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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum levels of IgE, other immunoglobulins and C'3 were measured in 36 MS patients, and the results compared with those of 40 age- and sex-matched patients hospitalized on Neurology Service. Diagnoses among controls included cerebral infarction, cervical spondylosis, nonmigrainous headache, seizure disorders and peripheral neuropathy. Six patients in the MS group and seven in the non-MS group had a past history of allergy to food, drugs, dust or other substances. IgE levels were measured by double-antibody radioimmunoassay. Other immunoglobulins (G, M, D and A) and C'3 were quantitated by Mancini's method. Results indicate that the median IgE and C'3 levels of MS patients were slightly lower than those for non-MS subjects. Concentrations of other immunoglobulins were similar for the two groups. CSF samples from 12 MS and five non-MS patients were studied and none of these contained measureable (greater than 7.5 U/ml) IgE. In view of: 1) recent reports describing mast cells in MS plaques, 2) the suggested role of biogenic amines in the pathogenesis of demyelinating diseases, and 3) because IgE exists in free and cell bound state, it is suggested that tissue surveys of MS plaques for IgE deposits similar to those seen in glomeruli in nephrotic syndromes may provide a clue to the pathogenesis of MS.
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PMID:Circulating IgE, allergy and multiple sclerosis. Serum levels of IgE, other immunoglobulins and complement (C's) in patients with multiple sclerosis in exacerbation and other neurologic diseases. 125 79

Iloprost, a stable prostacyclin analog, was evaluated clinically for its ability to ameliorate the symptoms of peripheral neuropathy associated with diabetes. In an open, nonrandomized trial, 13 diabetic patients with neuropathy but without proliferative retinopathy received an intravenous infusion of Iloprost at a dose of 10 micrograms, at a rate of 0.1 micrograms/kg/h, twice daily for two weeks. The administration of Iloprost relieved the majority of such subjective symptoms as pain, numbness or sensation of cold and to a lesser extent, such autonomic symptoms as dizziness. In contrast, there was little evidence of objective improvement, e.g., in motor nerve conduction velocity. Iloprost treatment significantly inhibited the platelet aggregation rate stimulated by collagen in vitro. In the one patient tested, thermography revealed an increase in skin temperature by more than 2 degrees C. Side effects associated with Iloprost included headache (3 patients) or aggravation of pain in the extremities (2 patients) and could be ameliorated by slowing the infusion rate or by discontinuing the drug (one patient). Iloprost appears to be safe and effective for relieving the symptoms of diabetic neuropathy. Our results provide the rationale for a double-blind, clinical trial in larger populations of diabetics with peripheral neuropathy.
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PMID:Clinical efficacy of a stable prostacyclin analog, iloprost, in diabetic neuropathy. 170 9

Results of Yusho annual inspection were reviewed from the view point of correlation of PCBs, PCQs and PCDFs concentration in blood or subcutaneous adipose tissue and clinical findings. To make discussion quantitative, fifteen terms of clinical findings on Yusho disease were quantified on the severity by evaluating (+) as 2 points, (+-) as 1 point and (-) as 0 point. First, the temporal variations of the severity of clinical findings on 5 Yusho patients were figured. Additionally, the temporal variations of blood triglyceride and PCBs concentration, and GOT were also surveyed. The adopted terms of clinical findings were general malaise, cough, sputum, headache, abdominal pain, peripheral neuropathy, soreness of joints, deformity of nails, comedo formation, acne-like eruption, secondary infection, scar formation, disorder of Meibomian glands, edema of eye lids and increased discharge from the eyes. During the investigated period from 1972 to 1988 the total score of clinical findings clearly decreased on two patients who had high score, tended to decrease on two other patients, and was not clear on another patient. Secondly, the correlation coefficients were calculated between each of PCDFs, PCBs or PCQs concentration in subcutaneous adipose tissue or blood and the total score at the year in which the adipose tissue and blood were taken. For the female patients the correlation coefficient of PCDFs concentration in subcutaneous adipose tissue and total score of clinical findings was the highest of all (r = 0.9885). However, for the male patients it was not available because the number of the subjects was only two. Thus far it has been reported that the powers of PCBs gas chromatogram pattern and PCQs concentration as criteria for Yusho diagnosis are low as for the subjects who belonged to the border area between Yusho patients and normal persons. This survey suggests that PCDFs concentration in subcutaneous adipose tissue can be a potent criterion that has a high correlation with the clinical findings of Yusho.
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PMID:[Studies on the application of residual PCBs, PCQs and PCDFs concentrations to Yusho diagnosis]. 191 1

Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100-150 mg/day have shown minimal or no toxicity in five- to 10-year studies. Women self-medicating for PMS taking 500 to 5000 mg/day have shown peripheral neuropathy within one to three years. It would appear from this retrospective analysis that pyridoxine is safe at doses of 100 mg/day or less in adults. In children there is not enough data to make any sort of suggestion. Because the major neurologic complication is a peripheral neuropathy and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition.
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PMID:Vitamin B6 in clinical neurology. 216 44

We studied 61 patients with complications of Semple-type postexposure rabies immunization. Thirty-six had neurologic signs, and 25 had only fever, headache, or myalgia. Thirty-two patients had CNS complications, and 4 had an acute peripheral neuropathy. Disease was acute and monophasic in 33, but 3 patients had progressive disease, including 1 patient with a relapsing-remitting course. No clinical features, including CSF content of myelin basic protein, were prognostic indicators. In three of six patients with encephalomyelitis, lymphocytes showed a proliferative response to myelin.
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PMID:Neurologic complications of Semple-type rabies vaccine: clinical and immunologic studies. 243 91

Renal failure and its treatment are associated with a number of neurologic complications that must be differentiated from the nervous system complications of the disease leading to renal failure. Uremic encephalopathy is characterized by clinical signs of depressed brain function coexisting with excitation, often in the form of generalized epileptic seizures. Peripheral neuropathy, due to axonal involvement, is common and is characterized by ascending sensory and motor dysfunction. The treatment of renal failure also may lead to the development of neurologic abnormalities in the form of dialysis disequilibrium characterized by headache, nausea, irritability that may progress to seizures, coma, and death, which is caused by the entry of free water into the brain and swelling. Dialysis dementia, caused by the toxic effects of aluminum, is now rare. Renal transplant recipients may develop cerebrovascular disease, infections by opportunistic organisms, or malignant neoplasms, particularly primary lymphoma of the brain. As transplant recipients live longer and more operations are performed, additional complications may be seen in the future.
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PMID:Neurologic complications of renal disease. 254 62

The three best-described genetic polymorphisms of drug metabolism--the debrisoquin/sparteine type of oxidative polymorphism (hereafter referred to as the debrisoquin polymorphism), the polymorphism of N-acetylation, and the mephenytoin type of oxidative polymorphism--are reviewed. For all three polymorphisms, the poor-metabolizer phenotype is inherited as an autosomal recessive trait. The debrisoquin and mephenytoin oxidative polymorphisms involve defects in two separate cytochrome P450 enzymes. The prevalence of the poor-metabolizer phenotype for debrisoquin ranges between 2% and 10% for groups of various ethnic origins. The poor-metabolizer phenotype for mephenytoin comprises about 5% of the Caucasian population and about 20% of the Japanese population. N-acetyltransferase is a cytosolic enzyme whose clinical polymorphism was discovered using isoniazid as the substrate probe. The prevalence of the slow-acetylator phenotype among American and European Caucasian and American black groups is about 50%; among the Japanese it is about 10%. More than 20 agents are substrates for debrisoquin hydroxylase, about 15 for N-acetyltransferase, and 3-5 for mephenytoin. In poor metabolizers, debrisoquin can cause hypotension, and sparteine can cause blurred vision, headache, and dizziness. Clinical consequences of the slow-acetylator phenotype include increased susceptibility to systemic lupus erythematosus induced by procainamide and hydralazine, peripheral neuropathy induced by isoniazid, hydralazine, and dapsone, and sulfasalazine-induced dose-related leukopenia, nausea, vomiting, headache, and vertigo. After administration of mephenytoin, poor metabolizers have increased somnolence and intellectual impairment. Awareness of genetic polymorphisms of drug metabolism should improve understanding of interindividual variability in drug disposition and response.
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PMID:Polymorphic drug metabolism. 268 60

The neurological features of acromegaly are reviewed and two cases are reported. The most common neurological complications of active hypersomatotropism are headache, acroparesthesia and visual disturbance. Primary peripheral neuropathy, myopathy, entrapment myelopathy and/or cauda equina syndrome are uncommon, especially in young acromegalics. It is postulated that peripheral neuropathy in acromegaly is due to the entrapment of a nerve secondary to a soft tissue edematous mechanism by traumatic compression, angulation and/or stretching of the nerve in acquired extraspinal intermuscular, fibrous or osseofibrous tunnel stenosis; and/or in acquired spinal lateral recess stenosis, rather than true primary neuropathic or secondary endocrinological complications of hypersomatotropism. Proximal weakness is more likely arthropathic rather than myopathic, neuropathic or endocrinologic. Differential diagnosis of backache is briefly discussed. Further investigations of the mechanisms and the conservative treatment for neurological involvements in acromegaly are needed.
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PMID:Neurological features of acromegaly: a review and report of two cases. 284 43

Among the various reported neuropsychological effects of electroconvulsive therapy are amnesia, delirium, peripheral neuropathy, headaches, and seizures. A case history is presented that describes a previously unreported neurological sequela: the development of intractable yawning during a course of electroconvulsive therapy. Neuropathophysiological mechanisms possibly relating to this phenomenon are discussed.
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PMID:Yawning as a complication of electroconvulsive therapy and concurrent neuroleptic withdrawal. 289 29

Carbaryl, a widely used insecticide, is reputed to have a wide safety margin. It can induce acute cholinesterase poisoning, which is rapidly reversible on discontinuation of exposure. Long-term sequelae from long-term exposure have not previously been described in humans. This report describes the experience of a 75-year-old man who had long-term excessive exposure to carbaryl and in whom a debilitating syndrome, including headaches, memory loss, proximal muscle weakness, muscle fasciculation, muscle cramps, and anorexia with marked weight loss, developed. At the time of diagnosis, serum pseudocholinesterase levels were low, and his major symptoms resolved on termination of exposure. Late clinical features were sleep apnea and progressive development of a peripheral neuropathy. The difficulty in diagnosing the cause of a group of relatively nonspecific symptoms raises the question of whether chronic carbaryl neurotoxicity might be occurring more frequently than previously suspected.
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PMID:Subacute neurotoxicity following long-term exposure to carbaryl. 308 76


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