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      The Value of Terminal Latency Index and Sensory Electrophysiology in Idiopathic and Diabetic Chronic Inflammatory Demyelinating Polyradiculoneuropathy

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          Abstract

          Highlights • CIDP and diabetes can be seen together. • It is difficult to diagnose CIDP in patients with diabetes. • Clinical presentation, nerve conduction studies, and spinal fluid analysis are the best approaches to diagnose CIDP even in patients with diabetes. • Terminal latency index and sensory electrophysiology may vary in idiopathic and diabetic CIDP cases. • Diagnosis of CIDP can be missed in patients with diabetes due to underlying or existing neuropathy.

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          Biology of the blood-nerve barrier and its alteration in immune mediated neuropathies.

          Takashi Kanda (2013)
          The blood-nerve barrier (BNB) is a dynamic and competent interface between the endoneurial microenvironment and the surrounding extracellular space or blood. It is localised at the innermost layer of the multilayered ensheathing perineurium and endoneurial microvessels, and is the key structure that controls the internal milieu of the peripheral nerve parenchyma. Since the endoneurial BNB is the point of entry for pathogenic T cells and various soluble factors, including cytokines, chemokines and immunoglobulins, understanding this structure is important to prevent and treat human immune mediated neuropathies such as Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal protein and skin changes) syndrome and a subset of diabetic neuropathy. However, compared with the blood-brain barrier, only limited knowledge has been accumulated regarding the function, cell biology and clinical significance of the BNB. This review describes the basic structure and functions of the endoneurial BNB, provides an update of the biology of the cells comprising the BNB, and highlights the pathology and pathomechanisms of BNB breakdown in immune mediated neuropathies. The human immortalised cell lines of BNB origin established in our laboratory will facilitate the future development of BNB research. Potential therapeutic strategies for immune mediated neuropathies manipulating the BNB are also discussed.
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            Chronic inflammatory polyradiculoneuropathy.

            David J. Dyck, J A Bastron, T R Groover … (1975)
            The diagnostic criteria, natural history, nerve conduction characteristics, pathology, laboratory features, and efficacy of corticosteroid treatment have been evaluated personally in 53 patients with chronic inflammatory polyradiculoneuropathy (CIP) who were followed up for an average of about 7.5 years. These were patients whose monophasic neurologic deficit had not crested by 6 months, patients with recurrences, and patients with a steady or stepwise progression. The typical features of CIP include absence of an associated disease, frequent history of preceding infection or receipt of foreign protein, and tendency to involve cranial, truncal, and proximal as well as distal limb structures and to have diffusely slow conduction velocity of peripheral nerves. The most marked slowing is often very proximal. The pathologic features include serous edema, mononuclear cell infiltrates (especially in perivascular areas, but without evidence of vasculitis), macrophage-induced segmental demyelination, and hypertrophic neuritis. If our patients are representative, complete recovery occurs only infrequently; about 60% of patients are able to be ambulatory and work, 25% become confined to a wheelchair or become bedridden, and approximately 10% die from their disease. Although the bulk of the pathologic changes affect spinal roots and proximal nerves, the brain and spinal cord may be involved also. Degeneration into linear rows of myelin ovoids is the predominant type of myelinated fiber degeneration of the sural nerve at the ankle.
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              Elevation of plasma 1-deoxy-sphingolipids in type 2 diabetes mellitus: a susceptibility to neuropathy?

              M F Dohrn, Adil A. Othman, S Hirshman … (2015)
              Diabetic distal sensorimotor polyneuropathy (DSPN) is a frequent, disabling complication of diabetes mellitus. There is increasing evidence that sphingolipids play a role in insulin resistance and type 2 diabetes (T2DM). Whether neurotoxic 1-deoxy-sphingolipids are elevated in DSPN patients' plasma and whether levels correlate to the DSPN stage were examined.
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                Author and article information

                Journal
                Title: Clinical Neurophysiology Practice
                Abbreviated Title: Clinical Neurophysiology Practice
                Publisher: Elsevier BV
                ISSN (Print): 2467981X
                Publication date Created: September 2019
                Publication date (Print): September 2019
                Article
                DOI: 10.1016/j.cnp.2019.08.002
                SO-VID: 2cfaa0c8-a887-47dc-8fca-05133d81d4e8
                Copyright © © 2019
                License:

                https://www.elsevier.com/tdm/userlicense/1.0/

                http://creativecommons.org/licenses/by-nc-nd/4.0/

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