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Motor neuropathy

Vasculitic mononeuritis multiplex Multifocal motor neuropathy... [Pg.622]

Diabetes mellitus is the most common cause of peripheral neuropathy in the United States. Approximately half of all diabetics demonstrate evidences of neuropathy. The usual clinical pattern is that of a slowly progressive, mixed sensorimotor and autonomic polyneuropathy. More acute, asymmetrical motor neuropathies are also seen, usually affecting the lumbosacral plexus, particularly in older persons with type 2 (non-insulin-dependent) diabetes mellitus. Patients with diabetes mellitus are also prone to develop isolated palsies of cranial nerve III or VII, and there is a high incidence of asymptomatic focal demyelin-ation in the distal median nerve. [Pg.624]

Mutant Tbce mice. Progressive motor neuropathy (PMN), an autosomal recessive murine disease, manifests as weakness beginning within a few weeks of birth [14, 136]. These mice are homozygous for a Trp 524 Gly substitution of Tbce (tubulin-specific chaperone E), localized to mouse chromosome 13 [14]. Tbce mRNA is present in neurons in the spinal cord. Degenerative changes are conspicuous in motor axons, and ultrastructural studies of peripheral nerves of PMN mice disclose reduced numbers of microtubules in these axons. Mutations of the highly conserved Trp524 residue, which appears to influence... [Pg.737]

Anonymous. 1974. Solvent causes motor neuropathy in workers at clothing factory. J Am Med Assoc 229 247-248. [Pg.75]

Neuropathic disorders Administer with caution in individuals with peripheral motor neuropathic diseases (eg, amyotrophic lateral sclerosis, motor neuropathy) or neuromuscular junctional disorders (eg, myasthenia gravis, Lambert-Eaton syndrome). Patients with neuromuscular disorders may be at increased risk of clinically significant P.787... [Pg.1342]

Kennel P, Revah F, Bohme GA, et al (2000) Riluzole prolongs survival and delays muscle strength deterioration in mice with progressive motor neuropathy (pmn). J Neurol Sci 180 55-61... [Pg.293]

Tremors of the hands and sleep disturbances in the form of vivid dreams, nightmares, and insomnia have been reported in association with the use of amiodarone. Ataxia, staggering, and impaired walking have been noted. Peripheral sensory and motor neuropathy or severe proximal muscle weakness develops infrequently. Both neuropathic and myopathic changes are observed on biopsy. Neurological symptoms resolve or improve within several weeks of dosage reduction. [Pg.188]

Ferdinandusse S, Denis S, Clayton PT, Graham A, Rees JE, Allen JT, Mclean BN, Brown AY, Vreken P, Waterham HR, Wanders RJA (2000) Mutations in the gene encoding peroxisomal alpha-methylacyl-CoA racemase cause adult-onset sensory motor neuropathy. Nat Genet 24 188-191... [Pg.230]

Pentachlorophenol (PCP) has been used as an insecticide, a fungicide, defoliant, herbicide and wood preservative. As a street drug of abuse it is known as angel dust. PCP is a metabolic stimulant and has caused deaths from hypothermia. It can also produce peripheral motor neuropathies when absorbed via the skin. [Pg.325]

In Tg, motor neuropathy, hind limb Null, Tg-weakness T105M... [Pg.355]

Herbicides, or weed killers, may be classified as pesticide chemicals. They can kill plants on contact, or they can be translocated (i.e absorbed by one part of the plant and carried to other parts where they exert their primary toxic effect). Most commonly used herbicides have a low toxicity and have caused few adverse effects in users. Some herbicides pose more serious problems to the central nervous system (CNS) and can cause depression. The skin absorption of herbicides also may cause skin irritation, dermatitis, and photosensitization in addition to peripheral motor neuropathies. [Pg.157]

Tangier disease is a rare autosomal recessive disorder characterized by the near absence of plasma HDL and the storage of esterified cholesterol in foam cells in many tissues. Clinical features include enlarged orange-colored tonsils, splenomegaly and a relapsing sensory-motor neuropathy. The clincial aspects of Tangier disease have been reviewed elsewhere (H24, S10). [Pg.229]

Paterson, G., Wilson, G., Kennedy, P.G.E., Willison, H.J. Analysis of anti-GMi antibodies cloned from motor neuropathy patients demonstrates diverse variable region gene usage with extensive somatic mutation. J Immunol 155 (1995) 3049-3059. [Pg.238]

Polyneuropathy with both sensory and motor involvement is much more common among cancer patients than pure SN [83, 110, 111]. SCLC is the most common associated tumor, although other solid tumors may be found [112]. Sensory-motor neuropathy is a quite common paraneoplastic feature in patients with onconeural antibodies, especially Hu and CRMP-5 antibodies. The CRMP-5 antibody is particularly associated with SCLC and thymoma [30]. The CRMP-5 antibody binds to oligodendrocytes as well as to neurons in specific brain regions and the retina and Schwann cells of the peripheral nervous system. In accordance with this, the clinical characteristics are heterogeneous. Many patients exhibit mixed axonal and demye-linating sensory-motor neuropathy, optic neuritis, or cerebellar dysfynction [85, 113], as well as extrapyramidal symptoms (Chapter 5.3). [Pg.156]

In lymphoproliferative disease, sensory-motor neuropathy may be a result of diffuse malignant nerve infiltration or immune-mediated mechanisms [120], Syndromes similar to Guillain Barre syndrome sometimes occur among patients with lymphoproliferative disease, but in this group, it is uncertain whether cancer by itself favors the development of Guillain-Barre syndrome by suppressing immunosurveillance mechanisms [121]. [Pg.157]

Neurotoxic chemicals and motor neuropathy Chlorpyrifos, dichlorvos (DDVP), EPN, n-hexane, 2-hexanone, lead, lead chromate, lead II thiocyanate, leptophos, methamidophos, mipafox, omethoate, parathion, trichlor-fon, trichloronate, triorthocresyl phosphate Neurotoxic chemicals and sensorimotor neuropathy acrylamide, allyl chloride, arsenic and compounds, arsenic trichloride, calcium arsenate, carbon disulfide, dichloroacetylene, ethylene oxide, gallium arsenide, lead arsenate, mercuric chloride, mercuric nitrate, mercurous nitrate, mercury, nitrous oxide, phenyl arsine oxide, thallium and soluble compounds, thallous nitrate... [Pg.183]

CMT diseases are the most frequent hereditary sensory-motor neuropathies. They are distinguished from other types of genetic neuropathies, either purely motor, mainly distal and dysautonomous neuropathies which mainly alter sensory and sympathetic fibers of the peripheral nerves. We only deal here with CMT diseases and among the many genetic causes, those that give rise to primary demyelinating diseases of the peripheral nervous system (PNS). [Pg.544]

Ogino M, Orazio N, Latov N (1995) IgG anti-GMl antibodies ffom patients with acute motor neuropathy are predominantly of the IgGl and IgG3 subclasses. J Neuroimmunol 58 77-80. [Pg.279]

There have been reports of HIV-associated neuromuscular weakness, probably associated with symptomadc lacdc acidosis (Estanislao et al., 2004). Lethal cases have been reported in associadon with stavucUne. Usually the cases have occurred after several months of use of the mecUcadon and have been associated vith sensory motor neuropathy and elevated serum lactate levels. It is tempdng to include this concUdon as another manifestadon of mitochoncUial damage induced by NRTIs. [Pg.611]

Uncini A, Santoro M, Corbo M, Lugaresi A, Latov N (1993) Conduction abnormalities induced by sera of patients with multifocal motor neuropathy and anti-GMl antibodies. Muscle Nerve 16 610-615. [Pg.280]

Braun R, Arechalde A, French LE. Reversible ascending motor neuropathy as a side effect of systemic treatment with ciclosporine for nodular prurigo. Dermatology 1999 199(4) 372-3. [Pg.763]

Neuropathy has not been reported in patients with leprosy taking the usually recommended dosage of 100 mg/day. Isolated cases of dapsone-induced peripheral neuropathy, including motor and minor sensory defects, have been published (15,16). The clinical characteristics include a motor neuropathy affecting the extremities with onset within 5 years after the start of dapsone therapy in doses of over 300 mg/day. Complete recovery from the neuropathy almost always occurs after the dose is reduced or the drug is withdrawn. [Pg.1051]

Saqueton AC, Lorincz AL, Vick NA, Hamer RD. Dapsone and peripheral motor neuropathy. Arch Dermatol 1969 100(2) 214-7. [Pg.1052]


See other pages where Motor neuropathy is mentioned: [Pg.664]    [Pg.646]    [Pg.965]    [Pg.153]    [Pg.140]    [Pg.1230]    [Pg.232]    [Pg.360]    [Pg.1382]    [Pg.227]    [Pg.143]    [Pg.156]    [Pg.157]    [Pg.164]    [Pg.553]    [Pg.721]    [Pg.264]    [Pg.329]    [Pg.264]    [Pg.329]    [Pg.1719]   


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Acute Motor Axonal Neuropathy (AMAN)

Axonal motor neuropathy

Guillain-Barre syndrome acute motor axonal neuropathy

Hereditary motor and sensory neuropathy

Motor neuropathy, peripheral

Multifocal motor neuropathy

Multifocal motor neuropathy with conduction block

Neuropathy acute motor axonal

Neuropathy acute motor-sensory axonal

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