By: Caimen R. Wigington
Sensory Processing Disorder (SPD) and epilepsy represent two complex neurological conditions that significantly impact some people’s lives. While traditionally studied in isolation, emerging research suggests potential connections between these disorders. This paper explores their relationship, using recent scientific studies to understand their neurological intersections.
Sensory Processing Disorder presents a neurological challenge where the brain struggles to receive and respond to sensory information effectively. Individuals may experience heightened sensitivity to certain stimuli or, conversely, minimal response to others, creating challenges in daily life. The condition extends beyond simple sensory irregularities, affecting behavior, learning, and social interactions. Assessment of SPD typically involves standardized screening tools such as the Sensory Processing Measure (SPM) and the Sensory Profile 2, which evaluate sensory skills across multiple domains. Occupational therapists with specialized training in sensory integration are the primary professionals who assess and diagnose SPD, often working alongside developmental pediatricians, child psychologists, and neurologists to provide a comprehensive evaluation. Notably, research by Miller et al. (2012) highlighted compelling similarities in behavioral and physiological responses between children with ADHD and those experiencing sensory modulation disorders, suggesting potential underlying neurological parallels. These findings point to broader patterns of sensory dysregulation across multiple conditions, raising questions about shared neurobiological mechanisms. However, some researchers argue that SPD’s distinct neural signatures require further clarification before drawing strong comparisons with other disorders.
Epilepsy is characterized by recurrent seizures that might seem distinctly different from SPD, however, investigations reveal subtle yet significant connections. Seri et al. (1998) discovered that epileptic activity can substantially interfere with auditory sensory processing in specific epilepsy syndromes. This suggests that disruptions in sensory pathways are not exclusive to SPD but may also occur as a consequence of abnormal electrical activity in epilepsy. This overlap suggests seizures and sensory disturbances may stem from shared neural pathways rather than being distinct disorders. Nonetheless, some studies indicate that sensory dysfunction in epilepsy may be secondary to seizure activity rather than a primary characteristic, warranting further exploration.
A particularly compelling area of research centers on neuroinflammation as a potential common denominator. Recent studies, including Liew et al.’s (2023) work, emphasize neuroinflammation’s critical role in various neurological conditions. Specifically, inflammation-related changes in the hippocampus appear to influence both seizure activity and sensory processing challenges. The shared mechanisms of hippocampal changes and neuronal responses suggest deeper relationships between neurological disorders than previously understood. However, further research is needed to determine whether neuroinflammation serves as a root cause or a secondary effect in these conditions. Some researchers propose that while neuroinflammation is involved in both disorders, its role in SPD remains less defined compared to epilepsy (Vezzani, Balosso, & Ravizza, 2019).
Microglia, the brain’s resident immune cells, play a key role in these neurological processes. Masuda et al. (2019) revealed how these cells dynamically interact with their microenvironment, changing molecular structures during developmental and disease stages. Under chronic stress conditions, such as those present in epilepsy or sensory processing disorders, microglial activation can become problematic, potentially exacerbating symptoms. Lannes et al. (2017) emphasized how activated microglia contribute to a range of neurological and mental health challenges. If microglial dysfunction plays a role in both SPD and epilepsy, treatments targeting neuroinflammation could hold promise for managing both conditions.
While neither SPD nor epilepsy currently has a definitive cure, understanding their potential connections opens new avenues for treatment. Current epilepsy treatments focus on seizure control, but recognizing sensory processing complexities could lead to more comprehensive management strategies. Similarly, SPD interventions might benefit from considering potential neurological inflammation and epileptic activity. A more integrative approach could improve outcomes for individuals experiencing both conditions.
Several areas warrant further investigation to deepen our understanding of the relationship between SPD and epilepsy. First, studies examining the co-occurrence of these conditions across developmental stages could reveal temporal relationships and potential causal mechanisms. Second, neuroimaging research comparing brain activity patterns in individuals with both conditions versus those with either condition alone may identify specific neural signatures of overlap. Third, genetic studies could explore whether shared genetic vulnerabilities predispose individuals to both epilepsy and sensory processing challenges. Fourth, clinical trials investigating whether anti-inflammatory treatments used in epilepsy could benefit SPD patients may provide new therapeutic approaches for both conditions. Finally, research into how sensory interventions might influence seizure frequency or severity could lead to innovative non-pharmacological management strategies. These research directions could significantly advance our understanding of neurological comorbidities and potentially revolutionize treatment approaches for both conditions.
Although direct research linking Sensory Processing Disorder and epilepsy remains limited, emerging neuroscientific evidence suggests intricate neurological connections. Shared mechanisms involving neuroinflammation and microglial activity provide a promising framework for future research. A better understanding of these links could improve diagnostic precision, lead to more effective, tailored interventions, and improve people’s quality of life.
References:
Lannes, N., Eppler, E., Etemad, S., Yotovski, P., & Filgueira, L. (2017). Microglia at center stage: A comprehensive review about the versatile and unique residential macrophages of the central nervous system. Oncotarget, 8(69), 114393-114413. https://www.oncotarget.com/article/22592/text/
Liew, Y., Retinasamy, T., Arulsamy, A., Ali, I., Jones, N. C., O’Brien, T. J., & Shaikh, M. F. (2023). Neuroinflammation: A common pathway in Alzheimer’s disease and epilepsy. Journal of Alzheimer’s Disease, 94(Supplement 1), S253–S265. https://journals.sagepub.com/doi/10.3233/JAD-230286
Masuda, T., Sankowski, R., Staszewski, O., Böttcher, C., Amann, L., Sagar, Scheiwe, C., Nessler, S., Kunz, P., van Loo, G., Coenen, V. A., Reinacher, P. C., Michel, A., Sure, U., Gold, R., Grün, D., Priller, J., Stadelmann, C., & Prinz, M. (2019). Spatial and temporal heterogeneity of mouse and human microglia at single-cell resolution. Nature, 566(7744), 388-392. https://www.nature.com/articles/s41586-019-0924-x
Miller, L. J., Nielsen, D. M., & Schoen, S. A. (2012). Attention deficit hyperactivity disorder and sensory modulation disorder: A comparison of behavior and physiology. Research in Developmental Disabilities, 33(3), 804-818. https://www.sciencedirect.com/science/article/abs/pii/S0891422211004318?via%3Dihub
Seri, S., Cerquiglini, A., & Pisani, F. (1998). Spike-induced interference in auditory sensory processing in Landau-Kleffner syndrome. Electroencephalography and Clinical Neurophysiology, 108(5), 506-510. https://pubmed.ncbi.nlm.nih.gov/9780021
Vezzani, A., Balosso, S., & Ravizza, T. (2019). Neuroinflammatory pathways as treatment targets and biomarkers in epilepsy. Nature Reviews Neurology, 15(8), 459–472. https://doi.org/10.1038/s41582-019-0217-x
