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A. Leland Albright, Yasser Awaad, Michael Muhonen, William R. Boydston, Richard Gilmartin, Linda E. Krach, Michael Turner, Kathryn A. Zidek, Ed Wright, Dale Swift and Karen Bloom

Object. The objectives of this multicenter study were to monitor the performance of a 10-ml pump infusing intrathecal baclofen to treat 100 children with cerebral spasticity, to monitor complications associated with the pump, and to correlate pump-related complications with body habitus.

Methods. Age at implantation of the pump ranged from 1.4 to 16.8 years (mean 8.1 years). The effects of ITB on spasticity in the upper and lower extremities were evaluated using the Ashworth Scale. Data were collected regarding implant site, infection, complication, and body mass index (BMI). Ashworth Scale scores decreased significantly in the upper and lower extremities at 6 and 12 months after pump implantation (p < 0.001). There were four serious system-related complications, all specific to catheters. There were 32 serious procedure-related complications in 21 patients: 11 complications were infections that occurred in nine patients. Four of nine pump-induced infections were treated with pump removal and antibiotic therapy; five infections were treated successfully with antibiotic therapy alone, without pump removal. In children younger than 8 years of age there was a significantly higher incidence of serious procedure-related adverse events than in older children. There was no significant correlation between BMI and the incidence of pump pocket—related complications or infections.

Conclusions. The 10-ml pump can be used therapeutically in small children, particularly those weighing less than 40 lbs, with greater ease and less wound tension, than the conventional 18-ml pump. The incidence of complications associated with the 10-ml pump in younger children appears to be similar to that previously reported with the 18-ml pump in larger-sized children.

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Brandon P. Lucke-Wold, Ryan C. Turner, Aric F. Logsdon, Linda Nguyen, Julian E. Bailes, John M. Lee, Matthew J. Robson, Bennet I. Omalu, Jason D. Huber and Charles L. Rosen

OBJECT

Chronic traumatic encephalopathy is a progressive neurodegenerative disease characterized by neurofibrillary tau tangles following repetitive neurotrauma. The underlying mechanism linking traumatic brain injury to chronic traumatic encephalopathy has not been elucidated. The authors investigate the role of endoplasmic reticulum stress as a link between acute neurotrauma and chronic neurodegeneration.

METHODS

The authors used pharmacological, biochemical, and behavioral tools to assess the role of endoplasmic reticulum stress in linking acute repetitive traumatic brain injury to the development of chronic neurodegeneration. Data from the authors’ clinically relevant and validated rodent blast model were compared with those obtained from postmortem human chronic traumatic encephalopathy specimens from a National Football League player and World Wrestling Entertainment wrestler.

RESULTS

The results demonstrated strong correlation of endoplasmic reticulum stress activation with subsequent tau hyperphosphorylation. Various endoplasmic reticulum stress markers were increased in human chronic traumatic encephalopathy specimens, and the endoplasmic reticulum stress response was associated with an increase in the tau kinase, glycogen synthase kinase–3β. Docosahexaenoic acid, an endoplasmic reticulum stress inhibitor, improved cognitive performance in the rat model 3 weeks after repetitive blast exposure. The data showed that docosahexaenoic acid administration substantially reduced tau hyperphosphorylation (t = 4.111, p < 0.05), improved cognition (t = 6.532, p < 0.001), and inhibited C/EBP homology protein activation (t = 5.631, p < 0.01). Additionally the data showed, for the first time, that endoplasmic reticulum stress is involved in the pathophysiology of chronic traumatic encephalopathy.

CONCLUSIONS

Docosahexaenoic acid therefore warrants further investigation as a potential therapeutic agent for the prevention of chronic traumatic encephalopathy.