NEUROBIOLOGY of AUTISM
The core neurological deficit in the brain of Asperger’s person is a lack of social relatedness due to abnormalities in the amygdala and anterior cingulate cortex. Both people with autism or Asperger’s have decreased metabolism in the anterior cingulate.
The circuit between the anterior cingulate in the frontal cortex and the amygdala is not completely connected. As a result, people with autism or Asperger’s have decreased metabolism in the anterior cingulate cortex.
What is different about the autistic brain is how it functions with respect to its neurophysiology. In a neurotypical brain, the anterior cingulate gyrus (ACG) acts like an automatic transmission that seamlessly switches attention back and forth between frontal lobes, as required.
David Rowland (Canadian Association for Neuroscience, Independent Researcher).
He presents a very restrictive view of autism and Asperger’s that is not in accordance with most other experts but gives an interesting viewpoint. There is truth in his theory of left brain “trapping” and is presented here primarily to present another theory in the neurobiology of autism. His views are certainly at odds with those of Temple Grandin who sees ASD on a continuum. His “clinical signs” are also all or nothing. Few high-functioning Asperger’s people could accept his dogmatic views.
According to Rowland, the autism spectrum idea is counterproductive and needs to be scrapped. This erroneous concept has been a major contributor to the epidemic of false diagnoses of autism.
Autism does not belong on any spectrum. There is only one kind of autism, not several. There are no shades of autism, nor any such thing as autistic tendencies. Autism is 100 percent. Either one is autistic, or s/he is not. There is no middle ground in autism, a dysfunctional anterior cingulate gyrus keeps the person trapped in his/her left frontal lobe, the intellectual, analytical, problem-solving part of the brain – with no ability to access the emotional/creative processing right frontal lobe, which plays a central role in spontaneity, social behaviour, and nonverbal abilities.
Some neurotypical people are left-brain dominant whereas others are right-brain dominant. Autistic people, however, are left brain-exclusive.
This inherent neurophysiological anomaly creates a perpetual state of hyperfocus: intense single-minded concentration fixated on one thought pattern at a time to the exclusion of everything else, including one’s feelings. Hyperfocus is the sole factor responsible for the autistic person’s withdrawal into an inner world that is entirely mental. Hyperfocus keeps a person’s awareness trapped in the intellectual/analytical left frontal lobe with no ability to access whatever may be happening in the right frontal lobe, where emotions and social connectivity are felt. Autistic hyperfocus explains all 11 traits of Asperger syndrome as first described by Lorna Wing, a British clinician whose ideas were years ahead of her American counterparts.
Being left brain exclusive means that one can only process his/her emotions intellectually, by deduction or inference, a process that can take about 24 hours. Failure to process emotions causes anxiety, which is an upsetting physiological response (different from emotion) that bypasses the intellect.
Hyperfocus is so intensely single-minded that an autistic person cannot divide attention between two trains of thought. An autistic person takes everything you say literally because s/he cannot also be running a second mental program questioning how you use words. While talking at length about a favorite topic, autistic people are incapable of running a second mental program asking how they are being received or perceived by their audience. Autistic people require structured activities because they cannot divide their attention between what they are doing and trying to figure out what may be about to happen next.
Hyperfocus also causes various kinds of sensory overload. A sudden loud or high-pitched noise switches hyperfocus to the noise, which the autistic person then experiences with many times the intensity than does a neurotypical person. Seeing too many words on a page can cause cognitive impairment whereby the autistic person’s mind goes disturbingly blank. Too many products on shelves and overhearing unwanted conversations in stores can trigger anxiety. Lighting displays in hardware stores can trigger intense anxiety. For some, hyperfocus exaggerates the sense of touch, making close-fitting clothing irritating and hugs unbearable.
Non-communicative autistic children are the ones most intensely trapped in hyperfocus, Intensely autistic children cannot be taught to speak; however, some spontaneously start to speak on their own initiative.
The most fitting description for autism is the word given to it in the Maori language: “takiwātanga”. It means “in his/her own space”.
Frontal Lobe. It controls higher executive functions including emotional regulation, planning, reasoning, and problem-solving.
Left Frontal Cortex/Lobe. In the autistic left frontal lobe, alpha frequencies (8-12 Hz) predominate over beta (12.5-30 Hz), which is the exact opposite of the neurotypical brain. Higher alpha frequencies in the left brain appear to be compensating for the inability to access creativity and intuition from the right brain (Rowland).
Right Frontal Cortex/Lobe. There is normal brainwave activity in the right frontal lobe, with alpha frequencies predominating over beta frequencies. However, the autistic person is unaware of anything that happens in his/her right frontal lobe, the place where emotions and social connectivity are experienced (Rowland).
Anterior Cingulate Cortex. It is involved in certain higher-level functions, such as attention allocation, reward anticipation, decision-making, ethics and morality, impulse control (e.g. performance monitoring and error detection), and emotion.
The anterior cingulate cortex can be divided anatomically into cognitive (dorsal) and emotional (ventral) components. The ventral part of the ACC is connected with the amygdala, nucleus accumben, hypothalamus, hippocampus, and anterior insula, and is involved in assessing emotion and motivational information. The ACC seems to be especially involved when effort is needed to carry out a task, such as in early learning and problem-solving.
It contains specialized neurons called spindle cells useful in addressing difficult problems.
A typical task that activates the ACC involves a conflict that can potentially result in an error. When the ACC receives conflicting input from control areas in the brain, it determines and allocates which area should be given control over the motor system. This evaluation is emotional in nature and highlights the amount of distress associated with a certain error.
Sagittal MRI slice with highlighting indicating the location of the anterior cingulate cortex
The ventral part of the ACC, on the other hand, is believed to be involved more with affective responses to errors. Frustration occurs when making mistakes and it may form the basis of self-confidence. It is likely the center of free will in humans. It appears to be involved in the emotional reaction to pain rather than in the perception of pain itself. The ACC may also be involved in monitoring painful social situations as well, such as exclusion or rejection.
Abnormalities of the ACC are associated with emotional instability, inattention, and akinetic mutism. schizophrenia, ADHD, obsessive-compulsive disorder, social anxiety, major depression, childhood trauma, and executive dysfunction. Impaired development of the anterior cingulate and the medial-frontal cortex may be the basis of the socio-cognitive deficits in autism.
Frontostriatal circuits are neural pathways that connect frontal lobe regions with the basal ganglia (striatum). They process information to control social behaviour and executive functions like working memory, planning and organization, behavioural control, adaptation to changes, and decision-making. They are responsible for the elaboration of the plan of actions responsible for goal-directed behaviour.
There are five circuits. Because of its role in affective-emotional processing, the circuit most pertinent to autism is the ventromedial prefrontal circuit that connects the prefrontal cortex to the amygdala.
Autopsies reveal that in both autism and Asperger’s there is immature development of the cerebellum, amygdala, and hippocampus. Autism has more immature hippocampus development than Asperger’s, which may explain the cognition problems seen in low-functioning autism. The situation is reversed for the amygdala, a part of the brain that processes emotion – the Asperger’s brain is often more abnormal than the autistic brain. The more normal hippocampus preserves cognitive function in Asperger’s, and the less normal amygdala causes social problems.
People with Asperger’s process emotional information differently than normal subjects. Functional MRI studies indicate that normal people activate the amygdala to judge the expression in another person’s eyes, but people with Asperger’s call on frontotemporal regions of the brain.
Amygdala and hypothalamus. The amygdala and hypothalamus are part of the limbic system – that part of the brain involved in our behavioural and emotional responses, especially when it comes to behaviours we need for survival: feeding, reproduction, caring for our young, and fight or flight responses. The left and right amygdala especially play a central role in our emotional responses, including feelings like pleasure, fear, anxiety, and anger. The amygdala also attaches emotional content to our memories, and so plays an important role in determining how robustly those memories are stored. Memories that have strong emotional meaning tend to stick.
The amygdala doesn’t just modify the strength and emotional content of memories; it also plays a key role in forming new memories specifically related to fear. Fearful memories are formed after only a few repetitions. This makes ‘fear learning’ a popular way to investigate the mechanisms of memory formation, consolidation, and recall. Suppressing or stimulating activity in the amygdala can influence the body’s automatic fear response, which kicks in when something unpleasant happens, such as a startling noise.
Cerebellum. Part of the hindbrain contains special neurons called Purkinje cells, capable of processing many signals at once due to their highly complex dendrite branches. The cerebellum coordinates our sensations with our muscles, enabling most of our voluntary movements. It also coordinates the inner ear with muscle movement, thus helping us maintain balance and posture.
Quantitative MRI and PPI testing
When healthy, unmedicated, intellectually able adults with Asperger’s syndrome are studied using quantitative MRI and PPI to measure sensorimotor gating to examine brain anatomy are compared to healthy controls of comparable age, IQ, gender, and handedness, differences in the anatomy and function of limbic circuitry has been demonstrated. Abnormalities in the anatomy of this entire neural system have been demonstrated in people with an autistic spectrum disorder.
People with Asperger’s syndrome have significantly less grey matter in medial temporal, and frontal lobe structures and cerebellar regions, and widespread differences in white matter. White matter projections to and from abnormal grey matter structures show white matter excesses are distributed bilaterally, but deficits appeared to be more prominent in the left hemisphere. This hemisphere normally develops later than the right and, perhaps as a consequence of evolving speech pathways, frontotemporal pathways reach maturation later than those linking lower-order regions.
Thus the neuro‐developmental delay in autism may particularly impact the left hemisphere and consequently explain some of the developmental language anomalies found in the disorder. Significant frontotemporal white matter deficits include the left superior temporal lobe speech area.
People with Asperger’s syndrome have significant reductions in grey matter volume of frontostriatal and cerebellar regions. In addition, people with Asperger’s syndrome have white matter excesses bilaterally around the basal ganglia, whereas they had deficits mainly in the left hemisphere. The concentration of abnormalities in the frontostriatal circuitry observed most likely has functional consequences. PPI is thought to depend in part on intact frontostriatal pathways, and significant impairment in sensorimotor gating in Asperger’s syndrome.
The limbic circuitry, proposed by some as the biological substrate of autism, plays an important role in sensorimotor gating. This mechanism is used to suppress motor responses to irrelevant stimuli, and similar processes may underlie cognitive gating.
These findings fit broadly with a growing consensus that limbic system and cerebellar abnormalities may be important determinants of autism.
Megaloencephaly is not a universal feature of autistic spectrum disorders, and no bulk regional brain volume differences between Asperger’s syndrome and controls have been found. Past reports of megalocephaly in autism may therefore reflect an effect of disease severity (e.g. mental retardation) that is not evident in the Asperger’s sample studied.
Age‐related differences in whole brain and grey matter volume in the controls were not evident in people with Asperger’s syndrome. The reason for this is unknown but may include neurodevelopmental differences in neurogenesis and programmed cell death.
Frontal and striatal brain regions are reciprocally connected and the thalamus. Dysfunction in a system incorporating the basal ganglia and the mesial frontal lobe is responsible for the clinical symptoms of autism, including motor disturbances such as dystonia, bradykinesia and hyperkinesias, and impaired social communication.
The frontostriatal regions identified as abnormal are known to have intimate and reciprocal links with the cerebellum, and the cerebellum has been implicated in higher-order cognitive functions, including executive functions such as planning and shifting attention. Abnormalities in the cerebellum may be related to the behavioural phenotype of people with an autistic spectrum disorder, but cerebellar pathology may best be viewed in the context of system‐wide pathology, rather than in isolation.
Sensorimotor Gating is the normal protective mechanism in the brain by which a neural system screens or ‘gates’ irrelevant external (sensory) and internal (cognitive, motor) information from higher-order processing. This prevents information overload, the misinterpretation of sensory information, and facilitates mental and behavioural integration. This enables coherent thought – the uninterrupted processing of the most salient aspects of the external and internal environment.
Filtering out relevant from irrelevant information is deficient in multiple neuropsychiatric disorders including autism and Asperger’s syndrome, schizophrenia, and obsessive-compulsive disorder.
Sensorimotor gating is significantly impaired in Asperger’s syndrome due to abnormalities in frontostriatal pathways. Sensorimotor gating deficits in autism may reflect similar difficulties with cognitive gating, rendering the individual unable to inhibit or ‘gate’ the repetitive thoughts, speech, and actions characteristic of the disorder. The subsequent information ‘overload’ may lead to higher cognitive difficulties, such as executive function and ‘theory of mind” (ToM) abnormalities, reported in autism. ToM is conceptualizing the thoughts, feelings, knowledge, and beliefs of others. Neurotypicals use context, knowledge of the person, and whether a particular comment or action had benevolent or malicious intent, to make character judgments. This is impaired in autism. It makes them naive and prone to be attracted to and imitate children who may not demonstrate good friendship skills.
ToM and executive function accounts of autism together explain quite well the socio‐communicative and flexibility problems in this disorder. However, neither account can explain why people with autism are so good at certain tasks.
Autism presents a strikingly uneven cognitive profile, with typical peaks on Wechsler block design and digit span. One theoretical account of autism attempts to explain these skills in terms of a bias toward featural versus configural processing. This cognitive style of ‘weak central coherence is demonstrated through the success of individuals with autism on tasks favouring detail focus, and relative inability on tasks requiring processing of information in context for global form or meaning. Impaired sensorimotor gating permits stimuli indiscriminate access to response output systems without regard for the context of presentation.