Sensorimotor neuropathy

Chronic inflammatory demyelinating polyradiculopathy Mononeuritis multiplex Early pre-AIDS Subacute or chronic Sensorimotor neuropathy NCS show demyelinating features Immune dysfunction demyelinating neuropathy... 

DIES-associated neuropathy has a variety of chnical presentations, including painful symmetric or asymmetric sensorimotor neuropathy, distal sensory neuropathy, mononeuritis multiplex, and demyelinating polyneuropathy (Gherardi et al. 1998). Cranial neuropathy without evidence of a more generahzed neuropathy may occur, typically as a facial nerve palsy in association with parotidomegaly (Itescu et al. 1990 Brew 2003). The neuropathy develops subacutely over days to weeks. In some cases, muscle weakness may be a result of an inflammatory myositis (Kazi et al. 1996). 

Drowsiness dizziness sensorimotor neuropathy sleepiness paresthesia 1 12.7... 

Anti-CRMP5/CV2 CRMP5 Cytoplasm of oligodendrocytes Encephalomyelitis, cerebellar degeneration, LE, chorea, sensory neuronopathy, sensorimotor neuropathy, optic neuritis, gastrointestinal pseudo-obstruction SCLC, thymoma, gynecological tumors... 

Peterson K, Forsyth PA, Posner JB. Paraneoplastic sensorimotor neuropathy associated with breast cancer. J Neurooncol 1994 21 (2) 159—170. 

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... 

Repeated low-dose administration of OP compounds can produce symptoms and signs that are not seen after single exposures to the same doses. For example, subjects given dally injections of DFF reported the additional symptoms of insomnia, excessive dreaming, emotional lability. Increased libido, paresthesias, visual hallucinations, and tremor (90) and prolonged administration in animals induces sensorimotor neuropathy. 

In a slow acetylator, an axonal sensorimotor neuropathy could have been due to sulfasalazine (SEDA-17, 424). 

Symptoms suggestive of severe sensorimotor neuropathy developed in a 40-year-old woman 15 days after admission for a severe exacerbation of asthma (7). During this time she was given isoflurane 0.5-3% in oxygen, vecuronium bromide 4-6 mg/hour, and fentanyl 100 micrograms/hour. The neuropathy resolved spontaneously over the next 3 months. 

Nitrous oxide inactivates the enzyme methionine synthetase, and caution is urged in giving nitrous oxide to patients who may be deficient in vitamin B12. Low serum vitamin B12 concentrations have previously been reported in patients with sickle cell disease, but the reason for this is uncertain. Three cases of peripheral neuropathy have been reported in patients with sickle cell disease who received nitrous oxide (12-14). AU three had a history of frequent painful sickle crises, for which they received nitrous oxide for prolonged periods. Serum vitamin B12 concentrations were slightly reduced in two patients and very low in the third. The patients aU presented with difficulty in walking and paresthesia. Peripheral sensorimotor neuropathy was confirmed by nerve conduction studies. The patients all responded well to vitamin B12 injections and avoiding further exposure to nitrous oxide. Caution is therefore recommended when using nitrous oxide in patients with sickle cell disease or who are suspected of vitamin B12 deficiency. Two cases of polyneuropathy have also been reported after the use of nitrous oxide for 80 minutes and 3 hours in patients who were subsequently found to have pernicious anemia. They both responded well to hydroxocobalamin. 

The neurological health of painters has been extensively studied. Painters have been found to suffer from impaired behavioral effects, I86 87 93 sensory and sensorimotor neuropathies, t89l psychiatric function,I90,91,94 and learning and memory deficiency 92 problems. In the studies just cited, as well in many other similar ones, exposures were generally low level, occurring over a period of years, and exposures were to mixtures of lipophilic and hydrophilic chemicals. Other studies on exposures to single... 

Gagnaire, F., B. Marignac, and J. de Ceaurriz. 1990. Diethylbenzene-induced sensorimotor neuropathy in rats. J. Appl. Toxicol. 10(2) 105-112. 

Not only peripheral sensorimotor neuropathies are beneficially affected by the ACTH 4-9 analog Org 2766 but autonomic neuropathies, such as the crushed parasympathetic fibers of the oculomotor nerve are responsive to treatment with this neuropeptide, especially in the initial stages of regeneration. However, if the oculomotor nerve is sectioned, systemic treatment with Org 2766 improves neither the rate nor quality of functional recovery as determined by pupil diameter (Vandertop et al., 1994). 

A 22-year-old man developed a severe sensorimotor neuropathy following ingestion of podophyllin that had been prescribed for topical application for genital condylo-mata. The initial toxic symptoms were vomiting and diarrhea, followed by peripheral neuropathy. The neuropathy was still present 18 months later. Nerve conduction studies and sural nerve biopsy confirmed the presence of axonal degeneration (O Mahony et al. 1990). 

Indomethacin and chloroquine have been implicated in causing mild sensorimotor neuropathy as well as vascular myopathy. Peripheral neuropathy has been reported in patients treated with penicillamine, but less often than the myasthenic syndrome that develop in some patients treated with this drug. Paresthesiae and muscle weakness have been reported in some patients treated with phenylbutazone (Argov and Mastaglia 1979). In all these sydromes, little evidence exists that they are caused by allergic mechanisms. 

CT-2103 was administered as a 30-minute intravenous infusion once every 21 days starting at a dose of 11 mg/m paclitaxel-equivalent. The dose was doubled in each successive patient through doses of 22, 44, 89, and 176 mg/m. The dose was then increased by 50% to 266 mg/m, and 6 patients were enrolled at that dose. Two patients had dose-limiting toxicides at that dose. One patient with an unusual, abmpt onset sensorimotor neuropathy that was consistent with a paraneoplastic syndrome, and an uncomplicated neutropenia. A cohort of six patients was treated at the next lower dose of 233 mg/m. Two patients experienced uncomplicated grade 4 neutroperua lasting more than 5 days. Thus the MTD for heavily pre-treated patients lies... 

We recently identified a new peroxisomal disorder in two patients suffering from on adult-onset sensorimotor neuropathy [17]. The enzyme involved catalyzes the interconversion of (2R)- and-(2S)-stereoisomers of a-methyl-branched-chain fatty acids like pristanic acid, THCA and DHCA whereas this enzyme is not involved in VLCFA / -oxidation, which explains the accumulation of THCA, DHCA and pristanic acid but not C26 0 in these patients. The clinical picture has some resemblance to that of Refsum disease with sensorimotor neuropathy. 

Vignette 16. Chronic sensorimotor neuropathy and myelopathy, caused by vitamin B12 insufficiency or deficiency... 

Chronic sensorimotor neuropathy can result from vitamin B12 (cobalamin) deficiency, and can easily be treated by subcutaneous B12 injections (using insulin syringes with 31 needles). B12 deficiency or insufficiency can also cause myelopathy and cerebral involvement. 

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