What is SPD?

Sensory Processing Disorder (SPD) refers to a cluster of
disorders relating to processing of sensory information. According to the
updated nosology for SPD put forth in 2007, there are three main subgroups:
sensory modulation disorder (SMD), sensory-based motor disorder (SBMD), and
sensory differentiation disorder (SDD) (Miller, Anzalone, Lane, Cermak, & Osten, 2007). There are three types of SMD
disorders: sensory under-responsivity (SUR), sensory over-responsivity (SOR),
and sensory seeking (SS). The two types of SBMDs are dyspraxia and postural
disorders. Finally, it is possible to have a sensory differentiation disorder
in any of the following senses: vision, audition, tactile, vestibular,
proprioception, taste/smell.


While this is the most recent classification of this
disorder, the term sensory integration
dysfunction goes back to the year 1963 when Ayres described it (Ayres, 1963). Ayres, a psychologist and
neuroscientist, observed a relationship between sensory integration and
developmental disorders.

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Neither SPD nor RD are or have been included in the
Diagnostic Statistical Manual. Prior to the revision of the Diagnostic
Classification of Mental Health and Developmental Disorders of Infancy and
Early Childhood (DC:0-3) in 2005, sensory processing symptoms were included, categorized
under a broader umbrella of regulation disorder (RD), which also includes
problems sleeping, feeding, mood regulation, and other aspects of
self-regulation (Zero to Three (Organization), 1994). Simply termed “Sensory
Over-responsivity Disorder” and “Sensory Under-responsivity Disorder” in the
most recent version of this diagnostic manual, they are still not recognized in
the DSM.


The Sensory Profile is a useful tool in diagnosing SPD (Dunn & Westman, 1997). It has been estimated that
just over 5% of kindergarteners meet the criterion for SPD (Ahn, Miller, Milberger, & McIntosh, 2004). More recently, it has been
suggested that up to 16% of 7-11 year old children meet the criterion (Ben-Sasson, Carter, & Briggs-Gowan, 2009). One paper estimates that
about 8% of infants seen at the Infant Psychiatry Clinic at British Columbia
Children’s hospital are diagnosed with RD (Reebye & Stalker, 2007).


Although SPD can be seen alone with no co-morbid disorders,
it is commonly seen alongside other developmental disorders, including Fragile
X syndrome (Baranek et al., 2002, 2008), ADHD (Lane, Reynolds, & Thacker, 2010; Miller, Nielsen,
& Schoen, 2012),
and Autism Spectrum Disorders (ASD) (Baranek, Little, Diane Parham, Ausderau, &
Sabatos-DeVito, 2014; Ben-Sasson et al., 2008; Ben-Sasson, Cermak, Orsmond,
& Tager-Flusberg, 2007; Green, Ben-Sasson, Soto, & Carter, 2012; Kern
et al., 2006; Kirby, Boyd, Williams, Faldowski, & Baranek, 2017; Leekam,
Nieto, Libby, Wing, & Gould, 2007; Matsushima & Kato, 2013; McCormick,
Hepburn, Young, & Rogers, 2016). In fact, most children
diagnosed with ASD also have SPD (Al-Heizan, AlAbdulwahab, Kachanathu, & Natho,
2015; Kern et al., 2006). It is also sometimes seen with anxiety, with
the relationship between social anxiety and sensory dysfunction being modulated
by level of autism symptoms (Ludlow, Roberts, & Gutierrez, 2015), and associations between
sensory symptoms and general anxiety symptoms (Levit-Binnun, Szepsenwol, Stern-Ellran, &
Engel-Yeger, 2014).


While sensory dysfunction is sometimes seen with ADHD (Lane et al., 2010), they are distinct disorders.

Children with ADHD but not SPD tend to have more attentional symptoms, and
children with SPD (subtype SMD) have more sensory symptoms (Miller et al., 2012).


Sensory processing disorder is similar to some other
developmental disorders with mainly behavioral symptomology in that they
traditionally cannot be diagnosed before a certain age when social development
surpasses a certain level. With the more recent development of early markers
this has changed some, but it is still mostly true that data and symptomology
for infants relies on either studies using at-risk populations, such as younger
siblings of those who have been diagnosed, retrospective studies, or
longitudinal studies. Given the prevalence of SPD co-occurring with other
developmental disorders, it often makes sense to talk about SPD within a
context of co-morbid disorders.


Risk Factors/Early Indicators


Risk for developing SPD can be traced to the pre-natal
period. Prematurity, low birth weight, maternal stress etc. are all possible
risk factors (Hulle, Lemery-Chalfant, & Goldsmith, 2015;
May-Benson, Koomar, & Teasdale, 2009).


Hours of fussing, but not crying, as an infant (4-12 weeks
old) significantly correlated with decreased sensory processing (DeSantis, Coster, Bigsby, & Lester, 2004). In another study, sensation
avoiding and higher levels of sensory sensitivity were associated with more
fussing (McGeorge, Milne, Cotton, & Whelan, 2015). But, there inconsistent
results among other papers. Interestingly, jaundice occurred three to four
times more often in infants who went on to be diagnosed with ASD or SPD than
typically developing children (May-Benson et al., 2009).




Many behavioral symptoms of ASD do not emerge until a child
is at least a toddler, but it has been suggested that because sensory symptoms
tend to emerge before behavioral ones, identification of these symptoms could
help in earlier diagnosis of ASD (Germani et al., 2014).


Sensory dysfunction has been found to be one of a group of
early indicators of a later autism diagnosis (Baranek, 1999). In a retrospective study,
12-month-old high-risk infants who go on to be diagnosed with ASD show higher
sensory seeking behavior at 20-24 months (Baranek et al., 2017). Early risk factors can
predict later diagnosis of SPD (Bolaños,
Gomez, Ramos, & Rios del Rio, 2016). One of the first symptoms
seen is the inability to integrate the two sides of the body, starting in the
early months of life and sometimes persisting until 4 years of age.


While many studies investigate sensory systems associated
with other developmental disorders, few have examined children only diagnosed
with SPD. By far the most prevalent of SPDs, sensory over-responsivity (SOR) in
infancy has been found to be associated with clinical SOR in children, and
symptoms are relatively stable over the first three years (Ben-Sasson, Carter, & Briggs-Gowan, 2010). Further, in a sample of
toddlers diagnosed with autism, anxiety symptoms increased over a one year
period while symptoms of SOR did not change significantly over time (Green et al., 2012), suggesting that symptoms of
SOR appear earlier than symptoms of anxiety in an autism population. Another
study has corroborated these results, finding sensory processing abnormalities
across the senses; however, sensory symptoms seemed to decrease in individuals
with autism later on in life (Kern et al., 2006).


Neuronal Substrates


Event-related potentials can reliably be used to measure
multisensory integration in children, including those who are over-responsive
to sensory stimuli (Brett-Green, Miller, Schoen, & Nielsen, 2010). Sensory gating, the brain’s
ability to respond to important information while filtering out irrelevant
stimuli, has been measured in children and adults with and without SPD to
determine how this process develops over the lifespan. ERP experiments have
observed sensory gating as early as 1-4 months in infants (Kisley, Polk, Ross, Levisohn, & Freedman, 2003), with abnormal sensory gating
around 70 days old being correlated with attention symptoms 3 years later (Hutchison et al., 2017). In another ERP experiment, children
with and without SPD showed less sensory gating overall compared to adults, and
children with SPD showed less sensory gating than typically developing children
(Davies, Chang, & Gavin, 2009).


Other studies by the same group were able to use EEG
measures to discriminate between those with SPD and those without, with one
study correctly classify over 90% of participants as either a typically
developing child, a child with SPD, or an adult (Davies, Chang, & Gavin, 2010), another study discriminated
children with and without SPD with 86% accuracy (Davies & Gavin, 2007), and a third study differentiating
children with SPD from typically developing children with 77% accuracy, showing
decreased P300 amplitudes and shorter N200 latencies in children with SPD
relative to typically developing children (Gavin et al., 2011). In this last study, not only
were there differences in ERP measures, but these differences correlated with
behavioral tasks.


Further, other neuroimaging methods are capable of
uncovering structural differences in the brain. One such method is diffusion
tensor imaging (DTI) which measures white matter tracts. It has been shown that
a group of 8-11 year old boys with SPD had abnormal white matter structure
primarily in posterior cerebral tracts compared to a typically developing
age-matched group (Owen et al., 2013). Further, in a study that
examined white matter tractography in boys with autism and boys with SPD but
not autism, it was found that both groups had disrupted tracts in sensory
processing pathways, such as parietal-occipital tracts, but only the group of
boys with autism showed deficient connectivity in socio-emotional pathways,
such as more temporal tracts (Chang et al., 2014). This corroborates previous
evidence suggesting that even though SPD and autism may share some sensory
systems, they are distinct disorders. (ref?)


Additionally, those with autism have attenuated sensory
responses to auditory stimuli (Donkers et al., 2015).


Do symptoms persist over time without treatment?


Symptoms of sensory dysregulation tend to emerge early and
remain stable over early development. Data suggest that, while symptoms of
sensory dysfunction decrease over time in typically developing children, they
do not change in children diagnosed with autism or other developmental
disorders (McCormick et al., 2016). Given that more sensory
symptoms are present in children with ASD than in developmentally delayed or
typically developing children at age 2, this suggests that the early emergence
of these symptoms in children with autism may be unique to ASD, although this
sample does not include children who are diagnosed with SPD only.


One particular study found that 50% of infants who had
moderate to severe regulatory dysfunction at 7 months continued to show
symptoms at 36 months (DeGangi, Breinbauer, Roosevelt, Porges, &
Greenspan, 2000).

Another study from the same group assessed regulatory disordered infants at
8-11 months and then again 4 years later and found that eight out of 9 of the
RD group had sensorimotor deficits. The RD group and typical group differed on
many measures of RD, including sensorimotor deficits and tactile sensitivity (DeGangi, Porges, Sickel, & Greenspan, 1993). Importantly, studies suggest
that sensory sensitivity scores for a sample randomly obtained from hospital
records remain relatively stable over the period from one to two years old (Carter, Briggs-Gowan, Jones, & Little, 2003). This allows researchers to
compare infants and children with sensory dysfunction to a normative sample. In
another study using the same sample as this study, 39% of 1- to 2-year-olds who
had elevated ITSEA scores still had elevated scores a year later (Briggs-Gowan, Carter, Bosson-Heenan, Guyer, &
Horwitz, 2006).

Goldsmith sensory
defensiveness paper?


In a sample of boys with fragile X syndrome, sensory
symptoms increased over time, worsening from infancy to late preschool age (Baranek et al., 2008).


More recent research suggests the need to examine the
heterogeneity of SPDs, especially with SOR, which can have varied symptoms
depending on various risk factors and the severity of symptoms during
toddlerhood (Hulle et al., 2015). Importantly, being at risk
for SOR as a toddler did not necessarily suggest the presence of SOR later in
childhood; at-risk toddlers and low symptom toddlers scored the same on sensory
sensitivity tests at the second time point. However, children who scored in the
at-risk category at both 2 years old and 7 years old both showed more symptoms
of sensory-motor related disorders at age 4 than did children who were not
at-risk at both time points and were more likely to be born premature or
underweight. Interestingly, children who only scored into the at-risk category
at age 7 did not differ from other groups on birth characteristics, suggesting
another mechanism may be at play. Temperament characteristics were associated
with SOR symptoms in early but not middle childhood.



While early diagnosis of SPD is still difficult, some tools
have helped and conducting both retrospective studies and longitudinal studies
have given rise to a developmental trajectory for this group of disorders. No
matter if SPD is seen on its own or with a co-morbid disorder such as ASD,
sensory dysfunction symptoms seem to appear early in life, even in the first
few months, and remain stable over at least the first few years of life. There
is some data to suggest a lessening of symptoms in later life, although this
could be due to a multitude of factors such as successful interventions in
school and beyond, coping strategies, etc.


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