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A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
Published on: November 9, 2017
[Autonomic dysfunction in acute inflammatory demyelinating polyneuropathy]
1Universitatea de Medicină şi Farmacie Gr.T. Popa Iaşi, Facultatea de Medicină, Disciplina de Neurologie.
Abstract:
Acute inflammatory demyelinating polyneuropathy (AIDP) is an autoimmune process that is characterized by progressive weakness, mild sensory changes and autonomic dysfunction. It is a rare disorder, afflicting about 1 person in 100,000. Yet, since the decline in the number of polio cases, it represents the most common cause of acute neuromuscular paralysis. AIDP is thought to arise as a result of the production of antibody to bacterial Campylobacter jejuni, sugar-containing surface antigen(s) that, due to molecular mimicry, cross-react with the myelin sheath and the axons of nerve cells. Antibody and/or cell mediated immune reactions are believed to produce degeneration of the nerve or interruption of neurotransmission. Autonomic dysfunction include: transient hypertension or, less often, hypotension, sinus tachycardia, bradycardia, urinary retention who usually improves in parallel with motor and sensory function. Our purpose was to study the disturbances of autonomic function of the patients with acute idiopathic demyelinating polyneuropathy. We had studied 36 patients with AIDP admitted in I-st Clinic of Neurology, Iassy, between 1998 and 2002. Analyzing the evolution of these autonomic disturbances we observed the early onset together with motor symptoms, tachycardia and tachypnea was more persistent and a real vital risk factor.
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