I’ve been at university for 2 and a half years and although I have done plenty of my own academic pursuits outside of my degree scheme mainly in the way of my own reading and the like, I have never took the initiative to branch out and attend one of the many lectures and seminars put on by various schools that involve guest speakers or researchers from the particular area putting the talks on. However tonight I seized the chance to attend a public lecture given by one of the leading psychiatrists in the UK; Sir Robin Murray. His talk entitled ‘What Makes People Mad’ was centered around Psychosis and in particular schizophrenia. I have come across these disorders a fair bit in my degree and knew alot of the theories behind the causes and obviously the affects of such disorders but I knew that this talk would (hopefully) not be dealing with these aspects too much, due to the fact that it was a public lecture and was likely to have a crowd primarily taken up by people who have a vocational or academic interest in the subject. Both of my assumptions were correct, although there was a business student present; my housemate Jack, who even though was not involved in the sciences was very impressed and interested in the talk. So was I.

Professor Murray gave a talk that while not heavily steeped in scientific jargon or overcomplicated theorem was appropriate enough for the intended audience - a group of academics who were I take it all very interested in such a current and important topic. 

The information about the main pathways that physiologically cause this disorder were secondary in the talk to what could possibly be the causes bringing about these changes in neurochemical processes, that range from social hardships to excessive drug consumption. In short, the main accepted theory as to what causes schizophrenia is an overproduction and release of dopamine in the striatal pathways of the brain. As dopamine is involved in reward systems it is also important in establishing stimuli that are important to the person in terms of survival and interaction with the outside world. This excess of dopamine thus makes everything, even the most innocuous of events and occurrences, of the utmost importance to the sufferer. This can then exhibit itself as feelings of paranoia and persecution as every little part of their interaction of the world is blown out of proportion in their mind. These experiences can then manifest itself in the most well known symptom of psychosis and schizophrenia, that of hearing voices and conspiracies, due to interrupting auditory and visual processes in the cortex of the brain, and again this over emphasising of such normal occurrences as a cough or a word that may signify to the sufferer an intent of hurt against them.

But this is just the chemical process by which the disorder manifests itself. The most interesting parts to me, and I would like to think the rest of the audience too, was what is causing this dysfunction to occur. I knew that there was genetic, social and behavioural factors, but as is too often the case with such important medical matters, I, like most people. only know what is fed to us in the social sphere, the easiest way to explain such abnormal behaviour. As Sir Murray explained, for a long time the view that psychiatrists held was the view held by everyone else. That schizophrenics were categorically different to sane people. That you were either mad or not mad. That the difference between these two groups of people came ultimately down to genetic alterations in the sufferers that produced the disorder. Of course, like most things in life, such complicated behaviours and actions cannot be explained by one limited cause. That this view was held for around 30 years, and enabled sufferers to be denigrated as human beings, speaks volumes for what is wrong with alot of the scientific community, that of not being able to accept any causes out side of some chemical or physiological malfunction, that of being closed off to the ‘non-scientific’ world. 

Genetic malfunctions have been found to play a large role in producing psychosis, with over a hundred genes discovered to play a role in producing the disorder. But instead of being just ‘psychosis genes’ they are normal every day genes that would code for normal everyday neurological processes, except that in a sufferer some part of the gene is not encoded properly or is missing, or some other form of genetic alteration has occurred to produce this abnormal phenotype. In some cases these alterations account almost solely for the display of the disorders symptoms. But it is the outside effects that can interact with these genes, that are seen to produce psychosis in a lot of sufferers. 

The professor produced study after study after study that showed how different causes from the outside world can interact with these malfunctioning genes. He showed that people who have had a traumatic experience, an abusive childhood, an isolated upbringing all have a greater risk of suffering from psychosis, and these results all coming from people who have not been screened for the psychosis genes, all normal people going about everyday lives. Any largely abnormal experience during development into an adult can result in schizophrenia at a later point in life. He addressed the much talked about topic of drug use and psychosis, in particular cannabis. Studies had shown that taking cannabis form an early age increased risk of psychosis in later life and that the consumption of skunk, which is high in concentration of THC, dramatically increased the incidence of psychosis by aorund 2 to 3 fold. Also taking cannabis for a long period of time dramatically increased the risk. He never said that taking cannabis would necessarily give you psychosis which can be an attitude of medical professionals, but like all sane people said that in moderation it will probably not harm you in this way. I had a problem with one of the studies on this drug use in south london that showed a risk with more skunk consumed. I wondered what the reasons for these subjects smoking weed were; isolation, bad upbringing, low prospects in life, deprivation socially and culturally. Could these factors have impacted greater than the cannabis use in producing psychosis? And was the cannabis use greater in people who thought they might have psychosis and were self medicating? These questions were not really answered and though would not really invalidate the results should be taken into account when studying such a sensitive topic. Aside from this, the views expressed mirrored my own on the link of psychosis and cannabis use and were no big surprises.

What was a surprise to me was the studies he showed that indicated an increased risk of psychosis in ethnic minorities in this country. At first I thought I’d stumbled into a bio-racism seminar until he went on to explain that this increase in risk was only present in immigrant ethnicities. The increased risk was found nowhere else in the world where the majority of the country was of these races. In particular the risk was greatly increased in african and afro-Caribbean people but not seen in africa and the Caribbean. This led them to surmise that it was only when people migrated to this country that the risk of contracting the disorder increased. This was backed up by a study where communities where the ethnicity was in the majority the risk was much lower than if they were the minority in the community, hinting that the social isolation and feelings of outsider ship were the factors contributing to the psychosis. Added to this is the higher incidence of psychosis in cities where isolation and individualism is greater which in light of alot the studies produced, seems a credible cause of developing psychosis.  This whole race factor made me recall somethign I’d learnt at A-level psychology of all places, whereby this increase in schizophrenia in ethnic minorities, in particular those from africa, may have been attibuted purely to cultural differences. It was theorised that in some african cultures hearing voices was encouraged whereas in western culture it is wholly frowned upon. When diagnosing schizophrenia, hearing voices is a very good indicator, and so such people may have only been acting what is considered sane in their culture and may not have had other symptoms of schizophrenia but were still diagnosed anyway. Another talking point in this whole psychotic mess.

Alike to cultural differences is a topic only touched on briefly in the talk but one that veers very much away from the scientific core of the disorder. That of what is abnormality, and what is defined as psychosis. The idea that at all points in our lives we have psychotic episodes, thinking people are against us primarily, and that such a thing as psychosis is too hard a thing to define as A and B, Black and White. You get into a very grey area when you start talking about definitions of insanity as it can get hijacked to easily by people who want to sound ‘alternative’ and have no real grasp of science. But it is true that psychosis and schizophrenia are the extreme degrees of a cumulative scale with variances of mental health problems. There are no two categories of insane and sane. It is only when you get to these extremes of behaviour that psychosis presents itself. The scale of mental health only becomes a problem when the persons life is detrimentally effected. People with symptoms of psychosis can go about their lives sometimes as long as it is not destroying their lives, and this was all, albeit briefly, touched upon in the talk.

This definitions of insanity and the social causes of schizophrenia are what interested me the most about this talk. Genetics can sometimes really make a cold matter about hot topics. If you went around purely using genetics as an explanation for all behaviours you would encounter many great problems and no societal progress will be done. You just have to look at thatchers ‘there is no society’ remark in relation to genetic theories of the time that postulated that we were nothing but vessels for our genes and they were all that mattered. Genes controlled our lives and the hell to everyone else. As in this, so is schizophrenia. You could get yourself tied up in knots while trying to think about whether psychosis can be considered normal. The behaviour is only abnormal to the norms of our society, but that is how we function as human beings, as part of a larger group and so any behaviour that limits our ability to do so, even if the term abnormal is considered harsh, is detrimental to our lives and our interactions with others. The fact that a large social factor shown to be involved in an increased risk of psychosis is isolation  and trauma is especially pertinent in contemporary times. As our society becomes ever more individualistic and we become ever more isolated from social interaction could the incidence of schizophrenia become greater? As we look inwardly to save our selves in bleak economic times will those more susceptible  to madness get left behind creating a whole cohort of mentally unstable people that could have been saved with a little more human compassion from us and our leaders? The ever increasing expansion of cities, coupled with technological innovations that decrease out need to fully socially interact, only increases this loneliness for those without a strong social group to exist in. For those for whom this is true that are unlucky enough to have the dangerous cocktail of malfunctioning psychosis genes it may be a dark future for their minds.

Aside from all the unhappiness that is always involved when someone is suffering from any debilitating illness I thoroughly enjoyed this lecture. Although not overly informative it was extremely thought provoking, exemplified by the continuous conversations we had on the topic on the way home. It was great to see amongst the crowd of middle aged medical professionals and academics a fairly good number of people my own age who I can only presume are students. It restores a little of my faith in my peers. This sort of activity is a great countenance to the quickly boring social facade that is the student clubbing/partying experience. I love the socialising aspect of Uni but it has taken me too long to extend myself academically in this way and I will not be leaving such a gap between my next experience of this nature. 

Keep Sane!!

D.F.W would have been 50 today if he hadn’t bloody hung himself a few years ago. Here’s an excerpt from Infinite Jest. It’s not verbatim, it has a few sections of text edited out just so the quote makes sense in its entirety, but its the message that comes across properly I think. One about communication and emotions that is all too valid in our world. (The character speaking is Avril Incandenza to her physically disabled son Mario)

“Well, love, but you know the idiom “not yourself” - “He’s not himself today”, for example. There are, apparently, persons who are deeply afraid of their own emotions, particularly the painful ones. Grief, regret, sadness. Sadness, especially, perhaps. Dolores describes these people as afraid of obliteration, emotional engulfment. As if something truly and thoroughly felt would have no end or bottom. Would become infinite and engulf them.
Such Persons usually have a fragile sense of themselves as persons. As Existing At all.
My point here is that certain types of persons are terrified even to poke a big toe into genuinely felt regret or sadness, or to get angry. This means they are afraid to live. They are imprisoned in something, I think. Frozen inside, emotionally. 
The irony, of course, being that the very imprisonment that prohibits sadness’s expression must itself feel intensely sad and painful. For the hypothetical person in question.”

I thoroughly fucking suggest reading this novel. It’s a fucking stormer. This fucking part is from page 765-766.

Wankiness seems to be a favourite term recently. Fitting is following:

Personal transcendence, the loftiness of thought. The feeling of a full mind. A mind gorged on the truth and knowledge that is sought by our murky grey matter. Unrivalled acceptance of the inadequate lot given to us by chaos. Lifting you up higher by mind than any star that first engendered your curiosity as a wild eyed sprat into the intangible, unimaginable eloquence of a seemingly unknowable reality. That feeling a curious consciousness gets when it has comatosed its interactions with the outside world and has inwardly searched for the nagging truth of a meaningless existence, going ever deeper into the dark depths of thought, until it reaches that almost epiphanic realization of all that forever remains out of reach, and then is snapped back into this reality unknowing but confirmed. That all consuming want to know what was just a finger tip of lucidity away that produces that feeling, that enveloping feeling. That personal transcendence.

As one of the most largely used recreational drugs in the world, 3,4-methylenedioxymethamphetamine (MDMA/ecstasy) is the subject of many studies that want to evaluate its long-term effects and whether they are detrimental to the users brain. Given the fact that it is now being considered as a potential therapeutic agent for anxiety disorders, the determining of whether this substance is neurotoxic is of an even greater importance.

            The potential problems envisaged with MDMA use is down to its action on the brain signalling chemical serotonin and the possibility of this action causing a neurotoxic effect on the brain. The loss of serotonin nerve axons has been seen in animal studies, and humans have been shown to have serotonin alterations that are similar to the ones viewed in animals. However, altered brain neurophysiology has not been found using functional neuroimaging methods. These studies give an insight into how the brain is actively working, and so would give a good account of any abnormalities in brain function caused by MDMA.

            In this study, neuroimaging equipment was used, but in this case the study was focused on the visual system as evidence has indicated that it may be ideal for revealing chronic MDMA effects. This is due to a dense collection of serotonin nerves on structures in the system such as the LGN of the thalamus region and the primary and secondary visual cortical regions. If MDMA had caused serotonin toxicity then damage in these areas would be a good indicator. Damage is indicated by increased visual cortical excitability due to the loss of the mechanisms which are involved in removing the serotonin from the region.

            With MDMA users in one group and non MDMA users in another, the subjects were shown red and blue flashing lights at low, medium and high intensity levels while being scanned by functional MRI scanners that detect blood flow to brain areas, indicating brain activity. The results were then analysed to see the activation of the LGN and Brodmann Area (BA) which would indicate stimulation. The higher the intensity of activation the more damage to the regions would have been caused.

            The results initially indicated that there was no difference in cortical excitability between MDMA users and non-MDMA users, which would have allowed the conclusion that MDMA is not toxic in this way. However, by further splitting the MDMA users into high and low usage, the results showed a greater cortical excitability for those who had a greater lifetime usage of the drug. Also found was that within those who had used MDMA those who had also used Methampthemine, which also acts largely on serotonin, had a higher level of cortical excitability, thus adding weight to the conclusions. This lead the researchers to suggest that the damage caused by MDMA is present when excessive usage has occurred and in moderation, ecstasy use may not cause long lasting neurotoxicity. They do also say however, that larger and more extensive research needs to be undertaken before any definitive conclusions can be wrought into whether MDMA is safe or not, which with the clinical implications being brought about, is a particularly pressing matter.

This is my own condensing of a research article from a journal of the same name:

Bauernfeind AL, Dietrich MS, Blackford JU, Charboneau EJ, Lillevig JG, Cannistraci CJ, Woodward ND, Cao A, Watkins T, Di Iorio CR, Cascio C, Salomon RM, Cowan RL (2011). Human Ecstasy Use is Associated with Increased Cortical Excitability: An fMRI study, Neuropsychopharmacology, 1 - 15.

MDMA under a microscope from Florida State University.