Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cas is reported of a 23-year-old man who voluntarily took a massive dose of arsenic (at least 8 g). In spite of the ingested amount and the acute nature of the poisoning, the patient survived 8 days. Gastrointestinal, neurologic and cardiac features were predominant including nausea, vomiting, choleroid diarrhoea, encephalopathy, peripheral neuropathy, and finally a fatal toxic cardiomyopathy. Metabolic acidosis, moderate cytolysis and an anticoagulant effect were also observed. This unique characteristic was partly due to a circulating anticoagulant with prothrombinase activity, as well as direct antivitamin K activity. Postmortem examination revealed: a congestive oesophagitis; a necrosing gastritis involving all the stomach wall; diffuse hepatic steatosis; skin lesions with vascular congestion and dermoepidermal detachment; discrete subepicardial congestive lesions. Arsenic was found in all tissues.
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PMID:[Subacute arsenic poisoning]. 185 59

We describe a man with essential mixed cryoglobulinemia who developed peripheral neuropathy and multiinfarctual encephalopathy. Vasculitis was observed in the vasa nervorum and in the small vessels of the brain. The possible pathogenetic role of the cryoglobulins in the nervous system lesions is discussed.
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PMID:Peripheral and central nervous system involvement in essential mixed cryoglobulinemia: a case report. 188 25

Physicians and surgeons have long recognized that septic illness may be accompanied by abnormal brain functions; however, no systematic, comprehensive study has been done to define the clinical and laboratory features of the syndrome of sepsis-associated encephalopathy. We undertook such a prospective study in a tertiary care hospital and found that of 69 patients with fever and microbial cultures, 32 had marked brain dysfunction, 17 showed mild encephalopathy, and 20 were clinically nonencephalopathic. Severe cases showed obtundation and paratonic rigidity while milder cases showed confusion, inappropriate behavior, inattention, disorientation, and writing errors. There were no focal neurological deficits. The following factors correlated with the severity of brain dysfunction: adult respiratory distress syndrome; fatal outcome; certain types of EEG abnormality; axonal peripheral neuropathy; elevated peripheral white blood cell count; elevated serum levels of alkaline phosphatase, bilirubin, creatinine, phosphate, potassium, and urea; reduced blood pressure and reduced serum albumin level. Our data suggest that brain functions fail with dysfunction of other organs in septic illness. Pathogenetic mechanisms are discussed. The brain dysfunction should be regarded as potentially reversible, even in severely encephalopathic cases. Prompt control of the infection is the most important measure in controlling the encephalopathy and in preventing the increased mortality found with severely encephalopathic patients.
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PMID:The encephalopathy associated with septic illness. 207 9

Treatment of lead intoxication with intravenous ethylene-diamine-tetra-acetic acid (EDTA) depends on the urinary excretion of chelated lead. This route of excretion was absent in a 48-year-old patient with childhood lead exposure and end stage renal failure who developed encephalopathy and a rapidly progressive neuropathy thought to be due to acute lead intoxication. Diagnosis was confirmed by lead chelation with EDTA and neurophysiological studies. EDTA was added by the patient to her chronic ambulatory peritoneal dialysis (CAPD) fluid each week and chelated lead excreted in the dialysate. Intraperitoneal administration of EDTA was 70% as efficient in removing lead as intravenous administration. Four months of home chelation therapy was associated with resolution of the encephalopathy but no improvement in the peripheral neuropathy.
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PMID:Lead intoxication in an anuric patient: management by intraperitoneal EDTA. 212 76

Neurological investigations were performed for 53 cases with chronic lymphocytic thyroiditis diagnosed by pathology and serum antithyroid antibodies determination. Of the 53 cases, 29 had different types and severity with neurological findings, which could be divided into 5 groups: 1) Elevated levels of acetylcholine receptor antibody in 13 cases (24.1%); 2) Myopathy and weakness accompanied by elevated serum enzyme levels (GOT, CPK, LDH and alpha-HBDH) in 7 cases (13%); 3) Peripheral neuropathy in 6 cases (11.1%); 4) Encephalopathy in 2 cases (3.7%); and 5) The changes in sella turcica in 2 cases. Our data showed that the neuropathy was not closely correlated to the duration of chronic lymphocytic thyroiditis and seemed that it had no relation with the thyroid function and titer of antithyroid antibodies. However, neuropathy occurred more often in cases with both chronic lymphocytic thyroiditis and some other autoimmune disorders, suggesting that abnormal immune function might be the common background patients with chronic lymphocytic thyroiditis and neuropathy. The aforementioned data suggest that the hypothyroid function and high titer of antithyroid antibodies might not be a prerequisite for developing neuromyopathies.
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PMID:[Neuropathy and myopathy in patients with chronic lymphocytic thyroiditis]. 214 91

An 18-year-old male with mitochondrial myopathy, encephalopathy and lactic acidosis was studied by electromyography (EMG) along with histological and biochemical studies on his biopsied muscle. Mitochondrial cytochrome c oxidase deficiency with a decrease in the amounts of the subunits 2, 6, and 7 was discovered. Although no apparent symptoms of peripheral neuropathy were present, EMG revealed high-amplitude motor unit action potentials with a reduced interference pattern and the histochemical study revealed fiber type grouping without grouped atrophy. These findings indicated lower motor neuron damage, probably due to the mitochondrial disorder, followed by reinnervation. Coenzyme Q10 administration was effective in reducing both the lactate and pyruvate levels and for recovering the muscle atrophy.
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PMID:A case of mitochondrial myopathy, encephalopathy and lactic acidosis due to cytochrome c oxidase deficiency with neurogenic muscular changes. 215 48

We review the English-language literature on antibiotic-associated adverse reactions in patients with renal insufficiency in order to highlight this important but often overlooked clinical problem. Because many adverse reactions to antibiotics are not dependent on renal function, we have attempted to review only those reactions that are believed to be associated with renal insufficiency or that have been reported in patients with impaired renal function. Adverse effects of antibiotics in this setting can be divided into six major categories: neurologic toxicity, coagulopathy, nephrotoxicity, hypoglycemia, hematologic toxicity, and aminoglycoside inactivation by penicillins. Neurologic toxicity can be further divided into central nervous system toxicity consisting primarily of encephalopathy and seizures, ototoxicity, peripheral neuropathy, and neuromuscular blockade/respiratory depression. We explore the factors in uremia that may contribute to the susceptibility of patients with renal insufficiency to the adverse effects of antibiotics. Moreover, we make general recommendations regarding the use of the discussed antibiotics in patients with compromised renal function.
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PMID:Adverse antibiotic effects associated with renal insufficiency. 192 3

At least 60% of patients infected with the human immunodeficiency virus (HIV) develop neurologic disorders. These may be the direct result of human immunodeficiency virus (HIV) infection, opportunistic infections, neoplastic disorders, or cerebrovascular complications. Neurologic diseases associated with HIV infection include encephalopathy, aseptic meningitis, vacuolar myelopathy, peripheral neuropathy, and myopathy. The pathogenesis of these diseases is not known, but it is likely that they will differ. There is evidence that HIV is the etiologic agent of HIV-associated meningitis and subacute encephalitis, but to date there is little evidence to implicate HIV directly as the cause of vacuolar myelopathy, peripheral neuropathies, and myopathies. The results of preliminary clinical studies suggest that treatment with zidovudine (Retrovir) may cause improvement in some patients.
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PMID:Neurologic disorders associated with HIV infections. 219 51

1. The main neurological disorders associated with chronic VSA are peripheral neuropathy, cerebellar disease, chronic encephalopathy and dementia. Apart from peripheral neuropathy, the clinical features are non-specific, evidence for solvent-related toxicity is in most cases circumstantial and there is no clear dose/response relationship. 2. Peripheral neuropathy is mainly associated with n-hexane and methyl n-butyl ketone. 3. Cerebellar disease is usually associated with toluene exposure; in the more severe cases there is often radiological evidence of irreversible cerebellar atrophy. 4. Chronic encephalopathy and dementia are the most serious consequence of solvent exposure, particularly to toluene in abusers and to mixed solvents in industrial workers. Postmortem studies in some abusers have shown generalized axonal degeneration, demyelination and brain atrophy. 5. Further studies on low level solvent exposure are needed as little is known about the neurological consequences of mild VSA, especially as regards individual susceptibility and possible interactions between solvents and other toxins such as ethanol.
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PMID:Chronic neurological toxicity associated with exposure to volatile substances. 255 Mar 57

A cross sectional field study of workers exposed to styrene was performed to evaluate possible acute and chronic neurotoxic effects. A total of 36 workers of four companies handling polyester resin materials for one to 16 years (median: 7 years) and two control groups were each examined on a Monday. The control group 1 (formed to compare acute effects) consisted of 20 men from two companies with no exposure to neurotoxic chemicals. To compare chronic effects, a second control group was formed by "one to one matching" with respect to age, socioeconomic status, and pre-exposure intelligence level. Ambient air monitoring using active sampling (short time) and passive samplers (long time) showed styrene in air concentrations as follows: range 3-251 ppm (median: 18 ppm) and concentrations 140-600 ppm during lamination of the inside of boats. For biological monitoring the results were as follows (postshift samples: range/median): styrene in blood: 5-482 micrograms/dl (39 micrograms/dl), mandelic acid urine: 0.01-3.64 g/l (0.21 g/l), and phenylglyoxylic acid urine: 0.01-0.87 g/l (0.19 g/l). The clinical examination found no signs or symptoms of peripheral neuropathy or encephalopathy. The principal work related health complaints were acute, reversible irritation of the eyes that occurred after exposure to styrene concentrations of 200 ppm or more. The neurobehavioural tests showed no significant differences in acute effects (p greater than 0.05) between the two groups or between preshift and postshift testing. Nor were there any significant differences in the relevant neurobehavioural variables between the styrene workers and the controls. It is concluded that occupational exposure to styrene concentrations in air up to 100 ppm causes no adverse acute or chronic effects on the central nervous system.
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PMID:Clinical and neurobehavioural study of the acute and chronic neurotoxicity of styrene. 259 Jun 45


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