Autism and epilepsy

Sundelin, Heléne E.K.; Larsson, Henrik; Lichtenstein, Paul; Almqvist, Catarina; Hultman, Christina M.; Tomson, Torbjörn; Ludvigsson, Jonas F.

doi:10.1212/wnl.0000000000002836

Cited by 68 publications

(11 citation statements)

References 31 publications

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“…It has been shown that the rates of neural response to input increase following administrations of glutamate agonists [ 41 ] and GABA antagonists [ 42 ]. It is noteworthy that our result of greater neural responsivity to increasing sensory input resembles those previously reported in epilepsy patients in a similar paradigm [ 43 , 44 ] while shared etiology between epilepsy and ASD has been discussed by some authors [ 45 ]. Further, our finding parallels observations from a meta-analysis of fMRI studies, which indicates that enhanced activation in visual cortex is one of the most frequently reported findings in ASD [ 46 ].…”

Section: Discussionsupporting

confidence: 86%

Neurophysiological hyperresponsivity to sensory input in autism spectrum disorders

Takarae

Sablich

White

et al. 2016

J Neurodevelop Disord

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BackgroundAtypical sensory processing is a common clinical observation in autism spectrum disorder (ASD). Neural hyperexcitability has been suggested as the cause for sensory hypersensitivity, a frequently reported clinical observation in ASD. We examined visual evoked responses to parametric increases in stimulus contrast in order to model neural responsivity of sensory systems in ASD.MethodsThirteen high-functioning individuals with ASD and 12 typically developing (TD) individuals completed a steady-state visual evoked potential study. Stimuli were vertical circular gratings oscillating at 3.76 Hz at varying contrasts (5, 10, 20,…, 90 % contrast, 10 levels). The average spectral power at the stimulus oscillation frequency was calculated for each contrast level.ResultsThe magnitude of evoked sensory responses increased at a significantly greater rate and resulted in disproportionately elevated activation with higher contrasts in the ASD group. Approximately 45 % of ASD participants had rates of response increases greater than any TD participant. This alteration was highly associated with parental reports of these participants’ sensory difficulties.ConclusionsGreater increases in visual responses over contrast manipulation suggest heightened excitability in the sensory cortex in ASD participants. Heightened neural excitability was observed in a substantial portion but not all of the ASD participants. This pattern suggests that individuals with higher excitability may constitute a neurobiologically distinct subgroup requiring individualized treatment interventions.

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Section: Discussionsupporting

confidence: 86%

Neurophysiological hyperresponsivity to sensory input in autism spectrum disorders

Takarae

Sablich

White

et al. 2016

J Neurodevelop Disord

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“…that seizures may cause ASD [ 16 , 25 ]. Others have argued against this because the relationship is bi-directional and individuals with ASD are at increased risk of future epilepsy and seizures may occur in adolescence or adulthood [ 21 , 22 , 45 , 46 ]. This study highlights the importance of considering the additive effects of the underlying genetic aetiology and seizures contributing to autism symptoms in AS, which may be relevant also for other conditions [ 15 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of epilepsy on autism symptoms in Angelman syndrome

et al. 2018

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BackgroundAutism spectrum disorder and epilepsy often co-occur; however, the extent to which the association between autism symptoms and epilepsy is due to shared aetiology or to the direct effects of seizures is a topic of ongoing debate. Angelman syndrome (AS) is presented as a suitable disease model to explore this association.MethodsData from medical records and questionnaires were used to examine the association between age of epilepsy onset, autism symptoms, genetic aberration and communication level. Forty-eight participants had genetically verified AS (median age 14.5 years; range 1–57 years). A measure of autism symptoms (the Social Communication Questionnaire; SCQ) was completed for 38 individuals aged ≥ 4 years. Genetic cause was subgrouped into deletion and other genetic aberrations of the 15q11-q13 area. The number of signs used to communicate (< 20 sign and ≥ 20 signs) was used as a measure of nonverbal communication.ResultsMean age of epilepsy onset was 3.0 years (range 3 months–7.8 years). Mean SCQ score for individuals without epilepsy was 13.6 (SD = 6.7) and with epilepsy 17.0 (SD = 5.6; p = 0.17); 58% used fewer than 20 signs to communicate. There were no age differences between groups according to presence of epilepsy, level of nonverbal communication or type of genetic aberration. SCQ scores were higher in individuals with the deletion than in those with other genetic aberrations (18.7 vs 10.8 p = 0.008) and higher in the group who used < 20 signs to communicate (19.4 vs 14.1 p = 0.007). Age of epilepsy onset was correlated with SCQ (r = − 0.61, p < 0.001). Multiple regression showed that age of seizure onset was significantly related to SCQ score (β = − 0.90; p = 0.006), even when the type of genetic abnormality was controlled (R2 = 0.53; F = 10.7; p = 0.001).ConclusionsThe study provides support for the notion that seizures themselves contribute more to autism symptoms than expected from the underlying genetic pathology alone. The study demonstrates how a rare genetic syndrome such as Angelman syndrome may be used to study the relation between epilepsy and autism symptomatology.

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“…An interesting population-based, nationwide cohort study was carried out in Sweden by Sundelin et al 40 The study design was unusual. They examined follow-up data for 85,201 individuals with epilepsy, 80,511 siblings of these individuals and 98,534 offspring.…”

Section: What Is the Role Of Genetics In Determining Conditions That mentioning

confidence: 99%

Epilepsy in patients with autism: links, risks and treatment challenges

Besag¹

2017

NDT

121

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Autism is more common in people with epilepsy, approximately 20%, and epilepsy is more common in people with autism with reported rates of approximately 20%. However, these figures are likely to be affected by the current broader criteria for autism spectrum disorder (ASD), which have contributed to an increased prevalence of autism, with the result that the rate for ASD in epilepsy is likely to be higher and the figure for epilepsy in ASD is likely to be lower. Some evidence suggests that there are two peaks of epilepsy onset in autism, in infancy and adolescence. The rate of autism in epilepsy is much higher in those with intellectual disability. In conditions such as the Landau–Kleffner syndrome and nonconvulsive status epilepticus, the epilepsy itself may present with autistic features. There is no plausible mechanism for autism causing epilepsy, however. The co-occurrence of autism and epilepsy is almost certainly the result of underlying factors predisposing to both conditions, including both genetic and environmental factors. Conditions such as attention deficit hyperactivity disorder, anxiety and sleep disorders are common in both epilepsy and autism. Epilepsy is generally not a contraindication to treating these conditions with suitable medication, but it is important to take account of relevant drug interactions. One of the greatest challenges in autism is to determine why early childhood regression occurs in perhaps 25%. Further research should focus on finding the cause for such regression. Whether epilepsy plays a role in the regression of a subgroup of children with autism who lose skills remains to be determined.

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Autism and epilepsy

Cited by 68 publications

References 31 publications

Neurophysiological hyperresponsivity to sensory input in autism spectrum disorders

Neurophysiological hyperresponsivity to sensory input in autism spectrum disorders

Effect of epilepsy on autism symptoms in Angelman syndrome

Epilepsy in patients with autism: links, risks and treatment challenges

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