Abnormal sensory-based behaviors are a defining feature of autism spectrum disorders (ASD). Dr. A. Jean Ayres was the first occupational therapist to conceptualize Sensory Integration (SI) theories and therapies to address these deficits. Her work was based on neurological knowledge of the 1970’s. Since then, advancements in neuroimaging techniques make it possible to better understand the brain areas that may underlie sensory processing deficits in ASD. In this article, we explore the postulates proposed by Ayres (i.e., registration, modulation, motivation) through current neuroimaging literature. To this end, we review the neural underpinnings of sensory processing and integration in ASD by examining the literature on neurophysiological responses to sensory stimuli in individuals with ASD as well as structural and network organization using a variety of neuroimaging techniques. Many aspects of Ayres’ hypotheses about the nature of the disorder were found to be highly consistent with current literature on sensory processing in children with ASD but there are some discrepancies across various methodological techniques and ASD development. With additional characterization, neurophysiological profiles of sensory processing in ASD may serve as valuable biomarkers for diagnosis and monitoring of therapeutic interventions, such as SI therapy.
Fascinating research adds to and challenges our existing knowledge. This recently published research is suggesting that the fight and flight response in vertebrates may in part be triggered by osteocalcin release via bones. This research raises so many questions regarding the evidence about why sensory integration may help support self regulation. It makes me wonder about the role of the heavy muscle work we all use as part of therapy and the sensory strategies we recommend to support self regulation at home and school.
Does activating proprioception sensors found in the muscles and tendons around our bones have a role in inhibiting release of osteocalcin? Does proprioception andvdeep pressure touch signalling via DCML alter or impact on osteocalcin release? And what’s the impact on GABA ?
A layman’s article about this interesting research can be found here:
Read the original research: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30441-3
Meeting the needs of children with sensory integration and processing difficulties when they need cate for acute illness can be challenging for parents and medical teams. This study explores the development of a sensory care pathway to address this need.
“Objective: To identify pediatric patients with sensory sensitivities during a hospital visit, and to implement a clinical pathway that can meet their sensory needs. The goal is to remove barriers to care delivery that is related to the sensory need for pediatric patients who present with an acute medical illness.
Methods: The clinical pathway (identified as ‘Sensory Pathway’) was developed as a joint effort between key stakeholders within the community and medical providers. The pathway was conducted in a tertiary pediatric hospital from September 2016-April 2019. The main components of this pathway included- 1. Staff training; 2. Provision of sensory toolkits and story board; 3. Early collaboration with allied professionals; and 4. Early and continuous parental involvement. The Sensory Pathway was implemented first in the emergency department, followed by inpatient units. Patients triggered the pathway through caregiver or staff identification. Demographic of patients who triggered the pathway was extracted. A detailed qualitative analysis of any parents’ feedback received was performed.
Results: A cohort of patients with sensory needs was identified amongst pediatric patients who presented to the hospital with an acute illness. The most common comorbidity associated with sensory sensitivity/need was Autism Spectrum Disorder (48%), followed by cerebral palsy (22.8%) and Attention-Deficit/Hyperactivity Disorder (16%). 1337 patients (51.8%) had a single comorbidity while 45.9% patients had more than one comorbidity. Only 1.3% patients had a known diagnosis of sensory processing disorder. The pathway was triggered in 2,580 patient visits with 1643 patients and 937 repeat visits. The vast majority of patients who triggered the pathway had a medical presenting complaint (vs. behavioral). The following themes emerged from the parents’ feedback: 1. Additional help received specific to the child’s sensory needs; 2. Feeling of comfort; and 3. Improved overall experience.
Conclusion: The Sensory Pathway identified a unique profile of pediatric patients who have sensory needs during their hospital stay. The pathway was successfully implemented for children with sensory need in our hospital across a wide range of demographic and with varied medical illness.”
Pain and sensory integration difficulties including sensory sensitivity are thought to be features in many disorders including CFS/ME and hyper mobility. Recent research and evidence is exploring the links.
Abstract “Sensory modulation disorder (SMD) affects sensory processing across single or multiple sensory systems. The sensory over-responsivity (SOR) subtype of SMD is manifested clinically as a condition in which non-painful stimuli are perceived as abnormally irritating, unpleasant, or even painful. Moreover, SOR interferes with participation in daily routines and activities (Dunn, 2007; Bar-Shalita et al., 2008; Chien et al., 2016), co-occurs with daily pain hyper-sensitivity, and reduces quality of life due to bodily pain. Laboratory behavioral studies have confirmed abnormal pain perception, as demonstrated by hyperalgesia and an enhanced lingering painful sensation, in children and adults with SMD. Advanced quantitative sensory testing (QST) has revealed the mechanisms of altered pain processing in SOR whereby despite the existence of normal peripheral sensory processing, there is enhanced facilitation of pain-transmitting pathways along with preserved but delayed inhibitory pain modulation. These findings point to central nervous system (CNS) involvement as the underlying mechanism of pain hypersensitivity in SOR. Based on the mutual central processing of both non-painful and painful sensory stimuli, we suggest shared mechanisms such as cortical hyper-excitation, an excitatory-inhibitory neuronal imbalance, and sensory modulation alterations. This is supported by novel findings indicating that SOR is a risk factor and comorbidity of chronic non-neuropathic pain disorders. This is the first review to summarize current empirical knowledge investigating SMD and pain, a sensory modality not yet part of the official SMD realm. We propose a neurophysiological mechanism-based model for the interrelation between pain and SMD. Embracing the pain domain could significantly contribute to the understanding of this condition’s pathogenesis and how it manifests in daily life, as well as suggesting the basis for future potential mechanism-based therapies.”
Read more here: Sensory Modulation Disorder (SMD) and Pain: A New Perspective