The Brain in Autism: Part I

This was originally provided as a handout to accompany my presentation “Abnormalities of cortical circuitry in the brains of autistic individuals” at the Autism One conference in May, 2006.


The first few paragraphs of this introduction summarize some of our initial research findings in autism. If you feel lost regarding some of the terminology used, do not despair for you are in good company. The next few sections are aimed at dispelling any doubts that you may have. For those that already have some knowledge in terms of neuroscience, you may want to skip to the section on autism and minicolumns after reading this introduction.

The brains of autistic patients have “minicolumns” that are smaller and more numerous than normal. Furthermore, brain cells (neurons) within each minicolumn are reduced in size. Since the efficiency of connections among neurons is a function of cell size, the presence of smaller neurons in the brains of autistic patients has a dramatic effect on the way that different parts of the brain work together. Brain activities that require longer projections (e.g., face recognition) may be impaired while those that depend on shorter connections (e.g., visual discrimination) may be preserved or reinforced.

The outer covering of the brain or neocortex is arranged as a hierarchy of interdependent modules. Studies suggest that many faculties that define cognition and behavior are located within the neocortex. The smallest module capable of processing information is called a minicolumn. These small modules or minicolumns are composed of both cells (neurons) and their projections. They were given the descriptive name minicolumns because of their microscopic proportions (mini) and rectilinear arrangement (columns).

The total number of minicolumns is defined during the first forty days of fetal development. This window of vulnerability coincides with reports of autistic behaviors in fetal/developmental conditions such as rubella babies, infants exposed to thalidomide, and tuberous sclerosis. In all of these conditions a defect is presumed to have arisen at an early stage of development, one that coincides with the formation of minicolumns.

Information is transmitted through the core of the minicolumn and is prevented from activating neighboring units by surrounding inhibitory fibers. In autism minicolumnar size reduction involves primarily the peripheral compartment that provides the inhibitory surround. This means that stimuli are no longer contained within specific minicolumns but rather overflow to adjacent minicolumns thus providing an amplifier effect. This may explain the hypersensitivity of some autistic patients as well as their seizures.

The following paragraphs provide the background information needed in order to understand how minicolumns behave in both the normal and abnormal state. I will start with a short section on brain development and then describe how different areas of the brain acquire particular functions. A subsequent section will describe how minicolumns are altered in autism. I will finalize with a short section on how these findings may be of use in providing for putative therapeutic interventions. The latter sections will published in part II of this blog.

Brain development

The outer covering of the brain or neocortex is arranged as a hierarchy of interdependent modules. These modules originate at a very early stage of development when newly formed cells near the core of the brain migrate towards its outer margin. Since the corresponding cells migrate along a radial guiding process, their ultimate arrangement is columnar. Because these cells develop together and are in close apposition most of their connections are bound together into what has been called a canonical or representative circuit. Connectivity of elements within these vertical arrays exceeds connectivity between them by several orders of magnitude. Unsurprisingly, voltage recording microelectrodes indicate that cells within these rectilinear arrangements share similar stimulus response properties. This means that all of the neurons within a particular minicolumn receive information from the same source. Also, stimulating one element of a minicolumn will provide for a rapid cascade of connections and the transmission of information among its component cells. These functional and anatomical characteristics define minicolumns as the smallest units or systems capable of information processing within the brain.

Minicolumns are analogous to microprocessors in modern day computers. In their function they represent the holistic properties of the brain as a whole: receiving stimuli from elsewhere in the body, processing information, and providing for some type of response. Whenever any of these functions is altered the whole minicolumn becomes dysfunctional. It is believed that Alzheimer’s disease is the result of a minicolumnar abnormality. Degenerative changes know as neurofibrillary tangles occur primarily in those cells that provide for the response or output of the minicolumn. By targeting and damaging these few cells, the whole minicolumn ceases to function. This helps explain both the rapid deterioration of mental faculties observed in this condition and why cognitive impairment seems out of proportion to the amount of cell loss.

A main advantage to the modular organization of the neocortex entails a reduced metabolic expenditure by limiting connectivity. Instead of connecting every single cell within the cortex to different brain regions in a haphazard fashion, projections are organized into modules. Single cells project to target sites and information gained or transmitted is transferred to other neurons within the same modules. Another advantage for dividing the cortex into modular arrangements is that of plasticity or the ability to recover from injury. The fact that minicolumns exhibit the same circuitry allows them to replace each other in case of injury. This implies a spectrum of injury severity where mild lesions cause no major loss of function, i.e., the prevailing minicolumns take over the function from missing minicolumns. As in logic circuitry, where a single type of logic gate (either NAND or NOR) suffices to construct networks for any Boolean function, so it has been argued that the circuitry of a minicolumn acts as a component having the same function regardless of its location in the cortex.This is a common theme in evolution in which complex variations come into being from tinkering with a limited reservoir of components. They take inputs and guide them through the same logic-level registration. The end result is an output that appears modulated by the source of the input, output target, and inhibitory influences. Our mental activities are therefore primarily dependent on connectivity, that is, on how we putt these logic gates together in different combinations. The view of canonical circuits having the same function regardless of cortical location was first espoused in the literature by O. D. Creutzfeldt [1].

V. Ramachandran [2] tells the story of a patient whose arm had been amputated above his elbow. When touching the patient’s cheek as part of the neurological examination, the patient felt a sensation on the thumb of his amputated, and otherwise “non-existent”, arm. Experimental evidence sustains that the representation of the face on the surface of the brain (neocortex) is near the hand. Ramachandran believes that, in this particular patient, the vacated area in the neocortex corresponding to the hand is invaded by sensory input from the adjacent facial skin. Still the information coming to the neocortex and its minicolumns has to be processed exactly the same way for this phantom limb phenomenon to work.

The above mentioned explanations should not be not be construed as saying that minicolumns are clone-like entities. Different brain regions exhibit a certain degree of minicolumnar variability, e.g. in their width and cell density. Comparison across species indicates that this variability may, in part, reflect the complexity of the information being processed. At any given age minicolumar variability is thus more prominent in humans than in other primates. However, regardless of any minicolumnar variability, all mammalian species have cortices that are arranged in terms of the same rectilinear arrangements. This has been the case for all brain regions thus far examined. Non-mammalian species, i.e. reptiles, lack this minicolumnar arrangement.

Variability among the multiple components of the minicolumn (e.g., number of neurons and amount of synapses) may contribute to the fault tolerance of larger networks such as macrocolumns. Redundant systems can be reliable even when the underlying components are error-prone. McCulloch [3] characterized unreliable networks of threshold elements as “logically stable” when elements’ thresholds could vary in tandem—not changing the function computed by the network as a whole—and “logically unstable” when thresholds could vary independently. He showed that, provided that individual components are more than 50 % reliable, redundant systems of unstable nets could be designed for greater reliability than redundant systems of stable nets of the same size. Paradoxically though it first appears, the functional plasticity of minicolumns, their ability to compute different functions than other minicolumns within the same module, can be used to the module’s advantage with respect to sensitivity to error.

Thus far one study has indicated a trend toward significant differences when comparing the variability of minicolumns among brains of autistic patients and controls. One possibility is that the limited number of patients within that series decreased the power thus necessitating a larger outcome measure (i.e., variability) than available in the sample. If lack of variability was proven in larger series it could help explain certain behavioral traits observed in autistic patients, e.g. the insistence on sameness, repetitive movements, and restricted range of interests.



  1. Otto D. Creutzfeldt. Generality of the functional structure of the neocortex. Naturwissenschaften 64 (October, 1977) 507–517.
  2. V. S. Ramachandran. A brief tour of human consciousness: From impostor poodles to purple numbers. New York: Pi Press, 2004.
  3. W. S. McCulloch. Agatha Tyche: of nervous nets— the lucky reckoners. In: National Physical Laboratory. Mechanisation of thought processes. London: H. M. Stationery Office, 1959. p 611–625.

4 responses to “The Brain in Autism: Part I

  1. Minicolumn abnormalities have also been implicated in schizophrenia I read, in some ways they are similar, in other ways they are like opposites…well more like two sides of the same coin, counterparts. Too much of the opposite in some ways.

    The autistic brain would be like a chopped salad (poor long range communication and excessive local functions). A healthy brain is a soup with chunks, the schizophrenic brain a puree where information flood arounds, chaotic, hence the schizophrenic tendency to move from idea to idea rapidly instead of staying fixated on one area, and gravitate towards absurd thinking instead of literalmindedness like autism.

    I read some article saying what we call Asperger Syndrome may be a form of autism with some slight overlap with mild schizophrenic features from a brain scan study.

    Cell cultures from autistic brains show synapses growing too long, getting all tangled and excessive, not pruning. Schizophrenic brain cell cultures show the opposite, short watery few synapse that keep dying too fast.

    It’s interesting, do you think these disorders are somehow counterparts in a way Manuel? What is your theory about it?

    Liked by 1 person

    • Complicating the issue, it is known that some individuals with Asperger’s may exhibit the positive symptoms of schizophrenia. They do seem to have the same inhibitory deficit and have a gamma abnormality similar to autism. However, there are intrinsic differences in each of these manifestations. I am not ready to conflate both. Would like to do more research on the subject.


  2. Unfortunately the novel space-time event method has not been applied to the parameters of neuropsychiatric or degenerative pathologies. This method exponentially simplifies large nerve net time factors with precise space and time event coordinates. A decade of brain imaging studies support this method. However the diagnostic uncertainty confounds psychiatric disorders.


  3. Pingback: The Brain in Autism: Part II | Cortical Chauvinism·

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