This study was performed to evaluate the long-term functional nerve recovery after reconstruction of a 10-mm gap in the sciatic nerve of the rat, with a thin-walled nerve guide, composed of a biodegradable copolymer of DL-lactide and epsilon-caprolactone [p(DLLA-epsilon-CL)]. To evaluate both motor and sensory nerve recovery, walking track analysis and electrostimulation tests were carried out after implantation periods ranging from 3 to 52 weeks postoperatively. The first signs of both motor and sensory nerve recovery could be observed after 5 weeks. After 15 weeks, 70% of the sciatic function and 90% of the sensory nerve function had been recovered. After this period, the sciatic function index (SFI) did not improve further, whereas the sensory nerve function appeared to return to normal. When the results of the SFI measurements, minus those obtained from rats with severe automutilation, are extrapolated, further improvement of the SFI might be expected after 52 weeks. The fact that 100% sensory nerve recovery was obtained, as measured by the electrostimulation test, could be explained by sensory reinnervation from surrounding areas. The SFI was not fully reestablished because automutilation had a great impact on the use of walking track assessment.

The previously published studies regarding CRPS-I as a reason for amputation all represent Level-IV evidence, and they do not clearly delineate the beneficial and adverse affects of an amputation performed for this diagnosis. Whether to amputate or not in order to treat long-standing, therapy-resistant CRPS-I remains an unanswered question.

Our results suggest a common sequence, in which formation of cytoplasmic and nuclear inclusions precede proteasomal impairment and induction of the cellular stress response. Clearly, impairment of the PQC is not the primary cause for inclusion formation, but rather a consequence that might contribute to neuronal dysfunction and death. Notably, the inclusion pathology is not directly correlated to the severity of the degeneration in different areas, implying that different populations of neurones respond to polyQ aggregation with varying efficacy and that protein aggregation outside the neuronal perikaryon (e.g. axonal aggregates) or other effects of polyQ aggregation, which are more difficult to visualize, may contribute to neurodegeneration.

Despite the fact that pilocytic astrocytoma showed a different vessel architecture compared with glioblastoma, a critical overlap in vessel immaturity/instability and the angiogenic profile was seen between both tumours. These findings suggest encouraging possibilities for targeting angiogenesis (for instance with anti-VEGF) as a therapeutic strategy in pilocytic astrocytoma.

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