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NEUROLOGY 1976;26:905
© 1976 American Academy of Neurology

Neuropathology of experimental vitamin B12 deficiency in monkeys

D. P. AGAMANOLIS, M.D., E. M. CHESTER, M.D., M. VICTOR, M.D., J. A. KARK, M.D., J. D. HINES, M.D. and J. W. HARRIS, M.D.

From the departments of Pathology (Neuropathology), Medicine, Neurology and Hematology, Cleveland Metropolitan General Hospital, and Case Western Reserve University School of Medicine, Cleveland, Ohio.

We have produced severe vitamin B12 deficiency in rhesus monkeys by feeding them a defined experimental diet under controlled conditions. Five years after institution of the deficient diet, the morphology and counts of peripheral blood and bone marrow are normal. Gross visual impairment appeared in five of the monkeys between 33 and 45 months after the Institution of the vitamin B12 deficient diet. Subsequently, in three of the visually impaired animals, a gradually progressive spastic paralysis of their hind limbs developed. Autopsies of six deficient animals showed degeneration of the peripheral visual pathway in all and of white matter in the spinal cord in four. Degeneration of several cranial nerve roots was found in four monkeys and a mild diffuse degeneration of cerebral white matter in four. The lesions in all affected parts of the central nervous system were bilaterally symmetrical and were indistinguishable from those due to B12 deficiency in the human. No abnormalities were found in one B12 supplemented control animal.

Reprint requests should be addressed to Dr. D. P. Agamanolis, Cleveland Metropolitan General Hospital, Cleveland, OH 44109.

This study was supported by NIH Grant No. AM-00745.

Received for publication December 22, 1975.




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