Brain Differences in Autism 2: Fusiform Gyrus

A review of: van Kooten, I.A., Palmen, S.J., von Cappeln, P., Steinbusch, H.W., Korr, H., Heinsen, H., Hof, P.R., van Engeland, H., Schmitz, C. (2008). Neurons in the fusiform gyrus are fewer and smaller in autism. Brain DOI: 10.1093/brain/awn033

The fusiform gyrus is an area of the temporal lobes of the brain that has been extensively associated to people’s ability to recognize faces. The authors of this paper proposed that abnormalities in the fusiform gyrus may explain some social deficits in Autism. Although people with autism can correctly complete face processing tasks, the authors noted that people with autism display reduced activation of the fusiform gyrus during these tasks. This alteration could be responsible for atypical behaviors such as reduced eye contact. To examine the underlying hypothesis further, the authors examined the post-mortem brains of 7 children and adults with autism as compared to 10 matched controls. They found significantly reduced neuron density and total neuron number in areas of the fusiform gyrus but not in other cortical areas. The authors presented a very interesting alternative interpretation. Although the reduced neural density and number in the fusiform gyrus could reflect neurodevelopmental impairments in the fusiform itself resulting in specific functional impairments, it is also possible that this atrophy is related to ‘loss of targets’ to which the fusiform gyrus projects. That is, the fusiform gyrus sends neural projections to the amygdale, which play an important role in monitoring eye gaze and other social behaviors. Thus, is the finding of reduced neural density and total number of the fusiform gyrus a reflection of dysfunction of this area of the brain, or simply a byproduct of alterations in other related areas such as the amygdale?

Brain Differences in children with Autism: White Matter – Gray Matter

A review of: BONILHA, L., CENDES, F., RORDEN, C., ECKERT, M., DALGALARRONDO, P., LI, L., STEINER, C. (2008). Gray and white matter imbalance – Typical structural abnormality underlying classic autism?. Brain and Development DOI: 10.1016/j.braindev.2007.11.006

The authors of this study discussed the relative inconsistent results from studies trying to examine brain differences in children with and without Autism. For example, although many post-mortem studies have found brain differences, the differences they find vary significantly between studies. The same is true of studies using imaging techniques such as MRI. However, the most consistent finding is an overall larger brain volume in children with autism, leading some researchers to propose deficits in cell pruning as a possible cause of autism (more of this below). In this study the authors used MRI (Magnetic Resonance Imaging) to compare 12 children with Autism (average age 12) to 16 matched typically developing children. The results showed that children with autism had increased generalized bilateral gray matter. Specifically increased gray matter was observed in the cingulated gyrus, caudate, cerebellum, claustrum, cuneus, fusiform gyrus, inferior, middle and superior frontal gyri, inferior and superior temporal gyri, inferior and superior parietal lobules, pre and post-central gyrus, precuneus, putamen, thalamus, insula and occipital cortex. The results also showed decreased generalized bilateral white matter in the cuneus, medial and superior frontal gyri, pre- and post-central gyri, inferior parietal lobule, supramarginal gyrus, cingulote gyrus, middle occipital gyrus, parahippocampal gyrus, and the middle and superior temporal gyri. The authors concluded that their data provides strong evidence for increased gray matter and reduced white matter in children with autism when compared to typically developing kids. Similar results have been used as evidence of the cell pruning theory of autism. This theory indicates that children with autism have an atypical brain development process during early infancy. Specifically, during a typical post-natal period, there is considerable removal of connections between cells in the brain leading to more efficiency in cell connectivity and cell communication. Researchers argue that abnormal brain growth during early development in autism is due to limited pruning of such synaptic connections.

Asperger’s Syndrome and Language Skills.

A review of: Saalasti, S., Lepistö, T., Toppila, E., Kujala, T., Laakso, M., Nieminen-von Wendt, T., Wendt, L., Jansson-Verkasalo, E. (2008). Language Abilities of Children with Asperger Syndrome. Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-008-0540-3

One of the diagnostic criteria of Asperger’s syndrome (AS) is normative language development, or more specifically: no evidence of language delays. However, the authors of this study argued that there is evidence to suggest that people with AS have impairment in various aspects of language including production and comprehension, making their language fluent but “pragmatically impaired.” Their interpretation of utterances is literal, leading to problems with the understanding of humor, metaphors, idioms, etc. To better understand the nature of these deficits the researchers compared the language skills of 22 children with AS (16 boys) between 7 and 10 years of age (diagnosed via ADOS and ADI) against 22 typically developing children of similar ages and IQ who were recruited from elementary schools. The researchers examined vocabulary, phonological processing, comprehension, repetition (phonological and sentence), fluency, and auditory processing. Children with AS performed significantly worse than typically developing children in the comprehension test (Comprehension of Instructions from the NEPSY) and tended to perform worse in the phonological processing test. No other differences were found. The authors argued that lower scores in the comprehension test are likely due to deficits in self-regulation and executive function, since both skills are necessary for successful performance on the comprehension and phonological processing tests.

Limited processing of facial expressions may explain limited gaze following in children with Austim

A review of: de JONG, M.C., van ENGELAND, H., KEMNER, C. (2008). Attentional Effects of Gaze Shifts Are Influenced by Emotion and Spatial Frequency, but Not in Autism. Journal of the American Academy of Child & Adolescent Psychiatry, 47(4), 443-454. DOI: 10.1097/CHI.0b013e31816429a6

This elegant experimental study comes to us from the Rudolf Magnus Institute of Neuroscience in the Netherlands. The researchers wanted to address a paradox in the Autism research literature: Although gaze following difficulties (specifically limited or absent gaze following) is a clinical hallmark of ASDs, many experimental studies have failed to replicate this phenomena in the laboratory (see for example Kemmer et al., 2006 & Senju et al., 2004). Gaze following refers to the re-direction of one’s attention towards the same location of someone else’s gaze direction. For example, if you are talking to a 2-year-old child and abruptly turn your head (or you eyes) to your left to see something, the child will immediately turn, arguably “to see what you are looking at.” The authors hypothesized that a possible explanation for problems with gaze following in children with ASDs is that these children have difficulty processing the emotional content intrinsic to facial expressions, and that such emotional content plays a critical role in triggering a re-orientation of attention by the observer. Specifically, the authors argued that this difficulty in the processing of emotional information is due to a bias towards processing local (detail) information instead of global information. So when looking at a face, research suggests that children with ASDs focus on details such as wrinkles and shapes, etc) instead of the ‘whole’ expression of the face. To test this hypothesis, the researchers examined 30 children with ASDs (diagnosed by a psychiatrist via ADI) with IQ over 80 and matched controls (matched for sex, age, and IQ). The children were presented with naturalistic pictures of faces with either a neutral of fearful expression and with straight or averted eye direction. Two conditions were presented, a neutral-to-fear condition and a fear-to-neutral condition. In the neutral-to-fear condition, a neutral face with straight gaze was followed by a fearful face with averted gaze. In the fearful-to-neutral condition, a fearful face with straight gaze was followed by a neutral face with averted gaze. An additional condition was also added: blurriness. In some pictures the face was blurry, making it more difficult to focus on the details of the picture (I did not review the results of these last conditions). The overall results were in partly line with the researchers' hypotheses. Although the authors concluded that "impaired gaze following in ASDs is related to impaired emotion processing," this conclusion was based on 1) a pattern of neruphysiological data that I did not review in this summary and 2) a differential pattern in 'cue validity' effect. Although a full explanation of cue validity effects goes beyond the scope of this review, the findings suggest that for typically developing children, when a discrepant emotional cue was presented (incorrect cue)a delay in reaction time in gaze following was observed when comparing reaction time to a fear face with the divergent gaze vs. a neutral face with divergent gaze. The children with ASDs did not show this pattern. That is, the speed of gaze following of typically developing children was affected when the presentation of the fear face was preceded by an incorrect cue. This is the traditional effect that you expect. However, the children with autism did not seem to be affected by this incorrect cue.