Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.
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PMID:[Folate and the nervous system (author's transl)]. 22 16

Severe neurological complications (either peripheral neuropathy, subacute combined degeneration of the cord or cerebral changes) are a characteristic feature in some patients with marked vitamin B12 deficiency. Although Addisonian pernicious anaemia (PA) is the major cause of this neurological syndrome, the disorder has been described in association with other conditions in which there is a profound depletion of vitamin B12 stores. Sixteen patients with vitamin B12 neuromyelopathy, associated with PA, have been HLA-typed for 27 alleles of the A and B loci and compared with 53 cases of PA without neurological damage and 60 controls of the same ethnic group. There is a significantly increased frequency of the HLA phenotype. A12;B12 (44% instead of 4% in PA patients without neurological damage) in the disease group studied (P less than 0.0005). The signficance of these findings in relation to the pathogenesis of vitamin B12 neuromyelopathy is discussed.
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PMID:HLA phenotype A2;B12 in vitamin B12 neuromyelopathy. 86 92

In the 1990s, HIV has replaced syphilis as the "great masquerader." Virtually every level of the neuraxis may be affected in a patient with HIV infection. The superimposition of multiple levels of neuropathology further complicate the bedside neurologic diagnosis of an AIDS patient. This article has reviewed the variety of forms of peripheral neuropathy that may be associated with HIV infection and its treatment. Distal symmetrical polyneuropathy may be produced in patients with HIV infection by neurotoxic drugs (e.g., vincristine, INH, ddC, or ddI) or by vitamin B12 deficiency or may develop in the later stages of HIV infection without identifiable cause. GBS and CIDP occur with increased frequency in early HIV infection owing to presumed autoimmunity, and these IDPs respond to plasmapheresis or prednisone, similar to HIV-seronegative patients. A limited distribution of mononeuropathy simplex or multiplex occurs in patients with CD4 counts greater than 200; the neuropathy will usually spontaneously improve in these patients. Widespread mononeuropathy multiplex may occur in patients with AIDS and CD4 counts less than 50 and is then usually caused by CMV infections; those neuropathies are usually progressive unless antiviral treatment is given. Progressive polyradiculopathy usually occurs in patients with AIDS and low CD4 counts. If the cerebrospinal fluid has a polymorphonuclear pleocytosis, CMV infection is almost always present, and progression is expected unless ganciclovir therapy is promptly started. Finally, mild autonomic neuropathy is commonly present in HIV-infected patients. Protocols for the evaluation and therapy of cranial and peripheral neuropathies are presented (Figs. 6 and 7). It is unfortunate but likely that increasing numbers of "neuro-AIDS" patients will be encountered, not only in urban medical centers but also in general community practice. The pace at which research in the field of HIV research has proceeded is unprecedented. It is, therefore, important that neurologists stay at the forefront of investigation and clinical care of these complex disorders.
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PMID:Peripheral neuropathies associated with human immunodeficiency virus infection. 132 49

The case of a 59-year-old Japanese woman with post-gastrectomy megaloblastic anaemia having urinary and faecal incontinence and paraesthesia in four extremities is described. While the haematological abnormalities were improved by administration of a total dose of 17 mg of intramuscular mecobalamin, the neurological abnormalities remained unchanged. Five months later, a total dose of 7.5 mg of mecobalamin was injected intravenously over a period of 5 weeks, although the serum level of vitamin B12 was greater than 1180 pmol l-1. Immediately after initiation of the therapy, the urinary and faecal incontinence were gradually improved, and were completely cured within 2 months. The peripheral neuropathy was also ameliorated. The effectiveness of intravenous vitamin B12 injection for the neurological abnormalities due to vitamin B12 deficiency is emphasized.
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PMID:Complete cure of urinary and faecal incontinence after intravenous vitamin B12 therapy in a patient with post-gastrectomy megaloblastic anaemia. 155 28

An increased prevalence of vitamin B12 deficiency has been reported in patients infected by the human immunodeficiency virus (HIV). We report an unexpectedly high prevalence (20%) of such abnormal vitamin B12 metabolism in a population of HIV-infected patients referred for neurological evaluation. This abnormality was associated with both peripheral neuropathy and myelopathy. A majority of those treated with cyanocobalamin had a therapeutic response. Selected neuropathological results suggest a relationship between vitamin B12 deficiency and vacuolar myelopathy. Vitamin B12 deficiency may be a frequent and treatable cause of neurological dysfunction in patients with HIV infection.
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PMID:Abnormal vitamin B12 metabolism in human immunodeficiency virus infection. Association with neurological dysfunction. 184 71

The association of Crohn's disease and peripheral neuropathy is a rare event and the pathogenic factors often implicated are vitamin B12 deficiency or metronidazole treatment. We report a case of severe axonal polyneuropathy associated with Crohn's disease and unrelated to vitamin deficiency or metronidazole treatment. This represents a very rare extra-digestive manifestation of Crohn's disease.
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PMID:[Colonic Crohn's disease complicated with peripheral neuropathy]. 212 51

We report on 7 patients suffering from chronic renal failure (2 females, 5 males; aged 35-75 (phi 53.5) years) who showed severe neuromyeloencephalopathy (NME) after high doses of a new Henle's loop diuretic, Muzolimine. The temporal and phenomenological development of these systems was strikingly parallel. The neurological deficit was revealed on neurophysiological, neuroradiological and in 2 cases on neuropathological tests (gross demyelinisation of the posterior column, mainly of the fasciculus gracilis, less in the lateral corticospinal tract and in some spinal roots). The critical drug dose for first neurological impairment was 52 g on average; at this point the patients had been treated for 78 days. The maximal daily dose was 1.440 mg. Dominant clinical features were pallhypaesthesia, ataxia, signs of peripheral neuropathy in combination with hyperreflexia and progressive para- to tetraspastic paresis. Constellation of symptoms, course of disease and findings of additional investigations, especially those of neuropathology, very much resemble Vitamin B12 deficiency and SMON-(Subacute Myelo Optic Neuropathy) syndrome. The rare entity of Muzolimine-NME is discussed in respect to other endogenous and exotoxic neuromyelopathies. We present the hypothesis of a toxic, partially dialysable metabolite of Muzolimine.
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PMID:[Neuromyeloencephalopathy caused by high-dose muzolimine medication in patients with renal failure]. 215 46

Somatosensory evoked potentials (SEPs) following median nerve stimulation were abnormal in 7 patients with sensory impairment due to vitamin B12 deficiency. Extensor plantar reflexes indicated a central sensory pathway lesion in 4 cases and absent tendon jerks suggested peripheral neuropathy in 4, but median nerve SEPs indicated a predominantly central lesion without marked peripheral nerve involvement in 6 and an axonal neuropathy without CNS involvement in 1. The latter had evidence of central slowing of conduction in SEPs following posterior tibial nerve stimulation. Consequently, it is suggested that the brunt of sensory pathway involvement usually falls on the CNS, although peripheral neuropathy may occur as the major abnormality in some cases. In 2 patients SEPs showed a marked improvement following treatment with vitamin B12 injections, one consistent with restored central conduction and the other with recovery from peripheral neuropathy. No peripheral or central SEP abnormalities were seen in 18 dairy-produce eating vegetarians with low vitamin B12 levels, although 6 reported mild sensory symptoms suggestive of peripheral neuropathy and 3 had corroborative clinical signs.
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PMID:Central and peripheral SEP defects in neurologically symptomatic and asymptomatic subjects with low vitamin B12 levels. 283 10

In five patients with peripheral neuropathy due to vitamin B12 deficiency, electrodiagnostic studies demonstrated severe reduction in sensory nerve conduction velocities compatible with a demyelinating disorder affecting sensory nerve fibres. It is suggested that in some patients lack of vitamin B12 may cause primary sensory demyelinating neuropathy.
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PMID:Sensory peripheral neuropathy of vitamin B12 deficiency: a primary demyelinating disease? 283 39

Peripheral neuropathy in Crohn's disease has been described, to date, only with vitamin B12 deficiency or as due to oral metronidazole treatment. We report the association of Crohn's disease and peripheral neuropathy in two patients in whom neither of these pathogenetic factors of nerve damage apply. The CSF of both was normal. Patient 1 has had Crohn's disease for 12 years with predominantly sensory distal neuropathy and recurrent course related to worsening and improvement of the enteritis. Patient 2 had Crohn's disease some years before symptoms of recurrent sensory loss in the feet. Axonal degeneration was the mechanism of nerve damage in both patients.
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PMID:Peripheral neuropathy associated with Crohn's disease. 303 9


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