Limb weakness

In severe cases, or those refractory to treatment, truncal and limb weakness may be accompanied by involvement of masticatory, bulbar, and respiratory muscles. However the most life-threatening clinical manifestations are those affecting the gastrointestinal tract, since stomach ulceration can occur and death from perforation and peritonitis are not unknown. Medication with steroidal antiinflammatory agents is necessary but weakens the childrens resistance to infection, so that systemic spread of usually self-limiting disorders, such as candidiasis, may occasionally occur. 

Primary hyperparathyroidism occurs as a result of hyperplasia or the occurrence of adenoma. Secondary hyperparathyroidism may result from renal failure because of the associated phosphate retention, resistance to the metabolic actions of PTH, or impaired vitamin D metabolism. The last-mentioned factor is primarily responsible for the development of osteomalacia. Muscle symptoms are much more common in patients with osteomalacia than in primary hyperparathyroidism. Muscle biopsy has revealed disseminated atrophy, sometimes confined to type 2 fibers, but in other cases involving both fiber types. Clinical features of osteomalacic myopathy are proximal limb weakness and associated bone pain the condition responds well to treatment with vitamin D. 

In humans, acute exposure to acrylonitrile results in characteristics of cyanide-type toxicity. Symptoms in humans associated with acrylonitrile poisoning include limb weakness, labored and irregular breathing, dizziness and impaired judgment, cyanosis, nausea, collapse, and convulsions (Baxter 1979). However, the doses that produce these effects were not clearly defined. Workers exposed to 16 to 100 ppm for 20 to 45 minutes complained of headaches and nausea, apprehension and nervous irritation (Wilson et al. 1948). The workers exposed to acrylonitrile vapors fully recovered. In a study with human volunteers exposed to acrylonitrile at doses of 2.3 and 4.6 ppm, no symptoms attributable to effects on the nervous system were observed (Jakubowski et al. 1987). 

Symptoms which have been associated with acrylonitrile poisoning in humans include limb weakness, labored and irregular breathing, dizziness and impaired judgment, cyanosis and nausea, collapse, and convulsions (Baxter 1979). Case studies of occupational exposure to acrylonitrile suggest that the acute nonlethal effects in humans may be fully reversible (Vogel and Kirkendall 1984 Wilson 1944 Wilson et al. 1948). 

Effects produced by exposure to acrylonitrile, particularly after acute exposures, are characteristic of cyanide toxicity. These effects can be detected in people exposed by evaluating signs and symptoms such as limb weakness, labored and irregular breathing, dizziness and impaired judgement, cyanosis and convulsions. While tests are not specific for acrylonitrile-induced toxicity, they do identify potential health impairment. Studies to develop more specific biomarkers of acrylonitrile-induced effects would be useful in assessing the potential health risk of acrylonitrile near hazardous waste sites. 

Short-chain 3-hydroxyacyl-CoA dehydrogenase deficiency has been described in three patients. It is associated with additional defects of (3-oxidation, which have been associated with limb weakness and attacks of myoglobinuria, and it is potentially fatal. 

Glutaric aciduria type II, which is a defect of P-oxida-tion, may affect muscle exclusively or in conjunction with other tissues. Glutaric aciduria type II, also termed multiple acyl-CoA dehydrogenase deficiency (Fig. 42-2), usually causes respiratory distress, hypoglycemia, hyperammonemia, systemic carnitine deficiency, nonketotic metabolic acidosis in the neonatal period and death within the first week. A few patients with onset in childhood or adult life showed lipid-storage myopathy, with weakness or premature fatigue [4]. Short-chain acyl-CoA deficiency (Fig. 42-2) was described in one woman with proximal limb weakness and exercise intolerance. Muscle biopsy showed marked accumulation of lipid droplets. Although... 

Motor neuron disease is characterized clinically by weakness, muscle atrophy and spasticity. This illness, often termed Lou Gehrig s disease in the United States, is the most common adult-onset form of MND with a prevalence of approximately 2-3 per 100,000 people [1-3,10, 25, 28]. Each year in the United States, in excess of 5,000 people are diagnosed with ALS. In parts of the United Kingdom, 1 in =500 deaths are attributed to some form of MND. The principal clinical signs of ALS include progressive limb weakness, which may be symmetrical or asymmetrical atrophy of appendicular, bulbar and respiratory muscles and spasticity [1,2,26,28]. The paralysis/muscle atrophy and spasticity are the result of degeneration of motor neurons in the spinal cord/brain stem and motor cortex respectively. The onset of this illness is typically in the fifth or sixth decade of life affected individuals usually... 

Rat 20 mg/kg diet After 7 days, decreased food intake after 3 to 4 weeks, hind limb weakness and some deaths on return to normal diet, signs of poisoning gone in 7 days with normal weight in 4 weeks 21... 

Dawley) 24 hr/d wadding gait, limb weakness, swollen axons, axonal degener ation) ... 

About 80% of MS patients have an episodic form of the disease called relapsing-remitting multiple sclerosis. An episode typically starts with sensory disturbances, limb weakness, and clumsiness symptoms evolve over several days, stabilize, and then often improve spontaneously or in response to corticosteroids. In the initial phase of the disease, relapses are generally followed by complete or nearly complete clinical recovery. However, persistent signs of CNS dysfunction may develop after a relapse, and the disease... 

An 87-year-old man developed progressive proximal limb weakness 1 year after starting leuprolide therapy for prostate cancer (60). Electromyography showed a moderately severe non-inflammatory myopathy without evidence of fiber necrosis or associated biochemical changes. Within 6 months after stopping leuprolide he was able to resume his usual activities. 

A TIA usually lasts less than 24 hours and there is full recovery of pre-TIA function. Symptoms may include facial or limb weakness, dysphagia and dysphasia as well as collapse. 

Thallium, atomic no. 81 This element is better known for its poisonous properties and links with almost undetected deaths and Agatha Christie -type murder mysteries.2 Thallium compounds are used in some countries as cheap insecticides, particularly for killing cockroaches. Intake of this element causes stomach pains, vomiting and nausea, painful soles and palms of hands, limb weakness, double vision, involuntary eye movements, hallucina tions, characteristic hair loss and white lines across the nails. The symptoms are often mis-diagnosed as other diseases. Treatment is with the chemical Prussian Blue... 

In most people the area of cerebral cortex associated with speech is located in the left cortex, so both the speech difficulties and the right limb weakness are consistent with damage to the left side of Grandpa s cerebral cortex. 

Phosphofructokinase deficiency (Tarui s disease) is an inborn error of glycogen metabolism characterised by a phosphofructokinase deficiency in the muscles, and associated with abnormal deposition of glycogen in muscle tissues, occasionally with myoglobinuria. The symptoms are similar to those seen in McArdle s disease. Classic Tarui s disease typically presents in childhood with exercise intolerance and anaemia. The fatal infantile variant presents in the first year of life. All reported patients have died by age four years. A late-onset variant manifests itself during later adulthood with progressive limb weakness without myoglobinuria or cramps. It is an autosomal recessive inheritance. Males are slightly more often affected than females. 

Limb weakness Epileptic seizures Fluid balance Electrolytes and urea Blood glucose Hematocrit... 

Neurotoxicity is the result of improper (careless) use, handling, and negligence in the management of chemical substances such as metals, food additives, pesticides, industrial solvents, cosmetics, radiation treatment, and drug therapies. Depending upon route and dose of exposure, the symptoms of neurotoxicity appear immediately after exposure or are delayed. The symptoms include limb weakness or numbness loss of memory, vision, and/or intellect headache cognitive and behavioral problems and sexual dysfunction. Children and workers with certain existing health disorders are more vulnerable to the adverse effects of neurotoxic chemicals. 

Nonocular muscle involvement is also prevalent, tanging from fluctuating dysarthria to dysphagia. Because of involvement of muscles that control breathing and swallowing, myasthenia is a potentially fetal condition. No specific pattern of limb weakness occurs, although the proximal muscles are most often affected. 

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