Introduction: Expanding the Boundaries of Chronic Traumatic Encephalopathy
The medical understanding of Chronic Traumatic Encephalopathy (CTE) has traditionally focused on the cerebral cortex, specifically the pathognomonic accumulation of hyperphosphorylated tau (p-tau) in neurons and astrocytes around small blood vessels at the depths of the cortical sulci. However, emerging clinical evidence suggests that individuals exposed to repetitive head impacts (RHI) often present with a constellation of symptoms that extend beyond cognitive and behavioral changes, frequently involving motor dysfunction reminiscent of amyotrophic lateral sclerosis (ALS) or parkinsonism. A groundbreaking study by Tanaka et al., published in JAMA Neurology (2026), provides critical evidence that the pathology of CTE is not confined to the brain but represents a systemic trauma-related encephalomyelopathy involving the spinal cord.
Exposure to RHI, common in contact sports and military service, is a known risk factor for various neurodegenerative diseases. While the cortical manifestations of CTE neuropathologic change (CTE-NC) are well-documented, the involvement of the spinal cord has remained a significant gap in our understanding of the disease’s natural history. This study addresses whether the spinal cord is a primary site of protein misfolding following trauma and how these pathologies correlate with clinical motor symptoms.
