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Drugs and their interactions may contribute in part or fully to the neurological demyelination, and treatment response may assist diagnostically or in future management plans. Rarely, immune-mediated demyelinating neuropathies occur during initial or maintenance treatment with immunomodulatory, immunosuppressive or antineoplastic agents. Medication-induced immune perturbation presumably triggers a dysimmune attack directed at unidentified peripheral nerve myelin epitopes; true peripheral nerve toxicity (i.e., dependent on accumulative dose or serum level) plays no identified role. Biomechanics In Organs, Biofluid mechanics, Biotribology are the wings included in Pharmacological and Toxicological Sciences including subtopics Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoepidemiology, Clinical pharmacology, Immunology¸ and Cardiovascular pharmacology.
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Scope and Importance:
Chronic inflammatory demyelinating polyradiculoneuropathy (cidP) is a term for a group of acquired, immune-mediated inflammatory demyelinating disorders of the peripheral nervous system. Most patients with cidP respond to ‘first-line’ therapy with intravenous immunoglobulin (iViG), plasmapheresis and/or corticosteroids. ‘conventional’ immunosuppressive drugs are of no proven benefit. Biological agents directed at key aspects of the cidP immunopathogenic pathway have gained increasing attention due to the unpredictable efficacy and overall health risks of non-targeted immunosuppressive drugs. Presently, there exists insufficient clinical experience with biological therapy to allow specific treatment recommendations for cidP. The challenge remains to identify drug-naïve or treatment-resistant cidP patients who will most likely respond to targeted immunotherapy.
Drug-induced peripheral neurotoxicity usually manifests as a length-dependent, "dying back" axonal, predominantly sensory polyneuropathy. Rarely, immune-mediated demyelinating neuropathies occur during initial or maintenance treatment with immunomodulatory, immunosuppressive or antineoplastic agents. Medication-induced immune perturbation presumably triggers a dysimmune attack directed at unidentified peripheral nerve myelin epitopes; true peripheral nerve toxicity (i.e., dependent on accumulative dose or serum level) plays no identified role.
Several neuroimaging studies have revealed that the brains of schizophrenic patients exhibit abnormalities in white matter pathways. Using magnetic resonance imaging (MRI) methods, such as T2-weighted imaging and diffusion tensor imaging (DTI), it is possible to objectively quantify white matter structural properties in patients as well as the pharmacological effect on white matter. In the preclinical domain, these strategies, however, have been hindered by a lack of in vivo imaging assays. Mainly demyelination diseases are due to medications uncommonly prescribed not used in the U.S(perhexline,almitrine), normally used in low doses with minimal toxicity(phenytoin,ara-c), or typically used for short duration(metronidazole).A number of other factors render some individuals more vulnerable to potentially toxic medications.
The global market for treatments for syndromes of neurological disorders was valued at 10.5 billion in 2011 and should reach $11.1 billion in 2012. Total market value is expected to reach $16.7 billion in 2017 after increasing at a five-year compound annual growth rate (CAGR) of 8.5%.
The global sales of drugs to treat progressive dementia with other neurological abnormalities expected to reach $537.2 million in 2012 and $913.7 million by 2017, at a CAGR of 11.2% over the five-year forecast period.
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This page was last updated on 11th Sep, 2015
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