All psychological traits are rooted in biology.  Francis Crick once famously said that, “You, your joys and sorrows, your memories and ambitions, your sense of personal identity and free will, are, in fact, no more than the behavior of a vast assembly of nerve cells.”  To a large extent, how you think and behave is dictated by how the brain is constructed.  Studies now suggest that the brains of autistic individuals differ from those of neurotypicals in regards to how different parts of the brain connect to each other.  The difference in connectivity is helpful in explaining how and why autistics think and behave in their own particular way.

In order to explain the workings of the brain, some people offer the analogy to a computer. It should help clarify that the analogy does not relate to a modern digital computer. Instead, the analogy is made to an older analog computer.  The analog computer of the 1960’s and 1970’s was bulky, noisy and gave an enormous amount of heat whenever it was used.  These analog computers had mechanical switches or relays inside of them that provided for a clickety-clack sound.  Hearing the cavalcade of clickety-clack sounds was a reassurance for those working with the computer that the computer was working properly.  If you ever opened the computer, you would find a mind boggling number of cables connecting the relays together. The intelligence of the analog computer resided in these cable connections.  Microprocessors and other integrated circuits had not been invented in this era.  Similar to the analog computer, the way our brain acts and the behaviors it engenders is to a large extent dictated by its underlying connectivity.

Disrupted connectivity is regarded as a key feature in the pathophysiology of autism spectrum disorder (ASD) (Kana et al., 2011; Vasa et al., 2016). This point of view was first proposed by Belmonte et al. (2004) in a model where reduced information transfer in the brains of ASD individuals was seen as a consequence of local overconnectivity and long-range-underconnectivity. According to the disrupted connectivity hypothesis, weaker functional connections among disparate brain regions hamper their ability to integrate complex cognitive tasks (Just et al., 2004). Belmonte’s explanatory framework relied heavily on Brock et al (2002) studies suggesting the presence of underconnectivity between distant brain regions as reflected in a lack of EEG synchrony in the gamma band. The concept was further elaborated by Rippon et al. (2007) as an “impaired connectivity” hypothesis of autism by tying together the relevance of gamma band activity to the excitatory/inhibitory balance of cortical activity (Rubenstein and Merzenich, 2003, Casanova et al., 2003, Casanova et al., 2013). Neuropathological studies of neuronomorphometry and columnar structure give credence to the disrupted connectivity hypothesis and its possible ties to the excitatory inhibitory balance of the cerebral cortex (Casanova et al., 2006). According to researchers a shift in cell/minicolumnar size has biased brain connectivity so as to develop an “intrahemispheric modus operandi” (Casanova et al., 2006; Doty, 2007, p.282).

This peculiar pattern of circuitry, one  connecting closely adjacent areas of the cerebral cortex and bypassing longer connections, imparts an autistic individual with certain aspects of their personality.  I have often used it as a way of explaining the emphasis on details as opposed to the organized whole or gestalt.  This is a type of verbatim memory proficient in autism that excels in extracting details, but loses itself when trying to integrate these details into a pattern.

One of my good friends, Olga Bogdashina, is a world renowned teacher and a mother of an autistic adult.   Many years ago, Olga told me that she had to provide ample time for processing after giving her students a question.  A rather innocuous question as to attending a recent movie theater might propel the autistic individual into a step by step description of the whole event. More importantly, if interrupted, the autistic individual would have to start all over again in an attempt to answer the question.

In dealing with autistic individuals it is important to realize that their pattern of connectivity confers to some a way of thinking that colors their desires, aspirations, and talents. Pedagogic attempts should play to the strengths of autistic individuals, to do otherwise would frustrate them and prove unrewarding.

References

Brock J, Brown CC, Boucher J, Rippon G (2002) The temporal binding deficit hypothesis of autism. Dev Psychopathol 14:209-224, 2002.

Casanova MF, van Kooten IA, Switala AE, van England H, heinsen H, Steinbusch HW, Hof PR, Trippe J, Stone J, Schmitz C. Minicolumnar abnormalities in autism. Acta Neuropathologica. 112(3):287-303, 2006.

Casanova MF, Baruth J, El-Baz AS, Sokhadze GE, hensley M, Sokhadze EM. Evoked and induced gamma-frequency oscillations in autism. In Manuel Casanova, Ayman El-Baz and Jasjit Suri (eds) Imaging the Brain in Autism, Springer Publishing, ch.5, p. 87-106, 2013.

Doty RW. Cortical commisural connections in primates, in Evolution of Nervous Systems: A Comprehensive Reference, Vol. 4, Primates, eds J. H. Kaas and L. A. Krubitzer (Amsterdam: Elsevier), 277–289. 2007.

Just MA, Cherkassky VL, Keller TA, Minshew NJ. Cortical activation and synchronization during sentence comprehension in high-functioning autism: evidence of underconnectivity. Brain 127(pt8):1811-21, 2004.

Kana RK, Libero LE, Moore MS. Disrupted cortical connectivity theory as an explanatory model for autism spectrum disorders. Phys Life Rev 8(4):410-37, 2011.

Rippon G, Brock J, Brown C, Boucher J. Disordered connectivity in the autistic brain: challenges for the “new psychophysiology”. Int J Psychophysiol 63(2):164-172, 2007.

Rubenstein JL, Marzenich MM. Disordered connectivity in the autistic brain: challenges for the “new Psychophysiology”. Int J Psychophysiol 63(2):164-72, 2007.

Vasa RA, Mostofsky SH, Ewen JB. The disrupted connectivity hypothesis of autism spectrum disorder: time for the next phase in research. Biol Psychiatry Cogn Neurosci Neuroimaging 1(3):245-252, 2016