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      Value of terminal latency index and sensory electrophysiology in idiopathic and diabetic chronic inflammatory demyelinating polyradiculoneuropathy

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          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.

          Abstract

          Objectives

          To evaluate sensory electrophysiology, terminal latency index (TLI), and treatment response in idiopathic and diabetic chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).

          Methods

          We performed a retrospective review of 147 patients with CIDP who underwent electrodiagnostic evaluation (January 2000–December 2015). Eighty-nine patients fulfilled electrophysiological criteria described by the Ad hoc Subcommittee of the American Academy of Neurology and Albers et al. Fifty-eight patients were divided into idiopathic (N = 40) and diabetic (N = 18) groups. These groups were compared for age, sex, cerebrospinal fluid protein, response to treatment, sensory response abnormalities, and TLI measurements using chi-square tests for binary and categorical variables and using t-tests and mixed-effects models for continuous variables.

          Results

          The difference in abnormal rates of sensory responses was significant for the sural nerve, with the idiopathic group having a lower rate than the diabetic group (80% vs. 100%, p < 0.001). No group differences in the TLI measurements were significant.

          Conclusions

          Sural sensory responses may have some value in differentiating idiopathic CIDP from diabetic CIDP. Larger prospective studies are needed to confirm our findings.

          Significance

          Our study suggests that abnormal sural sensory potentials may have some significance in differentiating idiopathic CIDP from diabetic CIDP.

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          Most cited references18

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

          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.

            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?

              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

                Contributors
                Journal
                Clin Neurophysiol Pract
                Clin Neurophysiol Pract
                Clinical Neurophysiology Practice
                Elsevier
                2467-981X
                09 September 2019
                2019
                09 September 2019
                : 4
                : 190-193
                Affiliations
                [a ]Department of Neurology, Henry Ford Health System, Detroit, MI, USA
                [b ]Wayne State University, School of Medicine, Detroit, MI, USA
                Author notes
                [* ]Corresponding author at: 2799 W Grand Blvd, Detroit, Michigan 48202, USA. amemon2@ 123456hfhs.org
                Article
                S2467-981X(19)30031-9
                10.1016/j.cnp.2019.08.002
                6920505
                2cfaa0c8-a887-47dc-8fca-05133d81d4e8
                © 2019 International Federation of Clinical Neurophysiology. Published by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 12 September 2018
                : 13 August 2019
                : 23 August 2019
                Categories
                Clinical and Research Article

                terminal latency index,sensory electrophysiology,cidp,nerve conduction study,sensory nerve action potential,myelin-associated glycoprotein

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