barcode in c# windows application DISEASES OF THE NERVOUS SYSTEM DUE TO NUTRITIONAL DEFICIENCY in Microsoft Office

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DISEASES OF THE NERVOUS SYSTEM DUE TO NUTRITIONAL DEFICIENCY
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do not become anemic, despite the prolonged period of vitamin B12 de ciency Also, in distinction to the human condition, involvement of the optic nerves is particularly severe in the monkey and probably precedes the degeneration of the spinal cord The optic nerve lesions appear rst in the papillomacular bundles, in the retrobulbar portions of the nerves; it subsequently spreads beyond the con nes of this bundle and caudally in the optic nerves, chiasm, and tracts These changes are much the same as those of tobaccoalcohol amblyopia (see above) The peripheral nerves were not affected in the experimentally produced vitamin B12 de ciency The paresthesias, impairment of deep sensation, and ataxia are due to lesions in the posterior columns Weakness, spasticity, increased tendon re exes, and Babinski signs depend on involvement of the corticospinal tracts The spinothalamic tracts may rarely be involved in the pathologic process, which explains the occasional nding of a sensory level for pain and temperature on the trunk, as already noted The distal and symmetrical impairment of super cial sensation and loss of tendon re exes that occur in some patients are best explained by involvement of peripheral nerves and are re ected in nerve conduction studies (see further on, under Diagnosis ) Pathogenesis Methylcobalamin is an essential cofactor in the conversion of homocysteine to methionine An impairment of this reaction due to a de ciency of cobalamin is thought to cause a failure of DNA synthesis, accounting for the hematologic abnormalities and particularly for the production of megaloblasts However, since neurons do not divide, this sequence of chemical events does not explain the central nervous system abnormalities One of the better-understood functions of vitamin B12 is its role as a coenzyme in the methylmalonyl CoA mutase reaction In this reaction, which is a key step in propionate metabolism, methylmalonyl CoA is transformed to succinyl CoA, which subsequently enters the Krebs cycle A lack of the cobalamin-dependent enzyme methylmalonyl CoA mutase leads to the accumulation of methylmalonyl CoA and its precursor, propionyl CoA According to this theorized mechanism, propionyl CoA displaces succinyl CoA, which is the usual primer for the synthesis of even-chain fatty acids; this results in the anomalous insertion of odd-chain fatty acids into membrane lipids, such as are found in myelin sheaths Conceivably this biochemical abnormality underlies the lesions of myelinated bers that characterize the disease However, Carmel and associates have described a hereditary form of cobalamin de ciency in which methylmalonyl CoA mutase activity was normal, despite the presence of typical neurologic abnormalities In their view, the primary failure is one of methylation of homocysteine to methionine, ie, a failure of the methionine synthetase reaction, for which the coenzyme methylcobalamin is necessary Evidence for the latter view comes also from the observations, mentioned earlier, that prolonged administration of nitrous oxide (N2O) may produce not only megaloblastic changes in the marrow (Amess et al) but also a sensorimotor polyneuropathy, often combined with signs of involvement of the posterior and lateral columns of the spinal cord (Layzer) Probably N2O produces its effects by inactivating the methylcobalamin-dependent enzyme methionine synthetase These and other hypotheses are discussed by Jandl, Carmel and colleagues, and Beck The role of folate de ciency in the genesis of SCD is less certain One known clinical mistake has been to treat pernicious anemia by giving folic acid; this corrects the anemia but may worsen or even evoke the spinal cord lesions There are, neverthe-
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less, a few reported examples of cerebral and spinal cord lesions indistinguishable from those due to vitamin B12 de ciency in patients with defective folate metabolism both in adults with acquired de ciency (Pincus) and in children with an inborn metabolic error (Clayton et al) Diagnosis The main differential diagnostic considerations of the combined sensory and motor features are cervical spondylosis (page 1073), multiple sclerosis of the cervical cord (page 778), rarities such as the female carrier state of adrenoleukodystrophy (adrenomyeloneuropathy, page 836), and non-B12 de cient combined system disease (page 1078) The last of these refers to an obscure myelopathic process that affects the posterior and lateral columns subacutely but is unassociated with any form of B12 de ciency or related enzyme derangement Recent reports suggest that this process may be the result of an incompletely understood acquired type of copper de ciency It has been as frequent, in our cases, as the classic type due to B12 de ciency This entity is mentioned on page 1078 with other diseases of the spinal cord The chief obstacle to early diagnosis is the lack of parallelism that may exist between the hematologic and neurologic signs, occurring particularly in patients who have taken dietary or medicinal folate Anemia may also at times be absent, sometimes for many months, even in patients who have not taken folate In a retrospective study of 141 patients with neuropsychiatric abnormalities due to cobalamin de ciency, there were 19 patients in whom both the hematocrit and mean red blood cell volume were normal (Lindenbaum et al); in these patients, subtle morphologic abnormalities hypersegmented polymorphonuclear leukocytes and megaloblastosis in bone marrow smears were almost always found if carefully sought Laboratory Diagnosis Serum cobalamin should be measured whenever the diagnosis of vitamin B12 de ciency is in question Microbiologic assay (using Euglena gracilis) is the most accurate measurement, but the method is time-consuming and cumbersome and has been largely replaced by a commercial radioisotope dilution assay (the inexpensive chemiluminescence assay is an alternative but slightly less dependable) With the radioassay, a serum B12 level of less than 100 pg/mL is usually associated with neurologic symptoms and signs of vitamin B12 de ciency A level below 200 pg/mL that is unassociated with symptoms calls for further investigation of cobalamin de ciency However, even serum levels of 200 to 300 pg/mL may still be associated (in 5 to 10 percent of cases) with cobalamin de ciency High serum concentrations of cobalamin metabolites methylmalonic acid (normal range, 73 to 271 nmol/L) and homocysteine (normal range 54 to 162 mmol/ L) are probably the most reliable indicators of an intracellular cobalamin de ciency and can be used to corroborate the diagnosis (Allen et al; Lindenbaum et al) It must be emphasized that the serum cobalamin level is not a measure of total body cobalamin In a patient who stops absorbing ingested cobalamin, the serum levels may remain in the normal range for a long time despite decreasing tissue reserves In patients who have received vitamin B12 parenterally, the two-stage Schilling test is a more reliable indicator of cobalamin de ciency, since it uncovers a defect in absorption of the vitamin; however, the Schilling test has been supplanted for routine diagnosis by the measurement of antibodies to intrinsic factor and parietal cells Achlorhydria is almost invariably present in patients with pernicious anemia; its presence can be detected by measuring the se-
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