Cranial nerve injuries in patients with moderate to severe head trauma - Analysis of 91,196 patients from the TraumaRegister DGU® between 2008 and 2017.

OBJECTIVE: Traumatic brain injury (TBI) constitutes a major cause of trauma-related disability and mortality. The epidemiology and implications of associated cranial nerve injuries　(CNI)　in moderate to severe TBI are largely unknown. We aimed to determine the incidence of CNI in a large European cohort of TBI patients as well as clinical differences between TBI cases with and without concomitant CNI (CNI vs. control group) by means of a multinational trauma registry. METHODS: The TraumaRegister DGU® was evaluated for trauma patients with head injuries ≥ 2 Abbreviated Injury Scale, who had to be treated on intensive care units after emergency admission to European hospitals between 2008 and 2017. CNI and control cases were compared with respect to demographic, clinical, and outcome variables. RESULTS: 1.0% (946 of 91,196) of TBI patients presented with additional CNI. On average, CNI patients were younger than control cases (44.3 ± 20.6 vs. 51.8 ± 23.0 years) but did not differ regarding sex distribution (CNI 69.4% males vs. control 69.1%). Traffic accidents were encountered more frequently in CNI cases (52.3% vs. 46.7%; p < 0.001; chi-squared test) and falls more commonly in the control group (45.2% vs. 37.1%; p < 0.001). CNI patients suffered more frequently from concomitant face injuries (28.2% vs. 17.5%; p < 0.001) and skull base fractures (51.0% vs. 23.5%; p < 0.001). Despite similar mean Injury Severity Score (CNI 21.8 ± 11.3; control 21.1 ± 11.7) and Glasgow Coma Scale score (CNI 10.9 ± 4.2, control 11.1 ± 4.4), there was a considerably higher proportion of anisocoria in CNI patients (20.1% vs. 11.2%; p < 0.001). Following primary treatment, 50.8% of CNI and 35.5% of control cases showed moderate to severe disability (Glasgow Outcome Scale score 3-4; p < 0.001). CONCLUSION: CNI rarely occur in the context of TBI. When present, they indicate a higher likelihood of functional impairment following primary care and complicating skull base fractures should be suspected.

Germline ablation of dermatan-4O-sulfotransferase1 reduces regeneration after mouse spinal cord injury.

Chondroitin/dermatan sulfate proteoglycans (CSPGs/DSPGs) are major components of the extracellular matrix. Their expression is generally upregulated after injuries to the adult mammalian central nervous system, which is known for its low ability to restore function after injury. Several studies support the view that CSPGs inhibit regeneration after injury, whereas the functions of DSPGs in injury paradigms are less certain. To characterize the functions of DSPGs in the presence of CSPGs, we studied young adult dermatan-4O-sulfotransferase1-deficient (Chst14(-/-)) mice, which express chondroitin sulfates (CSs), but not dermatan sulfates (DSs), to characterize the functional outcome after severe compression injury of the spinal cord. In comparison to their wild-type (Chst14(+/+)) littermates, regeneration was reduced in Chst14(-/-) mice. No differences between genotypes were seen in the size of spinal cords, numbers of microglia and astrocytes neither in intact nor injured spinal cords after injury. Monoaminergic innervation and re-innervation of the spinal cord caudal to the lesion site as well as expression levels of glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) were similar in both genotypes, independent of whether they were injured and examined 6weeks after injury or not injured. These results suggest that, in contrast to CSPGs, DSPGs, being the products of Chst14 enzymatic activity, promote regeneration after injury of the adult mouse central nervous system.