| 1. |
- Dahlin, Lars, et al.
(author)
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Compression of the lower trunk of the brachial plexus by a cervical rib in two adolescent girls : case reports and surgical treatment.
- 2009
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In: Journal of Brachial Plexus and Peripheral Nerve Injury. - : BioMed Central. - 1749-7221. ; 4, s. 14-
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Journal article (peer-reviewed)abstract
- Presence of a cervical rib in children is extremely rare, particularly when symptoms of compression of the lower trunk of the brachial plexus occur. We present two cases with such a condition, where two young girls, 11 and 16 years of age were treated by resection of the cervical rib after a supraclavicular exploration of the lower trunk of the brachial plexus. The procedure led to successful results, objectively verified with tests in a work simulator, at one year follow-up.
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| 2. |
- Saito, Harukazu, et al.
(author)
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Crossed over repair of the femoral sensory and motor branches influences N-CAM
- 2010
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In: NeuroReport. - 1473-558X. ; 21:12, s. 841-845
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Journal article (peer-reviewed)abstract
- N-CAM, expressed by non-myelinating Schwann cells, was investigated by immunohistochemistry in transected rat femoral nerves, which were repaired either using a straight or a crossed over technique. N-CAM staining covered 30 and 11% of the cross-sectional area of and motor branches, respectively, in uninjured nerves. After 3 days there was a transient smaller area of N-CAM staining following both the repairs. After a straight repair N-CAM area increased to the control values in both branches. In contrast, a crossed over repair resulted in a continuous increase of N-CAM in the motor branch, whereas the area in the sensory branch returned slowly to control values. N-CAM is influenced by an intentionally misdirected outgrowth of motor and sensory axons after nerve repair. NeuroReport 21:841-845 (C) 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
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| 3. |
- Saito, Harukazu, et al.
(author)
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Delayed nerve repair increases number of caspase 3 stained Schwann cells
- 2009
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In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 456:1, s. 30-33
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Journal article (peer-reviewed)abstract
- Caspase 3 staining in Schwann cells was investigated with immunohistochemistry, as a measure of Schwann cell apoptosis, after transection and immediate (day 0) or delayed rat sciatic nerve repair (30, 90 and 180 days post injury). Cleaved caspase 3 stained Schwann cells significantly increased at the site of lesion (SNL; median [IQR], 15.2 [7.0] %) and in the distal nerve segment (SND; 9.5 [3.6] %) 10 days after immediate repair. The number of cleaved caspase stained Schwann cells also increased significantly after delayed repair, irrespective of length of delay, at both locations (SNL: 22.0-27.1%; SND: 18.5-22.1%; p < 0.05). Some cleaved caspase 3 stained satellite cells were seen in dorsal root ganglia on the injured side, but no stained motor or sensory neurons were observed at any time-point. Delayed nerve repair is associated with more pronounced Schwann cell apoptosis which may explain impaired nerve regeneration after nerve injury and delayed repair. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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| 4. |
- Saito, Harukazu, et al.
(author)
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Expression of ATF3 and axonal outgrowth are impaired after delayed nerve repair
- 2008
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In: BMC Neuroscience. - : Springer Science and Business Media LLC. - 1471-2202. ; 9
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Journal article (peer-reviewed)abstract
- Background: A delay in surgical nerve repair results in impaired nerve function in humans, but mechanisms behind the weakened nerve regeneration are not known. Activating transcription factor 3 (ATF3) increases the intrinsic growth state of injured neurons early after injury, but the role of long-term changes and their relation to axonal outgrowth after a delayed nerve repair are not well understood. ATF3 expression was examined by immunohistochemistry in motor and sensory neurons and in Schwann cells in rat sciatic nerve and related to axonal outgrowth after transection and delayed nerve repair (repair 0, 30, 90 or 180 days post-injury). Expression of the neuronal cell adhesion molecule (NCAM), which is expressed in non-myelinating Schwann cells, was also examined. Results: The number of neurons and Schwann cells expressing ATF3 declined and the length of axonal outgrowth was impaired if the repair was delayed. The decline was more rapid in motor neurons than in sensory neurons and Schwann cells. Regeneration distances over time correlated to number of ATF3 stained neurons and Schwann cells. Many neurofilament stained axons grew along ATF3 stained Schwann cells. If nerve repair was delayed the majority of Schwann cells in the distal nerve segment stained for NCAM. Conclusion: Delayed nerve repair impairs nerve regeneration and length of axonal outgrowth correlates to ATF3 expression in both neurons and Schwann cells. Mainly non-myelinating Schwann cells (NCAM stained) are present in distal nerve segments after delayed nerve repair. These data provide a neurobiological basis for the poor outcomes associated with delayed nerve repair. Nerve trunks should, if possible, be promptly repaired.
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