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cyanocobalamin/atrophy

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页 1 从 35 结果
OBJECTIVE A case of subacute combined degeneration (SCD) of the spinal cord manifesting as severe ataxia and urinary retention in a patient with a history of heavy nitrous oxide abuse and self-supplementation with cyanocobalamin is reported. CONCLUSIONS A 27-year-old woman was treated in the
BACKGROUND Observational epidemiologic studies indicate a direct association between homocysteine concentration in the blood and the risk of age-related macular degeneration (AMD), but randomized trial data to examine the effect of therapy to lower homocysteine levels in AMD are lacking. Our
Cyanocobalamin deficiency is not rare in India. Patients present with megaloblastic anemia, pancytopenia and sometimes neuropsychiatric manifestations. Subacute combined degeneration of the cord, peripheral neuropathy, dementia, psychotic depression and paranoid schizophrenia are well reported. We
Neuropathic pain after nerve injury is severe and intractable, and current drugs and nondrug therapies offer substantial pain relief to no more than half of affected patients. The present study investigated the analgesic roles of the B vitamins thiamine (B1), pyridoxine (B6) and cyanocobalamin (B12)
BACKGROUND Subacute combined degeneration of the spinal cord associated with vitamin B12 deficit is well known. However a paraneoplastic induced cyanocobalamin malabsorption responsible for either subacute combined degeneration of the spinal cord, has not been reported. Moreover, the possibility of
Central and peripheral nerve conduction was studied in two patients with subacute combined degeneration by using the short-latency somatosensory evoked potentials and the peripheral nerve conduction study during treatment with cyanocobalamin. Before the treatment, somatosensory evoked potentials
BACKGROUND Cyanocobalamin (vitamin B12) is an essential cofactor of various metabolic pathways. Lack of it leads to symptoms which may be constitutional, of skin or mucous membranes, hematological or neuropsychiatric disorders. Neurological involvement in adults has been well described and analyzed
Autosomal dominant hereditary spastic paraplegia (AD-HSP) is due to mutations in the "spastin" gene (SPAST gene) encoding the AAA protein. The main clinical features of "pure" HSP are progressive lower-limb spasticity with corticospinal tracts and dorsal column degeneration without peripheral

Coma and axonal degeneration in vitamin B12 deficiency.

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A 23-year-old woman with pernicious anemia, previously treated with folic acid, demonstrated an unusually rapid and severe course of neurologic deterioration. She was first seen with coma, myelopathy, and peripheral neuropathy. Her EEG showed repetitive nonperiodic suppression bursts, probably

Leber's hereditary optic atrophy.

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Leber described a particular type of hereditary optic atrophy in 1871. The clinical features of all cases since reported are reviewed. There is characteristically acute visual loss, circumpapillary teleangiectatic micropathy, tortuosity of the retinal vessels and oedema in the retinal nerve fibres.
BACKGROUND Subacute combined degeneration (SCD) of the spinal cord has been reported to have distinctive characteristics on magnetic resonance imaging (MRI), such as an "inverted V sign", a "pair of binoculars sign", and a "dot sign". We report a 3-point sign as a novel MRI characteristic, expanding

BACKGROUND
Nitrous oxide (N2O) is a commonly used inhaled anesthetic in outpatient dental procedures. However, the increasing recreational use of N2O may result in vitamin B12 deficiency-related neurologic and psychiatric symptoms. The aim of this
Vitamin B12 (cyanocobalamin) is an integral component of two biochemical reactions in man: the conversion of L-methylmalonyl coenzyme A into succinyl coenzyme A and the formation of methionine by methylation of homocysteine. The transmethylation reaction is essential to DNA synthesis and to the
A method employing non-radioactive vitamin B(12) and microbiological assay is described for estimating intrinsic factor in gastric juice and for detecting antibody to intrinsic factor in serum. Satisfactory agreement was obtained between the results by this method and by a modification of the method
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