What Causes Sensory Processing Disorder: Key Factors

Sensory processing disorder (SPD) arises from differences in how the brain receives and organizes information from the senses. Rather than a single cause, it results from a combination of structural brain differences, prenatal influences, genetic factors, and nervous system patterns that affect how sensory signals travel and get interpreted. The condition is not yet recognized as a standalone diagnosis in the DSM-5 or ICD, but the neurological differences behind it are measurable and increasingly well understood.

Brain Wiring Differences in SPD

The most direct explanation for SPD lies in the white matter tracts that carry signals between brain regions. A neuroimaging study published in NeuroImage: Clinical found that children with SPD had significant structural differences in the connective tissue of the brain, particularly in posterior regions. The tracts most affected were those connecting sensory relay centers to the areas of the brain that process what you see, hear, and feel. These posterior pathways showed less organized fiber structure and more water diffusion, both signs that signals travel less efficiently.

What makes this finding especially telling is how tightly those structural differences correlated with real-world sensory behavior. Children with the most disrupted white matter in these tracts scored worst on measures of auditory processing, multisensory integration (the ability to combine input from multiple senses at once), and attention. The correlation was strong, with values ranging from 0.51 to 0.78, meaning the brain differences weren’t subtle or ambiguous. In practical terms, this means the wiring that helps a child filter background noise, process a teacher’s voice while watching their gestures, or shift attention smoothly between tasks is physically less efficient in children with SPD.

The Role of the Nervous System’s Alarm Response

Beyond brain structure, the autonomic nervous system plays a key role in sensory over-responsivity, the subtype of SPD where ordinary sensations feel overwhelming or even painful. Research shows that a child’s baseline arousal level, essentially how “revved up” their fight-or-flight system is at rest, directly influences how they respond to sensory input. A child whose nervous system runs at a higher baseline will react more intensely to sounds, textures, or movement that other children barely notice.

This isn’t just about the initial reaction. The intensity of that sensory response also affects how quickly the child can calm down afterward, and it mediates the relationship between sensory input and anxiety. So a child who overreacts to a fire alarm doesn’t just have a louder startle. Their nervous system takes longer to return to baseline, and repeated experiences like that can build into broader anxiety patterns. This creates a feedback loop: high baseline arousal leads to bigger sensory reactions, which leads to more anxiety, which keeps the nervous system running hot.

Prenatal and Birth Factors

Several prenatal exposures increase the likelihood of sensory processing difficulties. Alcohol exposure during pregnancy is the most well-documented teratogenic cause of developmental differences in children, disrupting the production and migration of neurons during fetal brain development. Children with fetal alcohol spectrum disorder frequently experience sensory processing problems alongside cognitive and behavioral challenges.

Prematurity is another significant risk factor. Between 39% and 52% of preterm infants show sensory processing difficulties, with sensory modulation problems being the most prominent type. A study comparing preterm and full-term infants at 12 months found that premature babies had significantly lower scores in overall sensory processing, reactivity to deep touch, and response to movement. The association was clear: prematurity correlated with poorer sensory processing across multiple domains.

Other birth complications that can contribute include oxygen deprivation during delivery, very low birth weight, serious infections during pregnancy, and birth trauma such as intracranial hemorrhage. These events can disrupt the early development of the neural pathways that later handle sensory integration. The common thread is anything that interferes with normal brain development during the critical prenatal and perinatal windows.

Genetic and Familial Patterns

SPD tends to run in families. Parents of children with sensory processing difficulties often report their own sensory sensitivities, whether it’s being bothered by clothing tags, overwhelmed in noisy environments, or unusually sensitive to certain foods. While no single gene has been identified as the cause, the familial clustering suggests a genetic component that likely involves multiple genes influencing how the nervous system develops and regulates sensory input. Twin studies have supported this heritability, though the genetics remain complex and not yet fully mapped.

Overlap With Autism and ADHD

Sensory symptoms are extremely common in both autism and ADHD, and this overlap is one reason SPD remains controversial as a standalone diagnosis. Sensory processing difficulties are so prevalent in autism that they were added to the diagnostic criteria in the DSM-5. In ADHD, sensory symptoms are also reported at high rates, including hypersensitivity to noise, difficulty filtering sensory distractions, and discomfort with certain textures.

Neuroimaging research has found shared neural patterns between the sensory symptoms in autism and ADHD, suggesting that overlapping brain mechanisms may drive the sensory difficulties seen in both conditions. This doesn’t mean SPD is “just” a feature of autism or ADHD. Many children have clinically significant sensory processing problems without meeting criteria for either condition. But the overlap means that when sensory difficulties are present, it’s worth considering whether they exist alongside or as part of a broader neurodevelopmental profile.

The Three Subtypes of SPD

Not all sensory processing difficulties look the same, and the cause may partly depend on which subtype a child has. The STAR Institute identifies three primary patterns:

  • Sensory modulation differences involve the brain’s ability to regulate its response to incoming stimuli. Children who are over-responsive react too intensely, too quickly, or for too long to ordinary sensations. Children who are under-responsive have muted or delayed reactions and may seem unaware of pain, temperature changes, or being touched.
  • Sensory discrimination differences affect the ability to interpret the subtle qualities of what you sense. This can show up across any modality: difficulty distinguishing similar sounds, trouble judging how hard to grip a pencil, or problems reading spatial information from touch or vision.
  • Sensory-motor differences involve the translation of sensory input into coordinated movement. This includes immature postural control and dyspraxia, which is difficulty planning and executing unfamiliar motor sequences despite having the physical ability to do so.

These subtypes likely involve different neural pathways. Modulation problems appear most connected to autonomic nervous system regulation and the brain’s filtering mechanisms. Discrimination problems point more toward the posterior white matter tracts that handle detailed sensory interpretation. Motor-based difficulties implicate the pathways between sensory input areas and motor planning regions. A child can have one subtype or a combination, which is part of why SPD presentations vary so widely from one person to the next.

Why No Single Cause Explains SPD

SPD is best understood as the result of multiple converging factors rather than one clear trigger. A child might inherit a genetic tendency toward nervous system sensitivity, experience a premature birth that disrupts white matter development, and then grow up with a nervous system that runs at a higher baseline arousal. Each factor compounds the others. This is also why the severity and type of sensory difficulty vary so much. Two children with SPD might share the same label but have entirely different sensory profiles, different triggers, and different underlying combinations of brain structure, nervous system regulation, and developmental history driving their experience.