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.

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.

Bilateral isolated phrenic neuropathy causing painless bilateral diaphragmatic paralysis.

The authors report four patients with a syndrome of painless bilateral isolated phrenic neuropathy. Electrophysiologic testing demonstrated active denervation restricted to the diaphragm. Long-term recovery was poor. The authors conclude that bilateral isolated phrenic neuropathy is a cause of painless diaphragmatic paralysis distinguishable from immune brachial plexus neuropathy and other neuromuscular disorders with similar clinical presentation.

Amyloidoma of the brachial plexus.

BACKGROUND: Amyloidomas of the peripheral nervous system are rare lesions. Most commonly, they involve the gasserian ganglion and the branches of the fifth cranial nerve. No association with systemic amyloidosis has been reported. CASE DESCRIPTION: We describe an amyloidoma of the lower trunk of the right brachial plexus. At the age of 34 years, this 71-year-old female had undergone radical right mastectomy for breast cancer with axillary lymph node dissection followed by radiotherapy. On admission, she presented with burning pain to the right hand and mild motor deficit to the ulnar-innervated intrinsic hand muscles. A palpable lesion was found in the supraclavicular region. On surgical inspection, the lesion appeared to originate from the lower trunk of the right brachial plexus. The middle and upper trunks were dislocated. Histologically, fibrous connective tissue embedded small nerve bundles featuring perineurial and endoneurial fibrosis as well as amyloid. Amyloid featured immunoreactivity for both lambda and kappa chains. DISCUSSION: Localized amyloidoma of brachial plexus has never been reported. Because of compressive rather than infiltrative growth of the present lesion, a conservative surgery was achieved. Our immunohistochemical findings indicated that peripheral nerve amyloidomas are not, by definition, monoclonal in nature.