A traditional line of work starting with the Gestalt school has shown that patterns vary in strength and salience; a difference in “Perceptual goodness.” The Holographic weight of evidence model quantifies goodness of visual regularities. The key formula states that W = E/N, where E is number of holographic identities in a pattern and N is number of elements. We tested whether W predicts the amplitude of the neural response to regularity in an extrastriate symmetry-sensitive network. We recorded an Event Related Potential (ERP) generated by symmetry called the Sustained Posterior Negativity (SPN). First, we reanalyzed the published work and found that W explained most variance in SPN amplitude. Then in four new studies, we confirmed specific predictions of the holographic model regarding 1) the differential effects of numerosity on reflection and repetition, 2) the similarity between reflection and Glass patterns, 3) multiple symmetries, and 4) symmetry and anti-symmetry. In all cases, the holographic approach predicted SPN amplitude remarkably well; particularly in an early window around 300–400 ms post stimulus onset. Although the holographic model was not conceived as a model of neural processing, it captures many details of the brain response to symmetry.

When actively classifying abstract patterns according to their regularity, alpha desynchronization (ERD) becomes right lateralized over posterior brain areas. This could reflect temporary enhancement of contralateral visual inputs and specifically a shift of attention to the left, or right hemisphere specialization for regularity discrimination. This study tested these competing hypotheses. Twenty-four participants discriminated between dot patterns containing a reflection or a translation. The direction of the transformation, which matched one half onto the other half, was either vertical or horizontal. The strategy of shifting attention to one side of the patterns would not produce lateralized ERD in the horizontal condition. However, right-lateralized ERD was found in all conditions, regardless of orientation. We conclude that right hemisphere networks that incorporate the early posterior regions are specialized for regularity discrimination.

Electrophysiological studies of symmetry have found a difference wave termed the Sustained Posterior Negativity (SPN) related to the presence of symmetry. Yet the extent to which the SPN is modulated by luminance-polarity and colour content is unknown. Here we examine how luminance-polarity distribution across the symmetry axis, grouping by luminance polarity, and the number of colours in the stimuli, modulate the SPN. Stimuli were dot patterns arranged either symmetrically or quasi-randomly. There were several arrangements: ’segregated’-symmetric dots were of one polarity and randomly-positioned dots were of the other; ‘unsegregated’-symmetric dots were of both polarities in equal proportions; ‘anti-symmetric’-dots were of opposite polarity across the symmetry axis; ‘polarity-grouped anti-symmetric’-this is the same as anti-symmetric but with half the pattern of one polarity and the other half of opposite polarity; multi-colour symmetric patterns made of two, three to four colours. We found that the SPN is: (i) reduced by the amount of position-symmetry, (ii) sensitive to luminance-polarity mismatch across the symmetry axis, and (iii) not modulated by the number of colours in the stimuli. Our results show that the sustained nature of the SPN coincides with the late onset of a topographic microstate sensitive to symmetry. These findings emphasise the importance of not only position symmetry, but also luminance polarity matching across the symmetry axis.

Symmetry is a highly salient feature in the visual world, abundant in both man-made and natural objects. In particular, humans find reflectional symmetry most salient. Electrophysiological work on symmetry perception has identified a difference wave known as the Sustained Posterior Negativity (SPN) originating from extrastriate areas. Amplitude is more negative for symmetrical than random patterns, from around 200 msec after stimulus onset. For the first time, we report responses to patterns presented exclusively in one hemifield. Participants were presented with reflection or random dot patterns to the left and right of fixation (3.2°). They judged whether the patterns were light red or dark red in colour. In Experiment 1, the pair always included one symmetrical and one random pattern. In Experiments 2 and 3 we varied the information presented contralaterally. The SPN was generated separately in each hemisphere in response to what was presented in the contralateral visual hemifield (a lateralised SPN). We conclude that a symmetry-sensitive network of extrastriate areas can be activated independently in each cerebral hemisphere.

Neurodevelopmental disorders are frequently associated with sleep disturbances. One class of neurodevelopmental disorders, the genetic synaptopathies, is caused by mutations in genes encoding proteins found at the synapse. Mutations in these genes cause derangement of synapse development and function. We utilized a validated sleep instrument, Children’s Sleep Habits Questionnaire (CSHQ) to examine the nature of sleep abnormalities occurring in individuals with two synaptopathies—Phelan–McDermid syndrome (PMD) (N = 47, male = 23, female = 24, age 1–46 years) and SYNGAP1-related intellectual disability (SYNGAP1-ID) (N = 64, male = 31, female = 33, age 1–64 years), when compared with unaffected siblings (N = 61, male = 25, female = 36, age 1–17 years). We found that both PMD and SYNGAP1-ID have significant sleep abnormalities with SYNGAP1-ID having greater severity of sleep disturbance than PMD. In addition, sleep disturbances were more severe for PMD in individuals 11 years and older compared with those less than 11 years old. Individuals with either disorder were more likely to use sleep aids than unaffected siblings. In conclusion, sleep disturbances are a significant phenotype in the synaptopathies PMD and SYNGAP1-ID. Improved sleep is a viable endpoint for future clinical trials for these neurodevelopmental disorders.

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Targeted treatments for fragile X syndrome (FXS) have frequently failed to show efficacy in clinical testing, despite success at the preclinical stages. This has highlighted the need for more effective translational outcome measures. EEG differences observed in FXS, including exaggerated N1 ERP amplitudes, increased resting gamma power and reduced gamma phase-locking in the sensory cortices, have been suggested as potential biomarkers of the syndrome. These abnormalities are thought to reflect cortical hyper excitability resulting from an excitatory (glutamate) and inhibitory (GABAergic) imbalance in FXS, which has been the target of several pharmaceutical remediation studies. EEG differences observed in humans also show similarities to those seen in laboratory models of FXS, which may allow for greater translational equivalence and better predict clinical success of putative therapeutics. There is some evidence from clinical trials showing that treatment related changes in EEG may be associated with clinical improvements, but these require replication and extension to other medications. Although the use of EEG characteristics as biomarkers is still in the early phases, and further research is needed to establish its utility in clinical trials, the current research is promising and signals the emergence of an effective translational biomarker.

Background SYNGAP1-related intellectual disability (ID) is a recently described neurodevelopmental disorder that is caused by pathogenic variation in the SYNGAP1 gene. To date, the behavioural characteristics of this disorder have mainly been highlighted via the prevalence of existing diagnoses in case series. We set out to detail the behavioural features of this disorder by undertaking interviews with those who have a child with SYNGAP1-related ID to allow them to describe their child’s behaviour. Methods We conducted 27 semi-structured interviews with parents and caregivers which covered basic information (e.g., age, gender), family history, perinatal history, past medical history, developmental history, epilepsy, behavioural history, and a general description of their child’s behaviour. Results Using a mixed quantitative and qualitative approach, the responses from the parents indicated that those with SYNGAP1-related ID showed high rates of autism spectrum disorder (52%), difficulties with fine and gross motor skills, delays in language development, and a high prevalence of epilepsy (70%). A qualitative analysis highlighted their general behaviour affected the themes of daily living skills, distress-related behaviours, emotional regulation, difficulties with change, a lack of danger awareness, and sensory differences. Sensory features described involved auditory, visual, tactile, gustatory, and proprioceptive themes. Conclusions Our findings and behavioural descriptions provide important insights as well as implications for the diagnosis and care of those with SYNGAP1-related ID.