Tag Archives: frontal

Putting thought in the right place, part 2

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CAP v2.1.2

In the last blog post, I discussed the Cognitive Action Pathways model, a schematic conceptual representation of the hierarchy of key components that underpin human thought and behaviour.

Small changes in the early processes within the Cognitive-Action Pathway model can snowball to effect every other part of the process. A real life example of this is ASD, or Autism Spectrum Disorder.

ASD has been present since time immemorial. Numerous bloggers speculate that Moses may have had ASD, while a couple of researchers proposed that Samson was on the spectrum (although their evidence was tenuous [1]). Thankfully, autism is no longer considered a form of demon possession or madness, or schizophrenia, or caused by emotionally distant “refrigerator mothers”, nor treated with inhumane experimental chemical and physical “treatments” [2, 3].

The autism spectrum is defined by two main characteristics: deficits in social communication and interaction, and restricted repetitive patterns of behaviour. People on the autism spectrum also tend to have abnormal sensitivity to stimuli, and other co-existing conditions like ADHD. The full diagnostic criteria can be found in DSM5. The new criteria are not without their critics [4-6], but overall, reflect the progress made in understanding the biological basis of autism.

ASD is recognized as a pervasive developmental disorder secondary to structural and functional changes in the brain that occur in the womb, and can be detected as early as a month after birth [7]. In the brain of a foetus that will be born with ASD, excess numbers of dysfunctional nerve cells are unable to form the correct synaptic scaffolding, leaving a brain that is large [8, 9], but out-of-sync. The reduced scaffolding leads to local over-connectivity within regions of the brain, and under-connectivity between the regions of the brain [10]. The majority of the abnormal cells and connections are within the frontal lobe, especially the dorsolateral prefrontal cortex and the medial prefrontal cortex [11], as well as the temporal lobes [12]. The cerebellum is also significantly linked to the autism spectrum [13]. There is also evidence that the amygdala and hippocampus, involved in emotional regulation and memory formation, are significantly effected in ASD [10].

There is also strong evidence for an over-active immune system in an autistic person compared to a neurotypical person, with changes demonstrated in all parts of the immune system, and the immune system in the brain as well as the rest of the body [14]. These immune changes contribute to the reduced ability of the brain to form new branches as well as develop new nerve cells or remove unnecessary cells.

There are a number of environmental and epigenetic associations linked to autism. These include disorders of folate metabolism [15, 16], pollutants [17], fever during pregnancy [18] and medications such as valproate and certain anti-depressants [19, 20] which are linked with an increase in autism[1]. Supplements such as folate [15, 21], omega-6 polyunsaturated fatty acids [22] and the use of paracetamol for fevers in pregnancy [18] have protective effects.

Although these factors are important, genes outweigh their influence by about 4:1. Twin studies suggest that between 70-90% of the risk of autism is genetic [23, 24]. Individual gene studies have only shown that each of the many single genes carry about a one percent chance each for the risk of autism [10]. It’s been proposed that the hundreds of genes linked with autism [10, 25] are not properly expressed (some are expressed too much, some not enough). The resulting proteins from the abnormal gene expression contribute to a different function of the cell’s machinery, altering the ability of a nerve cell to fully develop, and the ability of nerve cells to form connections with other nerve cells [26]. The effects are individually small, but collectively influential [24]. Autism is considered a complex genetic disorder involving rare mutations, complex gene × gene interactions, and copy number variants (CNVs) including deletions and duplications [27].

According to the Cognitive-Action Pathways model, the triad of the environment, epigenetics, and genes influence a number of processes that feed into our actions, thoughts, perceptions, personality and physiology. In ASD, the starting place is language processing.

New born babies from as young as two days old prefer listening to their own native language [28], which suggests that we are born already pre-wired for language. Auditory stimuli (sounds) are processed in the temporal lobes, including language processing. In neurotypical people, language processing is done predominantly on the left side, with some effect from the right side. But in people with autism, because of the abnormal wiring, there is only significant activity of the right temporal lobe [12]. Even more, from data so recent that it’s pending publication, loss of the processing of information of the left temporal lobe reversed the brains orientation to social and non-social sounds, like the sound of the babies name [7].

The change in the wiring of the left and right temporal lobes then alters the processing of language, specifically the social significance of language and other sounds. So already from a young age, people with autism will respond differently to environmental stimuli compared to a neurotypical person.

In the same way, the fusiform gyrus is part of the brain that processes faces. It’s quite specific to this task in a neurotypical person. However, the altered wiring of the brain in someone with autism causes a change, with different parts of the brain having to take up the load of facial processing [29].

Each time that one part of the brain can’t perform it’s normal function, the other parts take up the load. However that reduces the capacity for those parts of the brain to perform their own normal functions. In the case of the temporal lobes and the fusiform areas, this results in a reduced ability to discern subtleties especially those related to recognizing social cues. A neurotypical person and an autistic person could be standing in front of the same person, listening to the same words, and seeing the same facial expressions, but because of the way each persons brain processes the information, the perception of those words and cues can be completely different. This demonstrates how genetic changes can lead to changes in the perception of normal sensory input, resulting in differences in the physiological response, emotions, feelings, thoughts and actions, despite identical sensory input.

Physiology

The same changes that effect the cerebral cortex of the brain also have an influence on the deeper structures such as the hippocampus and the amygdala. The hippocampus is largely responsible for transforming working memory into longer term declarative memory. Studies comparing the size of the hippocampus in ASD children have shown an increase in size compared with typical developing children [30]. Combined with the deficits in the nerve cell structure of the cerebellum [13], autistic children and adults have a poor procedural memory (action learning, regulated by the cerebellum) and an overdeveloped declarative memory (for facts, regulated by the hippocampus). This has been termed the “Mnesic Imbalance Theory” [31].

The amygdala is also functionally and anatomically altered because of the changes to the nerve cells and their connections. The amygdala is larger in young children with ASD compared to typically developing children. As a result, young ASD children have higher levels of background anxiety than do neurotypical children [32]. It’s proposed that not only do ASD children have higher levels of background anxiety, they also have more difficulty in regulating their stress system, resulting in higher levels of stress compared to a neurotypical child exposed to the same stimulus [33].

Personality

On a chemical level, autism involves genes that encode for proteins involved in the transport of key neurotransmitters, serotonin and dopamine. Early evidence confirms the deficits of the serotonin and dopamine transporter systems in autism [34]. These neurotransmitters are integral to processing the signals of mood, stress and rewards within the brain, and as discussed in the last chapter, are significantly involved in the genesis of personality.

The abnormal neurotransmitter systems and the resulting deficiencies in processing stress and rewards signals contribute to a higher correlation of neuroticism and introverted personality styles in children with autism symptoms [35, 36].

So people with autism genes are going to process stress and rewards in a different way to the neurotypical population. As a result, their feelings, their thoughts and their resulting actions are tinged by the differences in personality through which all of the incoming signals are processed.

Actions

The underlying genes and neurobiology involved in autism also effect the final behavioural step, not only because genes and sensory input influence the personality and physiology undergirding our feelings and thoughts, but also because they cause physical changes to the cerebellum, the part of the brain involved in fine motor control and the integration of a number of higher level brain functions including working memory, behaviour and motivation [13, 37].

When Hans Asperger first described his cohort of ASD children, he noted that they all had a tendency to be clumsy and have poor handwriting [38]. This is a good example of how the underlying biology of ASD can effect the action stage independently of personality and physiology. The cerebellum in a person with ASD has reduced numbers of a particular cell called the Purkinje cells, effecting the output of the cerebellum and the refined co-ordination of the small muscles of the hands (amongst other things). Reduced co-ordination of the fine motor movements of the hands means that handwriting is less precise and therefore less neat.

A running joke when I talk to people is the notoriously illegible doctors handwriting. One of the doctors I used to work with had handwriting that seriously looked like someone had dipped a chicken’s toes in ink and let it scratch around for a while. My handwriting is messy – a crazy cursive-print hybrid – but at least it’s legible. I tell people that our handwriting is terrible because we spent six years at medical school having to take notes at 200 words a minute. But it might also be that the qualities that make for a good doctor tend to be found in Asperger’s Syndrome, so the medical school selection process is going to bias the sample towards ASD and the associated poor handwriting (Thankfully, those that go on to neurosurgery tend to have good hand-eye coordination).

But if your educational experience was anything like mine, handwriting was seen as one of the key performance indicators of school life. If your handwriting was poor, you were considered lazy or stupid. Even excluding the halo effect from the equation, poor handwriting means a student has to slow down to write neater but takes longer to complete the same task, or writes faster to complete the task in the allotted time but sacrificing legibility in doing so.

Either way, the neurobiology of ASD results in reduced ability to effectively communicate, leading to judgement from others and internal personal frustration, both of which feedback to the level of personality, molding future feelings, thoughts and actions.

Thought in ASD

By the time all the signals have gone through the various layers of perception, personality and physiology, they reach the conscious awareness level of our stream of thought. I hope by now that you will agree with me that thought is irrevocably dependent on all of the various levels below it in the Cognitive-Action Pathways Model. While thoughts are as unique as the individual that thinks them, the common genetic expression of ASD and the resulting patterns in personality, physiology and perception lead to some predictable patterns of thought in those sharing the same genes.

As a consequence of the differences in the signal processing, the memories that make their way to long-term storage are also going to be different. Memories and memory function are also different in ASD for other neurobiological reasons, as described earlier in the blog with the Mnesic Imbalance Theory.

Summary

The Cognitive-Action Pathways model is a way of describing the context of thoughts to other neurological processes, and how they all interact. It shows that conscious thoughts are one link of a longer chain of neurological functions between stimulus and action – simply one cog in the machine. The autistic spectrum provides a good example of how changes in genes and their expression can dramatically influence every aspect of a person’s life – how they experience the world, how they feel about those experiences, and how they think about them.

I used autism as an example because autism is a condition that’s pervasive, touching every aspect of a person’s life, and provides a good example of the extensive consequences from small genetic changes. But the same principles of the Cognitive-Action Pathways Model apply to all aspects of life, including conditions that are considered pathological, but also to our normal variations and idiosyncrasies. Small variations in the genes that code for our smell sensors or the processing of smells can change our preferences for certain foods just as much as cultural exposure. Our appreciation for music is often changed subtly between individuals because of changes in the structure of our ears or the nerves that we use to process the sounds. The genetic structure of the melanin pigment in our skin changes our interaction with our environment because of the amount of exposure to the sun we can handle.

So in summary, this blog was to set out the place that our thoughts have in the grand scheme of life. Thought is not the guiding or controlling force, it is simply a product of a number of underlying functions and variables.

References

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  6. Grzadzinski, R., et al., DSM-5 and autism spectrum disorders (ASDs): an opportunity for identifying ASD subtypes. Mol Autism, 2013. 4(1): 12 doi: 10.1186/2040-2392-4-12
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  9. Shen, M.D., et al., Early brain enlargement and elevated extra-axial fluid in infants who develop autism spectrum disorder. Brain, 2013. 136(Pt 9): 2825-35 doi: 10.1093/brain/awt166
  10. Won, H., et al., Autism spectrum disorder causes, mechanisms, and treatments: focus on neuronal synapses. Front Mol Neurosci, 2013. 6: 19 doi: 10.3389/fnmol.2013.00019
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  15. Schmidt, R.J., et al., Maternal periconceptional folic acid intake and risk of autism spectrum disorders and developmental delay in the CHARGE (CHildhood Autism Risks from Genetics and Environment) case-control study. Am J Clin Nutr, 2012. 96(1): 80-9 doi: 10.3945/ajcn.110.004416
  16. Mbadiwe, T. and Millis, R.M., Epigenetics and Autism. Autism Res Treat, 2013. 2013: 826156 doi: 10.1155/2013/826156
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  18. Zerbo, O., et al., Is maternal influenza or fever during pregnancy associated with autism or developmental delays? Results from the CHARGE (CHildhood Autism Risks from Genetics and Environment) study. J Autism Dev Disord, 2013. 43(1): 25-33 doi: 10.1007/s10803-012-1540-x
  19. Rai, D., et al., Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population based case-control study. BMJ, 2013. 346: f2059 doi: 10.1136/bmj.f2059
  20. Christensen, J., et al., Prenatal valproate exposure and risk of autism spectrum disorders and childhood autism. JAMA, 2013. 309(16): 1696-703 doi: 10.1001/jama.2013.2270
  21. Suren, P., et al., Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children. JAMA, 2013. 309(6): 570-7 doi: 10.1001/jama.2012.155925
  22. Lyall, K., et al., Maternal dietary fat intake in association with autism spectrum disorders. Am J Epidemiol, 2013. 178(2): 209-20 doi: 10.1093/aje/kws433
  23. Abrahams, B.S. and Geschwind, D.H., Advances in autism genetics: on the threshold of a new neurobiology. Nature Reviews Genetics, 2008. 9(5): 341-55
  24. Geschwind, D.H., Genetics of autism spectrum disorders. Trends Cogn Sci, 2011. 15(9): 409-16 doi: 10.1016/j.tics.2011.07.003
  25. Chow, M.L., et al., Age-dependent brain gene expression and copy number anomalies in autism suggest distinct pathological processes at young versus mature ages. PLoS Genet, 2012. 8(3): e1002592 doi: 10.1371/journal.pgen.1002592
  26. O’Roak, B.J., et al., Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations. Nature, 2012. 485(7397): 246-50 doi: 10.1038/nature10989
  27. Stankiewicz, P. and Lupski, J.R., Structural variation in the human genome and its role in disease. Annu Rev Med, 2010. 61: 437-55 doi: 10.1146/annurev-med-100708-204735
  28. Moon, C., et al., Two-day-olds prefer their native language. Infant behavior and development, 1993. 16(4): 495-500
  29. Pierce, K., et al., Face processing occurs outside the fusiform `face area’ in autism: evidence from functional MRI. Brain, 2001. 124(10): 2059-73 doi: 10.1093/brain/124.10.2059
  30. Schumann, C.M., et al., The amygdala is enlarged in children but not adolescents with autism; the hippocampus is enlarged at all ages. J Neurosci, 2004. 24(28): 6392-401 doi: 10.1523/JNEUROSCI.1297-04.2004
  31. Romero-Munguía, M.A.n., Mnesic Imbalance and the Neuroanatomy of Autism Spectrum Disorders, in Autism – A Neurodevelopmental Journey from Genes to Behaviour, Eapen, V., (Ed). 2011 Edition 1st, InTech. p. 425-44.
  32. Bal, E., et al., Emotion recognition in children with autism spectrum disorders: relations to eye gaze and autonomic state. J Autism Dev Disord, 2010. 40(3): 358-70 doi: 10.1007/s10803-009-0884-3
  33. Harms, M.B., et al., Facial emotion recognition in autism spectrum disorders: a review of behavioral and neuroimaging studies. Neuropsychol Rev, 2010. 20(3): 290-322 doi: 10.1007/s11065-010-9138-6
  34. Nakamura, K., et al., Brain serotonin and dopamine transporter bindings in adults with high-functioning autism. Arch Gen Psychiatry, 2010. 67(1): 59-68 doi: 10.1001/archgenpsychiatry.2009.137
  35. Austin, E.J., Personality correlates of the broader autism phenotype as assessed by the Autism Spectrum Quotient (AQ). Personality and Individual Differences, 2005. 38(2): 451-60
  36. Wakabayashi, A., et al., Are autistic traits an independent personality dimension? A study of the Autism-Spectrum Quotient (AQ) and the NEO-PI-R. Personality and Individual Differences, 2006. 41: 873-83
  37. De Sousa, A., Towards an integrative theory of consciousness: part 1 (neurobiological and cognitive models). Mens Sana Monogr, 2013. 11(1): 100-50 doi: 10.4103/0973-1229.109335
  38. Wing, L., Asperger’s syndrome: a clinical account. Psychol Med, 1981. 11(1): 115-29 http://www.ncbi.nlm.nih.gov/pubmed/7208735

[1] A word of caution: While there’s good evidence that valproate increases the risk of autism, and a possible link between some anti-depressants and autism, that risk has to be balanced with the risk to the baby of having a mother with uncontrolled epilepsy or depression, which may very well be higher. If you’re taking these medications and you are pregnant, or want to become pregnant, consult your doctor BEFORE you stop or change your medications. Work out what’s right for you (and your baby) in your unique situation.

Dr Caroline Leaf – Serious questions, few answers (Part 2)

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Yesterday I published the first part of an essay discussing the presentation of Dr Caroline Leaf, Audiologist, Communication Pathologist, and self-titled cognitive neuroscientist, at Kings Christian Church, Gold Coast.

Tonight I want to continue dissecting some of the more pertinent statements that she made, including her view of the mind-brain connection, a smattering of smaller issues, her over-reliance on case studies, and her opinion on the cause and treatment of ADHD.

Tomorrow I will publish the last, and most important part of my essay – That Dr Leaf believes that ‘toxic’ thoughts are sinful, and why this single statement unravels her most fundamental premise.

THE MIND IS IN CHARGE OF THE BRAIN

A large part of her sermon was based on her next premise, that the mind changes the brain, and not the other way around. That is half true. The mind influences the brain, and how we think will have effects on neural pathways within the brain. But for a cognitive neuroscientist to state that the brain does not influence the mind is somewhat concerning.

There are several reasons why her assertion is deeply flawed. For starters, where else does the mind or thought come from other than our neural networks? Thought is built on our neural connections. To say that the brain does not influence thought is like saying that the foundation of a building doesn’t influence the bricks.

There are clinical reasons as well. These come from a few areas – firstly the research that showed that newborn babies (who do not have thought like we have thoughts) are pre-wired for emotions which are refined as we learn. There is no time for neonates to have enough stimulation to form those emotions and reactions if it was from our mind.

Secondly, people with brain injuries or tumours can have personality or mood changes. The most famous was a man in the 1800’s called Phineas Gage, who on 13 September 1848 was packing explosives into rock with a tamping iron (a long, tapered, smooth crow-bar). History says that the explosives sent the tamping iron through his left face and skull, taking a fair chunk of his frontal lobe with it. Depending on who you believe, Gage’s personality changed after his physical recovery, reportedly from a moral, respectful man into a cursing, angry one (Kihlstrom 2010). Some reports of his story were that Gage made an almost full recovery, but assuming that some of the historical record is true, changes to his brain changed his mental function, ie: his thoughts.

Further, I have personally seen two patients with personality changes secondary to brain tumours. The first was a woman in her late 20’s who had six months of worsening anxiety, who did not seek help despite my referrals, until she had a seizure and the diagnosis was made. Then there was the sad case of a girl in her pre-teens who had only two weeks of rapidly escalating sullenness then aggression then violence. Her parents initially thought she was moody, and when they brought her into the Emergency Department they thought she was perhaps in the middle of a psychotic episode. It turned out that she had a very aggressive tumour near her frontal lobe.

It is clear from these cases, and from a basic understanding of the concept of thought, that changes to the brain result in changes to thoughts and the mind, and vice versa.

SOME MISCELLANEOUS ISSUES

If I had the time I would like to look at many others issues that she raised, but this isn’t a book. Suffice it to say that she claimed that stress prunes our “thought trees” although the evidence is only in animal models and only related to severe stress (Karatsoreos and McEwen 2011). She also stated that EVERY thought we EVER have is stored in ALL of our cells (so some random fibroblast in my big toe is somehow affected by my thought about tonights dinner), and that ALL our thoughts are stored in our gametes (our sperm and eggs) and are passed down to our 4th generation (but packed, like in a metaphysical zip-lock bag, and only opened if we choose to have the same thoughts.) And here I was thinking that nurture had something to do with learned behaviour.

ASD/ADHD – MORE OPINION THAN FACT?

She also claimed that 55-70% of ASD/ADHD cases are over-referred and the problem is in educational modeling. This one made me mad.

Not even professorial level researchers know exactly what’s going on in ASD/ADHD, so her statement is a brave one to make, especially without referencing her evidence.

She then espoused the party line of ADHD ignorance – that Ritalin is evil and all you need to do is stop their sugar intake and feed them organic foods and give them supplements. Ritalin isn’t perfect, to be sure, but it is the most effective treatment that’s currently available. If dietary measures and educational measures were effective, then ritalin wouldn’t be prescribed. I have never met a parent that has wanted their child on ritalin. Most of them have tried educational/psychological measures or dietary controls first. The reason why ritalin is prescribed is because dietary and psychological interventions on their own do not adequately control the symptoms, or fail altogether.

To confirm that I’m not just having a rant, there is published scientific literature to back me up. In their recently published meta-analysis, Nigg et al (2012) state, “An estimated 8% of children with ADHD may have symptoms related to synthetic food colors.” Eight percent. That’s all! That’s ninty-two percent of children with ADHD (real ADHD, not just rambunctious children with lots of energy) DID NOT have symptoms due to food colourings. Their conclusions: “A restriction diet benefits some children with ADHD. Effects of food colors were notable but susceptible to publication bias or were derived from small, nongeneralizable samples.” In terms of sugar, Kim and Chang (2011) note that, “children who consumed less sugar from fruit snacks or whose vitamin C intake was less than RI was at increased risks for ADHD (P < 0.05).” (emphasis added) The study was only of about 100 children, but the result was statistically significant. It wasn’t a chance effect.

The misinformation she stated as fact from the pulpit promotes scare-mongering and ignorance throughout the church, which has flow on effects. Church members with children with ADHD or ASD will avoid standard medical treatment on Dr Leaf’s advice. When her treatments fail in the majority of cases, those parents will either live with unnecessarily heightened stress because of their child’s poorly controlled condition, or the guilt of using ritalin, all the while believing that they are ruining their childs brain.

This also places the hosting church in a bind. Do they stand behind their guest speaker, or do they support the advice of the medical community? Is their duty of care to the reputation of the guest speaker or to the congregation under their protection? What would happen if Dr Leaf’s advice lead to the death or disability of a person in their congregation? Would they be libel?

CASE STUDIES – INSPIRATIONAL STORIES, BUT POOR SCIENTIFIC EVIDENCE

Dr Leaf also told a lot of stories of how everyone afflicted came to her and how she healed them all. If you took her at face value, she would have you believe that people with ASD, ADHD, anorexia, OCD, depression etc, just needed a glimpse of their self-worth and their inner gift and they would be cured. While her stories were inspirational, the world of scientific research demands more. If Dr Leaf’s insights are worth more than the hot air she produces when espousing them, then they should be put to the wider research community so they can pass through the fire of peer review. If peer review prove her insights to be valid, I would be happy to apply them and promote them.

Tomorrow, I will publish the last, and probably the most important part of my essay – that Dr Leaf believes that ‘toxic’ thoughts are sinful, and why this single statement unravels her most fundamental premise.

REFERENCES

Crum, A. J., P. Salovey and S. Achor (2013). “Rethinking stress: the role of mindsets in determining the stress response.” J Pers Soc Psychol 104(4): 716-733.

Karatsoreos, I. N. and B. S. McEwen (2011). “Psychobiological allostasis: resistance, resilience and vulnerability.” Trends Cogn Sci 15(12): 576-584.

Kihlstrom, J. F. (2010). “Social neuroscience: The footprints of Phineas Gage.” Social Cognition 28: 757-782.

Kim, Y. and H. Chang (2011). “Correlation between attention deficit hyperactivity disorder and sugar consumption, quality of diet, and dietary behavior in school children.” Nutr Res Pract 5(3): 236-245.

Leaf, C. (2009). Who Switched Off My Brain? Controlling toxic thoughts and emotions. Southlake, TX, USA, Inprov, Ltd.

Nigg, J. T., K. Lewis, T. Edinger and M. Falk (2012). “Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives.” J Am Acad Child Adolesc Psychiatry 51(1): 86-97 e88.