Peripheral motor neuropathy

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. 

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... 

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... 

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. 

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. 

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. 

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). 

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). 

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. 

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

GSLs, because they are shed into the CSF, may be potential markers for brain pathology. In addition, shed GSLs or bacterial GSL structural mimics may also act as antigens in peripheral neuropathies like Guillain-Barre syndrome and multifocal motor neuropathy. 

No bone marrow depression. Autonomic, peripheral and motor neuropathy, injection site necrosis. IV. Hepatic metabolism, biliary excretion. Acute lymphocytic leukemia, Hodgkin s lymphoma, some solid tumors. Isolated from periwinkle plant. 

Peripheral motor neuropathy, affeoting mainly the upper extremities, oan cause severe extensor muscle weakness ( wrist drop ). 

Nervons system Most studies of albumin-bound paclitaxel have used a higher dose of paclitaxel than with Cremophor-based paclitaxel, and this has correlated with a higher incidence of peripheral neuropathy. In phase II studies, 11-38% of patients had grade 2 or worse sensory neuropathy [9T, 98, 998], In a phase II comparison of 3-weekly cycles of albumin-bound paclitaxel 260 mg/rr and conventional Cremophor-based paclitaxel 175 mg/rr, grade 3 peripheral neuropathy was reported in 10% versus 2% of cases [100 ]. Neuropathy typically occurs in a glove-and-stocking distribution, with symptoms of numbness or pain. Perioral numbness has also been reported [95 "]. No cases of motor neuropathy have been reported so far. 

Nervous system Peripheral neuropathy has been common in studies to date and in some cases has been the dose-limiting adverse reaction. Sensory neuropathy is most common, of grade 2 or greater intensity in about 45% of cases. However, motor neuropathy and autonomic neuropathy have also been reported [153, 1545, I55 156 ]. In some phase II studies, some patients already had... 

Peripheral motor neuropathy from toxicanis results in secondary muscle wasting. In veterinary medicine, triorlhocresyl phosphate-delayed rreuropathy, some forms otgamphosphate toxicosis, arsanilic acid toxicosis, and selenium toxicosis On swind result in peripheral denervation wHh resultant mrside atrophy. 

Peripheral neuropathy is degeneration of peripheral nerves. Because motor and sensory axons tun in the same nerves, usually both motor and sensory functions are affected in this disease. Neuropathies may be either acute (e.g., Charcot-Marie-Tooth disease) or chronic (e.g., Guillain-Barre syndrome) and are categorized as demyelinating or axonal. 

Peripheral neuropathy primary dose-limiting toxicity motor sensory, autonomic, and cranial nerves may all be affected (paresthesias, ileus, urinary retention, facial palsies) may be irreversible mild emetogen SIADH vesicant extravasation injury... 

Other diseases with disruptions in neurofilament organization include diabetic neuropathy and Charcot-Marie-Tooth disease. For these diseases, the disruption of neuro filaments may be a secondary effect as in the case of trembler axons or a direct effect. For example, some forms of Charcot-Marie-Tooth peripheral neuropathy result from mutations in a neurofilament subunit [22, 43]. In most cases, neuronal degeneration is an eventual consequence, but neuronal function may be impaired prior to substantial loss of neurons. Generally, disruptions of neurofilaments have the most severe consequences in large motor neurons, which is consistent with the fact that the largest neurons have the highest levels of neurofilament expression. 

IGF I has recently been the focus of considerable interest due to its actions on motor neurons. It can prevent normal motor neuron cell death during development, reduce the loss of these cells following nerve injury and enhance axonal regeneration. In the adult, injection of IGF I results in sprouting of motor neuron terminals and increases the size of the neuromuscular junction. These and other studies suggest potential therapeutic applications of IGF I in several neurological diseases including amyotrophic lateral sclerosis and peripheral neuropathies. 

Peripheral neuropathies maybe widely disseminated or focal. Patients with disseminated polyneuropathy, whether demyelinative or axonal, usually demonstrate distal sensory and/or motor impairment. Multifocal neuropathy, also referred to as mononeuropathy multiplex, is often a consequence of lesions affecting the vasa nervorum, the blood vessels that supply peripheral nerves. The most common diseases to compromise the vasa nervorum and cause infarction of nerve fascicles are diabetes mellitus and periarteritis nodosa. Other frequent causes of mononeuropathy multiplex include infection (e.g. Lyme disease and leprosy) and multiple compression injury (e.g. bilateral carpal tunnel syndrome). When mononeuropathy... 

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