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Obstetrical brachial plexus palsy occurs at a frequency of 0.6 to 2.5 per 1000 births. 80 to 95% of these lesions recover spontaneously. If spontaneous recovery does not occur within the first six months of life, investigations like electrophysiology, and CT-myelography and surgical exploration of the brachial plexus are recommended. During the last ten years 73 children with obstetrical brachial plexus lesions were examined in our department. 29 newborns underwent surgery on the brachial plexus. In 20 out of 29 children nerve root avulsions were diagnosed preoperatively. We performed in 16 cases nerve grafting after neuroma excision, in four cases nerve grafting combined with neurotization, in seven cases external or internal neurolysis, and in the remaining two cases neurotization and plexo-plexal transfer, respectively. The children were followed up between 18 and 50 months (range 27 months) in 18 cases. Elbow function according to Gilbert scale achieved one half of the patients four to five points and the other half two to three points. We found shoulder function with abduction between 45 degrees to 128 degrees and external rotation in 61% (Grade II to V, according to Gilbert scale). In 31% hand function showed Grade III and IV (Gilbert and Raimondi scale). We recommend decision for surgery at the age of six months. Operation should be planned between six to nine months of life. In addition, physical therapy and options including muscle transfers and orthopaedic procedures must be available to ensure the optimal outcome for these children.

Object: Severe nerve injury induces the formation of a neuroma. Some neuromas cause excruciating pain. Overexpression of Na+ channels leads to hyperexcitability and painful phenomena. Ankyrin G, a multifunctional transmembrane protein of the axolemma, might be a key protein in neuroma formation because it binds Na+ channels in the initial segments of a regenerating axon and links with neuronal cell adhesion molecules. The authors wanted to determine if ankyrin G could be detected in neuroma, and if present, whether there would be differences in distribution between nonpainful neuromas, painful neuromas, and normal nerve., Methods: First, frozen sections of nine nerve specimens obtained from six patients (six nonpainful neuromas, one painful neuroma, and two normal nerves) were immunocytochemically screened for ankyrin G by using confocal laser scanning microscopy. Second, specimens from 29 patients (seven painful neuromas, 15 nonpainful neuromas, and seven normal nerves) were examined using immunoblot analysis for their ankyrin G content. Western blot analysis detected ankyrin G, which was visualized by applying the enhanced chemiluminescence technique. Computerized densitometry was used to quantitate ankyrin G expression by comparing band intensities. Normal nerve served as control. Neurofilament was used as a marker for nerve tissue content. Ankyrin G could be detected and was found to be increased in neuromas. The mean band intensity values were 1838 for painful neuromas, 1166 for nonpainful neuromas, and 411 for normal nerves. In two cases the authors were able to compare specimens of painful neuroma and normal nerve from the same patient. The painful neuromas exhibited considerably higher levels of ankyrin G. Painful neuroma and normal nerve densitometry values were 499 and 165, respectively, for one patient, and 4254 and 821, respectively, for the other patient. Painful neuromas were also found to have higher neurofilament values than nonpainful neuromas., Conclusions: Altered regulation of ankyrin G after nerve injury may lead to hyperexcitability and painful phenomena via clustering of Na+ channels. A propensity to overexpress ankyrin G after peripheral nerve trauma may turn out to be a factor in the development of painful neuromas and neuropathic pain. The relevant literature regarding the importance of ankyrin G for nerve regeneration and nerve membrane remodeling is reviewed.

Background: The axolemmal distribution and density of voltage-gated sodium channels largely determines the electrical excitability of sprouting neurites. Recent evidence suggests that accumulation of sodium channels at injured axonal tips may be responsible for ectopic axonal hyperexcitability and the resulting abnormal sensory phenomena of pain and paresthesias. For future improvement in pain management it is necessary to identify structurally significant generators of autorhythmicity. A first step in this regard will be to determine the predominant types of sodium channels in injured axons. The opportunity to test human specimens from painful and non-painful neuroma is of great value., Methods: We employed immunocytochemical methods to investigate if two types of highly specific voltage-gated sodium channel subtypes could be detected in sections of human neuroma., Findings: Both subtypes of sodium channels PN1 and PN3 accumulated abnormally in human neuromas. The immunoreactive pattern was more pronounced in painful neuromas. This is in contrast to previous reports that focused either on PN1 or PN3 as main generators of hyperexcitability induced pain., Interpretation: Both, PN1 and PN3 seem to be involved in hyperexcitability induced pain. It can be expected that a variety of other highly specific voltage gated sodium channel subtypes will be detected in regenerating peripheral nerve in the near future, which contribute to the development of neuropathic pain states. Thus, in order to therapeutically control hyperexcitability induced neuropathic pain, it might be worthwhile to develop pharmaceuticals that can selectively block different sodium channel subtypes and subunits.A review of the role of sodium channels in neuropathic pain is implemented in the discussion.

We tested if ankyrin G could be detected in human neuroma, if it colocalized with site-specific peripheral nerve sodium channels that accumulate at axon tips of injured nerve, and if there are differences in the distribution of these proteins in non-painful neuroma and painful neuroma tissue vs. normal nerve. Frozen sections from one painful, six non-painful, and three normal nerves were immunocytochemically examined. A double labeling technique with highly specific antibodies against peripheral nerve type 1 (Na(v)1.7), and peripheral nerve type 3 (Na(v)1.8) sodium channels and anti-ankyrin G antibodies detected sodium channels and ankyrin G on the same section, using confocal laser scanning microscopy. Ankyrin G colocalized with both types of sodium channels. Neuroma specimens exhibited considerably larger immunofluorescence for both sodium channels and ankyrin G compared with normal nerve. The painful neuroma presented an even more pronounced immunolabeling in clusters. Findings support results from animal models that link ankyrin G with clustering of sodium channels at axon tips of unmyelinated, sprouting fibers. A common (repair-) mechanism that exists throughout the human nervous system for clustering sodium channels at a high density is assumed. A dysregulation in this membrane remodeling mechanism might be an initial step in a cascade that leads to a painful rather than a non-painful neuroma.

Object: The purpose of this study was to discover the number and types of iatrogenic nerve injuries that were surgically treated during a 9-year period at a relatively busy nerve center. The specific nerves involved, their sites of injury, and the mechanisms of injury were also documented., Methods: The authors retrospectively evaluated the surgically treated iatrogenic lesions by reviewing case histories, operative reports, and follow-up notes in 722 cases of trauma. These cases were treated between January 1990 and December 1998 because of pain, dysesthesias, and sensory and/or motor deficits. latrogenic injury was a much larger category of trauma than predicted. One hundred twenty-six (17.4%) of the 722 surgically treated cases were iatrogenic in origin. Most of these injuries occurred during a previous operation. To a major extent, nerves of the extremities were affected, and a relatively large number of injuries occurred in the neck and groin. Incidence was highest in the spinal accessory nerve (14 cases), the common peroneal nerve (11 cases), the superficial radial nerve (10 cases), the genitofemoral nerve branches (10 cases), and the median nerve (nine cases). At least two thirds of the patients did not undergo surgery for the iatrogenic injury within an optimal time interval due to delayed referral. Follow-up data were available in 97 of the 126 patients. Surgical outcomes demonstrated improvement in 70% of patients. Operative results were especially favorable in patients suffering from iatrogenic injuries to the accessory and superficial sensory radial nerves., Conclusions: latrogenic injuries should be corrected in a timely fashion just like any other traumatic injury to nerve.