![]() Median, ulnar, radial, peroneal, peroneal superficial, tibial, and sural nerves were selected for evaluation (sensory nerve data are not shown). Surface electrodes were used to record the wave forms of fully relaxed muscles after stimulation. Lumbar puncture was performed under the informed consent of subjects, and cerebrospinal fluid (CSF) was quantitatively analyzed to determine albumin protein concentration.Īll subjects received a nerve conduction test by (Natus, CA, USA) in a quiet room with a temperature >20☌. ![]() Blood immunofixation electrophoresis was tested for subjects to meet the exclusion terms. A panel of various kinds of anti-gangliosidosis (GM1, GM2, GM3, GD1a, GD1b, GQ1b, GD1b) was used, and a positive result was determined by the visible band in the GM1 area. Gangliosidosis antibody examination was semiquantitative by blot and was fulfilled by the KingMed Diagnostics (Guangdong, China). Routine blood tests, liver and kidney function, blood electrolytes, thyroid function, vitamin B 12, folic acid, and blood glucose were evaluated to ensure that patients met the inclusion and exclusion criteria. Meticulous physical examinations were performed to determine the tendon reflex as well as other positive neurological signs. Detailed clinical history was investigated to collect disease duration and onset and to determine neurological manifestations of weakness, numbness, and atrophy. General information on gender, age, and height were recorded. The exclusion criteria were peripheral neuropathy family history alcohol abuse toxic and neurotoxic exposure tumor metabolic disorders including pathoglycemia (diabetic mellitus and impaired glucose tolerance) and paraproteinemia (monoclonal gamma-globulin related polyneuropathy). The LSS and CIDP diagnoses were based on the 2010 European Federation of Neurological Societies (EFNS)/Peripheral Nerve Society (PNS) guidelines on CIDP, and the MMN diagnosis was based on the 2010 EFNS/PNS guidelines on MMN. A total of 107 nerves of LSS subjects, 176 nerves of MMN subjects, and 110 nerves of CIDP-CB subjects were analyzed. Written informed consent for data and sample collection was obtained from the patients on admission.įifteen LSS subjects, 24 MMN subjects and 17 CIDP-CB subjects admitted to the Renji Hospital, Shanghai Jiaotong University School of Medicine from 2013 to 2017 were included in the study. This was a retrospective cross-sectional study performed under the principles of the Declaration of Helsinki and was approved by the Institutional Review Board of Renji Hospital, Shanghai Jiaotong University School of Medicine. Thus, in this study, by using many well-established electrophysiological indicators, for example, distal motor latency (DML), terminal latency index (TLI), F-wave latency, and nerve conduction velocity (NCV) as well as CB, we aimed to investigate the demyelinating distribution and selectivity of nerves and segments in patients with LSS, MMN, and CIDP with CB (CIDP-CB). This phenomenon has been observed in other neuropathies, but it has not been fully studied in focal demyelination by electrophysiology methods. Differing nerve involvement among demyelinating polyneuropathies was proposed in a morphological study, in which the authors suggested different demyelination distributions and selective vulnerability of nerves. Their limb onset selectivity is well known, although reciprocal differentiation is not efficient. Distinct from common peripheral neuropathies, the motor impairments in these focal neuropathies are clinically non-uniform, that is, non-length dependent and asymmetric. Multifocal motor neuropathy (MMN) and Lewis-Sumner syndrome (LSS) are the most representative chronic acquired focal neuropathies, while many of the classic chronic inflammatory demyelinating polyradiculoneuropathies (CIDPs) also present with CB. ![]() As a hallmark of peripheral nerve focal demyelination, conduction blocks (CBs) have been observed in both acquired and hereditary demyelinating neuropathies. The pathological features of peripheral nerve myelin lesions are known as diffuse and focal demyelination. ![]()
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