My background is in vision (optometry) and in blindness (orientation and mobility). I am not an expert on autism (far from it) and I am not an expert on the human brain. I have worked in a center for handicapped children since 1980; many of the kids I taught had "autistic behaviors". This page was created as a collection of ideas and speculations about vision and autism.
Autism is a general term under which we categorize many children in special education. These children can be very different, so there are levels of severity in autism and differences in the extent to which brain areas are impaired. Each child must be looked at as unique and teaching strategies need to be carefully tailored for the individual. Diagnostic information is critical to help determine the best assistive strategies.
Given the complexity of autism and the unique situation of each student, we must conclude that there is no magic cure for all people with the autism label. Furthermore, autism is a set of behaviors (unexplained symptoms) and not an active disease state. The sole common attribute that gives the label some coherence is sensory dysfunction (sensory distortion): one (or a combination) of the senses is not working normally; poorly sensed information cannot easily be organized or processed in higher brain centers.
MRI and other brain imaging studies strongly implicate the cerebellum as the impaired organ that causes a cascade of irregularities in the developing brain. Damage (incomplete development?) to neural loops (afferent and efferent) that connect the cerebellum to the rest of the brain eventually causes secondary damage in higher brain centers. If research findings hold up over time and the cerebellum remains heavily implicated in the development of autistic brains, we will need a deeper understanding of the role the cerebellum plays in human development and behavior.
The cerebellum has long been understood to be the organ responsible for smooth control of muscles. It was a surprise when imaging studies pinpointed the cerebellum as a locus of damage in autistic brains. Autistic behaviors are so sensorially intensive and so socially irregular that the cerebellum was low on the list of suspects. Researchers overlooked the phylogenetic and embryological evidence that the cerebellum is a sensory brain organ.
The cerebellum is a center for "tracking" relevant sensory information and for aligning the sensory system with the object of attention. Smooth, accurate muscle coordination is required to spot and keep track of the location of relevant sensory input, as well as to align the body correctly and appropriately. If the input is dangerous (a hungry lion, for example), it is best to keep careful track of the animals movements and to align the body in escape position. If the object of regard is wild game for the hunter, the tracking skill is needed to maintain the position of the animal and to position the human body in attack mode.
These primitive examples of the human being as a hunter or as the potential prey of another animal are very appropriate for the cerebellum. It is a very old evolutionary brain structure. It evolved before consciousness. It is part of a very basic survival network that has been successful throughout mammalian evolution. It evolved into a master organ that controls subconscious human navigation A healthy cerebellum is crucial for the development and maintenance of posture, balance, subconscious motor control, and fine coordination (hand and eye for example). It also controls muscle tone.
Not only does the cerebellum track the location and movement of objects in the environment, but it also predicts what might happen in the future given further movement. Which way is the lion facing, and is it slowly drifting in a specific direction? What does this circumstance predict for future activity of the lion? Where do I shoot an arrow at a running rabbit? The cerebellum feeds these predictions to higher centers for motor processing.
If the autistic brain has damage to tissues in the cerebellum, then the ability to track and to predict will be impaired to various degrees. Wrong predictions sent to higher motor processing centers will cause "under and over shooting" of the muscles; a dysfucntion of the motor system will occur. Gait might be affected, as in the characteristic "cerebellar gait" of children with cerebral palsy, or the blind gait of children with severe vision impairments. The ability to smoothly track with the eyes will be affected, and a cascade of visual challenges will affect reading, writing, hand and eye activities, accurate pointing, and navigation errors (and many more behaviors).
Damage in the cerebellum is to the Purkinje cells, as well as in the vellum, the two hemispheres, and specifically in lobes 6 and 7 (of the vellum; these two lobes are the oldest part of the mammalian cerebellum and the location where visual and auditory signals converge ). Speculation is that tissue and cell damage causes functional problems in the brain's higher level attentional system. Autistic individuals have difficulty shifting attention (slow re-orienting of attention); they cannot easily drop what they are attending to so that they can take on another object of attention.
Blind individuals, particularly congenitally blind children, lack peripheral retinal processing which is responsible for subconscious navigation. Peripheral vision normally works in conjunction with the cerebellum and vestibular system (via specialized neural pathways) to align the body and position it in space. The cerebellum relies in part on the peripheral retina to tell it where the body is in space, where it is going, and how fast and in what direction. Visual input is coordinated with muscle signals and vestibular inflow. When peripheral vision is lost, the cerebellum must make these calculations based solely on muscular and vestibular data. In a way, blindness causes a functional loss of ability in the cerebellum. It is as if the cerebellum had sustained damage so that it cannot do its full job (this is speculation on my part, I am not a cerebellar expert). There are also syndromes in which blindness and aqutism exist in the same individual.
Cerebellar damage causes a characteristic gait; a wide stance and a shuffling walk. This sounds like (and looks like) what we have come to call the blind gait. We reason that blind children shift their center of gravity back because they are blind; they move their face out of harms way. This leads to a widened stance and a shuffling gait. There may, however, be another (deeper?) explanation for the blind gait. It may come from the loss of the peripheral visual processing system, and its link with the cerebellar pathways. It is also interesting to note that cerebellar damage causes a characteristic veer either to the right or left. It could be that the veering tendencies of some blind individuals are also due to the disruption of the cerebellar pathways. The low tone seen in many congenitally blind children may also be related to this loss of peripheral, subconscious processing, since low tone is a consequence of cerebellar damage.
Nystagmus also results from cerebellar damage. It is interesting to speculate that nystagmus may also be related to the disruption of the subconscious pathways for navigation. The very fine micro-oscillations of the eyeballs that are necessary for perception are controlled by the cerebellum. Disruption of the cerebellar pathways would lessen smooth control, resulting in a coarser, widened ocular oscillation.
The pathway from the retina to the vestibular system to the cerebellum is called the vestibulo-ocular pathway. One of its functions is to rapidly refixate, so that the eye is able to track a moving object while the head is also turning. Damage to the vestibulo-ocular pathway causes an inability to smoothly track moving objects.
The older cerebellar brain includes the basal ganglia which abut against the cerebral ventricles. Subconscious motor and navigational pathways flow to and from the basal ganglia. When a child has hydrocephalus there is pressure on the ventricles which then expand, killing cells that line the walls. This may explain why children with a history of hydrocephalus have not only poor motor control, but also have characteristic problems with navigation (spatial awareness, left right discrimination, etc.).
When the cerebellum is damaged (or its pathways disrupted) then subconscious, automatic movements are reduced or lost. This means that children with reduced cerebellar function must will actions. They must use higher cognitive areas and voluntarily command their muscles to perform functions. This is obviously an inefficient and exhausting task. Watching children with cerebral palsies or other neuromotor damage, you quickly see how debilitating loss of cerebellar functioning can be.
I noticed something else about the use of vision in physically impaired children. I used to say that many of these kids did not know where their eyes were in their heads; that they did not have ocular proprioception. The eyes of these kids seemed to drift all over the place. I had to repeatedly ask them to look at me or an object, which they seemed fleetingly able to do. I now realize that when asked to voluntarily direct their eyes they can do so. It is hard and exhausting, but they can do it. Most of the time however, the subconscious lower pathways of the cerebellum are inoperable; so most of the time oculomotor control is on "drift".
If hearing is affected, a common set of symptoms are often observed:
1. A hypersensitivity to sound; a higher than normal hearing acuity; sometimes painIf vision is affected:
2. Inability to full the salient sounds from the background sounds
3. If you can't pull the figure from the ground acoustically it can affect the learning of speech, (input and out of auditory information; communication), voice tone;and ability to follow directions
1. Sensory play is common: spinning, twirling, head shaking, head tilt, flipping through booksIf touch is affected:
2. Don't look directly at objects of regard; overdeveloped peripheral vision, underdeveloped central vision
3. Cannot focus on the figure in the ground
4. Obsession with the features of the peripheral system: fascination with movement, edges, etc.
5. Higher level processing inability in the central system (visual training of the central system while dampening the peripheral system?)
1. Hyper or hypo reaction to touch; an extreme in one direction or the other (also to temperature)If taste and smell are affected:
2. Often hypersensitive to soft touch (tactile defensiveness may result); consequently may avoid physical contact
3. May not be able to feel deep pressure
1. Many do not have a sensation of taste (smell?)Cerebellar implications:
2. Some have a hypersensitivity to taste and/or smell
1. Coordination of movement across joints, and the integration of composite movements are abnormal at an early age
2. The odd movement patterns and postures of autistic children are often normal for an earlier developmental stage
3. The social "dance" of communicating, interacting (in the same space), the psychic "pull and push" of humans in a shared space has to be coordinated by the cerebellum. Autistic people often unable to participate in these social "dances".
4. The reading and sending of body language and facial gestures, as well as eye and pupil fluctuations (that convey social and emotional messages) would be impaired in people with cerebellar damage
Besides the cerebellum, autopsy records indicate involvemnt with the pons, amygdala, and frontotemporal lobes.
Autistic people have poor communication skills and poor social skills. We know that when there is blindness, one of the biggest loses is the ability to use the face to send and receive non-verbal communication signals. The face is a social organ, it is a powerful avenue for telling others what we feel and what we think. Autistic people seem to have an inability to read faces and to use their own face to send signals, as if the eyes were blind. Indeed, there is evidence that the area of the brain that "sees" faces is damaged. It could be the feedback loop from Cerebellum to retina that is damaged.
Autism seems to go deeper than this however, since autistics seem incapable of caring (loving) others; their "urge to love" system is impaired. They cannot read others on a deeper level than just face analysis; they cannot understand that others have plans, thoughts and different points of view. They do not understand that others have beliefs, emotions, and attitudes. On the other hand their cognitive problem solving skills can be "normal".
The tract that is involved with attention goes to and from the cerebellum and is called the olivoponto-cerebello-thalamocortical tract.
There is universal dyspraxia in autism.
A hallmark of cerebellar functioning, classical eye blink conditioning, is abnormal in autism, both in amplitude and in latency of conditioned responses and in the rate of extinction.
Autistics have a general insensitivity to pain.
The eyes have a strong connection to the amygdala (part of the basal ganglia) that is related to strong emotional response.
Navigational tracts interconnect the eyes, the vestibular inner ear systems, the cerebellum, the pons, and the basal ganglia. From the basal ganglia the tracts go through the thalamus to the frontal cortex (frontal eye fields, premotor and motor areas). The basal ganglia are a collection of paired cell clusters buried deep below the cortex in white matter. The basal ganglia are spaced at a distance from each other but are interconnected by neural tracts. The basal ganglia include the corpus striatum, the globus pallidus, the substantia nigra, and the subthalamic nucleus. Together, these ganglia control complex patterns of movements such as walking. They control smooth voluntary movements.