Cytokine profile and glial activation following brachial plexus roots avulsion injury in mice.

Inflammation and tissue infiltration by various immune cells play a significant role in the pathogenesis of neurons suffering the central nervous systems diseases. Although brachial plexus root avulsion (BPRA) leads to dramatic motoneurons (MNs) death and permanent loss of function, however, the knowledge gap on cytokines and glial reaction in the spinal cord injury is still existing. The current study is sought to investigate the alteration of specific cytokine expression patterns of the BPRA injured spinal cord during an acute and subacute period. The cytokine assay, transmission electron microscopy, and histological staining were utilized to assess cytokine network alteration, ultrastructure morphology, and glial activation and MNs loss within two weeks post-injury on a mouse unilateral BPRA model. The BPRA injury caused a progressively spinal MNs loss, reduced the alpha-(α) MNs synaptic inputs, whereas enhanced glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor molecule-1 (IBA-1), F4/80 expression in ipsilateral but not the contralateral spinal segments. Additionally, cytokine assays revealed BPRA significantly altered the level of CXCL1, ICAM1, IP10, MCP-5, MIP1-α, and CD93. Notably, the elevated MIP1-α was mainly expressed in the injured spinal MNs. While the re-distribution of CD93 expression, from the cytoplasm to the nucleus, occasionally occurred at neurons of the ipsilateral spinal segment after injury. Overall, these findings suggest that the inflammatory cytokines associated with glial cell activation might contribute to the pathophysiology of the MNs death caused by nerve roots injury.

Fortuitous Diagnosis of Preexisting Neuropathy During Ultrasound-Guided Regional Anesthesia Performance: A Case Report.

Ultrasound-guided regional anesthesia requires the anesthesia provider to interpret new information. This article reports on the case of a 38-year-old man scheduled for a fifth metacarpal fracture repair. Ultrasound nerve examination revealed abnormal pathology of the axillary brachial plexus consisting of an increased volume of the terminal nerves of the brachial plexus. Ultrasound scanning initiated the subsequent diagnosis of multifocal motor neuropathy. Regional anesthesia was abandoned in favor of general anesthesia. Ultrasonography training needs to be expanded in the coming years to include awareness of the abnormal pathology, as it might impact the choice of anesthetic procedure and patient outcome.

The neuralgic amyotrophy consultation.

Neuralgic amyotrophy is a distinct clinical syndrome with acute severe pain and patchy paresis in the shoulder and arm region. The clinical phenotype was recently found to be more comprehensive and the long-term prognosis less optimistic than usually assumed for many patients. The disorder can be idiopathic or hereditary in an autosomal dominant fashion, with only few phenotypical variations between the two. This article provides a practical overview of current knowledge on the clinical presentation, diagnosis, pathogenesis and the treatment of pain and complications.

Paraneoplastic rhombencephalitis and brachial plexopathy in two cases of amphiphysin auto-immunity.

Amphiphysin, a synaptic vesicle protein, is an auto-immune target in rare cases of paraneoplastic neurological disorders. We report two additional cases with distinct neurological syndromes and paraneoplastic anti-amphiphysin antibodies. The first patient, a 59-year-old man, presented with cerebellar and cranial nerve dysfunction and small cell lung carcinoma. The second, a 77-year- old woman, presented with left brachial plexopathy followed by sensorimotor neuropathy and breast carcinoma.

Prostanoid receptor EP1 and Cox-2 in injured human nerves and a rat model of nerve injury: a time-course study.

BACKGROUND: Recent studies show that inflammatory processes may contribute to neuropathic pain. Cyclooxygenase-2 (Cox-2) is an inducible enzyme responsible for production of prostanoids, which may sensitise sensory neurones via the EP1 receptor. We have recently reported that while macrophages infiltrate injured nerves within days of injury, they express increased Cox-2-immunoreactivity (Cox-2-IR) from 2 to 3 weeks after injury. We have now investigated the time course of EP1 and Cox-2 changes in injured human nerves and dorsal root ganglia (DRG), and the chronic constriction nerve injury (CCI) model in the rat. METHODS: Tissue sections were immunostained with specific antibodies to EP1, Cox-2, CD68 (human macrophage marker) or OX42 (rat microglial marker), and neurofilaments (NF), prior to image analysis, from the following: human brachial plexus nerves (21 to 196 days post-injury), painful neuromas (9 days to 12 years post-injury), avulsion injured DRG, control nerves and DRG, and rat CCI model tissues. EP1 and NF-immunoreactive nerve fibres were quantified by image analysis. RESULTS: EP1:NF ratio was significantly increased in human brachial plexus nerve fibres, both proximal and distal to injury, in comparison with uninjured nerves. Sensory neurones in injured human DRG showed a significant acute increase of EP1-IR intensity. While there was a rapid increase in EP1-fibres and CD-68 positive macrophages, Cox-2 increase was apparent later, but was persistent in human painful neuromas for years. A similar time-course of changes was found in the rat CCI model with the above markers, both in the injured nerves and ipsilateral dorsal spinal cord. CONCLUSION: Different stages of infiltration and activation of macrophages may be observed in the peripheral and central nervous system following peripheral nerve injury. EP1 receptor level increase in sensory neurones, and macrophage infiltration, appears to precede increased Cox-2 expression by macrophages. However, other methods for detecting Cox-2 levels and activity are required. EP1 antagonists may show therapeutic effects in acute and chronic neuropathic pain, in addition to inflammatory pain.

Is IgG anti-GT1a antibody associated with pharyngeal-cervical-brachial weakness or oropharyngeal palsy in Guillain-Barré syndrome?

The pharyngeal-cervical-brachial variant (PCB) of Guillain-Barré syndrome (GBS) has clinical features similar to those of botulism and diphtheria. Mizoguchi et al. (1994) [Mizoguchi, K., Hase, A., Obi, T., Matsuoka, H., Takatsu, M., Nishimura, Y., Irie, F., Seyama, Y., Hirabayashi, Y., 1994. Two species of antiganglioside antibodies in a patient with a pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. J. Neurol. Neurosurg. Psychiatry 57, 1121-1123] reported a patient with PCB-like symptoms who had serum IgG anti-GT1a antibodies which did not cross-react with GQ1b. We assumed that PCB is associated with anti-GT1a antibodies that do not have reactivity to GQ1b and made a serological study of a PCB patient. We searched for PCB patients prospectively and found one with PCB. This patient had IgG anti-GT1a antibodies which were not absorbed with GQ1b in an absorption study, whereas IgG anti-GT1a antibodies from Fisher's syndrome patients were. The frequency of positive IgG anti-GT1a antibody did not differ in patients with and without bulbar palsy. Our findings indicate that IgG anti-GT1a antibodies which do not cross-react with GQ1b are specifically detectable in PCB and can be used as a diagnostic marker of PCB.

Blood lymphocytes are sensitized to branchial plexus nerves in patients with neuralgic amyotrophy.

The percentage of lymphocytic subsets in the blood of cases with neuralgic amyotrophy (NA), and the proliferative response of blood lymphocytes cultured with different nerve extracts, obtained from normal subjects at postmortem, were examined in 6 patients with NA and in 18 age-matched controls with shoulder pain not related to NA. Most (5/6) NA patients had decreased CD3 values and increased CD4/CD8 ratios due to a decreased of the CD8 subset. Lymphocytes of NA patients increased their blastogenic activity in cultures with nerve extracts from different brachial plexus nerves and its branches, but not in cultures with extracts of sacral plexus nerves. Cultures did not respond to nerve extracts in any of the control cases, although mitogenic activity was similarly elicited in cultured lymphocytes stimulated with phytohemagglutinin in both control cases and NA patients. These results suggest that NA is probably an immune mediated disease.

Immunocytochemical studies of human peripheral nerve with serum from patients with polyneuropathy and paraproteinemia.

Immunohistochemical binding of IgM paraproteins to nerve was studied using the immunoperoxidase technique with serum from 10 patients with benign plasma cell dyscrasia and neuropathy. We stained the myelin sheaths of peripheral nerves and roots fo five patients who had myelin-absorbable IgM paraproteins. Two patients with IgM paraproteins that did not react with myelin showed predominant staining of axons, while three were completely negative. Serum specimens from normal volunteers and patients with paraproteinemias or ALS were also unreactive. Immunocytochemical methods can detect IgM paraproteins with an affinity for nerve antigens and may assist in the diagnosis and classification of plasma cell dyscrasia associated neuropathy.