Sensory processing disorder is one of those peculiarly modern diseases caught in the purgatory between legitimacy and quackery. It’s widely accepted that some children have difficulty handling external stimuli. Kids diagnosed with autism and ADHD have trouble managing sensory experiences that others deal with easily. They cover their ears on the playground, for example, or complain that their clothing is intolerably scratchy. That much is uncontroversial. In the 1970s, however, a UCLA psychologist claimed that sensory processing failure is not merely a symptom of other disorders but is more often a freestanding disease with its own neurologic basis. After 40 years of debate, we still don’t know whether she was right.
This debate sounds like a medical technicality, but the distinction between symptom and disorder matters a great deal. It matters because tens of thousands of parents are convinced that their children’s behavioral issues are the result of sensory processing difficulties. They don’t believe, or can’t believe, that the real problem is anxiety, ADHD, or autism. It also matters because barrel-loads of money are on the line. Advocates claim that up to 16 percent of American children suffer from SPD, but few insurance companies will pay for therapy until mainstream doctors are convinced that the disease is real and treatment works.
Official recognition seems distant, however, because the good ship SPD has come upon choppy seas of late. Two years ago, the American Academy of Pediatrics issued a position paper concluding that there was insufficient evidence that sensory processing challenges represent an independent disorder. The organization warned pediatricians against diagnosing children with the disease and advised parents that there is limited evidence to support existing therapies. SPD experienced a more significant setback in 2013, when the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders excluded the disease on the basis of inadequate evidence.
The series of rejections has set up a pitched battle between the medical “establishment” (if that term can be used non-pejoratively) and angry families. The current standoff is a good example of why the Internet is a terrible medium for debating medical issues. The stakes are highest, and the need for a resolution most urgent, for the people who are least able to understand the science. That’s not a dig at families who are struggling with major behavioral problems—it’s simply a fact of modern life and scientific practice. Doctors need time and money to untangle complicated psychiatric issues.
A brief look at the literature reveals why these issues are impossible for laypeople to adjudicate. There are dozens of papers addressing the disorder in peer-reviewed journals. Quality and quantity are not the same thing, though. Even Lucy Miller, director of the Sensory Therapies and Research Center and one of the leading advocates for SPD, acknowledges that the early research was “not rigorous.” Those shortcomings put advocates in a hole, as major journals and many medical experts came to think of SPD research as unscientific.
SPD research has unquestionably improved in recent years. Advocates have better outlined categories of sensory processing problems, improving the framework for research. The National Institutes of Health have funded some of the research, granting it no small degree of legitimacy. Last year, a paper in the journal Neuroimage: Clinical purported to identify structural brain abnormalities in children with clinical evidence of sensory processing issues.
Many hopeful parents think that means victory, but it’s not even close. Despite 40 years of discussion, SPD researchers have yet to agree on a proven, standardized diagnostic tool. This undermines researchers’ ability to define the boundaries of the disease. It makes correlation studies, like the one about structural brain abnormalities, less convincing. It also makes it impossible to test the effectiveness of the therapies, many of which, to be frank, look a little loopy to stuffy scientific types. (Spinning? Swinging?) If you can’t prove that the therapies work, insurance companies are not going to pay for them.
Larry Desch, a pediatrician and co-author of the 2012 report that declined to recognize SPD, acknowledges that some of the recent research, which uses a blinded approach to distinguish between SPD and other disorders, is of a high quality. But, he muses, “Has there been enough clear data to determine that what we are seeing in some children is truly a disorder and not just a temporary issue or a variation of normal?” That question will take many more years to answer.
There have also been some public relations setbacks for SPD. In 2007, New York Times science writer Benedict Carey described sensory processing disorder as belonging to “the special-needs vernacular,” which also included attention deficit hyperactivity disorder. It’s not clear whether Carey intended to be critical, but it’s bad press for a childhood psychiatric disorder to appear in a sentence with ADHD, the stand-in for our national preoccupation with over-medicalizing childhood behavioral problems.
Backers of the disorder also haven’t helped themselves. The checklist of symptoms on the website of the SPD Foundation, one of the primary advocacy groups for the disorder, is almost impossibly broad. It includes such warning signs as “My infant/toddler has problems eating,” “My child has difficulty being toilet trained,” “My child is in constant motion,” and “My child gets in everyone else's space and/or touches everything around him.” These read more like the day-to-day complaints of an average parent than a symptom screen for a legitimate psychiatric disorder. The estimate that 16 percent of children suffer from SPD also seems hard to accept, contributing to the perception among skeptics that the SPD diagnosis stigmatizes children who are simply sensitive to noise or poorly behaved.
Desch uses the word waiting when describing the state of play. Pediatricians and psychologists are waiting for more studies, waiting for a standardized diagnostic tool, waiting to learn whether the therapies heal behavioral issues better than the passage of time alone. Thousands of concerned parents are waiting, too.
It’s difficult to predict where SPD will go from here. It could become the next fibromyalgia, a once-mocked diagnosis that has achieved general—if begrudging—acceptance. Or it could go the way of chronic lyme, a would-be disease that saw its proponents’ hopes for official recognition effectively ended in a comprehensive debunking by the Infectious Diseases Society of America in 2006. Even so, chronic lyme advocates continue to accuse physicians of colluding with insurance companies to deny them needed coverage.
There have already been similar rumblings among devotees of sensory processing disorder. “Probably paid off by the insurance companies,” grumbled one commenter beneath a story about the 2012 report.
Don’t join these conspiracy theorists. There’s no evidence of corruption, bias, or incompetence on either side. Give the professionals time to do their work. You may know your child, but they know the science.
Current research on the underlying neurobiology of SPD has been guided by the overarching hypothesis that both autonomic and central nervous system processes are affected in SPD. These hypotheses are based on Ayres’ proposal that children with SPD may have an impaired ability to integrate stimuli from multiple sensory modalities, leading to atypical behavioral responses to ordinary environmental stimuli (Ayres, 1963). Those with SPD-SOR are easily overwhelmed by daily sensory experiences, while those with SPD-SUR tend to “tune-out” or not notice the same sensory experiences (Miller et al., 2007b).
Autonomic nervous system research
The first line of this phase of research, which started in 1995, examined physiologic mechanisms of autonomic nervous system regulation in response to sensory stimulation in children with SPD-SOR. This research was based on Ayres’ original theoretical constructs, as well as current clinical observations that many children with SPD-SOR exhibit “fight or flight” responses to everyday stimuli (Ayres, 1963). Atypical sympathetic and parasympathetic nervous system function were documented in children with SPD-SOR compared to typically developing controls (McIntosh et al., 1999; Miller et al., 2001; Schaaf et al., 2003). The sympathetic (increased reactivity) and parasympathetic responses (less vagal variability) were hypothesized to contribute to the inability of children with SPD-SOR to modulate the degree, intensity, and type of response to typical environmental sensory stimuli. When further investigated in relation to other established diagnostic categories, children with SPD-SOR exhibited different physiological patterns than children with attention deficit/hyperactivity disorder (ADHD; Mangeot et al., 2001) as well as children with autism spectrum disorder (ASD; S.A. Schoen et al., submitted). These discriminant validity studies comparing SPD to ADHD and comparing SPD to ASD used both phasic and tonic electrodermal activity as outcome measures. Results of these studies suggest that children with SPD-SOR have more phasic reactivity to sensory stimulation than children with ASD or typically developing children, In addition, children with ASD have lower tonic arousal levels than both typically developing children and children with SPD (S.A. Schoen et al., submitted). On the other hand, children with ADHD displayed atypically large reactions to the initial presentation of a sensory stimulus, but habituated following subsequent presentations of the stimuli (Mangeot et al., 2001; Miller et al., 2001). This finding differentiated children with ADHD from children with SPD-SOR who had larger reactions to all stimuli and did not habituate to recurring sensory stimulation (McIntosh et al., 1999).
Central nervous system research
Studies of the central nervous system (CNS) were then implemented to examine potential brain processes that may underlie SPD. These studies were predicated on Ayres’ theory (Ayres, 1972b, 1979) that behavioral expressions of SPD-SOR, such as frequent meltdowns, withdrawal from others, and severe aggression observed after being touched, might be related to immaturity or malfunction in brain processes (Ayres, 1963). Hypotheses were developed for the SPD-SOR and SPD-SUR subtypes, since these children clinically have difficulty integrating multisensory stimuli, or filtering background stimuli. It was hypothesized that auditory stimulation would result in atypical brain activity and that sensory gating and MSI would be abnormal in theses subtypes. Hypotheses were studied in both children (Davies and Gavin, 2007; Brett-Green et al., submitted) and adults (Kisley et al., 2004).
Sensory gating, a measure of the ability of the CNS to inhibit responses to redundant or irrelevant sensory stimuli, manifests electrophysiologically as a reduction in amplitude of a specific evoked potential component (e.g., P50) in response to paired stimuli. When typically developing children were presented with tones at different frequencies and intensities, distinct brain responses were elicited for each intensity (Davies et al., 2009). However, children with SPD-SOR and SPD-SUR did not exhibit the typical increased response to an increased intensity of stimulation, strongly suggesting that their brain processing of simple auditory stimuli is less organized (Davies et al., 2009). The clinical sample also demonstrated less auditory sensory gating than typically developing children (Davies and Gavin, 2007; Davies et al., 2009), suggesting that children with SPD have more difficulty filtering out repeated or irrelevant sensory information. While sensory gating improved with age for typically developing children, sensory gating did not improve with age in the clinical group, indicating that the maturational course of sensory gating in SPD may be quite different than typical controls (Davies and Gavin, 2007; Davies et al., 2009). The brain activity measured in the intensity and gating paradigms correctly classified children with SPD vs. typically developing children with 86% accuracy (Davies and Gavin, 2007). Moreover, findings suggested that children with SPD could be either over-responsive or under-responsive when responding to sensory input compared to typically developing children (Davies and Gavin, 2007). These studies support Ayres’ theories suggesting that the CNS has a deficit in processing sensory stimuli and validates the SOR and SUR subtypes in the current clinical nosology groupings (Miller et al., 2007c).
Sensory gating was also investigated in adults who endorsed high rates of SOR. Adults with greater SPD-SOR symptoms exhibited less efficient sensory gating (i.e., lower suppression of auditory ERP P50 and N100 components in a paired click paradigm; Kisley and Cornwell, (2006)). Notably, decreased P50 responses were correlated with higher endorsement of “perceptual modulation” difficulties (feelings of being flooded by sounds), whereas decreased N100 responses were correlated with increased endorsement of an inability to filter out background sounds. These data suggest that two distinct neural processes might account for these two distinctive types of abnormal auditory information processing.
Additionally, sensory gating was evaluated in rats using pre-pulse inhibition (PPI), a functional measure of sensorimotor gating that provides a way to investigate how the brain normally suppresses over-reactivity to sensory stimuli. SP deficits and PPI deficits in particular were hypothesized to involve disrupted nicotinic acetylcholine signaling in the CNS (see for review Heath and Picciotto, 2009). PPI was pharmacologically impaired and unimodal (auditory startle with auditory prepulse) and bimodal (tactile startle with auditory prepulse) PPI responses to clozapine and nicotine were evaluated. Bimodal PPI impairments in sensory gating were attenuated only by clozapine (Levin et al., 2007), but unimodal PPI impairments in sensory gating were attenuated by a combination of nicotine with clozapine (Levin et al., 2005). While the basic neurotransmitter mechanism of each of these pharmacological agents in isolation is relatively well known, the specific mechanisms of their interactions in modifying unimodal and biomodal PPI needs further study. A better understanding of the basic neurobiology, neurotransmitter interactions, and pharmacology of unimodal versus bimodal PPI may lead to insights about the underlying mechanisms of SPD and perhaps future pharmacological interventions.
Studying MSI in children with SPD was also a logical line of research to pursue given Ayres’ fundamental premise that SPD reflects a disorder in “intersensory/MSI.” Additionally, clinical observations report children identified with SPD-SOR are overwhelmed in situations where sensations from multiple modalities are present (e.g., a busy mall or a school cafeteria). Below is a brief overview of some preliminary findings that provide a basis for the ongoing research studies of MSI in individuals with SPD.
The ability of the brain to integrate sensory stimuli is a fundamental neural function that must be intact for a person to function adaptively in the environment by responding to meaningful stimuli and ignoring stimuli that are incidental. Recent research based on electroencephalography using event-related potentials (ERPs) suggests that impaired MSI in children with SPD-SOR may be based on differences in the spatio-temporal pattern of MSI responses in SPD compared to typically developing children (B. Brett-Green, personal communication). In a preliminary study of typically developing children auditory-somatosensory MSI was identified based on differences between multisensory and summed unisensory responses (Brett-Green et al., 2008), a classic approach commonly used in MSI research (Stein and Meredith, 1993). MSI was found contralateral to the side of somatosensory stimulation over the caudo-medial auditory cortex in typically developing children (Brett-Green et al., 2008) whereas in children with SPD, frontal regions were activated (B. Brett-Green, submitted). The location of MSI in typically developing children is consistent with recent MSI reports in typical adults (Foxe and Schroeder, 2005; Murray et al., 2005).
In typically developing children, MSI was found in the ipsilateral cortex and in midline cortical regions (Brett-Green et al., 2008). Children with SPD-SOR showed smaller amplitude MSI responses in midline and frontal cortical regions, and showed an absence of ipsilateral integration (B. Brett-Green, submitted). These studies suggest that the automatic integration of multisensory stimuli occurring early in sensory information processing in lower level cortical regions may not occur in children with SPD-SOR. Instead, higher-level frontal MSI processes may be engaged. The possible ramification of this finding may explain why children with SPD-SOR tend to attend to all environmental stimuli, meaningful or not. However, the exact consequence of the differences between typically developing children and those with SPD-SOR or SPD-SUR in MSI is not yet known. The lack of ipsilateral MSI in children with SPD-SOR needs further study.
The evidence that abnormalities in MSI exist in SPD provided the impetus for this special journal issue of Frontiers in Integrative Neuroscience. The comingling of ideas from basic science and from the clinical perspective will benefit research in both fields.