Assessment and management of pain in the home care setting

Garon, Maryanne

doi:10.1097/00004650-199110000-00010

Cited by 3 publications

(1 citation statement)

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“… 69 Previous cases in the literature showed an overlap between ASD and chronic pain, particularly among adolescents. 6 , 70 , 72 As previously mentioned, ASD has a strong genetic contribution, and advances of arrays and sequencing technologies have provided tools to elucidate both de novo single nucleotide variants and copy number variations and other genetic variants that contribute to approximately 10% to 40% of cases. 49 , 73–75 Sodium channels in ASD research have gained significant traction, with SCN2A , a gene that encodes a voltage-gated sodium channel subtype 2 alpha protein (Na v 1.2), becoming a front runner due to the sheer amount of de novo single nucleotide variants that occur in patients.…”

Section: The Autism Spectrum Disorder Risk Gene Scn9a and Pain Comorbiditiesmentioning

confidence: 99%

A mini-review: Bridging the gap between autism spectrum disorder and pain comorbidities

Brown

Singh

2020

Canadian Journal of Pain

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Background Pain is a complex neurobiological response with a multitude of causes; however, patients with autism spectrum disorder (ASD) often report chronic pain with no known etiology. Recent research has been aimed toward identifying the causal mechanisms of pain in mouse and human models of ASD. In recent years, efforts have been made to better document and explore secondary phenotypes observed in ASD patients in the clinic. As new sequencing studies have become more powered with larger cohorts within ASD, specific genes and their variants are often left uncharacterized or validated. In this review we highlight ASD risk genes often presented with pain comorbidities. Aims This mini-review bridges the gap between two fields of literature, neurodevelopmental disorders and pain research. We discuss the importance of the genetic landscape of ASD and its links to pain phenotypes. Results Among the numerous genes implicated in ASD, few have been implicated with varying severities of pain comorbidity. Mutations in these genes, such as SCN9A, SHANK3 , and CNTNAP2 , lead to altered neuronal function that produce different responses to pain, shown in both mouse and human models. Conclusion There is a necessity to use new technologies to advance the current understanding of ASD risk genes and their contributions to pain. Secondly, there is a need to power future ASD risk genes associated with pain with their own cohort, because a better understanding is needed of this subpopulation.

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