Neuromuscular dysfunction

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

Autoantibodies are directed against nicotinic acetylcholine receptors in myasthenia gravis, resulting in receptor loss, skeletal muscle paralysis, and dysfunction (100). In addition, antibodies directed against voltage-gated Ca " channels produce similar neuromuscular dysfunction of Lambert-Eaton... 

Barbara, G., Vallance, B.A. and Collins, S.M. (1997) Persistent intestinal neuromuscular dysfunction after acute nematode infection in mice. Gastroenterology 113,1224-1232. 

Johnson and colleagues have summarized the major toxicological observations made after administration of vinblastine or vincristine to other animals Ib). In rabbits and cats intravenous doses of 0.2 mg/kg vincristine were lethal after the second to the fifth dose on a schedule involving drug administration two to three times a week. Signs consistent with neurotoxicity were observed in rabbits and cats for example, a head drop phenomenon, characteristic of neuromuscular dysfunction, was observed in rabbits, and clonic convulsions were observed in cats. Vincristine is lethal to dogs when administered at 0.05 mg/kg, intravenously, five times in a 1-week period. Vincristine is lethal to monkeys when administered five times on a schedule of 1 mg/kg weekly comparable toxicity is observed when the drug is administered more frequently (daily) at lower doses (e.g., 0.2 g/kg). 

Vitamin E deficiency is normally associated with diseases of fat malabsorption and is rare in humans. Deficiency is characterized by erythrocyte haemolysis and prolonged deficiency can cause neuromuscular dysfunction. Hypervitaminosis E is not common, despite an increased intake of vitamin E supplements. Extremely high doses of the vitamin may interfere with the blood clotting process. 

Wecker, L., Laskowski, M.B., Dettham, W-D. (1978h). Neuromuscular dysfunction induced by acetylcholinesterase inhibition. Fed. Proc. 37 2818-22. 

Deficiency—may result in neuromuscular dysfunction. Excess—may result in hypertension and fluid retention. 

Uchitel OD, Scomik F, Proth DA, Fumberg CG, Alvarez V, Appel SH (1992) Long-term neuromuscular dysfunction produced by passive transfer of amyotrophic lateral sclerosis immunoglobulins. Neurology 42 2175-2180. 

Dc Wilde, V, Vogelaers, D Coiardyn, F., Van Den Neucker, K., Vanderstraeten, G Dc Bleecker, J, Dc Reuck, J, and Van Den Hcode, M. (1991), PosLsynaptic neuromuscular dysfunction in organopho.sphbte induced iniermediate. syndrome. Klin, Wockenxchr. 69, 177-183. 

Despite the relatively detailed understanding of iodine metabolism and the action of THs at the molecular level, their action on the human nervous system remains poorly understood. At the clinical interface, the neuromuscular manifestations of THs are quite common. Their incidence depends primarily on how extensively and rigorously the symptoms are sought. Overall, neuromuscular dysfunction occurs in 20—80% of cases (Aminoff, 2002). In hypothyroidism, it is as high as 79%, and in hyperthyroidism it is 67%. The predominant symptoms are sensorimotor axonal neuropathy in both extremes of thyroid dysfunction. Most of these resolve with treatment for the thyroid condition. Although not documented, most patients with thyroid disease often complain of neuromuscular-type symptoms. 

The neuromuscular dysfunction is a very interesting phenomenon in this enigmatic condition. This condition presents with a classical triad of marked hypokalemia, TTX and severe quadraparesis. Quadraparesis may involve any muscle group, including the bulbar muscles and infrequently the cranial nerves, but the lower limbs are the most affected. Although the condition is often not life-threatening,... 

Similar to TTX, thyroid underactivity can result in significant neuromuscular dysfunction, which is generally better appreciated by clinicians. The prevalence of neuromuscular disease in... 

Neuromuscular dysfunctions in thyroid disorders are more common than often thought, occurring in up to 70% of cases. 

In hyperthyroidism, the commonest neuromuscular dysfunction is proximal myopathy. 

The reason for this toxic reaction is not known but the authors of the report postulate a transient brain stem or neuromuscular dysfunction caused by both drugs. It is an uncommon reaction and reversible, so that concurrent use need not be avoided but both drugs should be stopped if it happens. The report cited here seems to be the only report of this interaction. 

As mentioned, GABA is an important neural transmitter and deficiencies in GABA are associated with diseases that exhibit neuromuscular dysfunction such as epilepsy, Huntington s disease and Parkinson s disease. S-Aminopentanoic acid (S-aminovaleric acid, DAVA) is also a neurotransmitter and used for treatment of neuromuscular disease. In at least one study, 3-alkyl-4-aminobutanoic acid derivatives were shown to be in vitro activators of f glutamic acid decarboxylase and they showed anti-convulsant activity. ... 

There have been numerous attempts to identify the anatomical changes underlying the neuromuscular dysfunction of clinical... 

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