Neurodiversity is a movement that offers a perspective about autism that differs from that espoused by the medical profession. The ideology seems rooted in the anti-psychiatry movement ( see https://en.wikipedia.org/wiki/Anti-psychiatry ) that claimed that many psychiatric disorders were constructs of the medical profession but otherwise fell within the normal range of human behaviors.
The offshoot of the antipsychiatry movement, neurodiversity, claims that autism falls within the normal variability intervals of the human genome/connectome (the blueprint of white matter connectivity). The term is attributed to an Australian sociologist by the name of Judy Singer, herself diagnosed within the spectrum and also having a child on the spectrum. Neurodiversity had initially the good intention of avoiding terms with negative connotations (e.g., disorder, disability) that prejudged and demeaned affected individuals. The use of negative terms pathologized autism and ultimately insulted the sensitivities of many autistic individuals who clearly understood the nuances of medical verbiage. Self-advocacy groups, primarily from within the Aspie community, took advantage of the popularity of the neurodiversity movement in order to challenge the conventional thinking that autism needed to be cured. In effect, many high functioning autistic individuals, such as Temple Grandin, do not regret being autistic and, in fact, consider it a gift. This has lead to endless philosophising as to whether we should try to “cure” autism or better focus our efforts on acceptance and accommodations (http://conversations.psu.edu/episodes/temple_grandin/ ).
The neurodiversity movement calls into question whether higher functioning autistic individuals are representative of the autistic population at large. Would proponents of neurodiversity feel the same way if riddled with seizures, self-injurious behaviors, or tremendously diminished cognitive processing? Would they try to find a cure if suffering with any of the aforementioned handicaps? Curiously, some people from within the neurodiversity movement would hold steadfast to their beliefs. According to some neurodiversity proponents autism is caused by outside (environmental) exigencies and taking them out of the picture would promote a cure for autism.
It is difficult to argue with people who base their opinion on philosophical perspectives and know very little about brain functioning.Most of their arguments shift the onus of a scientific debate to discussing the meaning of words rather than facts. These arguments portray wishful thinking rather than the analysis of available evidence. Overall, neurodiversity flies in the face of present day scientific knowledge that firmly places autism within the spectrum of neurodevelopmental conditions.
Curiously some of the evidence in favor of neurodiversity has been provided by my own work (see http://bit.ly/1bitCvg ). I have argued in several articles that there is a ratio of short to long connections joining different parts of the cortex that help define cognitive styles. At one end of the spectrum you have people with supernumerary short connections at the expense of longer ones who show an “autistic cognitive style”. The latter is manifested as being quite concrete and mentally inflexible but excelling at functions that can be performed within a given brain parcellation (embedded block design, finding Waldo within a picture). At the other tail end of the connectivity spectrum we have people that manifest supernumerary long connections at the expense of shorter ones. These people usually exhibit a cognitive style characteristic of dyslexics/attention deficit disorders. They excel at synthesizing and are the prototype of the absent-minded professor; they see the forest but loose sight of the tree. These observations are meant to help explain differences in cognitive or thinking styles, that is, the way people perceive or remember information. This is what many people within the neurodiversity movement try to defend. They are clearly satisfied with their way of thinking and see attempts at changing the same as menticide (mental genocide). However understandable is their feeling of being threatened nobody is trying to change the way they think. Divergent thinkers always add to society and probably account for its advancement (see Thomas West, “Thinking Like Einstein).
Let me go back to the subject of pathology. Some of the early neuroimaging series of autistic individuals uncovered significant portions of the brain as having unidentified bright objects or UBO’s in their scans. It is now known that UBO’s represent a migratory defect where large cluster of cells become arrested and never reach their final destinations. Higher resolution studies using postmortem material have shown that these islands of malpositioned cells are found in some 75% of patients. (Wegiel et al., 2012) (figure 1). If considered alone, the presence of single cells may actually cloud the boundary between the gray and white matter making the same indistinct (figure 2). When quantitative methods are applied this abnormality may be present in all autistic patients.
Figure 1. (Double click on the picture for a larger image). It is said that one picture is worth a thousand words.The different panels (taken from Wegiel et al., 2010) illustrate cross sections of brain tissue in different autistic individuals. Each one illustrate how islands of migrating neurons (heterotopias) fail to reach their final destination and settle midstream. This is akin to having a hernia (i.e., a protrusion of an organ where it should not be). The findings are of importance for many reasons. First, these cell clusters are seen in all brain regions (e.g. frontal lobe in panel a, cerebellum in panel f) and clearly illustrate a disorder of neuronal migration. Although the final result may be an insidious malformation of the cortex (e.g., abnormally constructed cortical modules or minicolumns) and differences in brain connectivity, they are still the result of pathology. There are no grey boundaries here between normal and abnormal. These clusters and resultant malformations are clearly abnormal. Second, all of the previously described abnormalities occur during brain development, while cells are migrating to form the cerebral cortex. They are thus present and hardwired by the time a patient is born. Although postnatal event could, under certain circumstances, trigger expression of symptoms, the underlying defect is present from birth. Third, proposed causative insults should be able to explain the presence of this pathology. In this regard, mercury, could be excluded from the potential list of inciting agents. The pathology of mercury is well known and does not explain observed findings in the brains of autistic individuals (see https://corticalchauvinism.wordpress.com/2013/02/16/autism-it-is-not-about-mercury/ ). Lastly, these findings are of importance because of their explanatory powers. Their presence along with resultant cortical malformations can easily explain the presence of multifocal seizures and sensory abnormalities in autism. The fact that these abnormalities differ by location and severity also help explain the clinical heterogeneity of autism.
Figure 2. Computer generated binary images each black dot representing the position of cells cells within the cerebral cortex. The upper panel is that of a neurotypical individual and the one at the bottom for a person within the autism spectrum. The sigmoid function generated by a computer demarcates the boundary in-between the grey and white matter of the brain. The white matter immediately beneath the cortex of autistic individuals contain many more neurons than that of neurotypicals.
I think neurodiversity arose from the need of humans to believe themselves to be special. Several people have often used the quote that we think of ourselves as fallen angels rather than risen apes. For me that seems to be a human right. I also believe in many of the positive aspects of neurodiversity. However, I do not believe in the minority faction of neurodiversity bent on imposing their ideas over those of others, especially when they are based on a shaky scientific foundation. In the last few paragraphs I have tried to illustrate a clear-cut migrational abnormality for neurons in autism. This is something that anybody postulating a cause for autism will have to explain, be it mercury, immunological abnormalities, high oxidative load, or gene mutations. Valid arguments have to incorporate scientific knowledge (just ask the Dalai Lama about his conviction in neuroscience).
In a future blog I will talk about how we can put all of these findings together and what may be causing them.