{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T18:45:33Z","timestamp":1777920333378,"version":"3.51.4"},"reference-count":36,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[1988,1,1]],"date-time":"1988-01-01T00:00:00Z","timestamp":567993600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Vet Pathol"],"published-print":{"date-parts":[[1988,1]]},"abstract":"<jats:p>Chickens fed a riboflavin-deficient diet from hatching had leg weakness and paralysis as early as 12 days of age. Signs worsened through day 16; after 35 days, recovery was evident. Sciatic nerves from affected chickens were enlarged. Significant microscopic lesions were confined to peripheral nerves and included tissue separation (suggesting interstitial edema), Schwann cell swelling, perivascular leukocytic infiltration, and segmental demyelination accompanied by accumulation of osmiophilic debris in Schwann cell cytoplasm. Axon degeneration was present, but was not a primary lesion. Acid phosphatase enzyme activity of Schwann cells was increased in affected nerves. These results demonstrate that dietary riboflavin deficiency causes a demyelinating peripheral neuropathy in young, rapidly growing chickens.<\/jats:p>","DOI":"10.1177\/030098588802500102","type":"journal-article","created":{"date-parts":[[2010,1,26]],"date-time":"2010-01-26T17:39:07Z","timestamp":1264527547000},"page":"9-16","source":"Crossref","is-referenced-by-count":25,"title":["Peripheral Neuropathy Associated with Dietary Riboflavin Deficiency in the Chicken I. Light Microscopic Study"],"prefix":"10.1177","volume":"25","author":[{"given":"W. 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