Current research in<unk><unk>  is focused on finding the genetic and neurological causes of SPD. Electroencephalography (EEG), measuring event-related potential (ERP) and magnetoencephalography (MEG) are traditionally used to explore the causes behind the behaviors observed in SPD . Differences in tactile and auditory over-responsivity show moderate genetic influences, with tactile over-responsivity demonstrating greater heritability. Differences in auditory latency (the time between the input is received and when reaction is observed in the brain), hypersensitivity to vibration in the Pacinian corpuscles receptor pathways and other alterations in unimodal and multisensory<unk>  have been detected in autism populations. People with<unk><unk>  deficits appear to have less<unk>  gating than typical subjects, and atypical neural integration of<unk>  input. In people with<unk>  over-responsivity, different neural generators activate, causing the automatic association of causally related<unk>  inputs that occurs at this early<unk> -perceptual stage to not function properly. People suffering from<unk>  over-responsivity might have increased D2 receptor in the striatum, related to aversion to tactile stimuli and reduced habituation. In animal models, prenatal stress significantly increased tactile avoidance. Recent research has also found an abnormal white matter microstructure in children with SPD, compared with typical children and those with other developmental disorders such as autism and ADHD. One hypothesis is that multisensory stimulation may activate a higher-level system in the frontal cortex that involves attention and cognitive<unk> , rather than the automatic integration of multisensory stimuli observed in typically developing adults in the auditory cortex.
Sensory processing disorder
Somatosensory disorder
Motor disorder
Cognitive reserve
Communication disorder
Catastrophic illness
Stroke recovery
Pollutant-induced abnormal behaviour