or “functions”) are located in different cortical areas.
H.M. was born in 1928, and was 10 when he first started having epileptic seizures. These were extremely debilitating, and although several medications were tested, none had any affect. When H.M. was 27, a pioneering neuroscientist called William Scoville worked out where the seizures in H.M.’s brain were coming from, and decided that the best way to stop them was to operate, and cut out the parts of the brain that was responsible.
In terms of removing his seizures, this surgery was largely successful. However it came at a cost: H.M. could no longer form new long term memories, nor remember anything from X years before his operation. The image below is a scan taken of H.M.’s brain, and shows the lesions made during surgery, and how this differs from a normal brain scan.
memory-hm-anatomy2
As you can see from this image, H.M. was left with extensive damage to the central parts of his brain – this area is known as the medial temporal lobe. By analysing the brain damage, neuroscientists were able to make inferences about where certain brain functions are located. As H.M.’s memory was impaired, but other cognitive functions such as language were not, the medial temporal lobe was identified as being important in the formation of long term memories.
Perhaps unsurprisingly, things aren’t as simple as this. H.M.’s long term memory was affected, so severely that he was unable to remember things that happened a few minutes ago. However his short term memory was intact, with a normal digit span (a string of numbers that you can keep in your mind at once) of 7 +/- 2. Therefore, the structures damaged can’t be involved in short term memory.
There are also distinctions that can be made within long term memory. This can be divided into 3 different types of memory: semantic, which is general knowledge about the world; episodic, which are memories about ourselves and our lives; and procedural, which are learned physical movements e.g. riding a bike. Only H.M.’s episodic and semantic memory were damaged, which shows that our procedural memory must be located elsewhere. Other brain areas such as the cerebellum have been identified as involved in this. Not only was his procedural memory intact, he could also improve it by practicing new movements over time. The image below shows a mirror drawing task, where participants have to trace an image by only looking at its reflection in a mirror.
starmirror
H.M.’s performance improved each time he did this task, even though he had no recollection of ever doing the task before! This illustrates nicely the different between the automatic, learned ‘procedural’ memories, and the episodic memories about previous experiences.
One last question remains – why did H.M. lose his episodic memories from the years before the operation, but not ones from when he was much younger? There are several theories for this, with one being that older memories are ‘consolidated’ into the rest of the cortex – only newer memories remain in medial temporal structures such as the hippocampus. Therefore, when this area of brain was destroyed, so were the newer long term memories.
When H.M. died in 2008 aged 82, scientists were able to reveal his real name – Henry Molaison. He made a massive contribution to the field of neuroscience, and is thought to have been one of the most tested patients in medical history.
For those interested in reading more about H.M., I would recommend this article, written while he was still alive: Corkin, S. (2002). What’s new with the amnesic patient HM?. Nature Reviews Neuroscience3(2), 153-160.
And finally, I’ll leave you with a quote from H.M. himself, when he was asked “Are you happy?”
“Yes. Well the way I figure it is, what they find out about me helps them to help other people. And that’s more important.”
Advertisements

Epilepsy

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:

first-aid-for-seizures3_page_2

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).

deja-vu-experience1-e1407773003305.png

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!