Examination of peripheral nerve injuries

2007 ◽  
Vol 163 (5) ◽  
pp. 619
Author(s):  
A. Echaniz-Laguna
1990 ◽  
Vol 9 (2) ◽  
pp. 331-342 ◽  
Author(s):  
Francis X. Mendoza ◽  
Kenneth Main

2011 ◽  
Vol 106 (5) ◽  
pp. 2450-2470 ◽  
Author(s):  
Francisco J. Alvarez ◽  
Haley E. Titus-Mitchell ◽  
Katie L. Bullinger ◽  
Michal Kraszpulski ◽  
Paul Nardelli ◽  
...  

Motor and sensory proprioceptive axons reinnervate muscles after peripheral nerve transections followed by microsurgical reattachment; nevertheless, motor coordination remains abnormal and stretch reflexes absent. We analyzed the possibility that permanent losses of central IA afferent synapses, as a consequence of peripheral nerve injury, are responsible for this deficit. VGLUT1 was used as a marker of proprioceptive synapses on rat motoneurons. After nerve injuries synapses are stripped from motoneurons, but while other excitatory and inhibitory inputs eventually recover, VGLUT1 synapses are permanently lost on the cell body (75–95% synaptic losses) and on the proximal 100 μm of dendrite (50% loss). Lost VGLUT1 synapses did not recover, even many months after muscle reinnervation. Interestingly, VGLUT1 density in more distal dendrites did not change. To investigate whether losses are due to VGLUT1 downregulation in injured IA afferents or to complete synaptic disassembly and regression of IA ventral projections, we studied the central trajectories and synaptic varicosities of axon collaterals from control and regenerated afferents with IA-like responses to stretch that were intracellularly filled with neurobiotin. VGLUT1 was present in all synaptic varicosities, identified with the synaptic marker SV2, of control and regenerated afferents. However, regenerated afferents lacked axon collaterals and synapses in lamina IX. In conjunction with the companion electrophysiological study [Bullinger KL, Nardelli P, Pinter MJ, Alvarez FJ, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01097.2010], we conclude that peripheral nerve injuries cause a permanent retraction of IA afferent synaptic varicosities from lamina IX and disconnection with motoneurons that is not recovered after peripheral regeneration and reinnervation of muscle by sensory and motor axons.


2014 ◽  
Vol 120 (5) ◽  
pp. 1105-1112 ◽  
Author(s):  
Selçuk Göçmen ◽  
Ali Kıvanç Topuz ◽  
Cem Atabey ◽  
Hakan Şimşek ◽  
Kenan Keklikçi ◽  
...  

Object Nerve compressions due to osteochondromas are extremely rare. The aim of this retrospective study was to investigate the mechanisms, diagnostic evaluations, and treatment of nerve lesions due to osteochondromas, and to review the literature. Methods The authors retrospectively reviewed their clinic data archive from 1998 through 2008, and 20 patients who were operated on due to peripheral nerve injuries caused by osseous growth were enrolled in the study. Patients' age, duration of symptoms, localizations, intraoperative findings, and modified British Medical Research Council (MRC) and electromyography data obtained from hospital records were evaluated. The literature on this topic available in PubMed was also reviewed. All 20 patients underwent surgery, which consisted of tumor excision performed by orthopedic surgeons and nerve decompression performed by neurosurgeons. Results There were 17 men and 3 women included in the study, with a mean age of 21 years (range 18–25 years). Three patients had multiple hereditary exostoses, and 17 had a solitary exostosis. All of the patients underwent en bloc resection. The most common lesion site was the distal femur (45%). The peroneal and posterior tibial nerves were the structures that were affected the most frequently. The mean follow-up was 3.9 years (range 2–7 years). After the surgery, all patients (100%) experienced good sensory recovery (modified MRC Grade S4 or S5). Conclusions To the authors' knowledge, no large series have reported peripheral nerve compression due to exostoses. The authors have several recommendations as a result of their findings. First, all patients with peripheral nerve compression due to an osteochondroma should undergo surgery. Second, preoperative electromyographic examinations and radiographic evaluation, consisting of MRI and CT to provide optimal information about the lesion, are crucially important. Third, immediate treatment is mandatory to regain the best possible recovery. And fourth, performing nerve decompression first and en bloc resection of osteochondroma consecutively in a multidisciplinary fashion is strongly recommended to avoid peripheral nerve injury.


2016 ◽  
Vol 51 (1) ◽  
pp. 63-69
Author(s):  
Samuel Ribak ◽  
Paulo Roberto Ferreira da Silva Filho ◽  
Alexandre Tietzmann ◽  
Helton Hiroshi Hirata ◽  
Carlos Augusto de Mattos ◽  
...  

1997 ◽  
Vol 24 (6) ◽  
pp. 385-408 ◽  
Author(s):  
Joseph H. Feinberg ◽  
Scott F. Nadler ◽  
Lisa S. Krivickas

1993 ◽  
Vol 16 (2) ◽  
pp. 130-147 ◽  
Author(s):  
Matthew P. Lorei ◽  
Elliott B. Hershman

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