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1/15. copper deficiency myelopathy.

    BACKGROUND: In humans, Menkes disease is the well-recognized neurological disorder due to inherited copper deficiency. Myelopathy due to acquired copper deficiency is not a well-recognized entity in humans, although myelopathy due to copper deficiency is well documented in some animal species. patients: We describe 3 patients who developed a progressive spastic-ataxic gait with proprioceptive deficits. All patients had a severe reduction in serum ceruloplasmin and copper levels. RESULTS: All patients had evidence of posterior column dysfunction clinically and on somatosensory evoked potential studies. Two had a signal change in the posterior column on magnetic resonance imaging of the spinal cord. CONCLUSION: patients presenting with otherwise unexplained myelopathies should have their serum ceruloplasmin level measured.
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2/15. Peripheral neuropathy due to thiamine deficiency after inappropriate diet and total gastrectomy.

    Peripheral polyneuropathy due to vitamin B1 deficiency was encountered after total gastrectomy for gastric signet cell carcinoma in a patient with a history of breast-conserving surgery for breast cancer. She had greatly reduced her intake of animal foods, believing that would be effective for the prevention of re-occurrence of cancer. Her daily intake of vitamin B1 was less than half of the usual daily requirement. patients with malignancy tend to adopt unusual diets, and proper advice about food intake is important for such patients, especially those with gastrectomy.
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3/15. Severe ataxia, myelopathy, and peripheral neuropathy due to acquired copper deficiency in a patient with history of gastrectomy.

    BACKGROUND: In animal studies, copper absorption has been demonstrated to occur in the proximal gut via duodenal enterocytes. Acquired copper deficiency is known as "swayback" in ruminant animals and Menkes' disease in humans. copper is an essential micronutrient necessary for the hematologic and neurologic systems. Acquired copper deficiency in humans has been described, causing a syndrome similar to the subacute combined degeneration of vitamin B(12) deficiency. methods: This is a single case report. Our patient developed a neurologic constellation of ataxia, myelopathy, and peripheral neuropathy similar to vitamin B(12) deficiency many years after gastrectomy for severe peptic ulcer disease. The patient was maintained for decades with enteral feedings via jejunostomy that provided the recommended dietary allowance (RDA) for copper. RESULTS: copper deficiency was suspected, identified, and treated. Over 3 months of follow-up, serum copper levels increased from 4 microg/dL to 20 microg/dL (70-150 microg/dL), and ceruloplasmin increased from 6 mg/dL to 8 mg/dL (14-58 mg/dL). During this short time of follow-up, the patient has had no further progression of his neurologic symptoms. CONCLUSIONS: ataxia and myelopathy secondary to acquired copper deficiency are rare complications of major gastric resection. This is quite similar to the syndrome of vitamin B(12) deficiency. Vitamin B(12) repletion does not improve symptoms. Bariatric procedures such as gastric bypass surgery result in a similar functional anatomy of the proximal gut and may place more patients at increased risk. Early recognition and therapy with oral or parenteral copper may lead to a decrease in both neurologic and hematologic consequences.
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4/15. Peripheral nerve changes induced by methyl n-butyl ketone and potentiation by methyl ethyl ketone.

    A study of the sequential morphological changes in the peripheral nerve induced by experimental inhalation exposure of methyl n-butyl ketone (MBK) revealed that the earliest change was an increase in the number of neurofilaments in the large myelinated nerve fibers. This change occurred prior to axonal swelling or myelin thinning. As the duration of exposure lengthened the number of neurofilaments gradually increased and ultimately produced axonal swelling with secondary thinning of the myelin sheath. This appears to be the pathogenesis of the "giant axonal" neuropathy. Another change observed early in this neuropathy was the presence of inpouchings of the myelin sheath, which also increased in number in parallel to the duration of exposure. A careful study of the sequential changes in the entire motor unit did not show a predilection for early morphological changes at the axon terminal. Abnormalities at the neuromuscular junction occurred only after a full spectrum of changes were seen in the main nerve trunk, nerve roots and intramuscular nerves. An important observation was the marked potentiation of peripheral neurotoxicity observed when animals were exposed to MBK in combination with methyl ethyl ketone (MEK) at a ratio of 1:5, MBK:MEK. The latter solvent showed no neurotoxic effect alone. This might help explain a recent outbreak of a polyneuropathy affecting many workers. One further observation was that the sural nerve of a patient with prolonged exposure to MBK showed changes similar to those induced experimentally.
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5/15. "giant axonal neuropathy" caused by industrial chemicals: neurofilamentous axonal masses in man.

    Symmetrical polyneuropathy developed in two patients after they had been in contact with acrylamide and methyl n-butyl ketone, respectively. In sural nerve biopsy material from both patients, electron microscopy showed frequent focal axonal swellings containing masses of neurofilaments. Some axons undergoing axonal degeneration also were seen. These morphologic features are identical to those produced in experimental animals after exposure to these chemicals and are similar to those found in n-hexane neuropathy and in the three reported cases of giant axonal neuropathy. sural nerve biopsy is an important diagnostic test in identifying cases of peripheral neuropathy caused by these chemicals.
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6/15. Control of pain by direct electrical stimulation of peripheral nerves.

    Our results after implanting electrodes around peripheral nerves in 69 patients over a 10 year period are only fair with but 17 individuals maintaining relief until death or until the present time. Thirteen others had weeks or months of temporary relief. A continuing use of transcutaneous and better still of percutaneous electrodes to guide the decision regarding implantation is almost certainly advisable. Intensive efforts in laboratory animal studies with models of chronic pain are needed to improve our understanding of exactly what we should be doing. Empirical sustained work with the individual patient is likely to improve the figures we have presented, even in our present state of ignorance.
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7/15. diabetes mellitus following rodenticide ingestion in man.

    Ketotic, insulin-requiring diabetes mellitus and a severe peripheral neuropathy developed in a previously healthy 25-year-old man several days after he attempted suicide with rat poison containing N-3-pyridylmethyl N'-p-nitrophenyl urea. Study of islet-cell function ten months after ingestion showed a reduced disappearance rate of intravenous glucose and depressed c-peptide response to intravenous glucose when compared with a normal control but no impairment of glucagon release after intravenous arginine stimulation. Nerve conduction studies demonstrated severe sensory and mild motor neuropathy. Quadriceps capillary basement membrane thickness was in the diabetic range. Because at least 15 similar occurrences have been reported to the manufacturer, this agent appears to be diabetogenic in man, probably causing beta-cell destruction. niacinamide, which can prevent glucose intolerance in both streptozocin- and alloxan-treated animals and prevents death in rats given this rodenticide, may be a useful antidote.
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8/15. Immunoreactive myelin basic protein in tumor cells associated with carcinomatous neuropathy.

    Tumors from two patients with carcinomatous neuropathy were studied with an immunohistochemical method using anti-myelin basic protein (anti-MBP) sera. In both cases, immunoreactive MBP was clearly demonstrated in some of the tumor cells, which were widely distributed either singly or, more often, in clusters. The staining intensity varied from cell to cell. An autoimmune mechanism to nervous elements has been suggested in the pathogenesis of carcinomatous neuropathy. MBP is known to be a highly specific and potent antigen that can induce allergic neuritis in animals. In one patient the progressively worsening neurologic condition rapidly improved after gastrectomy removed the carcinoma. It is possible that immunoreactive MBP in tumor cells may function as an "antigen" in the development of carcinomatous neuropathy.
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9/15. Childhood giant axonal neuropathy. Case report and review of the literature.

    giant axonal neuropathy (GAN) is a rare autosomal recessive childhood disorder characterized by a peripheral neuropathy and features of central nervous system involvement. Typically seen are distal axonal swellings filled with 8-10 nm in diameter neurofilaments in central and peripheral axons, and intermediate filament collections in several other cell types. Many neurotoxins produce a morphologically similar neuropathy in humans and experimental animals. Defective nerve fiber energy metabolism has been postulated as a cause in these toxic neuropathies. It is possible that GAN represents an inborn error of metabolism of enzyme-linked sulfhydryl containing proteins, resulting in impaired production of energy necessary for the normal organization of intermediate filaments.
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10/15. Filamentous axonopathy in disulfiram neuropathy.

    A 52-year-old female developed a sensorimotor polyneuropathy while on treatment with disulfiram. Electron microscopic examination of a sural nerve biopsy disclosed occasional axons distended by intermediate filaments. Identical changes can be induced in animals by carbon disulfide (CS2), a metabolite of disulfiram. Our findings suggest that disulfiram neurotoxicity is mediated by CS2 and is exerted on the distal axon.
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