GdDO3NI Enhanced Magnetic Resonance Imaging Allows Imaging of Hypoxia After Brain Injury.

BACKGROUND: Brain tissue hypoxia is a common consequence of traumatic brain injury (TBI) due to the rupture of blood vessels during impact and it correlates with poor outcome. The current magnetic resonance imaging (MRI) techniques are unable to provide a direct map of tissue hypoxia. PURPOSE: To investigate whether GdDO3NI, a nitroimidazole-based T1 MRI contrast agent allows imaging hypoxia in the injured brain after experimental TBI. STUDY TYPE: Prospective. ANIMAL MODEL: TBI-induced mice (controlled cortical impact model) were intravenously injected with either conventional T1 agent (gadoteridol) or GdDO3NI at 0.3 mmol/kg dose (n = 5 for each cohort) along with pimonidazole (60 mg/kg) at 1 hour postinjury and imaged for 3 hours following which they were euthanized. FIELD STRENGTH/SEQUENCE: 7 T/T2 -weighted spin echo and T1 -weighted gradient echo. ASSESSMENT: Injured animals were imaged with T2 -weighted spin-echo sequence to estimate the extent of the injury. The mice were then imaged precontrast and postcontrast using a T1 -weighted gradient-echo sequence for 3 hours postcontrast. Regions of interests were drawn on the brain injury region, the contralateral brain as well as on the cheek muscle region for comparison of contrast kinetics. Brains were harvested immediately post-imaging for immunohistochemical analysis. STATISTICAL TESTS: One-way analysis of variance and two-sample t-tests were performed with a P < 0.05 was considered statistically significant. RESULTS: GdDO3NI retention in the injury region at 2.5-3 hours post-injection was significantly higher compared to gadoteridol (mean retention fraction 63.95% ± 27.43% vs. 20.68% ± 7.43% for gadoteridol at 3 hours) while it rapidly cleared out of the muscle region. Pimonidazole staining confirmed the presence of hypoxia in both gadoteridol and GdDO3NI cohorts, and the later cohort showed good agreement with MRI contrast enhancement. DATA CONCLUSION: GdDO3NI was successfully shown to visualize hypoxia in the brain post-TBI using T1 -weighted MRI at 2.5-3 hours postcontrast. EVIDENCE LEVEL: 1 TECHNICAL EFFICACY: Stage 1.

The effect of long-distance bicycling on ulnar and median nerves: an electrophysiologic evaluation of cyclist palsy.

BACKGROUND: Distal ulnar neuropathies have been identified in cyclists because of prolonged grip pressures on handlebars. The so-called cyclist palsy has been postulated to be an entrapment neuropathy of the ulnar nerve in the Guyon canal of the wrist. Previous studies utilizing nerve conduction studies have typically been either case reports or small case series. HYPOTHESIS: Electrophysiologic changes will be present in the ulnar and median nerves after a long-distance multiday cycling event. STUDY DESIGN: Cohort study; Level of evidence, 2. METHODS: A total of 28 adult hands from 14 subjects underwent median and ulnar motor and sensory nerve conductions, which were performed on both hands before and after a 6-day, 420-mile bike tour. A ride questionnaire was also administered after the ride, evaluating the experience level of the cyclist, equipment issues, hand position, and symptoms during the ride. RESULTS: Distal motor latencies of the deep branch of the ulnar nerve to the first dorsal interosseous were significantly prolonged after the long-distance cycling event. The median motor and sensory studies as well as the ulnar sensory and motor studies of the abductor digiti minimi did not change significantly. Electrophysiologic and symptomatic worsening of carpal tunnel syndrome was observed in 3 hands, with the onset of carpal tunnel syndrome in 1 hand after the ride. CONCLUSION: Long-distance cycling may promote physiologic changes in the deep branch of the ulnar nerve and exacerbate symptoms of carpal tunnel syndrome.