It has been proposed clinically that delayed surgery after traumatic brachial plexus injury may adversely affect functional outcome. In the present experimental study the neuroprotective and growth-promoting effects of early and delayed nerve grafting following proximal seventh cervical spinal nerve (C7) axotomy were examined. The ventral branch of C7 spinal nerve was transected and axons projecting out of the proximal nerve stump were labelled with Fast Blue (FB). At the same time, the biceps brachii muscle was denervated by transecting the musculocutaneous nerve at its origin. Neuronal survival and muscle atrophy were then assessed at 1, 4, 8 and 16 weeks after permanent axotomy. In the experimental groups, a peripheral nerve graft was interposed between the transected C7 spinal nerve and the distal stump of the musculocutaneous nerve at 1 week [early nerve repair (ENR)] or 8 weeks [delayed nerve repair (DNR)] after axotomy. Sixteen weeks after nerve repair had been performed, a second tracer Fluoro-Ruby (FR) was applied distal to the graft to assess the efficacy of axonal regeneration. Counts of FB-labelled neurons revealed that axotomy did not induce any significant cell loss at 4 weeks, but 15% of motoneurons and 32% of sensory neurons died at 8 weeks after injury. At 16 weeks, the amount of cell loss in spinal cord and dorsal root ganglion (DRG) reached 29 and 50%, respectively. Both ENR and DNR prevented retrograde degeneration of spinal motoneurons and counteracted muscle atrophy, but failed to rescue sensory neurons. Due to substantial cell loss at 8 weeks, the number of FR-labelled neurons after DNR was significantly lower when compared to ENR. However, the proportion of regenerating neurons among surviving motoneurons and DRG neurons remained relatively constant indicating that neurons retained their regenerative capacity after prolonged axotomy. The results demonstrate that DNR could protect spinal motoneurons and reduce muscle atrophy, but had little effect on sensory DRG neurons. However, the efficacy of neuroprotection and axonal regeneration will be significantly affected by the amount of cell loss already presented at the time of nerve repair.
Aim Assess current practice and views regarding checking Goldmann applanation tonometers for calibration errors in the United Kingdom. Design Questionnaire survey. Methods A total of 100 ophthalmology residents from England, Wales, and Scotland attending the 2004 Congress of the Royal College of Ophthalmologists, UK, responded to a structured questionnaire. They were asked the following: how often they used different tonometers between clinical sessions; how often they checked their tonometers for errors; and who they felt was responsible for checking tonometers for calibration errors. Results All respondents were using a different Goldmann tonometer for each clinic: 85% never check tonometers for errors; only 7% perform checks at the start of each clinical session; and 8% would only check the tonometer for calibration errors if they had suspicious or unexpected measurements. A total of 70% of respondents felt that calibration checks are not part of their responsibility. They believe that either nursing staff or other hospital staff should carry out calibration checks and ensure that tonometers are accurate. The remaining 30% felt that calibration checks should be carried out by the doctor using the tonometer. Conclusion Despite evidence that Goldmann tonometers lose accuracy during routine use in clinical practice, only a minority are checking the tonometers for calibration errors. There is no consensus as to who should be responsible for ensuring that tonometer calibration is maintained. We recommend that tonometers should be checked for calibration errors at least on a monthly basis by individuals identified by departmental protocols.
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