Acute inflammatory demyelinating polyneuropathy
Acute demyelinating polyneuritis
PREFERRED PRACTICE PATTERN
A 25-year-old woman is brought into the emergency department (ED) after sinking to the ground during a volleyball match. Her teammate notes that she had been stumbling and was starting to have more difficulty with her serve for the past week. On arrival, she can no longer raise her legs and labors to adjust herself in bed. She has also begun to complain of shortness of breath. She denies fever but states that 3 weeks ago the entire team suffered from abdominal cramps and diarrhea after a championship cookout. The patient denies previous health problems. Her temperature is 36.6°C (98°F); heart rate, 50 beats/min; respiration rate, 26 breaths/min; and blood pressure, 90/60 mmHg. She can only keep her arms up against gravity for 5 seconds, and her hands are limp. She has slight movement of her legs with decreased sensation of pain and fine touch in her lower legs. Her reflexes are absent. She has no skin lesions. Her heart and lung examinations are unremarkable except for bradycardia and poor inspiratory effort. MRI of the brain and spine is normal.2
Postulated immunopathogenesis of GBS associated with Campylobacter jejuni infection. B cells recognize glycoconjugates on C. jejuni (Cj) (triangles) that cross-react with ganglioside present on Schwann cell surface and subjacent peripheral nerve myelin. Some B cells, activated via a T cell–independent mechanism, secrete primarily IgM (not shown). Other B cells (upper left side) are activated via a partially T cell–dependent route and secrete primarily IgG; T cell help is provided by CD4 cells activated locally by fragments of Cj proteins that are presented on the surface of antigen-presenting cells (APCs). A critical event in the development of GBS is the escape of activated B cells from Peyer patches into regional lymph nodes. Activated T cells probably also function to assist in opening of the blood-nerve barrier, facilitating penetration of pathogenic autoantibodies. The earliest changes in myelin (right) consist of edema between myelin lamellae and vesicular disruption (shown as circular blebs) of the outermost myelin layers. These effects are associated with activation of the C5b–C9 membrane attack complex and probably mediated by calcium entry; it is possible that the macrophage cytokine tumor necrosis factor (TNF) also participates in myelin damage. B, B cell; MHC II, class II major histocompatibility complex molecule; TCR, T cell receptor; A, axon; O, oligodendrocyte. (From Longo DL et al., eds. Harrison’s Principles of Internal Medicine. 18th ed. http://www.accessmedicine.com. Copyright © McGraw-Hill Education. All rights reserved.)
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