Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0241981 (loss of balance)
 452 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A neurological disorder developed after prolonged exposure to nitrous oxide in 15 patients, all but 1 of whom were dentists. 13 patients had abused nitrous oxide to some extent for periods ranging from 3 months to several years, but 2 patients were exposed to nitrous oxide only professionally, by working in poorly ventilated surgeries. Symptoms included early sensory complaints, Lhermitte sign, loss of balance, leg weakness, gait ataxia, impotence, and sphincter disturbances. Neurological examination showed sensorimotor polyneuropathy, often combined with signs of involvement of the posterior and lateral columns of the spinal cord. Electrodiagnostic tests pointed to an axonal polyneuropathy, but other laboratory results were normal, including examination of the spinal fluid. The neurological picture is similar to that of subacute combined degeneration of the spinal cord, and it is possible that nitrous oxide interferes with the action of vitamin B12 in the nervous system.
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PMID:Myeloneuropathy after prolonged exposure to nitrous oxide. 8 36

Mefloquine is a quinoline derivative antimalarial which demonstrates promise for the treatment of schistosomiasis. Traditionally employed in prophylaxis and treatment of chloroquine-resistant Plasmodium falciparum malaria, recent changes to the approved European and U.S. product labeling for mefloquine now warn of a risk of permanent and irreversible neurological sequelae including vertigo, loss of balance and symptoms of polyneuropathy. The newly described permanent nature of certain of these neurological effects challenges the conventional belief that they are due merely to the long half-life of mefloquine and its continued presence in the body, and raises new considerations for the rational use of the drug against parasitic disease. In this opinion, it is proposed that many of the reported lasting adverse neurological effects of mefloquine are consistent with the chronic sequelae of a well characterized but idiosyncratic central nervous system (CNS) toxicity syndrome (or toxidrome) common to certain historical antimalarial and antiparasitic quinolines and associated with a risk of permanent neuronal degeneration within specific CNS regions including the brainstem. Issues in the development and licensing of mefloquine are then considered in the context of historical awareness of the idiosyncratic CNS toxicity of related quinoline drugs. It is anticipated that the information presented in this opinion will aid in the future clinical recognition of the mefloquine toxidrome and its chronic sequelae, and in informing improved regulatory evaluation of mefloquine and related quinoline drugs as they are explored for expanded antiparasitic use and for other indications.
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PMID:Idiosyncratic quinoline central nervous system toxicity: Historical insights into the chronic neurological sequelae of mefloquine. 2505 61

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease which involves multiple organs, including peripheral nervous system. Case presentation: We describe a 12-year-old boy with progressively worsening neurological symptoms as first manifestation. Legs pain, loss of balance, and lower extremity weakness were the reason for his admission in neurologic ward. The patient was started on intravenous immunoglobulin therapy due to the possibility of Guillain-Barre syndrome and acute inflammatory demyelinating polyneuropathy (AIDP). However, there was no appropriate response and he developed recurrent attacks of polyneuropathy again with diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). Then, he received intravenous pulse of methylprednisolone for 5 consecutive days followed by oral prednisolone for 3 months. One month after withdrawal of corticosteroid he admitted again with the same manifestations. Rheumatologic workup revealed the presence of leukopenia, hemolytic anemia, hematuria, proteinuria, positive antinuclear antibodies, and ds-DNA antibodies. On the basis of the American College of Rheumatology and Systemic Lupus International Collaborating Clinics Classification Criteria for SLE, the patient had underlying diagnosis of SLE. Eventually, he was treated by the pulse of methylprednisolone and cyclophosphamide, and oral hydroxychloroquine and prednisolone. His neurological and physical symptoms improved and complete neurological recovery occurred several months later. Conclusion: SLE and AIDP/CIDP are different entities, but ADP/CIDP can be part of the neurologic manifestations of the SLE. Although the association between AIDP/CIDP and SLE is very rare especially as a first manifestation of SLE, it should be early recognized for rapid appropriate treatment.
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PMID:Guillain-Barre syndrome as the first manifestation of juvenile systemic lupus erythematosus: a case report. 3111 4