Children with SCI or myelopathy may be at risk of cognitive dysfunction. Little is known about the frequency of cognitive dysfunction post-SCI, its etiology, and which cognitive domains are most affected. Cognitive dysfunction may arise from concurrent traumatic brain injury, from the etiology causing myelopathy, such as demyelination or central nervous system inflammation, from systemic effects of treatment for the etiology of SCI such as chemotherapy, and other causes not well-elucidated (Harder et al. 2013; Zonfrillo et al. 2014). Studies characterizing cognitive dysfunction post-SCI or post-myelopathy are summarized in the Tables below.
Only two studies have characterized the frequency and types of cognitive dysfunction post-SCI. Harder et al. (2013) evaluated cognition in children with transverse myelitis. Although transverse myelitis does not involve brain demyelination, more than half of patients had either mild (40.9%) or moderate (18.2%) attentional dysfunction, and nearly half of patients had mild (25%) or moderate (20%) reductions in verbal fluency, and more than half of patients had mild (33.3%) or moderate (20.8%) impairments in verbal memory. Abnormalities were also observed for processing speed and fine motor skills; however, much of this may be attributable to transverse myelitis and its impact on motor function rather than cognition. Zonfrillo et al. (2014) used a large observational database of children admitted for inpatient rehabilitation. Compared to children with traumatic brain injury, children with SCI (paraplegia and tetraplegia) had higher cognitive functioning at admission and at discharge from inpatient rehabilitation. More than half of children with paraplegia and tetraplegia improved to the highest Functional Independence Measure cognitive subscore on discharge. In a case report of a child with complete C2 tetraplegia, mental body representation was altered compared to age-matched controls (Salvato et al. 2017).